HEADACHES ORANGE COUNTY - HEADACHE TREATMENT IN ORANGE COUNTY - BEST HEADACHE TREATMENTS - HEAD ACHES ORANGE COUNTY, (949)589-9962, Orange County Headache, MIGRAINE HEADACHES- CERVICOGENIC HEADACHES - MUSCLE TENSION HEADACHES - POST-TRAUMATIC HEADACHES - CLUSTER HEADACHES, best headache treatments, rancho santa margarita headache, irvine headache, mission viejo headache, san juan capistrano headache, Laguna Beach Headaches, Leisure World Headaches, Laguna Woods headaches, Laguna Niguel Headaches, Costa Mesa Headaches, San Clemente Headaches, Aliso Viejo Headaches, Huntington Beach Headaches, anaheim headache, garden grove headache, buena park headache, fullerton headache, la palma headache, cypress headache, orange headache, Ladera Ranch headache, Coto De Caza headache, Dove Canyon headache, Tustin headache, Dana Point headache, Newport Beach headache, Balboa Island headache, Newport Coast headache, Huntington Beach headache, Brea headache, Anaheim Hills headache, Santa Ana headache, Seal Beach headache, Fountain Valley headache, El Toro headache, Villa park headache, Garden Grove headache,chronic headache, headache specialist orange county, headache help
 
UPPER CERVICAL CHIROPRACTIC
ORANGE COUNTY
"BLAIR CHIROPRACTOR"

CHIROPRACTOR RANCHO SANTA MARGARITA, MISSION VIEJO, LAKE FOREST

Back Pain, Neck Pain, Scoliosis, Headaches, Nagging Injury, Complaints of Fatigue, Reoccurring Illnesses or Disabilities, Specific Traumas, Work Related Injuries, Auto Accidents Injuries, Sports Injuries, Whiplash, Neck Pain, Low Back Pain, Arm Pain, Spasms, Leg Pain, Carpel Tunnel, Sciatica, Asthma, Disc Insury, Muscle Spasms, Foot Pain, Ankle Pain, Allergies, Numbness, Pinched Nerves
(949)589-9962
Free Estimates - Call Us Today!
HEADACHES, FATIGUE, BACK AND NECK PAIN
Email: Begin@UpperCervicalChiropracticOrangeCounty.com
NEW - TREATMENTS FOR HEADACHES - THE BRAIN TO BODY CONNECTION
MIGRAINE HEADACHES- CERVICOGENIC HEADACHES - MUSCLE TENSION HEADACHES - POST-TRAUMATIC HEADACHES - CLUSTER HEADACHES
 
CONTACT US:


UPPER CERVICAL
CHIROPRACTIC
ORANGE COUNTY
.com
Precision Chiropractic
Alfred W. Tomp, DC
30372 Esperanza
Rancho Santa Margarita, CA 92688


"Click Here for Directions"
MAP, PRINTER FRIENDLY


Telephone: (949) 589-9962

CALL US TODAY!
"Your Expert in Gentle Chriropactic"
 
 
   
 


  ARTICLES:
  GOTO HOME PAGE
ARTICLE 1:
SIGNS THAT YOU NEED A CHIROPRACTIC EXAM
ARTICLE 2:
ALL ABOUT HEADACHES

ARTICLE 3:
WHAT TO EXPECT FROM A BLAIR SPECIFIC TREATMENT

ARTICLE 4:
ABOUT THE UPPER CERVICAL SPINE
ARTICLE 5:
MOST FREQUENTLY ASKED QUESTIONS
ARTICLE 6:
FAQ'S ABOUT UPPER CERVICAL CARE
ARTICLE 7:
ABOUT THE BLAIR TECHNIQUE
ARTICLE 8:
TYPES OF HEADACHES
ARTICLE 9:
SCOLIOSIS
ARTICLE 10:
What You Can Do to Stay Well and Eliminate Pain - The Secret of Brain to Body Connection
 

Many of our patients come from
the Orange County - Southern California area which includes the following cities and zipcodes:

Anaheim 92801, 92802, 92803, 92804, 92805, 92806, 92807, 92808, 92809, 92812, 92814, 92815, 92816, 92817, 92825, 92850, 92899, Brea 92821, 92822, 92823, Buena Park 90620, 90621, 90622, 90623, 90624, Costa Mesa 92626, 92627, 92628, Cypress 90630, Fountain Valley 92708, 92728, Fullerton 92831, 92832, 92833, 92834, 92835, 92836, 92837, 92838, Garden Grove 92840, 92841, 92842, 92843, 92844, 92845, 92846, Huntington Beach 92605, 92615, 92646, 92647, 92648, 92649, La Habra 90631, 90632, 90633, La Palma 90623, Los Alamitos 90720, 90721, Orange 92856, 92857, 92859, 92861, 92862, 92863, 92864, 92865, 92866, 92867, 92868, 92869, Placentia 92870, 92871, Santa Ana 92701, 92702, 92703, 92704, 92705, 92706, 92707, 92708, 92711, 92712, 92725, 92728, 92735, 92799, Seal Beach 90740, Stanton 90680, Tusin 92780, 92781, 92782, Villa Park 92861, 92867, Westminister 92683, 92684, 92685, Yorba Linda 92885, 92886, 92887, Aliso Viejo 92653, 92656, 92698, Dana Point 92624, 92629, Irvine 92602, 92603, 92604, 92606, 92612, 92614, 92616, 92618, 92619, 92620, 92623, 92650, 92697, 92709, 92710, Laguna Beach 92607, 92637, 92651, 92652, 92653, 92654, 92656, 92677, 92698, Laguna Hills 92637, 92653, 92654, 92656, Laguna Niguel 92607, 92677, Laguna Woods 92653, 92654, Lake Forest 92609, 92630, Mission Viejo 92675, 92690, 92691, 92692, 92694, Newport Beach 92657, 92658, 92659, 92660, 92661, 92662, 92663, Rancho Santa Margarita 92688, San Clemente 92672, 92673, 92674, San Juan Capistrano 92675, 92690, 92691, 92692, 92693, 92694 Ladera Ranch 92694, Coto De Caza 92679 Anaheim Hills 92807, 92808, 92809, 92817 Dove Canyon 92679 Oceanside, CA:92049, 92051, 92052, 92054, 92055, 92056, 92057, 92058, San Diego, 92101, 92102, 92103, 92104, 92105, 92106, 92107, 92108, 92109, 92110, 92111, 92112, 92113, 92114, 92115, 92116, 92117, 92118, 92119, 92120, 92121, 92122, 92123, 92124, 92126, 92127, 92128, 92129, 92130, 92131, 92132, 92133, 92134, 92135, 92136, 92137, 92138, 92139, 92140, 92142, 92143, 92145, 92147, 92149, 92150, 92152, 92153, 92154, 92155, 92158, 92159, 92160, 92161, 92162, 92163, 92164, 92165, 92166, 92167, 92168, 92169, 92170, 92171, 92172, 92173, 92174, 92175, 92176, 92177, 92178, 92179, 92182, 92184, 92186, 92187, 92190, 92191, 92192, 92193, 92194, 92195, 92196, 92197, 92198, 92199

 

Problems in life show us who we are, How desparate our hearts can become, Shock us to see how low we can go, To get us to change for the better. EWB

 

The secret of Success is PERSISTANCE. The secret of persistance is VISION AND PURPOSE. Rick Warren

 

"A wise person will listen and continue to learn, and an understanding person will gain direction." - Proverbs 1:5 (GW)

 

"VISION is crucial to any enduring change and success. Our vision must involve the people who depend on us to make the vision come true. Who will be impacted? Why do we need to help them? How are they important to us? Imagine what will happen to them if you fail to create your vision. Step up and make your vision one of lasting greatness." - Michael P. Watson

 

"Love is patient, love is kind. It does not envy, it does not boast, it is not proud. It is not easily angered, it keeps no records of wrongs." 1 Corinthians 13: 4,5

.......
  ..

ALL ABOUT HEADACHES

 

Headache

A headache (cephalalgia in medical terminology) is a condition of pain in the head; sometimes neck or upper back pain may also be interpreted as a headache. It ranks amongst the most common local pain complaints and may be frequent for many people.

The vast majority of headaches are benign and self-limiting. Common causes are tension, migraine, eye strain, dehydration, low blood sugar, hypermastication and sinusitis. Much rarer are headaches due to life-threatening conditions such as meningitis, encephalitis, cerebral aneurysms, extremely high blood pressure, and brain tumors. When the headache occurs in conjunction with a head injury the cause is usually quite evident. A large percentage of headaches among women are caused by ever-fluctuating estrogen during menstrual years. This can occur prior to, or even during midcycle menstruation.

Treatment of an uncomplicated headache is usually symptomatic with over-the-counter painkillers such as aspirin, paracetamol (acetaminophen), or ibuprofen, although some specific forms of headaches (e.g., migraines) may demand other, more suitable treatment. It may be possible to relate the occurrence of a headache to other particular triggers (such as stress or particular foods), which can then be avoided.

Pathophysiology

The brain in itself is not sensitive to pain, because it lacks nociceptors. Several areas of the head can hurt, including a network of nerves which extend over the scalp and certain nerves in the face, mouth, and throat. The meninges and the blood vessels do have pain perception. Headaches often result from traction to or irritation of the meninges and blood vessels. The membrane surrounding the brain and spinal cord, called the dura mater, is innervated with nociceptors. Stimulation of these dural nociceptors is thought to be involved in producing headaches. Similarly the muscles of the head may be sensitive to pain.

Types


There are five types of headache: vascular, myogenic (muscle tension), cervicogenic, traction, and inflammatory.

Vascular

The most common type of vascular headache is migraine. Migraine headaches are usually characterized by severe pain on one or both sides of the head, an upset stomach, and, for some people, disturbed vision. It is more common in women. While vascular changes are evident during a migraine, the cause of the headache is neurologic, not vascular. After migraine, the most common type of vascular headache is the "toxic" headache produced by fever.

Other kinds of vascular headaches include cluster headaches, which are very severe recurrent short lasting headaches, often located through or around either eye and often wake the sufferers up at the same time every night. Unlike migraines, these headaches are more common in men than in women.

Muscular/myogenic

Muscular (or myogenic) headaches appear to involve the tightening or tensing of facial and neck muscles; they may radiate to the forehead. Tension headache is the most common form of myogenic headache.

Cervicogenic

ervicogenic headaches originate from disorders of the neck, including the anatomical structures innervated by the cervical roots C1–C3. Cervical headache is often precipitated by neck movement and/or sustained awkward head positioning. It is often accompanied by restricted cervical range of motion, ipsilateral neck, shoulder, or arm pain of a rather vague non-radicular nature or, occasionally, arm pain of a radicular nature.

Traction/inflammatory

Traction and inflammatory headaches are symptoms of other disorders, ranging from stroke to sinus infection. Specific types of headaches include:

  • Tension headache
  • Migraine
  • Idiopathic intracranial hypertension (headache with visual symptoms due to raised intracranial pressure)
  • Ictal headache
  • Cluster headache
  • "Brain freeze" (also known as: ice cream headache)
  • Thunderclap headache
  • Vascular headache
  • Toxic headache
  • Coital cephalalgia (also known as: sex headache)
  • Hemicrania continua
  • Rebound headache (also called medication overuse headache, abbreviated MOH)
  • Red wine headache
  • "Spinal headache" (or: post-dural puncture headaches) after lumbar puncture or related procedure that will lower the intracranial pressure
  • Hangover (caused by heavy alcohol consumption)

A headache may also be a symptom of sinusitis.

Like other types of pain, headaches can serve as warning signals of more serious disorders. This is particularly true for headaches caused by inflammation, including those related to meningitis as well as those resulting from diseases of the sinuses, spine, neck, ears, and teeth.

Diagnosis

While, statistically, headaches are most likely to be harmless and self-limiting, some specific headache syndromes may demand specific treatment or may be warning signals of more serious disorders. Some headache subtypes are characterized by a specific pattern of symptoms, and no further testing may be necessary, while others may prompt further diagnostic tests.

Headache associated with specific symptoms may warrant urgent medical attention, particularly sudden, severe headache or sudden headache associated with a stiff neck; headaches associated with fever, convulsions or accompanied by confusion or loss of consciousness; headaches following a blow to the head, or associated with pain in the eye or ear; persistent headache in a person with no previous history of headaches; and recurring headache in children.

The most important step in diagnosing a headache is for the physician to take a careful history and to examine the patient. In the majority of cases the diagnosis will be a "primary headache" which means that the headache, whilst unpleasant is not an occurring as a manifestation of a more serious condition. The main types of primary headache are tension headache, migraine and the trigeminal autonomic cephalalgias of which cluster headache is an example. As it is often difficult for patients to recall the precise details regarding each headache, it is often useful for the sufferer to fill-out a "headache diary" detailing the characteristics of the headache. When the headache does not clearly fit into one of the recognized primary headache syndromes or when atypical symptoms or signs are present then further investigations are justified.[1] Computed tomography (CT/CAT) scans of the brain or sinuses are commonly performed, or magnetic resonance imaging (MRI) in specific settings. Blood tests may help narrow down the differential diagnosis, but are rarely confirmatory of specific headache forms.

Treatment

TreatmentNot all headaches require medical attention, and many respond with simple analgesia (painkillers) such as paracetamol/acetaminophen or members of the NSAID class (such as aspirin/acetylsalicylic acid or ibuprofen).

In recurrent unexplained headaches, healthcare professionals may recommend keeping a "headache diary" with entries on type of headache, associated symptoms, precipitating and aggravating factors. This may reveal specific patterns, such as an association with medication, menstruation or absenteeism or with certain foods. It was reported in March 2007 by two separate teams of researchers that stimulating the brain with implanted electrodes appears to help ease the pain of cluster headaches.

Prevention

Some forms of headache, such as migraine, may be amenable to preventative treatment. On the whole, long-term use of painkillers is discouraged as this may lead to drug induced headaches and "rebound headaches" on withdrawal.[3] Caffeine, a vasoconstrictor, is sometimes prescribed or recommended as a remedy or supplement to pain killers in the case of extreme migraine. This has led to the development of paracetamol/caffeine analgesic.

Petasites, magnesium, feverfew. riboflavin, CoQ10, and melatonin are "natural" supplements that have shown some efficacy for migraine prevention; a 2006 review tentatively ranked petasites and magnesium with the best evidence, and melatonin with by far the least. Adverse events included sore mouth and tongue (including ulcers) and abdominal pain for feverfew.

Manual therapy

Headache sufferers often use manual therapy, such as spinal manipulation, soft tissue therapy, and myofascial trigger point treatment. A 2006 systematic review found no rigorous evidence supporting manual therapies for tension headache.[5] A 2005 structured review found that the evidence was weak for effectiveness of chiropractic manipulation for tension headache, and that it was probably more effective for tension headache than for migraine.[6] A 2004 Cochrane review found that spinal manipulation may be effective for migraine and tension headache, and that spinal manipulation and neck exercises may be effective for cervicogenic headache.[7] Two other systematic reviews published between 2000 and May 2005 did not find conclusive evidence in favor of spinal manipulation.[8]

Spinal manipulation is associated with frequent, mild and temporary adverse effects,[9] including new or worsening pain or stiffness in the affected region.[10] They have been estimated to occur in 34% to 55% of patients, with 80% of them disappearing within 24 hours.[11] Spinal manipulation, particularly on the upper spine, can also result in complications that can lead to permanent disability or death.[9] The incidence of these complications is unknown, due to high levels of underreporting and to the difficulty of linking manipulation to adverse effects such as stroke, a particular concern.[9] Weak to moderately strong evidence supports causation (as opposed to statistical association) between cervical manipulative therapy (whether chiropractic or not) and vertebrobasilar artery stroke.

Tension headache

Tension headaches, which were renamed tension-type headaches by the International Headache Society in 1988, are the most common type of primary headaches. The pain can radiate from the neck, back, eyes, or other muscle groups in the body. Tension-type headaches account for nearly 90% of all headaches. Approximately 3% of the population suffers from chronic-tension type headache.

Frequency and duration

Tension-type headaches can be episodic or chronic. Episodic tension-type headaches are defined as tension-type headaches occurring fewer than 15 days a month, whereas chronic tension headaches occur 15 days or more a month for at least 6 months. Tension-type headaches can last from minutes to days, months or even years, though a typical tension headache lasts 4-6 hours.

Pain and possible symptoms

Tension-type headache pain is often described as a constant pressure, as if the head were being squeezed in a vise. The pain is frequently bilateral which means it is present on both sides of the head at once. Tension-type headache pain is typically mild to moderate, but may be severe.

Cause and pathophysiology

Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor .

* Stress - Usually occurs in the afternoon after long stressful work hours
* Sleep deprivation
* Uncomfortable stressful position and/or bad posture
* Irregular meal time (hunger)
* Eyestrain
* Caffeine withdrawal

The exact cause of tension-type headaches is still unknown. It is suggested that abnormalities in the peripheral and central nervous systems may be involved in the pathophysiology of TTH. It has long been believed that they are caused by muscle tension around the head and neck. One of the theories says that the main cause for tension type headaches and migraine is teeth clenching which causes a chronic contraction of the temporalis muscle. Although muscle tension may be involved, scientists now believe there is not one single cause for this type of headache. Another theory is that the pain may be caused by a malfunctioning pain filter which is located in the brain stem. The view is that the brain misinterprets information, for example from the temporal muscle or other muscles, and interprets this signal as pain. One of the main molecules which is probably involved is serotonin. Evidence for this theory comes from the fact that chronic tension-type headaches may be successfully treated with certain antidepressants such as amitriptyline. However, the analgesic effect of amitriptyline in chronic tension-type headache is not solely due to serotonin reuptake inhibition, and likely other mechanisms are involved. Recent studies of nitric oxide (NO) mechanisms suggest that NO may play a key role in the pathophysiology of CTTH.. The sensitization of pain pathways may be caused by or associated with activation of nitric oxide synthase (NOS) and the generation of NO. Patients with chronic tension-type headache have increased muscle and skin pain sensitivity, demonstrated by low mechanical, thermal and electrical pain thresholds. Hyperexcitability of central nociceptive neurons (in trigeminal spinal nucleus, thalamus, and cerebral cortex) is believed to be involved in the pathophysiology of chronic tension-type headache. Recent evidence for generalized increased pain sensitivity or hyperalgesia in CTTH strongly suggests that pain processing in the central nervous system is abnormal in this primary headache disorder. Moreover, a dysfunction in pain inhibitory systems may also play a role in the pathophysiology of chronic tension-type headache.

Treatment

Episodic tension-type headaches generally respond well to over-the-counter analgesics, ibuprofen having been found more effective in providing relief than paracetamol/acetaminophen in controled studies. Other medications for chronic tension-type headaches include amitriptyline[6] mirtazapine, biofeedback, and sodium valproate (as prophylaxis).

Botulinum toxin is a treatment trialled by some tension-type headache sufferers, though results are varied. There are some reports of Botulinum toxin having the opposite effect, increasing tension.

Acupuncture has not been demonstrated as an effective treatment for tension headaches.

Prognosis

Tension headaches that do not occur as a symptom of another condition may be painful, but are not harmful. It is usually possible to receive relief through treatment. Tension headaches that occur as a symptom of another condition are usually relieved when the underlying condition is treated. Frequent use of pain medications in patients with tension-type headache may lead to the development of medication overuse headache or rebound headache.

Migraine

Migraine is a neurological syndrome characterized by altered bodily experiences, painful headaches, and nausea. It is a common condition which affects women more frequently than men.

The typical migraine headache is one-sided and pulsating, lasting 4 to 72 hours. Accompanying complaints are nausea and vomiting, and a heightened sensitivity to bright lights (photophobia) and noise (hyperacusis). Approximately one third of people who experience migraines get a preceding aura, in which a patient may sense a strange light or unpleasant smell.

Although the exact cause of migraine remains unknown, the most widespread theory is that it is a disorder of the serotonergic control system. Recently, PET scans have demonstrated the aura to coincide with spreading cortical depression after an episode of greatly increased blood flow (up to 300% higher than baseline). There also appear to be migraine variants that originate in the brainstem and involve dysfunction in calcium and potassium ion transport between cell membranes. Genetic factors may also contribute. Studies on twins show that genes have a 60 to 65% influence on the development of migraine. Fluctuating hormone levels show a relation to migraine in several ways: three quarters of adult migraine patients are female while migraine affects approximately equal numbers of boys and girls before puberty,[citation needed] and migraine is known to disappear during pregnancy in a substantial number of sufferers.

The treatment of migraine begins with simple painkillers for headache and anti-emetics for nausea, and avoidance of triggers if present. Specific anti-migraine drugs can be used to treat migraine. If the condition is severe and frequent enough, preventative drugs might be considered.

Classification

Migraines have been classified by the International Headache Society which periodically revises their classification.

Defining severity of pain

In addition to classifying the type of headache, the International Headache Society defines intensity of pain on a verbal 4-point scale:

Number Name Annotations
0 no pain
1 mild pain does not interfere with usual activities
2 moderate pain inhibits, but does not wholly prevent usual activities
3 severe pain prevents all activities

Migraine without aura

This is the most commonly seen form of migraine; patients who primarily suffer from migraine without aura may also have attacks of migraine with aura. The International Classification of Headache Disorders defines this condition as follows:

Description: Recurrent headache disorder manifesting in attacks lasting 4–72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia.

Diagnostic criteria:
A. At least five attacks fulfilling criteria B-D
B. Headache attacks lasting 4-72 hours [when untreated]
C. Headache has at least two of the following characteristics:

1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity...
D. During the headache at least one of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia
E. Not attributed to another disorder

When these criteria are only partially met, the document specifies possible alternative diagnoses, including "probable migraine without aura" or "episodic tension-type headache".

Migraine with aura

This is the second most commonly seen form of migraine: patients who primarily suffer from migraine with aura may also have attacks of migraine without aura. According to the International Classification of Headache Disorders it is a recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5–20 minutes and last for less than 60 minutes. Headache with the features of "migraine without aura" usually follows the aura symptoms. Less commonly, the aura may occur without a subsequent headache or the headache may be non-migrainous in type.

In order to diagnose migraine with aura, there must have been at least two attacks not attributable to another cause that fulfill the following criteria:

  1. Aura consisting of at least one of the following, but no muscle weakness or paralysis:
    • Fully reversible visual symptoms (e.g. flickering lights, spots, lines, loss of vision)
    • Fully reversible sensory symptoms (e.g. pins and needles, numbness)
    • Fully reversible dysphasia (speech disturbance)
  2. Aura has at least two of the following characteristics:
    • Visual symptoms affecting just one side of the field of vision and/or sensory symptoms affecting just one side of the body
    • At least one aura symptom develops gradually over more than 5 minutes and/or different aura symptoms occur one after the other over more than 5 minutes
    • Each symptom lasts from 5 to 60 minutes

Where these criteria are not fully met, a diagnosis of "probable migraine with aura" may be considered, although other neurological causes must also be considered. If the picture complies with the criteria but includes one-sided muscular weakness or paralysis, a diagnosis of "sporadic hemiplegic migraine" or "familial hemiplegic migraine" should be considered.

Basilar type migraine

Basilar type migraine (BTM), formerly known as basilar artery migraine (BAM) or basilar migraine (BM), is an uncommon type of complicated migraine with symptoms that result from brainstem dysfunction. Serious episodes of BTM can lead to stroke, coma, or even death. The use of triptans and other vasoconstrictors as abortive treatments in BTM is contraindicated. Abortive treatments for BTM often focus on vasodilation and restoration of normal blood flow to the vertebrobasilar territory and subsequent return of normal brainstem function.

Familial hemiplegic migraine

Familial hemiplegic migraine 'FHM' is a type of migraine with a possible polygenetic component. These migraine attacks may last 4–72 hours and are apparently caused by ion channel mutations, three types of which have been identified to date. Patients who experience this syndrome have relatively typical migraine headaches preceded and/or accompanied by reversible limb weakness on one side as well as visual, sensory or speech difficulties. A non-familial form exists as well, "sporadic hemiplegic migraine" (SHM). It is often difficult to make the diagnosis between basilar-type migraine and hemiplegic migraine. When making the differential diagnosis is difficult, the deciding symptom is often the motor weakness or unilateral paralysis which can occur in FHM or SHM. While basilar-type migraine can present with tingling or numbness, true motor weakness and/or paralysis occur only in hemiplegic migraine.

Abdominal migraine

According to the International Classification of Headache Disorders, abdominal migraine is a recurrent disorder of unknown origin which occurs mainly in children. It is characterised by episodes of moderate to severe central abdominal pain lasting 1–72 hours. There is usually associated nausea and vomiting but the child is entirely well between attacks.

In order to diagnose abdominal migraine, there must be at least five attacks, not attributable to another cause, fulfilling the following criteria:

  1. Attacks lasting 1–72 hours when untreated
  2. Pain must have ALL of the following characteristics:
    • Location in the midline, around the umbilicus or poorly localised
    • Dull or 'just sore' quality
    • Moderate or severe intensity
  3. During an attack there must be at least two of the following:
    • Loss of appetite
    • Nausea
    • Vomiting
    • Pallor

Most children with abdominal migraine will develop migraine headache later in life and the two may co-exist during adolescence.

Acephalgic migraine

Acephalgic migraine is a neurological syndrome. It is a variant of migraine in which the patient may experience aura symptoms such as scintillating scotoma, nausea, photophobia, hemiparesis and other migraine symptoms but does not experience headache. Acephalgic migraine is also referred to as amigrainous migraine, ocular migraine, or optical migraine.

Sufferers of acephalgic migraine are more likely than the general population to develop classical migraine with headache.

The prevention and treatment of acephalgic migraine is broadly the same as for classical migraine. However, because of the absence of "headache", diagnosis of acephalgic migraine is apt to be significantly delayed and the risk of misdiagnosis significantly increased.

Visual snow might be a form of acephalgic migraine.

If symptoms are primarily visual, it may be necessary to consult an ophthalmologist to rule out potential eye disease before considering this diagnosis.

Menstrual migraine

Menstrual migraine is distinct from other migraines. Approximately 21 million women in the US suffer from migraines, and about 60% of them suffer from menstrual migraines.

  • There are two types of menstrual migraine – Menstrually Related Migraine (MRM) and Pure Menstrual Migraine (PMM)
  • MRM is a headache of moderate-to-severe pain intensity that happens around the time of a woman’s period and at other times of the month as well.
  • PMM is similar in every respect but only occurs around the time of a woman’s period.
  • The exact causes of menstrual migraine are uncertain but evidence suggest there may be a link between menstruation and migraine due to the drop in estrogen levels that normally occurs right before the period starts.
  • Menstrual migraine has been reported to be more likely to occur during a five-day window, from two days before to two days after menstruation.

When compared with migraines that occur at other times of the month, menstrual migraines have been reported to

  • Last longer—up to 72 hours
  • Be more severe
  • Occur more often with nausea and vomiting
  • Be more difficult to treat—occur more frequently

Signs and symptoms

The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same migraineur:

  1. The prodrome, which occurs hours or days before the headache.
  2. The aura, which immediately precedes the headache.
  3. The pain phase, also known as headache phase.
  4. The postdrome.

Prodrome phase

Prodromal symptoms occur in 40–60% of migraineurs (migraine sufferers). This phase may consist of altered mood, irritability, depression or euphoria, fatigue, yawning, excessive sleepiness, craving for certain food (e.g. chocolate), stiff muscles (especially in the neck), constipation or diarrhea, increased urination, and other visceral symptoms. These symptoms usually precede the headache phase of the migraine attack by several hours or days, and experience teaches the patient or observant family how to detect that a migraine attack is near.

Aura phase

For the 20–30% of individuals who suffer migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes. The headache phase of the migraine attack usually begins within 60 minutes of the end of the aura phase, but it is sometimes delayed up to several hours, and it can be missing entirely. Symptoms of migraine aura can be visual, sensory, or motor in nature.

Visual aura is the most common of the neurological events. There is a disturbance of vision consisting usually of unformed flashes of white and/or black or rarely of multicolored lights (photopsia) or forma­tions of dazzling zigzag lines (scintillating scotoma; often arranged like the battlements of a castle, hence the alternative terms "fortification spectra" or "teichopsia"). Some patients complain of blurred or shimmering or cloudy vision, as though they were look­ing through thick or smoked glass, or, in some cases, tunnel vision and hemianopsia. The somatosensory aura of migraine consists of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the nose-mouth area on the same side. Paresthesia migrate up the arm and then extend to involve the face, lips and tongue.

Other symptoms of the aura phase can include auditory or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch.

Pain phase

The typical migraine headache is unilateral, throbbing, moderate to severe and can be aggravated by physical activity. Not all of these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and usually alternates sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides, and usually lasts between 4 and 72 hours in adults and 1 and 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several times a week, and the average migraineur experiences from one to three headaches a month. The head pain varies greatly in intensity.

The pain of migraine is invariably accompanied by other features. Nausea occurs in almost 90 percent of patients, while vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, osmophobia and seek a dark and quiet room. Blurred vision, nasal stuffiness, diarrhea, polyuria, pallor or sweating may be noted during the headache phase. There may be localized edema of the scalp or face, scalp tenderness, prominence of a vein or artery in the temple, or stiffness and tenderness of the neck. Impairment of concentration and mood are common. Lightheadedness, rather than true vertigo and a feeling of faintness may occur. The extremities tend to be cold and moist.

Postdrome phase

The patient may feel tired, have head pain, cognitive difficulties, "hungover", gastrointestinal symptoms, mood changes and weakness. Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise. Often, some of the minor headache phase symptoms may continue, such as loss of appetite, photophobia, and lightheadedness. For some patients, a 5 to 6 hour nap may reduce the pain, but slight headaches may still occur when standing or sitting quickly. Normally these symptoms go away after a good night's rest.

Diagnosis

Migraines are underdiagnosed and misdiagnosed. The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":

  • 5 or more attacks
  • 4 hours to 3 days in duration
  • 2 or more of - unilateral location, pulsating quality, moderate to severe pain, aggravation by or avoidance of routine physical activity
  • 1 or more accompanying symptoms - nausea and/or vomiting, photophobia, phonophobia

For migraine with aura, only two attacks are required to justify the diagnosis.

The mnemonic POUNDing (Pulsating, duration of 4–72 hOurs, Unilateral, Nausea, Disabling) can help diagnose migraine. If 4 of the 5 criteria are met, then the positive likelihood ratio for diagnosing migraine is 24.

The presence of either disability, nausea or sensitivity, can diagnose migraine with:

Migraine should be differentiated from other causes of headaches such as cluster headaches. These are extremely painful, unilateral headaches of a piercing quality. The duration of the common attack is 15 minutes to three hours. Onset of an attack is rapid, and most often without the preliminary signs that are characteristic of a migraine.

Pathophysiology

Migraines were once thought to be initiated exclusively by problems with blood vessels. The vascular theory of migraines is now considered secondary to brain dysfunction and claimed to have been discredited by others.

The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed.

Migraine headaches can be a symptom of hypothyroidism.

Depolarization theory

A phenomenon known as cortical spreading depression can cause migraines. In cortical spreading depression, neurological activity is depressed over an area of the cortex of the brain. This situation results in the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head.

This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. A French study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early stages.

Vascular theory

Migraines can begin when blood vessels in the brain contract and expand inappropriately. This may start in the occipital lobe, in the back of the brain, as arteries spasm. The reduced flow of blood from the occipital lobe triggers the aura that some individuals who have migraines experience because the visual cortex is in the occipital area.

When the constriction stops and the blood vessels dilate, they become too wide. The once solid walls of the blood vessels become permeable and some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation. With each heart beat, blood passes through this sensitive area causing a throb of pain.

The vascular theory of migraines is now seen as secondary to brain dysfunction.

Serotonin theory

Serotonin is a type of neurotransmitter, or "communication chemical" which passes messages between nerve cells. It helps to control mood, pain sensation, sexual behaviour, sleep, as well as dilation and constriction of the blood vessels among other things. Serotonin levels in the brain may lead to a process of constriction and dilation of the blood vessels which trigger a migraine. Triptans activate serotonin receptors to stop a migraine attack.

Neural theory

When certain nerves or an area in the brain stem become irritated, a migraine begins. In response to the irritation, the body releases chemicals which cause inflammation of the blood vessels. These chemicals cause further irritation of the nerves and blood vessels and results in pain. Substance P is one of the substances released with first irritation. Pain then increases because substance P aids in sending pain signals to the brain.

Unifying theory

Both vascular and neural influences cause migraines.

  1. stress triggers changes in the brain
  2. these changes cause serotonin to be released
  3. blood vessels constrict
  4. chemicals including substance P irritate nerves and blood vessels causing pain

Epidemiology

Migraine is an extremely common condition which will affect 12–28% of people at some point in their lives. However this figure — the lifetime prevalence — does not provide a very clear picture of how many patients there are with active migraine at any one time. Typically, therefore, the burden of migraine in a population is assessed by looking at the one-year prevalence — a figure that defines the number of patients who have had one or more attacks in the previous year. The third figure, which helps to clarify the picture, is the incidence — this relates to the number of first attacks occurring at any given age and helps understanding of how the disease grows and shrinks over time.

Based on the results of a number of studies, one year prevalence of migraine ranges from 6–15% in adult men and from 14–35% in adult women. These figures vary substantially with age: approximately 4–5% of children aged under 12 suffer from migraine, with little apparent difference between boys and girls. There is then a rapid growth in incidence amongst girls occurring after puberty, which continues throughout early adult life. By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men. After menopause, attacks in women tend to decline dramatically, so that in the over 70s there are approximately equal numbers of male and female sufferers, with prevalence returning to around 5%.

At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5:1 and 2:1Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without auraThus in pre-pubertal and post-menopausal populations, migraine with aura is somewhat more common than amongst 15–50 year olds.

There is a strong relationship between age, gender and type of migraine.

Geographical differences in migraine prevalence are not marked. Studies in Asia and South America suggest that the rates there are relatively low, but they do not fall outside the range of values seen in European and North American studies.

The incidence of migraine is related to the incidence of epilepsy in families, with migraine twice as prevalent in family members of epilepsy sufferers, and more common in epilepsy sufferers themselves.

Triggers

A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal. In the medical literature, these factors are known as 'precipitants.'

The MedlinePlus Medical Encyclopedia, for example, offers the following list of migraine triggers:

Migraine attacks may be triggered by:

* Allergic reactions
* Bright lights, loud noises, and certain odors or perfumes
* Physical or emotional stress
* Changes in sleep patterns
* Smoking or exposure to smoke
* Skipping meals
* Alcohol
* Menstrual cycle fluctuations, birth control pills, hormone fluctuations during the menopause transition
* Tension headaches
* Foods containing tyramine (red wine, aged cheese, smoked fish, chicken livers, figs, and some beans), monosodium glutamate (MSG) or nitrates (like bacon, hot dogs, and salami)
* Other foods such as chocolate, nuts, peanut butter, avocado, banana, citrus, onions, dairy products, and fermented or pickled foods.

Sometimes the migraine occurs with no apparent "cause". The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors and keeping a "headache diary" recording migraine incidents and diet to look for correlations in order to avoid trigger foods. It must be mentioned, that some trigger factors are quantitative in nature, i.e., a small block of dark chocolate may not cause a migraine, but half a slab of dark chocolate almost definitely will, in a susceptible person. In addition, being exposed to more than one trigger factor simultaneously will more likely cause a migraine, than a single trigger factor in isolation, e.g., drinking and eating various known dietary trigger factors on a hot, humid day, when feeling stressed and having had little sleep will probably result in a migraine in a susceptible person, but consuming a single trigger factor on a cool day, after a good night's rest with minimal environmental stress may mean that the sufferer will not develop a migraine after all. Migraines can be complex to avoid, but keeping an accurate migraine diary and making suitable lifestyle changes can have a very positive effect on the sufferer's quality of life. Some trigger factors are virtually impossible to avoid, e.g. the weather or emotions, but by limiting the avoidable trigger factors, the unavoidable ones may have less of an impact on the sufferer.

Food

A 2005 literature review found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients. Some suspected dietary trigger factors appear to genuinely promote or precipitate migraine episodes, but many other suspected dietary triggers have never been demonstrated to trigger migraines. The review authors found that alcohol, caffeine withdrawal, and missing meals are the most important dietary migraine precipitants, that dehydration deserved more attention, and that some patients report sensitivity to red wine. Little or no evidence associated notorious suspected triggers like chocolate, cheese, histamine, tyramine, nitrates, or nitrites with migraines. Some people may develop migraines from consuming aspartame. In a University of Parkinson's-Florida study, the incidence of migraine doubled for the majority of participants when they took aspartame, and their headaches lasted longer and were marked by increased signs of shakiness and diminished vision. Headaches are the most common side effect cited by those who consume aspartame-containing products. In a large and definitive study monosodium glutamate (MSG) in large doses (2.5 grams) was associated with adverse symptoms including headache more often than was placebo. The review authors also note that while general dietary restriction has not been demonstrated to be an effective migraine therapy, it is beneficial for the individual to avoid what has been a definite cause of the migraine.

The National Headache Foundation has a specific list of triggers based on the tyramine theory, detailing allowed, with caution and avoid triggers.

Weather

Several studies have found some migraines are triggered by changes in weather. One study noted 62% of the subjects thought weather was a factor but only 51% were sensitive to weather changes. Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:

  1. Temperature mixed with humidity. High humidity plus high or low temperature was the biggest cause.
  2. Significant changes in weather
  3. Changes in barometric pressure

Another study examined the effects of warm chinook winds on migraines, with many patients reporting increased incidence of migraines immediately before and/or during the chinook winds. The number of people reporting migrainous episodes during the chinook winds was higher on high-wind chinook days. The probable cause was thought to be an increase in positive ions in the air.

Other

One study found that for some migraineurs in India, washing hair in a bath was a migraine trigger. The triggering effect also had to do with how the hair was later dried.

Treatment

Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and preventive drugs. Patients who experience migraines often find that the recommended migraine treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all.

Children and adolescents, are often first given drug treatment, but the value of diet modification should not be overlooked. The simple task of starting a diet journal to help modify the intake of trigger foods like hot dogs, chocolate, cheese and ice cream could help alleviate symptoms

Abortive treatment

Migraine sufferers usually develop their own coping mechanisms for the pain of a migraine attack. Hot or cold water applied to the head, or resting in a dark and silent room may be helpful for some patients. Caffeine can be helpful during an attack, despite the fact that in general migraine-sufferers are advised to limit their caffeine intake.

For patients who have been diagnosed with recurring migraines, migraine abortive medications can be used to treat the attack, and may be more effective if taken early, losing effectiveness once the attack has begun. Treating the attack at the onset can often abort it before it becomes serious, and can reduce the near-term frequency of subsequent attacks.

Paracetamol or non-steroidal anti-inflammatory drug (NSAIDs)

The first line of treatment is over-the-counter abortive medication.

  • Regarding non-steroidal anti-inflammatory drugs, a randomized controlled trial found that naproxen can abort about one third of migraine attacks, which was 5% less than the benefit of sumatriptan.
  • Paracetamol, at a dose of 1000 mg, benefited over half of patients with mild or moderate migraines in a randomized controlled trial.
  • Simple analgesics combined with caffeine may help. During a migraine attack, emptying of the stomach is slowed, resulting in nausea and a delay in absorbing medication. Caffeine has been shown to partially reverse this effect, and probably accounts for its benefit.[citation needed] Excedrin is an example of an aspirin with caffeine product. Caffeine is recognized by the U.S. Food and Drug Administration as an Over The Counter Drug (OTC) treatment for migraine when compounded with aspirin and paracetamol.

Patients themselves often start off with paracetamol (known as acetaminophen in the USA), aspirin, ibuprofen, or other simple analgesics that are useful for tension headaches. OTC drugs may provide some relief, although they are typically not effective for most sufferers. It is one of doctors' practical diagnoses of migraine head pain when patients say typical OTC drugs "won't touch it".

Analgesics combined with antiemetics

Anti-emetics by mouth may help relieve symtoms of nausea and help prevent vomiting, which can diminish the effectiveness of orally taken analgesia. In addition some antiemetics such as metoclopramide are prokinetics and help gastric emptying which is often impaired during episodes of migraine. In the UK there are three combination antiemetic and analgesic preparations available: MigraMax (aspirin with metoclopramide), Migraleve (paracetamol/codeine for analgesia, with buclizine as the antiemetic) and paracetamol/metoclopramide (Paramax in UK). The earlier these drugs are taken in the attack, the better their effect.

Some patients find relief from taking other sedative antihistamines which have anti-nausea properties, such as Benadryl which in the US contains diphenhydramine (but a different non-sedative product in the UK).

Serotonin agonists

Sumatriptan and related selective serotonin receptor agonists are excellent for severe migraines or those that do not respond to NSAIDs[56] or other over-the-counter drugs.[57] Triptans are a mid-line treatment suitable for many migraineurs with typical migraines. They may not work for atypical or unusually severe migraines, transformed migraines, or status (continuous) migraines.

Ergot alkaloids

Until the introduction of sumatriptan in 1991, ergot derivatives (see ergoline) were the primary oral drugs available to abort a migraine once it is established.

Ergot drugs can be used either as a preventive or abortive therapy, though their relative expense and cumulative side effects suggest reserving them as an abortive rescue medicine. However, ergotamine tartrate tablets (usually with caffeine), though highly effective, and long lasting (unlike triptans), have fallen out of favour due to the problem of ergotism. Oral ergotamine tablet absorption is reliable unless the patient is nauseated. Anti-nausea administration is available by ergotamine suppository (or Ergostat sublingual tablets made until circa 1992). Ergot drugs themselves can be so nauseating it is advisable for the sufferer to have something at hand to counteract this effect when first using this drug. Ergotamine-caffeine 1/100 mg fixed ratio tablets (like Cafergot, Ercaf, etc.) are much less expensive per headache than triptans, and are commonly available in Asia. They are difficult to obtain in the USA. Ergotamine-caffeine can't be regularly used to abort evening or night onset migraines due to debilitating caffeine interference with sleep. Pure ergotamine tartrate is highly effective for evening-night migraines, but is rarely or never available in the USA. Dihydroergotamine (DHE), which must be injected or inhaled, can be as effective as ergotamine tartrate, but is much more expensive than $2 USD Cafergot tablets.

Steroids

Based on a recent meta analysis a single dose of iv dexamethasone, when added to standard treatment, is associated with a 26% decrease in headache recurrence.

Other agents

If over-the-counter medications do not work, or if triptans are unaffordable, the next step for many doctors is to prescribe Fioricet or Fiorinal, which is a combination of butalbital (a barbiturate), Paracetamol (in Fioricet) or acetylsalicylic acid (more commonly known as aspirin and present in Fiorinal), and caffeine. While the risk of addiction is low, butalbital can be habit-forming if used daily, and it can also lead to rebound headaches. Barbiturate-containing medications are not available in many European countries.

Amidrine (a cocktail of a pain reliever, a sedative, and a vasoconstrictor) is sometimes prescribed for migraine headaches.

Anti-emetics may need to be given by suppository or injection where vomiting dominates the symptoms.

Status migrainosus

Status migrainosus is characterized by migraine lasting more than 72 hours, with not more than four hours of relief during that period. It is generally understood that status migrainosus has been refractory to usual outpatient management upon presentation.

Treatment of status migrainosus consists of managing comorbidities (i. e. correcting fluid and electrolyte abnormalities resulting from anorexia and nausea/vomiting often accompanying status migr.), and usually administering parenteral medication to "break" (abort) the headache.

Although the literature is full of many case reports concerning treatment of status migrainosus, first line therapy consists of intravenous fluids, metoclopramide, and triptans or DHE.

Herbal treatment

The herbal supplement feverfew (more commonly used for migraine prevention, see below) is marketed by the GelStat Corporation as an OTC migraine abortive, administered sublingually (under the tongue) in a mixture with ginger. An open-label study (funded by GelStat) found some tentative evidence of the treatment's effectiveness, but no scientifically sound study has been done. Cannabis in addition to prevention, is also known to relieve pain during the onset of a migraine.

Comparative studies

Regarding comparative effectiveness of these drugs used to abort migraine attacks, a 2004 placebo-controlled trial reveals that high dose acetylsalicylic acid (1000 mg), sumatriptan 50 mg and ibuprofen 400 mg are equally effective at providing relief from pain, although sumatriptan was superior in terms of the more demanding outcome of rendering patients entirely free of pain and all other migraine-related symptoms.

Another randomized controlled trial, funded by the manufacturer of the study drug, found that a combination of sumatriptan 85 mg and naproxen sodium 200 mg was better than either drug alone.

Preventive treatment

Preventive (also called prophylactic) treatment of migraines can be an important component of migraine management. Such treatments can take many forms, including everything from taking certain drugs or nutritional supplements, to lifestyle alterations such as increased exercise and avoidance of migraine triggers. One such book that outlines these preventative measures quite well is "7 Steps To A Healthy Brain" by Dr. Winner.

The goals of preventive therapy are to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy. Another reason to pursue these goals is to avoid medication overuse headache (MOH), otherwise known as rebound headache, which is a common problem among migraneurs. This is believed to occur in part due to overuse of pain medications, and can result in chronic daily headache.

Prescription drugs

A 2006 review article by S. Modi and D. Lowder offers some general guidelines on when a physician should consider prescribing drugs for migraine prevention:

Following appropriate management of acute migraine, patients should be evaluated for initiation of preventive therapy. Factors that should prompt consideration of preventive therapy include the occurrence of two or more migraines per month with disability lasting three or more days per month; failure of, contraindication for, or adverse events from acute treatments; use of abortive medication more than twice per week; and uncommon migraine conditions (e.g., hemiplegic migraine, migraine with prolonged aura, migrainous infarction). Patient preference and cost also should be considered.

...Therapy should be initiated with medications that have the highest levels of effectiveness and the lowest potential for adverse reactions; these should be started at low dosages and titrated slowly. A full therapeutic trial may take two to six months. After successful therapy (e.g., reduction of migraine frequency by approximately 50 percent or more) has been maintained for six to 12 months, discontinuation of preventive therapy can be considered.

Preventive medication has to be taken on a daily basis, usually for a few weeks, before the effectiveness can be determined. Supervision by a neurologist is advisable. A large number of medications with varying modes of action can be used. Selection of a suitable medication for any particular patient is a matter of trial and error, since the effectiveness of individual medications varies widely from one patient to the next. Often preventive medications do not have to be taken indefinitely. Sometimes as little as six months of preventive therapy is enough to "break the headache cycle" and then they can be discontinued.

The most effective prescription medications include several drug classes:

Other drugs:

  • Sansert was withdrawn from the US market by Novartis, but is available in Canadian pharmacies. Although highly effective, it has rare but serious side effects, including retroperitoneal fibrosis.
  • Namenda, memantine HCI tablets, which is used in the treatment of Alzheimer's Disease, is beginning to be used off label for the treatment of migraines. It has not yet been approved by the FDA for the treatment of migraines.
  • ASA or Aspirin can be taken daily in low doses such as 80 mg, the blood thinners in ASA have been shown to help some migrainures, especially those who have an aura.

Trigger avoidance

Patients can attempt to identify and avoid factors that promote or precipitate migraine episodes. Moderation in alcohol and caffeine intake, consistency in sleep habits, and regular meals may be helpful. General dietary restriction has not been demonstrated to be an effective approach to treating migraine, and migraine is remarkably resistant to the placebo effect

Herbal and nutritional supplements

Butterbur

50 mg or 75 mg/day of butterbur (Petasites hybridus) rhizome extract was shown in a controlled trial to provide 50% or more reduction in the number of migraines to 68% of participants in the 75 mg dose group, 56% in the 50 mg dose group and 49% in the placebo group after four months. Native butterbur contains some carcinogenic compounds, but a purified version, Petadolex, does not.

Cannabis

Cannabis was a standard treatment for migraines from 1874 and 1942. It has been reported to help people through an attack by relieving the nausea and dulling the head pain, as well as possibly preventing the headache completely when used as soon as possible after the onset of pre-migraine symptoms, such as aura. A pharmaceutical company is currently conducting trials of a whole cannabis extract spray for migraine.

Coenzyme Q10

Supplementation of coenzyme Q10 has been found to have a beneficial effect on the condition of some sufferers of migraines. In an open-label trial, Young and Silberstein found that 61.3% of patients treated with 100 mg/day had a greater than 50% reduction in number of days with migraine, making it more effective than most prescription prophylactics. Fewer than 1% reported any side effects. A double-blind placebo-controlled trial has also found positive results.

Feverfew

The plant feverfew (Tanacetum parthenium) is a traditional herbal remedy believed to reduce the frequency of migraine attacks. A number of clinical trials have been carried out to test this claim, but a 2004 review article concluded that the results have been contradictory and inconclusive. However, since then, more studies have been carried out. As well as its prophylactic properties, feverfew is also touted as a migraine abortative.

Magnesium Citrate

Magnesium citrate has reduced the frequency of migraine in an experiment in which the magnesium citrate group received 600 mg per day oral of trimagnesium dicitrate. In weeks 9–12, the frequency of attacks was reduced by 41.6% in the magnesium citrate group and by 15.8% in the placebo group.

Riboflavin

The supplement Riboflavin (also called Vitamin B2) has been shown (in a placebo-controlled trial) to reduce the number of migraines, when taken at the high dose of 400 mg daily for three months.

Vitamin B12

There is tentative evidence that Vitamin B12 may be effective in preventing migraines.[82] In particular, in an open-label pilot study, 1 mg of intranasal hydroxocobalamin (a form of Vitamin B12), taken daily for three months, was shown to reduce migraine frequency by 50% or more in 10 of 19 participants. Although the study was not placebo-controlled, this response is larger than the typical placebo effect in migraine prophylaxis.

Surgical treatments

Surgery may be used to treat migraines by severing the corrugator supercilii muscle and zygomaticotemporal nerve The treatment may reduce or eliminate headaches in some individuals.

In 2005, research was published indicating that in some people with a patent foramen ovale (PFO), a hole between the upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines reduce in frequency if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without passing through the lungs.

Botulin toxin has been used to treat individuals with frequent or chronic migraines. It appears to be effective for chronic migraines but not useful in the treatment of episodic migraine.

Spinal cord stimulators are an implanted medical device sometimes used for those who suffer severe migraines several days each month.

Noninvasive medical treatments

Transcranial Magnetic Stimulation (TMS): At the 49th Annual meeting of the American Headache Society in June 2006, scientists from Ohio State University Medical Center presented medical research on 47 candidates that demonstrated that TMS — a medically non-invasive technology for treating depression, obsessive compulsive disorder and tinnitus, among other ailments — helped to prevent and even reduce the severity of migraines among its patients. This treatment essentially disrupts the aura phase of migraines before patients develop full-blown migraines. In about 74% of the migraine headaches, TMS was found to eliminate or reduce nausea and sensitivity to noise and light. Their research suggests that there is a strong neurological component to migraines. A larger study will be conducted soon to better assess TMS's complete effectiveness. In June 2008, a hand-held apparatus designed to apply TMS as a preemptive therapy to avert a migraine attack at the onset of the aura phase was introduced in California.

Biofeedback has been used successfully by some to control migraine symptoms through training and practice.

Hyperbaric oxygen therapy has been used successfully in treating migraines. This suggests that sufferers might be treated during an attack with a hyperbaric chamber of some sort, such as a Gamow bag (as is done in the treatment of "The Bends" and altitude sickness.

Bruxism, clenching or grinding of teeth, especially at night, is a trigger for many migraineurs. A device called a nociceptive trigeminal inhibitor (NTI) takes advantage of a reflex limiting the force of clenching. It can be fitted by dentists and clips over the front teeth at night, preventing contact between the back teeth. It has a success rate similar to butterbur and co-enzyme Q10, although it has not been subjected to the same rigorous testing as the supplements. Massage therapy of the jaw area can also reduce such pain.

There is a speculative connection between vision correction (particular with prism eyeglasses) and migraines. Two British studies, one from 1934 and another from 1956 claimed that many patients were provided with complete relief from migraine symptoms with proper eyeglass prescriptions, which included prescribed prism. However, both studies are subject to criticism because of sample bias, sample size, and the lack of a control group. A more recent study found that precision tinted lenses may be an effective migraine treatment. (Most optometrists avoid prescribing prism because, when incorrectly prescribed, it can cause headaches.

Behavioral treatments

Many physicians believe that exercise for 15–20 minutes per day is helpful for reducing the frequency of migraines.

Sleep is often a good solution if a migraine is not so severe as to prevent it, as when a person awakes the symptoms will have most likely subsided.

Diet, visualization, and self-hypnosis are also alternative treatments and prevention approaches.

Sexual activity has been reported by a proportion of male and female migraine sufferers to relieve migraine pain significantly in some cases.

In many cases where a migraine follows a particular cycle, attempting to interrupt the cycle may prolong the symptoms. Letting a headache "run its course" by not using painkillers can sometimes decrease the length of an episode. This is especially true of cases where vomiting is common, as often the headache will subside immediately after vomiting. Curbing the pain may delay vomiting, and prolong the headache.

Alternative medicine

A number of forms of alternative medicine, particularly bodywork, are used in preventing migraines.

Massage therapy and physical therapy are often very effective forms of treatment to reduce the frequency and intensity of migraines. However, it is important to be treated by a well-trained therapist who understands the pathophysiology of migraines. Deep massage can 'trigger' a migraine attack in a person who is not used to such treatments. It is advisable to start sessions as short in duration and then work up to longer treatments. Likewise, some migraine sufferers find relief through chiropractic care.

Frequent migraines can leave the sufferer with a stiff neck which can cause stress headaches that can then exacerbate the migraines. Claims have been made that Myofascial Release can relieve this tension and in doing so reduce or eliminate the stress headache element.

Some migraine sufferers find relief through acupuncture, which is usually used to help prevent headaches from developing. Sometimes acupuncture is used to relieve the pain of an active migraine headache. In one controlled trial of acupuncture with a sham control in migraine, the acupuncture was not more effective than the sham acupuncture but was more effective than delayed acupuncture.

Additionally acupressure is used by some for relief. For instance pressure between the thumbs and index finger to help subside headaches if the headache or migraine isn't too severe.

Incense and scents are shown to help. The smell and incense of peppermint and lavender have been proven to help with migraines and headaches more so than most other scents. However, some scents can be a trigger factor.

History

9000 year old skulls exist with evidence of trepanation. It is hypothesized that this drastic step was taken in response to headaches, though there is no clear evidence proving this.[citation needed]. Headache with neuralgia was recorded in the medical documents of the ancient Egyptians as early as 1200 BC. In 400 BC Hippocrates described the visual aura that can precede the migraine headache and the relief which can occur through vomiting. Aretaeus of Cappadocia is credited as the "discoverer" of migraines because of his second century description of the symptoms of a unilateral headache associated with vomiting, with headache-free intervals in between attacks. Galenus of Pergamon used the term "hemicrania" (half-head), from which the word "migraine" was derived. He thought there was a connection between the stomach and the brain because of the nausea and vomiting that often accompany an attack. For relief of migraine, Andalusian-born physician Abulcasis, also known as Abu El Qasim, suggested application of a hot iron to the head or insertion of garlic into an incision made in the temple. In the Medieval Ages migraine was recognized as a discrete medical disorder with treatment ranging from hot irons to blood letting and even witchcraft[citation needed]. Followers of Galenus explained migraine as caused by aggressive yellow bile. Ebn Sina (Avicenna) described migraine in his textbook "El Qanoon fel teb" as "... small movements, drinking and eating, and sounds provoke the pain... the patient cannot tolerate the sound of speaking and light. He would like to rest in darkness alone." Abu Bakr Mohamed Ibn Zakariya Râzi noted the association of headache with different events in the lives of women, "...And such a headache may be observed after delivery and abortion or during menopause and dysmenorrhea."

In Bibliotheca Anatomica, Medic, Chirurgica, published in London in 1712, five major types of headaches are described, including the "Megrim", recognizable as classic migraine. Graham and Wolff (1938) published their paper advocating ergotamine tart for relieving migraine. Later in the 20th century, Harold Wolff (1950) developed the experimental approach to the study of headache and elaborated the vascular theory of migraine, which has come under attack as the pendulum again swings to the neurogenic theory.

Economic impact

In addition to being a major cause of pain and suffering, chronic migraine attacks are a significant source of both medical costs and lost productivity. Medical costs per migraine sufferer (mostly physician and emergency room visits) averaged $107 USD over six months in one 1988 study,[citation needed] with total costs including lost productivity averaging $313. Annual employer cost of lost productivity due to migraines was estimated at $3,309 per sufferer. Total medical costs associated with migraines in the United States amounted to one billion dollars in 1994, in addition to lost productivity estimated at thirteen to seventeen billion dollars per year. Employers may benefit from educating themselves on the effects of migraines in order to facilitate a better understanding in the workplace. The workplace model of 9–5, 5 days a week may not be viable for a migraine sufferer. With education and understanding an employer could compromise with an employee to create a workable solution for both.

Migraine and cardiovascular risks

The risk of stroke may be increased two- to threefold in migraine sufferers. Young adult sufferers and women using hormonal contraception appear to be at particular riskThe mechanism of any association is unclear, but chronic abnormalities of cerebral blood vessel tone may be involved. Women who experience auras have been found to have twice the risk of strokes and heart attacks over non-aura migraine sufferers and women who do not have migraines. Migraine sufferers seem to be at risk for both thrombotic and hemorrhagic stroke as well as transient ischemic attacks. Death from cardiovascular causes was higher in people with migraine with aura in a Women's Health Initiative study, but more research is needed to confirm this

Idiopathic intracranial hypertension

Idiopathic intracranial hypertension (IIH), sometimes called benign intracranial hypertension (BIH) or pseudotumor cerebri (PTC) is a neurological disorder that is characterized by increased intracranial pressure (ICP), in the absence of a tumor or other diseases affecting the brain or its lining. The main symptoms are headache, pulsatile or pulse-synchronous tinnitus, double vision and visual loss. Diagnosis requires brain scans and lumbar puncture. There are various medical and surgical treatments.

Terminology

The terms "benign" and "pseudotumor" derive from the fact that increased intracranial pressure was, especially in the era before computed tomography (CT), associated with brain tumors. Those patients in whom no tumour was found were therefore diagnosed with "pseudotumor cerebri" (a disease mimicking a brain tumor). The disease was renamed "benign intracranial hypertension" to distinguish it from intracranial hypertension due to malignancy (i.e. cancer); this was also felt to be misleading because any disease that can blind someone should not be thought of as benign, and the name was therefore revised to "idiopathic (of no identifiable cause) intracranial hypertension".

Raised ICP due to another cause (e.g. meningitis, tumor) can be classified as "secondary intracranial hypertension".

Signs and symptoms

Characteristic symptoms of IIH are headache in 94%, transient visual obscurations or transient visual loss in one or both eyes usually lasting seconds (68%), pulse synchronous tinnitus (a "wooshing noise" in the ear) (58%) double vision (38%), and visual loss (30%).

If untreated, complete loss of vision is possible. While IIH may develop in any age group and in both males and females, it is more likely in females of fertile age (15-45) who are overweight or obese. Certain medications (hormonal contraception, vitamin A,[3] tetracycline antibiotics) may increase risk of IIH.

Physical findings in IIH are characterized by papilledema, loss of visual acuity and visual fields, and absence of focal neurological findings (e.g. face, arm or leg weakness, sensory disturbance or coordination loss). Diplopia (double vision), if present, may be due to abducens nerve palsy (the sixth cranial nerve). Absence of papilledema, while making IIH less likely, is possible.

Diagnosis

The diagnosis may be suspected on the basis of the history and examination. To confirm the diagnosis, as well as excluding alternative causes (such as a brain tumor), several investigations are required; more investigations may be performed if the history is not typical or the patient is more likely to have an alternative problem (e.g. children, the elderly).

Neuroimaging, usually with computed tomography (CT/CAT) or magnetic resonance imaging (MRI), rules out mass lesions. In IIH these scans may be normal, although small or slit-like ventricles and "empty sella sign" (flattening of the pituitary gland due to increased pressure) may be seen. Some propose MRI as preferred mode of imaging in atypical cases, and suggest performance of MR venography to exclude venous obstruction or cerebral venous sinus thrombosis.

Once a mass lesion has been ruled out, lumbar puncture is generally performed to measure the opening pressure, as well as to obtain cerebrospinal fluid (CSF) to exclude alternative diagnoses such as low-grade viral meningitis. If the opening pressure is increased, CSF may be removed for relief (see below).

Criteria

The original criteria for IIH were described by Dandy in 1937. They were modified by Smith in 1985 to become the "modified Dandy criteria".

1 Signs & symptoms of increased ICP – CSF pressure >25 cmH2O
2 No localizing signs with the exception of abducens nerve palsy
3 Normal CSF composition
4 Normal to small (slit) ventricles on imaging with no intracranial mass

A 2002 review proposed a 6-point set of criteria that required no unexplained symptoms or signs, measurement of the CSF opening pressure in the lateral decubitus (i.e. lying on the side), exclusion of any other causes on specific forms of imaging.

Pathogenesis

At least two primary mechanisms for the development of increased CSF pressure in primary IIH have been postulated: increased production of CSF and reduced resorption. Increased production may be the result of vasogenic extracellular brain edema, while decreased rebsorption may be due to low conductance of CSF outflow at the arachnoid villi.

Increased production

Sørensen et al found evidence for increased water diffusion in the brain of IIH patients when compared to normal subjects. It was argued that this evidence indicates abnormal convective transependymal water flow leading to brain edema.

However, this theory remains controversial, as a similar study conducted by Bastin et al that used significantly disparate MR imaging protocols was unable to reproduce these findings. Normal CSF flow involves production at the choroid plexuses and absorption at the cranial and spinal nerve root arachnoid villi and granulations.

Impaired CSF absorption

Impaired CSF absorption at the superior sagittal sinus or along the spinal nerve roots could therefore explain IIH and has been documented in 75-100% of IIH patients. Permeability along the blood-CSF barrier varies, producing an increasing oncotic pressure gradient between the CSF and venous system in a rostral to caudal progression. It is speculated that variations in this oncotic pressure contribute to or impede CSF absorption.

The mechanism remains unclear however, since high CSF protein concentrations, as commonly found in Guillain-Barré syndrome or spinal tumors, can manifest as intracranial hypertension, whereas individuals with IIH frequently present with normal-to-low CSF protein findings.

Treatment

The primary goal in treatment of IIH is the prevention of visual loss and blindness. IIH is treated mainly through the attempted reduction of CSF pressure and, where applicable, weight loss. IIH may resolve after initial treatment, may go into remission and relapse at a later stage, or may continue chronically. If the intracranial hypertension is secondary to medication, these need to be discontinued.

Lumbar puncture

CSF pressure may be temporarily decreased by repeated "therapeutic" (as opposed to diagnostic) lumbar punctures (to remove excessive cerebrospinal fluid). However, this is generally regarded as a "holding measure" until medical or surgical treatment has been instituted.

Medication

The best studied medical treatment is the carbonic anhydrase inhibitor acetazolamide, which reduces CSF production. Other drugs such as furosemide and various diuretics, and topiramate may be used in an attempt to reduce ICP. The long-term use of corticosteroids to treat chronic IH has fallen out of favor, unless there is a secondary inflammatory process caused by an underlying disease like lupus or Behcet disease. While corticosteroids may lower intracranial pressure in the short-term, the drawbacks to steroids include weight gain, fluid retention and a rebound in intracranial pressure during the drug’s withdrawal.

Surgery

Surgical treatments include optic nerve sheath decompression and fenestration. In this procedure, a slit is made in the sheath of the optic nerve, which can alleviate swelling and slow or halt loss of vision. Optic nerve sheath fenestration is less effective in controlling the CSF pressure (and in controlling most symptoms, such as headache), but is more effective in protecting the optic nerve from the effects of pressure.

Shunting is a neurosurgical procedure to facilitate the drainage of excess CSF (thereby reducing ICP). A shunt is essentially a silicone tube inserted somewhere in the fluid spaces of the central nervous system, which then drains CSF to the circulatory system or one of the body cavities. There are various types and configurations of shunts; lumboperitoneal (LP) shunts drain from the lumbar spine to the peritoneal cavity, while ventriculoatrial (VA) shunts run from the cerebral ventricles to the heart. Although shunts can dysfunction due to occlusion, infection, malfunction, etc., they are very effective in normalizing CSF pressures. The absence of papilledema or longstanding symptoms make successful shunting less likely. Studies have shown that shunting procedures are becoming more common as the rate of severe obesity rises.

In cases of severe obesity, gastric bypass surgery has been shown to lead to a marked improvement in symptoms.

Epidemiology

The reported annual incidence of IIH is <20 per 100,000 persons.

History

The first report of IIH is usually ascribed to the German physician Heinrich Quincke, who described it in 1893 under the name "serous meningitis". The term "pseudotumor cerebri" was introduced in 1904 by Max Nonne. Diagnostic criteria were developed in 1937 by the Baltimore neurosurgeon Walter Dandy.

Ictal headache

Ictal headaches are headaches associated with seizure activity. They may occur either before (pre-ictal) or after (post-ictal) a seizure, and in rare circumstances during a seizure. Many cases of ictal headache may be misdiagnosed as migraine with aura, or even cluster headache. However, while these conditions usually involve just one side of the head (are unilateral), an ictal headache may be centrally situated or cover the entirety of the head.

Severity of ictal headaches can vary from a slight pressure or "cloud" to an intensity far beyond migraine. Some have called it a "suicide headache" in the worst instances. Temporary blindness may also occur in some cases.

Ictal headaches can often be controlled with anticonvulsants.

Symptoms besides headache may be either present or absent, and may include unusual thoughts or experiences. In these cases it is especially important to obtain a correct diagnosis. Many people with these experiences are accidentally diagnosed with conditions such as psychosis or schizophrenia and given antipsychotic medications, which may actually increase seizure activity.

An EEG is recommended to detect other signs of epilepsy. Even when an EEG does not prove determinative, anticonvulsants may be a first line of treatment if these symptoms are present with headache.

Cluster headache

Cluster headache is a neurological disease that involves, as its most prominent feature, an immense degree of pain. "Cluster" refers to the tendency of these headaches to occur periodically, with active periods interrupted by spontaneous remissions. The cause of the disease is currently unknown.

Signs and symptoms

Cluster headaches are excruciating unilateral headaches, of extreme intensity. The duration of the common attack is 15 minutes to three hours. Onset of an attack is rapid, and most often without the preliminary signs that are characteristic of a migraine. However, some sufferers report preliminary sensations of pain in the general area of attack, often referred to as "shadows," that may warn them an attack is imminent. Though the headaches are almost exclusively unilateral, there are many documented cases of "side-shifting" between cluster periods, or, even rarer, simultaneously (within the same cluster period) bilateral headache. They are often initially mistaken for brain tumors and multiple sclerosis until patients are treated with corticosteroids and then imaged. Trigeminal neuralgia can also bring on headaches with similar qualities.

Pain

The degree of pain involved in cluster headaches is markedly greater than in other headache conditions, including migraine. It has been described by female patients as being more severe than childbirth. The pain is lancinating or boring in quality, and is located behind the eye (periorbital) or in the temple, sometimes radiating to the neck or shoulder. Analogies frequently used to describe the pain are a red-hot poker inserted into the eye, or a spike penetrating from the top of the head, behind one eye, radiating down to the neck, or sometimes having a leg amputated without any anaesthetic.The condition was originally named Horton's Neuralgia after Dr. B.T Horton who postulated the first theory as to their pathogenesis. His original paper describes the severity of the headaches as being able to take normal men and force them to suicide. Indeed, cluster headaches are also known by the nickname "suicide headaches".

From Horton's 1939 original paper on cluster headache:

Our patients were disabled by the disorder and suffered from bouts of pain from two to twenty times a week. They had found no relief from the usual methods of treatment. Their pain was so severe that several of them had to be constantly watched for fear of suicide. Most of them were willing to submit to any operation which might bring relief.

Other symptoms

The cardinal symptoms of the cluster headache attack are ptosis (drooping eyelid), conjunctival injection (redness of the conjuctiva - the covering of the eyeball), lacrimation (tearing), rhinorrhea (runny nose), and, less commonly, facial blushing, swelling, or sweating. These features are known as the autonomic symptoms. The attack is also associated with restlessness, the sufferer often pacing the room or rocking back and forth. Less frequently, he or she will have an aversion to bright lights and loud noise during the attack. Nausea is not typical of cluster headache, though it has been reported. The neck is often stiff or tender in the aftermath of a headache, with jaw or tooth pain sometimes present.

Cyclical recurrence and regular timing

Cluster headaches are occasionally referred to as "alarm clock headaches", because of the regularity of its timing and its ability to wake a person from sleep. Thus it has been known to strike at the same time each night or morning, often at precisely the same time during the day a week later. This has prompted researchers to speculate an involvement of the brain's "biological clock" or circadian rhythm. In some cases, cluster headaches remain "steady" without cyclical ups and downs for days.

Episodic or chronic

In episodic cluster headache, these attacks occur once or more daily, often at the same times each day, for a period of several weeks, followed by a headache-free period lasting weeks, months, or years. Approximately 10–15% of cluster headache sufferers are chronic; they can experience multiple headaches every day for years.

Cluster headaches occurring in two or more cluster periods lasting from 7 to 365 days with a pain-free remission of one month or longer between the clusters are considered episodic. If the attacks occur for more than a year without a pain-free remission of at least one month, the condition is considered chronic. Chronic clusters run continuously without any "remission" periods between cycles. The condition may change from chronic to episodic and from episodic to chronic. Remission periods lasting for decades before the resumption of clusters have been known to occur.

Ice-cream headache

ce-cream headache, also known as brain freeze, cold headache, shakeache, frigid face, freezie, frozen brain syndrome, cold-stimulus headache, or its given scientific name sphenopalatine ganglioneuralgia (meaning "nerve pain of the sphenopalatine ganglion"), is a form of brief cranial pain or headache commonly associated with consumption (particularly quick consumption) of cold beverages or foods such as ice cream.

Cause and frequency

An editorial was published in the British Medical Journal[1] on ice cream headache; it referenced several articles on the effect of rapid consumption of cold foods or beverages. It has been studied as an example of referred pain, an unpleasant sensation localised to an area separate from the site of the painful stimulation.

The effect occurs when something very cold, such as ice cream, touches the top palate in the mouth. The blood vessels constrict due to the cold. This makes the nerves send a signal to the brain to open blood vessels. But this rapid opening of the blood vessels makes fluid back up in the tissues that won't drain for thirty seconds to a minute. This causes a slight swelling in the forehead that causes pain.

It has been estimated that one in three people experience an ice-cream headache from consumption of ice cream. Some studies suggest that it is more common in people who experience migraines; other studies have shown the opposite. Experiments have shown that frozen yogurt, which will generally maintain a more liquid state than traditional ice cream at lower temperatures, will trigger this condition in test subjects more readily than dairy ice cream, cold drinks or ice. Food Detectives, A Food Network show that investigates food myths, dedicated an entire 375 minutes to find out what causes it and how to prevent, if at all possible, an Ice Cream headache. At the end of the episode, they commented that the best way to prevent one is to wear a warm hat, drink boiling hot water between bites, and take your time when eating something cold. Pressing the pad of your thumb firmly against the roof of your mouth is also said to work.

Thunderclap headache

A thunderclap headache is a headache that is severe and sudden (like a thunderclap). Because it may be a sign of a medical emergency, some sources recommend immediate medical attention.

In 25% of cases, a thunderclap headache is an indication of aneurysmal subarachnoid hemorrhage (SAH), which often leads to death or severe disability. Headaches which accompany SAH are "frequently described as being the worst headache of one's life, although other clinical presentations are possible."

Diagnosis is made via a process of exclusion with accompanying negative computed tomograph and lumbar puncture results

Vascular headache

A vascular headache is an outdated term to describe certain types of headache which were thought to be related to blood vessel swelling and hyperemia as cause of the pain.

It is not longer a recognized term and not mentioned in the Headache classification of the International Headache society (IHS), although it is still used by some physicians and still mentioned in some medical classification systems.

Headaches that were described as being vascular headaches include:

Toxic headache

A toxic headache is the least common type of vascular headache that usually comes from a fever from acute illnesses such as measles, mumps, pneumonia and tonsillitis. Common hazards in our environment also cause toxic headaches with exposure. These include chemicals, fumes, pollution, allergens and other health hazards. These toxins can be found in our communities, workplaces, and homes.

A chemical factor from the outside or inside of your body can result in a toxic headache. Internal body sources are harder to identify, but usually arise when an organ fails to function properly. When this happens, in the bowels, liver or kidneys for example, the body builds up toxicity because waste products are not being removed as they should. The increase in toxicity levels may cause a headache. To treat these headaches, the organ dysfunction must be corrected to eliminate toxic waste.

Toxic headaches are considered an environmental illness when it is caused by exposure to a toxin. These headaches can be caused by exposure to toxic chemicals, including lead, insecticides, organophosphate pesticides, chemical solvents, acetaldehyde from alcohol (a hangover), carbon tetrachloride, and some household cleaners. This often happens through destabilizing the magnesium metabolism of the cell, which triggers a cascade of biological and neurological reactions, culminating in a migraine, toxic headache, or worse (such as neurological damage). The effect of alcohol can be magnified by "congeners" from alcohol fermentation.

Several common chemicals are toxic headache culprits. Nitrite compounds dilate blood vessels, causing dull and pounding headaches with repeat exposure. Nitrite is found in dynamite, heart medicine and it is a chemical used to preserve meat. Poisons, like carbon tetrachloride, insecticides and lead can cause headaches with exposure also. Ingesting lead paint or having contact with lead batteries can cause headaches. Caffeine can be used to cure a headache by constricting dilated arteries. However, caffeine is also a chemical headache inducer for individuals who ingest lots of caffeine and are trying to cut back. Toxic shock syndrome can lead to headaches due to the staphylococcus aureus bacteria infection. Headaches are also a symptom of carbon monoxide poisoning. Toxic and polluted air can lead to toxic headaches with constant exposure.

Toxic headaches are treated by determining the cause of the headache and treating or removing it. But often the cause of a toxic headache is unknown because symptoms depend on the environmental or bodily cause. Symptoms may not appear for years or they can become gradually with more exposure. Many times the source of the headache will not be recognized until your symptoms continue or they only appear at specific places or times. Toxic headaches due to environmental causes are usually diagnosed by taking an exposure history, listing details about the places you frequent most days. Treatments vary based on symptoms and the cause of the headache.

Coital cephalalgia

Also known as "sexual headaches", coital cephalalgia is a rare type of severe headache that occurs at the base of the skull before orgasm during sexual activity, including masturbation. The pain usually moves from the base of the skull through the head towards the frontal lobes. Extremely severe and sharp pain behind the eyes is also a symptom. The headaches usually have an immediate onset, with some gradually worsening during intercourse and others (referred to as "explosive headaches") occurring almost instantaneously at the moment of orgasm. These headaches typically last for a few minutes to a few hours, although it is possible for such headaches to last up to a few days. It is most common for men to experience these headaches for the first time in their early 20s, or between the ages of 35-44; the reason for this is unclear.

More prevalent in men, by a ratio of 3:1, these headaches appear in roughly 1% of the population, though it has been suggested that the prevalence may be higher, due to the embarrassment of presenting with the disorder, especially in cases where spontaneous remission occurs after a few days. Up to 10% of patients taking medication for erectile dysfunction may experience these headaches. It is important to see a doctor if you have such symptoms in order to rule out a potential brain aneurysm, or tumors. In most cases, these headaches are benign. More serious symptoms include a stiff neck, confusion, and dizziness.

As for treatment, a doctor may recommend abstaining from sexual activities and masturbation for a short period of time ranging from a few days to a few weeks. In addition, doctors may recommend medications such as propanolol that can be taken in advance of sexual activity to prevent such headaches. Reduction in weight to a more ideal level and increased exercise may also reduce the likelihood of recurrences.

Coital cephalalgia can frequently occur in a timeframe that exertion headaches occur.

Hemicrania continua

Hemicrania continua (HC) is a persistent unilateral headache that responds to indomethacin. It is usually unremitting, but rare cases of remission have been documented. Hemicrania continua is considered a primary headache disorder, meaning that it's not caused by another condition.

Diagnostic criteria

International Headache Society's International Classification of Headache Disorders 2nd Edition, establishes the following diagnostic criteria for hemicrania continua:

  1. Headache for more than 3 months fulfilling other 3 criteria:
  2. All of the following characteristics:
    • Unilateral pain without side-shift
    • Daily and continuous, without pain-free periods
    • Moderate intensity, but with exacerbations of severe pain
  3. At least one of the following autonomic features occurs during exacerbations and ipsilateral to the side of pain:
  4. Complete response to therapeutic doses of indomethacin

A variant on hemicrania continua has also been described, in which the attacks may shift sides, although meeting the above criteria in all other respects.

Epidemiology

Hemicrania continua was first described in 1981, at that time around 130 cases were described in the literature. However, rising awareness of the condition has led to increasingly frequent diagnosis in headache clinics, and it seems that it is not as rare as these figures would imply. The condition occurs more often in women than men and tends to first present in adulthood, although it has also been reported in children as young as 5 years old.

Cause and diagnosis

The cause of hemicrania continua is unknown. There is no definitive diagnostic test for hemicrania continua. Diagnostic tests such as imaging studies may be ordered to rule out other causes for the headache. When the symptoms of hemicrania continua are present, it's considered "diagnostic" if they respond completely to indomethacin.

The factor that allows hemicrania continua and its exacerbations to be differentiated from migraine and cluster headache is that hemicrania continua is completely responsive to idomethacin. Triptans and other abortive medications do not affect hemicrania continua.

Symptoms

In addition to persistent daily headache of HC, which is usually mild to moderate, HC can present other symptoms. These additional symptoms of HC can be divided into three main categories:

  1. Autonomic symptoms:
    • conjunctival injection
    • tearing
    • rhinorrhea
    • nasal stuffiness
    • eyelid edema
    • forehead sweating
  2. Stabbing headaches:
    • Short, "jabbing" headaches superimposed over the persistent daily headache.
    • Usually lasting less than one minute.
  3. Migrainous features:

Treatment

Hemicrania continua generally responds only to indomethacin 25-300 mg daily, which must be continued long term. Unfortunately, gastrointestinal side effects are a common problem with indomethacin, which may require additional acid-suppression therapy to control.

In patients who are unable to tolerate indomethacin, the use of celecoxib 400-800 mg per day (Celebrex) and rofecoxib 50 mg per day (Vioxx - no longer available) have both been shown to be effective and are likely to be associated with fewer GI side effects. There have also been reports of two patients who were successfully managed with topiramate 100-200 mg per day (Topamax) although side effects with this treatment can also prove problematic.

Rebound headache

Rebound headaches, also known as medication overuse headaches, occur when pain medications (analgesics) are taken too frequently to relieve headache. Rebound headache can be caused by any painkiller or migraine abortive medication such as triptans as well as NSAIDs, antihistamines, and decongestants. Over-the-counter agents such as aspirin, paracetamol/acetaminophen (Tylenol) and ibuprofen (Advil, Motrin) as well as prescription medications such as Fioricet, Fiorinal, Imitrex and Vicodin can cause rebound headaches. The medications most likely to cause rebound appear to be the combination analgesics such as Fioricet, Fiorinal, and Excedrin, as well as narcotic medications. Rebound headaches frequently occur daily and can be very painful. They are a common cause of chronic daily headache. They typically occur in patients with an underlying headache disorder such as migraine, that "transforms" over time from an episodic condition to chronic daily headache due to more and more frequent analgesic use. Rebound headache was first described by Dr. Lee Kudrow.

Treatment

Rebound headache is common and can be treated. The overused medications must be stopped in order for the patient's headaches to resolve. This is usually done under the care of a neurologist. Often patients are started on preventive medications to ease their transition off the medications that induced the medication overuse / rebound cycle. It is important that the patient's physician be consulted before abruptly discontinuing medications as abruptly discontinuing some medications has the potential for creating another issue. Abruptly discontinuing butalbital, for example, can actually induce seizures in some patients, although simple over the counter analgesics can safely be stopped by the patient without medical supervision. A long acting analgesic/anti-inflammatory, such as Naproxen (500mg twice a day) can be used to ease headache during the withdrawal period.

Prevention

In general, any patient who has frequent headaches or migraine attacks should be considered as a potential candidate for preventive medications instead of being encouraged to take more and more painkillers or other rebound-causing medications. Preventive medications are taken on a daily basis. Some patients may require preventive medications for many years; others may require them for only a relatively short period of time such as six months. Effective preventive medications have been found to come from many classes of medications including neuronal stabilizing agents (aka anticonvulsants), antidepressants, antihypertensives, and antihistamines. Some effective preventive medications include Elavil (amitriptyline), Depakote (valproate), Topamax (topiramate), and Inderal (propranolol).

Red wine headache

Red wine headache ("RWH") is a bad headache often accompanied by nausea and flushing that occurs in many people after drinking even a single glass of red wine. This syndrome can sometimes develop within 15 minutes of consumption of the wine.

The condition does not occur after consumption of white wine or other alcoholic beverages. Some individuals report that they get a migraine headache hours later from drinking some red wines. No one knows for certain why this syndrome occurs. It probably has more than one cause.

Sulfites

Since wines contain a warning label about sulfites many people have assumed that sulfites are the cause of RWH. This is not the case. Almost all wine contains sulfites. Many sweet white wines have more sulfites than red wines. Dried fruit and processed food like lunchmeat have far more sulfites than red wine. Less than 1% of the population is sensitive to sulfites.

Histamines

There are no antihistamines in wine Fi. RWH is probably not caused by histamines except in rare cases. Red wine has 20 - 200% more histamines than white, and those who are allergic to them are deficient in a certain enzyme. Some experts believe that the combination of alcohol and that deficiency could cause headaches. However, a study of 16 people with an intolerance to red wine, reported in the Journal of Allergy and Clinical Immunology (Feb 2001), found no difference in reactions to low and high histamine wines. Taking loratadine (Claritin) an hour before drinking should reduce the reaction to histamines and the resulting symptoms. This would tell an individual whether histamines were the cause of their problem.

Another solution that has been advanced is to drink a cup of black tea before you drink the wine. If one will be drinking over the course of an evening, have another cup or two of black tea during the evening. Quercetin, a bioflavonoid found in black tea, significantly inhibits the headache/flush response (which is an inflammatory effect from histamines), according to Tareq Khan, M.D., a pain expert with St. Luke's Episcopal Hospital in Houston, Texas. Again, if histamine is not the cause of a given individual's reaction to wine, the antihistamine effects of black tea will be of no more help than the antihistamine effects of loratadine, just as in the example of the previous paragraph.

Tannins

Other experts think tannins are at the root of RWH. Tannins are the flavonoids in wine that give its degree of mouth-drying bitterness one tastes. The taste is the same as when you bite into a grape skin. Tannin is a chemical substance that comes from grape skins, stems, and seeds. The skins also impart color to wine, which is why red wines typically have a lot more tannin than whites. Red wines are fermented while in contact with the skins and seeds. Modern winemakers take care to minimize undesirable tannins from seeds by crushing grapes gently when extracting their juice.

Wines can also take on tannins from the oak or other woods used in wine barrels for storage. Different woods in different countries affect the type of tannins in the wine.

Tannins help prevent oxidation, an important role in a wine's aging potential. As age-worthy red wines mature, tannin molecules gradually accumulate and precipitate out of the wine into the harmless sediment (that black sludge at the bottom of older red wines.)

Certain wine styles have much less tannin content than others, due to reduced maceration time (grape juice contact with the grape pulp, including sources of tannin such as stems, seeds).

French reds from Bordeaux, and Italian reds like Barolo and Barbaresco, are particularly tannic. Vintage port is also very tannic when young, as are wines made from the syrah (shiraz) and cabernet sauvignon grapes.

French reds from Burgundy, and Italian wines like Dolcetto and Barbera, are less tannic. Wines made from Pinot Noir and Sangiovese grapes, as well as Spanish Riojas are less tannic. Beaujolais and Tempranillo are also lower tannin wines.

A quick way to identify these lower tannic wine bottles on a store shelf is to look for the sloped shoulder "Burgundy bottle". This is specially true for European wines, but several new world wineries have also adopted traditional bottle shapes to help consumers distinguish their wines.

There is a difference between the varieties and brands of red wine and the amount one can consume before the headache occurs, but the reports have not been consistent from person to person. Considering how the amount of tannins changes with aging, this would not be surprising.

The Harvard Health Letter notes several well-controlled experiments showing that tannins cause the release of serotonin, a neurotransmitter. High levels of serotonin can cause headaches and that may happen in people who also suffer from migraine headaches. But that does not explain why people who do not get migraines get RWH. Dr. Marion Nestle, chairwoman of the Department of Nutrition and Food Studies at New York University, added that no one complains about tea, soy, or chocolate headaches though all contain tannins.

The tannins that are extracted from grapes found in red wine are primarily condensed tannins which are polymers of procyanidin monomers. Hydrolysable tannins are extracted from the oak wood the wine is aged in. Hydrolysable tannins are more easily oxidised than condensed tannins.

Prostaglandins

RWH could be caused by the release of prostaglandins which some people are not able to metabolize. Prostaglandins are substances that can contribute to pain and swelling. Ibuprofen (Advil) and aspirin are prostaglandin inhibitors. Some people get good results taking a dose of ibuprofen an hour before consuming red wine.

Other possibilities

It has also been postulated that RWH could be caused by a strain of yeast or bacteria found in red wine.

Post dural puncture headache

Post dural puncture headache (PDPH) is a complication of spinal anesthesia, diagnostic spinal puncture, or epidural anesthesia.

PDPH typically occurs hours to days after puncture and presents with symptoms such as headache and nausea that typically worsen when the patient assumes an upright posture. It is thought to result from a leakage of cerebrospinal fluid into the epidural space. A decreased hydrostatic pressure in the subarachnoid space then leads to traction to the meninges with associated symptoms. The incidence of PDPH is higher with younger patients, complicated or repeated puncture, and use of large diameter needles. Modern, atraumatic needles such as the Sprotte spinal needle leave a smaller perforation and reduce the risk for PDPH.

Some patients require no other treatment than analgesics and bed rest. However, persistent and severe PDPH may require an epidural blood patch. A small amount of the patient's blood is injected into the epidural space near the site of the original puncture; the resulting blood clot then "patches" the meningeal leak. The procedure carries the typical risks of any epidural puncture but is highly effective, and further intervention is rarely necessary.

Hangover

A hangover (veisalgia) describes the sum of unpleasant physiological effects following heavy consumption of drugs, particularly alcoholic beverages. The most commonly reported characteristics of a hangover include headache, nausea, sensitivity to light and noise, lethargy, dysphoria, and thirst.

Hypoglycemia, dehydration, acetaldehyde intoxication, and vitamin B12 deficiency are all theorized causes of hangover symptoms. Hangovers may last up to two or three days after alcohol was last consumed. Roughly 25-30% of drinkers are resistant to hangover symptoms. Some aspects of a hangover are viewed as symptoms of acute ethanol withdrawal, similar to the longer-duration effects of withdrawal from alcoholism, as determined by studying the increases in brain reward thresholds in rats (the amount of current required to receive to electrodes implanted in the lateral hypothalamus) following ethanol injection.

Symptoms

An alcohol hangover is associated with a variety of symptoms that may include dehydration, fatigue, headache, nausea, vomiting, diarrhea, flatulence, weakness, elevated body temperature, hypersalivation, difficulty concentrating, anxiety, irritability, sensitivity to light and noise, erratic motor functions, trouble sleeping, and lack of depth perception. Many people will also be repulsed by the thought or taste of alcohol during a hangover. The symptoms vary from person to person, and occasion to occasion, usually beginning several hours after drinking. It is not clear whether hangovers directly affect cognitive abilities. In some rare cases, these symptoms can be additive to the point of hospitalization.

Causes

Ethanol has a dehydrating effect by causing increased urine production (such substances are known as diuretics), which causes headaches, dry mouth, and lethargy. Dehydration also causes fluids in the brain to be less plentiful. This can be mitigated by drinking water or an oral electrolyte solution after consumption of alcohol. Alcohol's effect on the stomach lining can account for nausea. Because of the increased NADH production during metabolism of ethanol by the enzymes alcohol dehydrogenase and aldehyde dehydrogenase, excess NADH can build up and slow down gluconeogenesis in the liver, thus causing hypoglycemia.

Another factor contributing to a hangover are the products from the breakdown of ethanol via liver enzymes. Ethanol is converted to acetaldehyde by the enzyme alcohol dehydrogenase, and then from acetaldehyde to acetic acid by the enzyme acetaldehyde dehydrogenase. Acetaldehyde (Ethanol) is between 10 and 30 times more toxic than alcohol itself, as well as being carcinogenic and mutagenic.

These two reactions also require the conversion of NAD+ to NADH. With an excess of NADH, the lactate dehydrogenase reaction is driven to produce lactate from pyruvate (the end product of glycolysis) in order to regenerate NAD+ and sustain life. This diverts pyruvate from other pathways such as gluconeogenesis, thereby impairing the ability of the liver to supply glucose to tissues, especially the brain. Because glucose is the primary energy source of the brain, this lack of glucose contributes to hangover symptoms such as fatigue, weakness, mood disturbances, and decreased attention and concentration.

Alcohol consumption can result in depletion of the liver's supply of glutathione and other reductive detoxification agents, reducing its ability to effectively remove acetaldehyde and other toxins from the bloodstream. Additionally, alcohol induces the CYP2E1 enzyme, which itself can produce additional toxins and free radicals.

There are various nervous system effects: the removal of the depressive effects of alcohol in the brain probably account for the light and noise sensitivity.

In addition, it is thought that the presence of other alcohols (such as fusel oils), by-products of the alcoholic fermentation also called congeners, exaggerate many of the symptoms (congeners may also be zinc or other metals added primarily to sweet liqueurs to enhance their flavor); this probably accounts for the mitigation of the effects when distilled alcohol, particularly vodka, is consumed instead.

Red wines have more congeners than white wines, and some people note less of a hangover with white wine. Some individuals have a strong negative reaction to red wine, distinct from hangover, called red wine headache that can affect them within 15 minutes after drinking a single glass of red wine. The headache is usually accompanied by nausea and flushing[citation needed].

In alcohol metabolism, one molecule of ethanol (the primary active ingredient in alcoholic beverages) produces 2 molecules of NADH, utilizing vitamin B12 as a coenzyme. Over-consumption of ethanol may cause vitamin B12 deficiency as well.

Possible remedies

There is debate about whether a hangover might be prevented or at least mitigated. There is currently no known proven mechanism for making oneself sober short of waiting for the body to metabolize ingested alcohol, which occurs via oxidation through the liver before alcohol leaves the body. However, drinking a large amount of water or a rehydration drink prior to sleep will effectively reduce a large proportion of the symptoms. This increases the need to urinate in the relevant timeline, thus cleaning the body and ridding it of many chemicals more quickly, including those that cause or heighten hangover symptoms.

A four page literature review in British Medical Journal on hangover cures by Max Pittler of the Peninsula Medical School at Exeter University and colleagues concludes: "No compelling evidence exists to suggest that any conventional or complementary intervention is effective for preventing or treating alcohol hangover. The most effective way to avoid the symptoms of alcohol induced hangover is to avoid drinking.

Potential beneficial remedies

* However, there is evidence that taurine taken before, during, or after alcohol consumption is able to reverse fatty liver deposits, liver disease.

* Rehydration: "Effective interventions include rehydration, prostaglandin inhibitors, and vitamin B6".

* Sodium bicarbonate; A slightly heaped teaspoon of baking soda suspended in a glass of water when consumed deals very effectively with the nausea, and indirectly with 'the shakes' associated with a hangover.

* Opioids: Codeine, dihydrocodeine, tilidine and other such medication directly work against many of the effects of alcohol hangover. It is believed that analgesic preparations containing acetaminophen (paracetamol/Tylenol) may predispose people to the risk of potentially fatal hepatotoxicity. Consumption of opioids along with alcohol or shortly after consumption thereof is potentially dangerous in itself because of added depressant effects on the central nervous system.

* Exercise: It is known that exercise after heavy intoxication helps the heart pump blood around the body and increases the amount of oxygen in the body. A light jog may alleviate hangover symptoms.

* Oxygen: In a double-blind random study of 231 patients at two Vienna hospitals, published in Anesthesiology in 1999 and reported by The New York Times, it was found that the side-effects of general anesthesia could be diminished by giving patients a mix of 80 percent oxygen and 20 percent nitrogen during the surgery, and for two hours afterward. Only 17 percent of the patients receiving supplemental oxygen experienced nausea and vomiting, compared with 30 percent of the group who were given the standard 30 percent oxygen and 70 percent nitrogen. The study's leader characterized the results for the Times, "Extra oxygen is cheap, risk-free and reduces the incidence of nausea as well as any known drug." A related study by members of Dr. Sessler's team, published in Anesthesiology in October 1999, indicated that patients given oxygen in amounts up to 80 percent did not suffer impaired lung function. In addition, there have been anecdotal reports, from doctors, nurses and SCUBA divers, that oxygen can also reduce the symptoms of hangovers sometimes caused by alcohol consumption. The theory is that the increased oxygen flow resulting from oxygen therapy improves the metabolic rate, and thus increases the speed at which toxins are broken down.

* Magnesium: It is well studied that excessive alcohol consumption can lead to a magnesium deficiency, or reduce levels of magnesium, as well as depleting zinc and other minerals.[citation needed] Individuals with lower magnesium levels may experience more severe hangovers. A healthy diet that contains an adequate intake of magnesium and other minerals may help in the long term to reduce the effects of hangovers. The hangover symptoms of headache, and light and sound sensitivity, are very similar to those of migraine. A common treatment for chronic migraine headaches is magnesium. Some scientists hypothesize that a hangover may be exhibiting at least some symptoms of an acute magnesium deficiency.

* Tolfenamic acid (TA): A study concludes, "TA was found significantly better than placebo in the subjective evaluation of drug efficacy (p<0.001) and in reducing the reported hangover symptoms in general (p < 0.01). In the TA group, significantly lower symptom scores were obtained for headache (p<0.01), and for nausea, vomiting, irritation, tremor, thirst, and dryness of mouth (all p < 0.05)."

* Vitamin B6 (pyritinol): Some studies have found large doses of Vitamin B6 (several hundred times the recommended daily intake) to reduce hangovers.

* Chlormethiazole: "Chlormethiazole was found to lower blood pressure and adrenaline output and, furthermore, to relieve unpleasant physical symptoms, but did not affect fatigue and drowsiness. The cognitive test results were only slightly influenced by this agent, while psychomotor performance was significantly impaired. Subjects with severe subjective hangover seemed to benefit more from the chlormethiazole treatment than subjects with a mild hangover." "However, all 8 subjects had unpleasant nasal symptoms following chlormethiazole, and it is therefore not an ideal hypnotic for this age group."

* Rosiglitazone: [Study in rats] "Rosiglitazone alleviated the symptoms of ethanol-induced hangover by inducing ALD2 expression…"

* Acetylcysteine: There are claims that N-acetylcysteine can relieve or prevent symptoms of hangover through scavenging of acetylaldehyde, particularly when taken concurrently with alcohol. Additional reduction in acetaldehyde toxicity can be achieved if NAC is taken in conjunction with vitamin B1 (thiamine).

* Food and Water: Simple consumption of foods such as eggs, which contain cysteine, and water may be enough to replenish lost moisture and at least rehydrate the body, making a hangover shorter.

* Milk, water and orange juice. The Calcium, re-hydration properties, and vitamin C contained in each product respectively is found to combat the symptoms of a hangover if taken shortly after consumption. Milk is also a dietary source of cysteine.

* According to a recent study a possible cure for a hangover is RU-21 supplement. "The Claim: It slows down the creation of a nasty by-product -- the one that causes headaches and nausea -- while speeding up the destruction of others." AOL Health

Possibly ineffective remedies

* Antipokhmelin: Also known under its tradename RU-21, it is an over-the-counter dietary supplement whose primary active ingredient is succinic acid, an extract of amber. It has been touted by internet marketers as a miracle cure for alcohol hangovers, alleged to have been produced by Soviet scientists for a KGB spy program. To-date, however, no double-blind, placebo-controlled scientific studies confirming the marketers' claims have been released.

* Globe artichoke (Cynara scolymus) extract: "Our results suggest that artichoke extract is not effective in preventing the signs and symptoms of alcohol-induced hangover."

* Artichoke and Sarsaparilla extract: A November 2004 issued U.S. Patent No. 6,824,798 states that the method described in the patent "results in complete elimination of veisalgia (hangover) in more than 80% of individuals". These plant extracts, when administered separately, do not seem to have a similar effect. The patent further states that the right combination of the extracts of both of these plants are required and that they then contain a complex of polyphenols, flavonoids, and phytosterols that are effective. However, no evidence is required for such statements to appear in a patent application or in the patent itself. The existence of a patent is merely legal evidence of intellectual property, not evidence of efficacy.

* Propranolol: "We conclude that propranolol does not prevent the symptoms of hangover."

* Fructose and glucose: A 1976 research has come to the conclusion that "The results indicate that both fructose and glucose effectively inhibit the metabolic disturbances induced by ethanol but they do not affect the symptoms or signs of alcohol intoxication and hangover." Nevertheless, consumption of honey (a significant fructose and glucose source) is often suggested as a way to reduce the effect of hangovers.

* Kudzu (Pueraria lobata): A study concluded, "The chronic usage of Pueraria lobata at times of high ethanol consumption, such as in hangover remedies, may predispose subjects to an increased risk of acetaldehyde-related neoplasm and pathology. … Pueraria lobata appears to be an inappropriate herb for use in herbal hangover remedies as it is an inhibitor of ALDH2.

Etymology

The term hangover was originally a 19th century expression describing unfinished business—something left over from a meeting—or ‘survival.’ In 1904, the meaning "after-effect of drinking too much" first surfaced.

Meningitis

Meningitis is a medical condition caused by inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. While some forms of meningitis are mild and resolve on their own, meningitis is often a potentially life-threatening condition due to the proximity of the inflammation to the brain and spinal cord. It is a medical emergency. The inflammation is usually caused by infection with bacteria, viruses or other microorganisms but also cancer, certain drugs, and other diseases.

The most common symptoms of meningitis are headache and neck stiffness, associated with fever, confusion or altered consciousness and inability to tolerate bright light (photophobia) or loud noises (phonophobia). Sometimes the only symptoms may be nonspecific, such as irritability and drowsiness. The presence of a rash may indicate particular causes, such as the non-blanching rash of meningitis caused by meningococcus bacteria. Meningitis is diagnosed by lumbar puncture, the removal with a needle of a sample of cerebrospinal fluid, the fluid that envelops the brain and the spinal cord.

Meningitis is treated promptly with antibiotics and often antiviral drugs. To prevent complications from overactive inflammation, corticosteroid drugs are given in some situations. Meningitis can lead to long-term complications such as deafness, epilepsy, hydrocephalus and cognitive deficit. Some forms of meningitis (such as those associated with meningococcus, Hemophilus influenzae type B, mumps virus or pneumococcus infections) may be prevented with immunization.

Signs and symptoms


Diagnostic features

In adults, severe headaches are the most common symptom of meningitis (87 percent) followed by nuchal rigidity ("neck stiffness", found in 83%). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever and altered mental status. All three features are present in only 44-46% of all cases of bacterial meningitis. If none of the three signs are present, meningitis is extremely unlikely. Other signs commonly associated with meningitis are photophobia (inability to tolerate bright light), phonophobia (inability to tolerate loud noises), irritability and delirium (in small children). In infants up to 6 months, bulging of the fontanelle (soft spot) may be present. Other features that might distinguish meningitis from less severe illness in young children are leg pain, cold extremities, and abnormal skin color.

Nuchal rigidity is the inability to flex the neck forward passively due to increased tone in the neck muscles. It occurs in 70% of adult cases. Other signs of meningism include Kernig's sign and Brudzinski's sign. Kernig's sign is typically assessed with the patient lying supine, with both hip and knee flexed to 90 degrees. In a patient with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary knee and hip flexion. Although commonly tested, the sensitivity of Kernig's and Brudzinski's tests are limited. They are, however, very specific: they rarely occur in other diseases. The patient may assume the "tripod position" (extending the neck, arching the spine backward and flexing knees and hips). A test known as the "jolt accentuation maneuver" is helpful in excluding meningitis in people reporting fever and headache: if the headache is not worsened by rapidly (2-3 times per second) rotating the head horizontally, meningitis is unlikely.

In "meningococcal" meningitis (i.e. meningitis caused by the bacteria Neisseria meningitidis), a rapidly spreading petechial rash is typical, and may precede other symptoms. It is not necessarily present. The rash consists of numerous small, irregular purple or red spots on the trunk, lower extremities, mucous membranes, conjunctiva, and occasionally on the palms of hands and soles of feet. The same kind of rash is rarely seen in other forms of bacterial meningitis, but may occur in meningitis due to Haemophilus bacteria (see below). Other clues to the nature of the cause may be the skin signs of hand, foot and mouth disease and genital herpes, both of which may be associated with viral meningitis.

Most people with meningitis have no obvious source for the infection. In a small proportion, there has been previous infection in the head and neck area, such as middle ear infection, or a recent trauma to the skull during which bacteria from the nasal cavity have entered the meningeal space. Those with a previously inserted cerebral shunt (a device that drains off excessive cerebrospinal fluid) or related devices (such as an extraventricular drain or Ommaya reservoir) are at increased risk of bacterial infection of these devices.

Early complications

People with meningitis may develop additional problems in the early stages of their illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature and rapid breathing. Very low blood pressure may occur early, especially but not exclusively in meningococcal illness; this may lead to insufficient blood supply to other organs. Disseminated intravascular coagulation (DIC), the excessive activation of blood clotting, may lead both to the obstruction of blood flow to organs and a paradoxical increase of bleeding risk. In meningococcal disease, gangrene of limbs can occur.

The inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves arising from the brain stem that supply the head and neck area and control eye movement, facial muscles and hearing, amongst other functions. Visual symptoms and hearing loss may persist after an episode of meningitis (see below). Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis), as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the affected area in the brain.

Seizures are common in children (30% of cases), but more unusual in adults, in whom it may indicate increasing intracranial pressure. Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-onset seizures and those that are difficult to control with medication are indicators of a poorer long-term outcome.

Causes


Infection

Meningitis is usually caused by infection with microorganisms. Most cases are due to infection with viruses (enterovirus, herpes simplex virus 2, mumps and HIV), followed by bacteria, fungi, or parasites.

Bacterial meningitis is caused by particular bacteria depending on age group. In premature babies and newborn up to three months, common bacteria are Group B streptococcus (subtype III)–especially in the first week of life–and bacteria that normally inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. Older children are more commonly affected by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in areas without vaccination, see below). Adults, too, are predominantly affected by N. meningitidis and S. pneumoniae, with increased risk of L. monocytogenes in those over 50. In trauma, neurosurgery, or other contact between the skin and the meninges, staphylococci are more likely, as well as infections with pseudomonas and related Gram-negative bacilli. The same pathogens are also more common in those with an impaired immune system. Tuberculous meningitis, meningitis due to infection with Mycobacterium tuberculosis, is more common in those from countries where tuberculosis is common, but is also encountered in those with immune problems, such as AIDS.

The term aseptic meningitis refers loosely to all cases of meningitis in which no bacterial infection can be demonstrated. This is usually due to viruses, but it may be due to bacterial infection that has already been partially treated, with disappearance of the bacteria from the meninges, or by infection in a space adjacent to the meninges (e.g. sinusitis). Endocarditis (infection of the heart valves with spread of small clusters of bacteria through the bloodstream) may cause aseptic meningitis. Aseptic meningitis may also result from infection with spirochetes, a type of bacteria that includes Treponema pallidum, the cause of syphilis, and Borrelia burgdorferi, the cause of Lyme disease. Meningitis may be encountered in cerebral malaria (malaria infecting the brain). Fungal meningitis, e.g. due to Cryptococcus neoformans is typically seen in people with immune deficiency, such as AIDS. Amoebic meningitis, meningitis due to infection with amoebae such as Naegleria fowleri, is contracted from freshwater sources.

Non-infectious

Meningitis may occur as the result of a number of non-infectious causes: spread of cancer to the meninges (malignant meningitis) and certain drugs (mainly non-steroidal anti-inflammatory drugs, antibiotics and intravenous immunoglobulins). It may also be encountered in several inflammatory conditions such as sarcoidosis (which is then called neurosarcoidosis), connective tissue disorders such as systemic lupus erythematosus, and certain forms of vasculitis (inflammatory conditions of the blood vessel wall) such as Behçet's disease. Rarely, migraine may cause meningitis, but this diagnosis is usually only made when other causes have been eliminated. Mollaret's meningitis is a syndrome of recurring episodes of meningitis; it is now thought to be caused by herpes simplex virus type 2.

Mechanism

In most cases, meningitis follows invasion of the bloodstream by organisms which live upon mucous surfaces such as the nasal cavity. This is often preceded further by viral infections. This allows organisms to invade spaces in the blood-brain barrier that lead to the subarachnoid space—such as the choroid plexus—that have been left vulnerable from prior infections. It can also develop as a result of CSF contamination of bacteria, such as by severe head trauma involving skull fractures or by congenital dural defects.

Large-scale inflammation occurs within the subarachnoid space during meningitis; however, this is not a direct result of bacterial infection but rather of the host's inflammatory pathways caused by pro-inflammatory cytokines. Upon entry to the host's central nervous system, pathogens rapidly replicate in cell walls or membrane components. Subsequently, when using antibiotics that affect the cell walls of bacteria, products can leak into the CSF. Furthermore, this causes an increased permeability to the blood-brain barrier (due to vascular endothelium injury), meningeal inflammation and cerebral vasculitis. This, when large numbers of leukocytes enter the subarachnoid space, contributes to overall edema and eventually an increased intracranial pressure (ICP). It is the increased ICP that then leads to perfusion and eventually neuronal injury and apoptosis (automated cell death).

Diagnosis

In someone suspected of having meningitis, blood tests are performed for markers of inflammation (e.g. C-reactive protein), as well as blood cultures. The most important test in identifying or ruling out meningitis, however, is analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap). If a person is at risk for a cerebral mass lesion or elevated intracranial pressure (recent head injury, a known immune system problem, localizing neurological signs, or evidence on examination of a raised ICP), a lumbar puncture may be contraindicated because of the possibility of fatal brain herniation. In such cases a CT or MRI scan is generally performed prior to the lumbar puncture to exclude these possibilities. If a CT or MRI is required before LP, or if LP proves difficult, professional guidelines suggest that antibiotics should be administered first to prevent delay in treatment, especially if this may be longer than 30 minutes. Often, CT or MRI scans are performed after the LP if not done previously to assess for complications of meningitis.

During the lumbar puncture procedure, the opening pressure is measured. A pressure between 200 and 500 mm H2O (20-50 cm) is consistent with a diagnosis of bacterial meningitis, although lower values are encountered in children. The initial appearance of the fluid may prove an indication of the nature of the infection: cloudy CSF indicates higher levels of protein, white and red blood cells and/or bacteria, and therefore may point at bacterial meningitis.

The cerebrospinal fluid (CSF) sample is examined for white blood cells (and which subtypes), red blood cells, protein content and glucose level. Gram staining of the sample may demonstrate bacteria in bacterial meningitis, but absence of bacteria does not exclude bacterial meningitis; microbiological culture of the sample may still yield a causative organism. The type of white blood cell predominantly present predicts whether meningitis is due to bacterial or viral infection. Other tests sometimes performed on the CSF sample include the latex agglutination test, the limulus lysate test and polymerase chain reaction (PCR) for bacterial or viral DNA. Apart from PCR, which is a highly sensitive and specific technique, guidelines recommend the routine use of these tests only if Gram stain and culture have not yielded a causative organism; in other circumstances they rarely lead to changes in the treatment of the patient.

In bacterial meningitis, the CSF glucose to serum glucose ratio is =<0.4; in neonates the cutoff of 0.6 is used. The Gram stain is positive in about 60% of cases; sensitivity of the Gram stain may be lower in particular infections, such as Listeria. Its sensitivity is reduced by 20% if the CSF is obtained after antibiotics have already been commenced. Cultures are more sensitive, with a reported sensitivity of 70–85%, but may take up to 48 hours to become available. Latex agglutination may be positive in meningitis due to Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli and Group B streptococci. Limulus lysates may be positive in Gram-negative meningitis. The various causes of viral meningitis may be identified by performing PCR or serology on CSF or blood for common viral causes of meningitis (enterovirus, herpes simplex virus 2 and mumps in those not vaccinated for this).[8] Diagnosis of cryptococcal meningitis requires an India ink stain of the CSF; alternatively, cryptococcal antigen may be detected in blood or CSF.

A diagnostic and therapeutic conundrum is the "partially treated meningitis", where there are meningitis symptoms after receiving antibiotics (such as for presumptive sinusitis). When this happens, CSF findings may resemble those of viral meningitis, but antibiotic treatment may need to be continued until there is definitive positive evidence of a viral cause (e.g. a positive enterovirus PCR).

Meninigitis can be diagnosed after death has occurred. The findings from a post mortem are usually a diffuse (widespread) inflammation of the pia-arachnoid area. Neutrophil leucocytes tend to have migrated to the cerebrospinal fluid and the base of the brain, along with cranial nerves and the spinal cord, may be surrounded with pus—as may the meningeal vessels.

Treatment


Initial treatment

Meningitis is a potentially life-threatening condition that has a high mortality rate if untreated; treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted. If meningococcal disease is supected in primary care, guidelines recommend that benzylpenicillin is administered before transfer to hospital. High-flow oxygen should be administered as soon as possible, along with intravenous fluids if hypotensive or in shock. Given that meningitis can cause a number of early severe complications, regular medical review is recommended to identify these complications early.

Bacterial meningitis

Empiric antibiotics must be started immediately, even before the results of the lumbar puncture and CSF analysis are known. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place. For instance, in the United Kingdom empirical treatment consists of a third-generation cefalosporin such as cefotaxime or ceftriaxone. In the USA, where resistance to cefalosporins is increasingly found in streptococci, addition of vancomycin to the initial treatment is recommended in some situations. Empirical therapy may be chosen on the basis of the age of the patient, whether the infection was preceded by head injury, whether the patient has undergone neurosurgery and whether or not there is a cerebral shunt present. For instance, in young children and those over 50 years of age, as well as those who are immunocompromised, addition of ampicillin is recommended to cover Listeria monocytogenes. Once the Gram stain results become available, it may be possible to change the antibiotics to those likely to deal with the presumed pathogen.

Once the results of the CSF analysis are known, empiric therapy may be switched to therapy targeted to the specific causative organism and its sensitivities. For instance, if the Gram stain shows H. influenzae, third generation cefalosporins are given and other antibiotics may be discontinued. The full culture and sensitivity results, which generally take longer to process, finally allow for the choice of specific antibiotics to which the pathogen has demonstrated definite sensitivty. For an antibiotic to be effective in meningitis, it must not only be active against the pathogenic bacterium, but also reach the meninges in adequate quantities; some antibiotics have inadequate penetrance and therefore have little use in meningits. Most of the antibiotics used in meningitis have not been tested directly on meningitis patents in clinical trials. Rather, the relevant knowledge has mostly derived from laboratory studies in rabbits.

Adjuvant treatment with corticosteroids (usually dexamethasone) reduces rates of mortality, severe hearing loss and neurological damage in adults, specifically when the causative agent is Pneumococcus. The use of corticosteroids has been proven in adults as well as in children from high-income countries. Their use in children from low-income countries is not supported by evidence. In adults, professional guidelines recommend the commencement of dexamethasone or a similar corticosteroid just before the first dose of antibiotics are given, and continued for four days. Given that most of the benefit of the treatment is confined to those with pneumococcal meningitis, American guidelines suggest that dexamethasone is discontinued if another cause for meningitis is identified. In tuberculous meningitis, there is a strong evidence base for treatment with corticosteroids, although this evidence is restricted to those without AIDS.

Other infections

Viral meningitis typically requires supportive therapy only, and tends to run a more benign course than bacterial meningitis. Most viruses responsible for causing meningitis are not amenable to specific treatment. Herpes simplex virus and varicella zoster virus may respond to treatment with antiviral drugs such as acyclovir, but there are no clinical trials that have specifically addressed whether this treatment is effective. Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of highly dosed antifungals, such as amphotericin B and flucytosine.

Complications


In children there are several potential disabilities which result from damage to the nervous system. These include sensorineural hearing loss, epilepsy, diffuse brain swelling, hydrocephalus, cerebral vein thrombosis, intra cerebral bleeding and cerebral palsy. Acute neurological complications may lead to adverse consequences. In childhood acute bacterial meningitis deafness is the most common serious complication. Sensorineural hearing loss often develops during the first few days of the illness as a result of inner ear dysfunction, but permanent deafness is rare and can be prevented by prompt treatment of meningitis.

Those who contract the disease during the neonatal period and those infected by S. pneumoniae and gram negative bacilli are at greater risk of developing neurological, auditory, or intellectual impairments or functionally important behaviour or learning disorders which can manifest as poor school performance.

In adults central nervous system complications include brain infarction, brain swelling, hydrocephalus, intracerebral bleeding; systemic complications are dominated by septic shock, adult respiratory distress syndrome and disseminated intravascular coagulation. Those who have underlying predisposing conditions e.g. head injury may develop recurrent meningitis. Case-fatality ratio is highest for gram-negative etiology and lowest for meningitis caused by H. influenzae (also a gram negative bacilli). Fatality for those over 60 years of age is more likely to be from systemic complications e.g. pneumonia, sepsis, cardio-respiratory failure; however in younger individuals it is usually associated with neurological complications. Age more than 60, low Glasgow coma scale at presentation and seizure within 24 hours increase the risk of death among community acquired meningitis.

Recurrent bacterial meningitis

Recurrent bacterial meninigitis may be caused by anatomical defects, either congenital or acquired, or by disorders in immune mechanisms. Anatomic defects are ususally those which allow continuity between the external environment and the nervous system, ususally with leakage of cerebrospinal fluid (which can be gross or mild, depending upon the defect). Skull fractures are the most common cause of recurrent meningitis, particularly those which affect the base of the brain, or those extending towards the sinuses and petrous pyramids.

Recurrent infections due to immune response may occur after a splenectomy, or in other conditions affecting the immune system. Leukemias and lymphomas have particularly high incidences of recurrent bacterial meningitis. When recurrent bacterial meningitis is caused by the same species of bacteria, it is likely to have been caused by inadequete therapy or resistence of the organism to previous treatment. A review of 363 reported cases of recurrent meningitis showed that 59% of cases occur due to anatomical abnormalities, 36% due to immune deficiencies, and 5% due to ongoing infectious in areas adjacent to the meninges.

Epidemiology

Meningitis occurs in localised outbreaks, whose scale depends on several factors including amount of contact with other people and varies seasonally. People with weaker immune systems are more susceptable, but during large epidemics Meningitis can affect any age group. In temperate climates winter and spring increase the number of cases.

In the area in sub-Saharan Africa stretching from Senegal to Ethiopia (largely coinciding with the Sahel region), large epidemics of meningococcal meningitis occur in the dry season, leading to it being labelled the Meningitis Belt. These outbreaks occur in a cyclic fashion, due to herd immunity from vaccinations, and have localised infection rates of up to 1 in 100 people.

The largest epidemic outbreak was in 1996, when over 250,000 cases occurred and 25,000 people died as a consequence of the disease.

Prevention


Immunization

Vaccinations against Haemophilus influenzae (Hib) have decreased early childhood meningitis significantly.

Vaccines against type A and C Neisseria meningitidis, the kind that causes most disease in preschool children and teenagers in the United States, have also been around for a while. Type A is also prevalent in sub-Sahara Africa and W135 outbreaks have affected those on the Hajj pilgrimage to Mecca. Immunisation with the ACW135Y vaccine against four strains is now a visa requirement for taking part in the Hajj.

Vaccines against type B Neisseria meningitidis are much harder to produce, as its capsule is very weakly immunogenic masking its antigenic proteins. There is also a risk of autoimmune response, and the porA and porB proteins on Type B resemble neuronal molecules. A vaccine called MeNZB for a specific strain of type B Neisseria meningitidis prevalent in New Zealand has completed trials and is being given to many people in the country under the age of 20 free of charge. There is also a vaccine, MenBVac, for the specific strain of type B meningococcal disease prevalent in Norway, and another specific vaccine for the strain prevalent in Cuba.[citation needed] Novartis has conducted preliminary clinical trials of a meningococcus type B vaccine in Britain with encouraging results.

Pneumococcal polysaccharide vaccine against Streptococcus pneumoniae is recommended for all people 65 years of age or older. Pneumococcal conjugate vaccine is recommended for all newborns starting at 6 weeks - 2 months, according to American Academy of Pediatrics (AAP) recommendations.

Mumps vaccination has led to a sharp decline in mumps virus associated meningitis, which prior to vaccination occurred in 15% of all cases of mumps.

Prophylaxis

In cases of meningococcal meningitis, prophylactic treatment of close relatives with antibiotics (e.g. rifampicin, ciprofloxacin or ceftriaxone) may reduce the risk of further cases.

Tension headache

Tension headaches, which were renamed tension-type headaches by the International Headache Society in 1988, are the most common type of primary headaches. The pain can radiate from the neck, back, eyes, or other muscle groups in the body. Tension-type headaches account for nearly 90% of all headaches. Approximately 3% of the population suffers from chronic-tension type headache.

Frequency and duration


Tension-type headaches can be episodic or chronic. Episodic tension-type headaches are defined as tension-type headaches occurring fewer than 15 days a month, whereas chronic tension headaches occur 15 days or more a month for at least 6 months. Tension-type headaches can last from minutes to days, months or even years, though a typical tension headache lasts 4-6 hours.

Pain and possible symptoms


Tension-type headache pain is often described as a constant pressure, as if the head were being squeezed in a vise. The pain is frequently bilateral which means it is present on both sides of the head at once. Tension-type headache pain is typically mild to moderate, but may be severe.

Cause and pathophysiology


Various precipitating factors may cause TTH in susceptible individuals . One half of patients with TTH identify stress or hunger as a precipitating factor .

* Stress - Usually occurs in the afternoon after long stressful work hours
* Sleep deprivation
* Uncomfortable stressful position and/or bad posture
* Irregular meal time (hunger)
* Eyestrain
* Caffeine withdrawal

The exact cause of tension-type headaches is still unknown. It is suggested that abnormalities in the peripheral and central nervous systems may be involved in the pathophysiology of TTH. It has long been believed that they are caused by muscle tension around the head and neck. One of the theories says that the main cause for tension type headaches and migraine is teeth clenching which causes a chronic contraction of the temporalis muscle. Although muscle tension may be involved, scientists now believe there is not one single cause for this type of headache. Another theory is that the pain may be caused by a malfunctioning pain filter which is located in the brain stem. The view is that the brain misinterprets information, for example from the temporal muscle or other muscles, and interprets this signal as pain. One of the main molecules which is probably involved is serotonin. Evidence for this theory comes from the fact that chronic tension-type headaches may be successfully treated with certain antidepressants such as amitriptyline. However, the analgesic effect of amitriptyline in chronic tension-type headache is not solely due to serotonin reuptake inhibition, and likely other mechanisms are involved. Recent studies of nitric oxide (NO) mechanisms suggest that NO may play a key role in the pathophysiology of CTTH.. The sensitization of pain pathways may be caused by or associated with activation of nitric oxide synthase (NOS) and the generation of NO. Patients with chronic tension-type headache have increased muscle and skin pain sensitivity, demonstrated by low mechanical, thermal and electrical pain thresholds. Hyperexcitability of central nociceptive neurons (in trigeminal spinal nucleus, thalamus, and cerebral cortex) is believed to be involved in the pathophysiology of chronic tension-type headache. Recent evidence for generalized increased pain sensitivity or hyperalgesia in CTTH strongly suggests that pain processing in the central nervous system is abnormal in this primary headache disorder. Moreover, a dysfunction in pain inhibitory systems may also play a role in the pathophysiology of chronic tension-type headache.

Treatment


Episodic tension-type headaches generally respond well to over-the-counter analgesics, ibuprofen having been found more effective in providing relief than paracetamol/acetaminophen in controled studies. Other medications for chronic tension-type headaches include amitriptyline mirtazapine, biofeedback, and sodium valproate (as prophylaxis).

Botulinum toxin is a treatment trialled by some tension-type headache sufferers, though results are varied. There are some reports of Botulinum toxin having the opposite effect, increasing tension.

Acupuncture has not been demonstrated as an effective treatment for tension headaches.

Prognosis


Tension headaches that do not occur as a symptom of another condition may be painful, but are not harmful. It is usually possible to receive relief through treatment. Tension headaches that occur as a symptom of another condition are usually relieved when the underlying condition is treated. Frequent use of pain medications in patients with tension-type headache may lead to the development of medication overuse headache or rebound headache.


NEW
-
TREATMENTS FOR HEADACHES - THE BRAIN TO BODY CONNECTION
MIGRAINE HEADACHES- CERVICOGENIC HEADACHES - MUSCLE TENSION HEADACHES - POST-TRAUMATIC HEADACHES - CLUSTER HEADACHES
UPPER CERVICAL CHIROPRACTIC
ORANGE COUNTY
"BLAIR CHIROPRACTOR"

CHIROPRACTOR RANCHO SANTA MARGARITA, MISSION VIEJO, LAKE FOREST

Back Pain, Neck Pain, Scoliosis, Headaches, Nagging Injury, Complaints of Fatigue, Reoccurring Illnesses or Disabilities, Specific Traumas, Work Related Injuries, Auto Accidents Injuries, Sports Injuries, Whiplash, Neck Pain, Low Back Pain, Arm Pain, Spasms, Leg Pain, Carpel Tunnel, Sciatica, Asthma, Disc Insury, Muscle Spasms, Foot Pain, Ankle Pain, Allergies, Numbness, Pinched Nerves
(949)589-9962
Free Estimates - Call Us Today!
HEADACHES, FATIGUE, BACK AND NECK PAIN
Email: Begin@UpperCervicalChiropracticOrangeCounty.com

"CHANGE - I have come from a place which I no longer wish to reside. I can sense and see the person I could be. I have tasted the virtues of change, growth, and service. I am no longer satisfied with just a taste or a morsel... I see a full and everlasting life of joy and prosperity. I see the mantle of greatness, accountability, and responsibility." - Michael P. Watson

UPPER CERVICAL CHIROPRACTIC ORANGE COUNTY
UPPER CERVICAL BLAIR CHIROPRACTOR RANCHO SANTA MARGARITA, CHIROPRACTIC
Serving Locally : RANCHO SANTA MARGARITA, MISSION VIEJO, LAKE FOREST, PORTOLA HILLS
SAN JUAN CAPISTRANO, IRVINE, NEWPORT BEACH
, LAGUNA BEACH, DANA POINT, SAN CLEMENTE
MY FRIENDLY HEADACHE SPECIALIST
HEADACHES ORANGE COUNTY - HEADACHE TREATMENT IN ORANGE COUNTY - BEST HEADACHE TREATMENTS - HEAD ACHES ORANGE COUNTY, (949)589-9962, Orange County Headache, MIGRAINE HEADACHES- CERVICOGENIC HEADACHES - MUSCLE TENSION HEADACHES - POST-TRAUMATIC HEADACHES - CLUSTER HEADACHES, best headache treatments, rancho santa margarita headache, irvine headache, mission viejo headache, san juan capistrano headache, Laguna Beach Headaches, Leisure World Headaches, Laguna Woods headaches, Laguna Niguel Headaches, Costa Mesa Headaches, San Clemente Headaches, Aliso Viejo Headaches, Huntington Beach Headaches, anaheim headache, garden grove headache, buena park headache, fullerton headache, la palma headache, cypress headache, orange headache, Ladera Ranch headache, Coto De Caza headache, Dove Canyon headache, Tustin headache, Dana Point headache, Newport Beach headache, Balboa Island headache, Newport Coast headache, Huntington Beach headache, Brea headache, Anaheim Hills headache, Santa Ana headache, Seal Beach headache, Fountain Valley headache, El Toro headache, Villa park headache, Garden Grove headache,chronic headache, headache specialist orange county, headache help

The Orange County Southern California area which includes the following:
Anaheim 92801, 92802, 92803, 92804, 92805, 92806, 92807, 92808, 92809, 92812, 92814, 92815, 92816, 92817, 92825, 92850, 92899, Brea 92821, 92822, 92823, Buena Park 90620, 90621, 90622, 90623, 90624, Costa Mesa 92626, 92627, 92628, Cypress 90630, Fountain Valley 92708, 92728, Fullerton 92831, 92832, 92833, 92834, 92835, 92836, 92837, 92838, Garden Grove 92840, 92841, 92842, 92843, 92844, 92845, 92846, Huntington Beach 92605, 92615, 92646, 92647, 92648, 92649, La Habra 90631, 90632, 90633, La Palma 90623, Los Alamitos 90720, 90721, Orange 92856, 92857, 92859, 92861, 92862, 92863, 92864, 92865, 92866, 92867, 92868, 92869, Placentia 92870, 92871, Santa Ana 92701, 92702, 92703, 92704, 92705, 92706, 92707, 92708, 92711, 92712, 92725, 92728, 92735, 92799, Seal Beach 90740, Stanton 90680, Tusin 92780, 92781, 92782, Villa Park 92861, 92867, Westminister 92683, 92684, 92685, Yorba Linda 92885, 92886, 92887, Aliso Viejo 92653, 92656, 92698, Dana Point 92624, 92629, Irvine 92602, 92603, 92604, 92606, 92612, 92614, 92616, 92618, 92619, 92620, 92623, 92650, 92697, 92709, 92710, Laguna Beach 92607, 92637, 92651, 92652, 92653, 92654, 92656, 92677, 92698, Laguna Hills 92637, 92653, 92654, 92656, Laguna Niguel 92607, 92677, Laguna Woods 92653, 92654, Lake Forest 92609, 92630, Mission Viejo 92675, 92690, 92691, 92692, 92694, Newport Beach 92657, 92658, 92659, 92660, 92661, 92662, 92663, Rancho Santa Margarita 92688, San Clemente 92672, 92673, 92674, San Juan Capistrano 92675, 92690, 92691, 92692, 92693, 92694 Ladera Ranch 92694, Coto De Caza 92679 Anaheim Hills 92807, 92808, 92809, 92817 Dove Canyon 92679 Oceanside, CA:92049, 92051, 92052, 92054, 92055, 92056, 92057, 92058, San Diego, 92101, 92102, 92103, 92104, 92105, 92106, 92107, 92108, 92109, 92110, 92111, 92112, 92113, 92114, 92115, 92116, 92117, 92118, 92119, 92120, 92121, 92122, 92123, 92124, 92126, 92127, 92128, 92129, 92130, 92131, 92132, 92133, 92134, 92135, 92136, 92137, 92138, 92139, 92140, 92142, 92143, 92145, 92147, 92149, 92150, 92152, 92153, 92154, 92155, 92158, 92159, 92160, 92161, 92162, 92163, 92164, 92165, 92166, 92167, 92168, 92169, 92170, 92171, 92172, 92173, 92174, 92175, 92176, 92177, 92178, 92179, 92182, 92184, 92186, 92187, 92190, 92191, 92192, 92193, 92194, 92195, 92196, 92197, 92198, 92199


Call US Today! (949)589-9962

Alfred W. Tomp, DC 30372 Esperanza, Rancho Santa Margarita, CA 92688

This Business was Awarded - Top 100 Best in Business, Orange County CA, Visit: OrangeCountyCABusinessDirectory.com

There is no deadlier poison than Words, There is no greater healer than words. EWB