NEUROPSYCHIATRIC ASPECTS OF HEADACHE

 Headache is one of the most common human afflictions. It is the condition that most
often leads people to seek medical advice.
 Because headache is commonly associated with psychiatric syndromes,
Psychiatrists are often consulted for the evaluation and treatment of people suffering
from headache.
 The most frequent primary headache syndromes are migraine, tension-type headache, and cluster
headache. The other headache subtypes described in the IHS system are secondary to a variety of
acute and chronic conditions.

MIGRAINE

Epidemiology:
 Epidemiological studies have shown that approximately 60 percent of the general population
reports a history of severe headaches. Milder headaches are reported by about 80 percent of the
general population.
 Migraine without aura and tension-type headache are the most common headache syndromes in the
general population.
 The lifetime prevalence of migraine derived from systematic population surveys is about 12
percent.
 Migraine is more common among women and persons between the ages of 20 and 45 years, with
the incidence decreasing after the fourth decade of life.
 Migraine may often begin in childhood when boys and girls are equally likely to suffer from
migraine headache.
 Migraine in childhood is more likely to be associated with gastrointestinal complaints, particularly
episodic bouts of stomach pain, vomiting, or diarrhea, and the duration is shorter than that
commonly observed in adults.
 In women, migraine is strongly associated with reproductive system function, with increased
incidence during puberty and the first trimester of pregnancy; migraine is also associated with
exogenous hormone use. After menopause, the frequency of migraine attacks generally decreases
dramatically, unless estrogen replacement therapy is administered.
 A family history of migraine is one of the most potent and consistent risk factors for migraine.
However, approximately 30 percent of migraine patients have no family history of this condition.
 Migraine is strongly associated with a variety of medical disorders, particularly asthma, allergies,
and cardiovascular disease.
 Comorbid psychiatric conditions include mood disorders (particularly the bipolar subtype),
phobias, and panic disorders.
 The course of migraine is variable. In general, the frequency and duration of migraine decrease at
midlife in both men and women, and the symptomatic manifestations may change substantially
over time.

Clinical presentation:
 Migraine is a complex debilitating condition characterized by either the presence or absence of aura
symptoms.
 Migraine presentation is multifaceted and symptoms emanate from multiple systems, including
vascular, neurological, gastrointestinal, endocrine, and visual manifestations. These symptoms may
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 be accompanied by a variety of changes in behavior and cognition, including mood alterations and
confusion.
 The core features of most definitions of migraine include recurrent headache, accompanied by
gastrointestinal symptoms such as nausea or vomiting, and hyperesthesia manifested by
photophobia or phonophobia.
 The headache generally has a pulsatile or throbbing quality exacerbated by routine physical activity
involving movement of the head, and is often unilateral.
 The new classification of migraine by the IHS no longer includes the common-classic distinction;
instead migraine is subtyped according to the presence or absence of aura symptoms (reversible
neurological dysfunction).
 Approximately 20% of people with migraines experience aura. Aura typically occurs between 5
and 30 minutes before the onset of migraine and is characterized by several symptoms, including
numbness or a pins-and-needles sensation in the head and alterations in the head and alterations in
auditory, olfactory, speech and visual senses.
 A recent study suggests a higher risk of cerebral infarction among migraine sufferers than in
controls.

Migraine without aura:

A. At least 5 attacks fulfilling criteria B – D.

B. Headache attacks lasting 4 – 72 hours (untreated or unsuccessfully treated)
C. Headache has at least 2 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 headache, at least one of the following:
1. nausea and/or vomiting
2. photophobia and phonophobia
E. Not attributed to another disorder.

Migraine with aura:

A. At least 2 attacks fulfilling criteria B – D.

B. Aura consisting of at least one of the following but no motor weakness:
1. fully reversible visual symptoms, including positive features (e.g., flickering lights, spots,
or lines) and/or negative features (i.e., loss of vision)
2. fully reversible sensory symptoms, including positive features (i.e., pins and needles) and/or
negative features (i.e., numbness).
3. fully reversible dysphasic speech disturbance.
C. At least two of the following:
1. homonymous visual symptoms and/or unilateral sensory symptoms
2. at least one aura symptom develops gradually over 5 or more minutes and/or different aura
symptoms occur in succession over 5 or more minutes.
3. each symptoms lasts 5 or more minutes and less than or equal to 60 minutes.

D. Headache fulfilling criteria B – D for migraine without aura begins during the aura or follows the
aura within 60 minutes.
E. Not attributed to another disorder.
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Etiology:
 The causes of the major types of headaches are still unknown.
 Migraine is believed to result from a combination of external trigger factors such as hunger,
sensory input, and hormonal fluctuations that activate serotonin and norepinephrine-containing
neurons in the brainstem.
 This activation alters the physiology of neurons, glia, and blood vessels, which provokes pain and
generates neuroinflammatory mediators in the brainstem, thalamus, cerebral cortex, and supporting
tissues.
 The activation of sensory vascular terminals within the blood vessel walls releases substance P and
other neuropeptides that trigger a sterile inflammatory process, causing prolonged pain.

Treatment:
 The mainstay of migraine treatment is pharmacological intervention.
 Treatment of migraine can be prophylactic, with medication taken daily; abortive, with medication
taken at the onset of an attack; or palliative, with medication taken after the pain has begun.
 The US Headache Consortium has identified the following goals of the long-term migraine
treatment:
 Reduce attack frequency and severity
 Reduce disability
 Improve quality of life
 Prevent headache
 Avoid headache medication escalation
 Educate and enable patients to manage their disease.
 There are also a variety of nonpharmacological approaches to reduce headache. These include
eliminating the triggers of attacks; maximizing the regularity of daily schedule, particularly with
respect to sleeping and eating habits; biofeedback; and relaxation treatment.
Symptomatic relief:
 The nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, naproxen, and
indomethacin and the analgesics aspirin and acetaminophen are commonly used as first-line
treatment of mild to moderate migraine.
 In 1998 the Food and Drug Administration (FDA) approved an acetaminophen-aspirin-caffeine
formulation (Exedrin) for the treatment of migraine.
 Other classes of drugs that are commonly prescribed for more severe attacks include ergot
derivatives, serotonin agonists, and narcotics. Combination agents generally comprised of
barbiturates, analgesics, and caffeine are also highly effective in the treatment of migraine
episodes.
 Ergotamine tartrate and dihydroergotamine (DHE) are two of the most commonly prescribed ergot
derivatives for moderate to severe attacks of migraine. In order to counterbalance the common
adverse effect of nausea, metoclopramide or prochlorperazine are recommended.
 The triptans are 5-HT 1D agonists that have been used for acute migraine. They act through
vasoconstriction to reduce the acute migraine attack. Triptans in current use include Sumatriptan,
Zolmitriptan, Naratriptan, Rizatriptan, Almotriptan, Eletriptan and Frovatriptan.
 Triptans compound in general are safe, but because they cause vasoconstriction they should be
avoided in individuals with vascular diseases.
Prophylaxis for migraine:
 Prophylactic treatment should be considered in patients:
 Who experience frequent, debilitating attacks on less than a monthly basis, particularly if
attacks occur more than twice a week.
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  Who miss a substantial amount of work or school due to headache (more than 3 days a
month)
 With comorbid disorders such as depression, anxiety or epilepsy.
 Who have had not success with acute treatments.
 Most of the migraine prophylaxis trials have shown that no agent has succeeded in reducing
migraine attacks or severity by more than 50%.
 There are several major classes of drugs that have been investigated in the prophylaxis of migraine
headaches. These include the ß – blockers, antidepressants, calcium channel blockers and
anticonvulsants. ß – blockers and calcium channel blockers have also been widely used to prevent
migraine.
 The ß – blockers are currently the most popular treatment of choice in migraine prophylaxis.
However, the effect of this class of drugs is moderate at best.

TENSION-TYPE HEADACHE

 Tension headache is characterized by episodes of bilateral pain lasting several days at a time.
 It is distinguished from migraine headache by its generally longer duration, the lack of pulsating
quality of the pain, the lack of worsening with physical activity, and the absence of gastrointestinal
concomitants. However, migraine and tension-type headache may often coexist, either
simultaneously or alternating over time.
 Tension-type headache is no longer believed to result from muscle tension; indeed, neck pain may
result from head movement to reduce headache pain.

Frequent episodic tension-type headache:

A. At least 10 episodes occurring on >1 but <15 days per month for at least 3 months and fulfilling
criteria B – D .
B. Headache lasting 30 minutes to 7 days.
C. Headache that ahs at least 2 of the following characteristics:
1. bilateral location
2. pressing/tightening (nonpulsatile) quality
3. mild or moderate intensity
4. not aggravated by routine physical activity such as walking or climbing stairs.
D. Both of the following:
1. no nausea or vomiting (anorexia may occur)
2. absence of photophobia and phonophobia.

Chronic tension-type headache:

A. headache occurring on > 15 days per month on average for more than 3 months and fulfilling
criteria B – D.
B. headache that lasts hours and may be continuous.
C. Headache that has at least 2 of the following characteristics:
1. bilateral location
2. pressing/tightening (nonpulsatile) quality
3. mild or moderate intensity
4. not aggravated by routine physical activity such as walking or climbing stairs.
D. Both of the following:
1. no more than one of photophobia, phonophobia or mild nausea
2. neither moderate or severe nausea nor vomiting.
E. Not attributed to another disorder
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Epidemiology:
 Compared to studies of migraine, far fewer studies have investigated the epidemiology and risk
factors associated with tension-type headache.
 The prevalence of tension-type headache has been estimated to range from approximately 30 to 80
percent depending on the definitions used.
 It is difficult to estimate the true prevalence of tension-type headache given that migraine and
tension-type headaches may co-occur in the same individual.
 Tension-type headaches are also more common in women and young adults, but there is a less
steep decrement in prevalence with age.
Etiology:
 Far less is known about the etiology of tension-type headache. It is clear however, that the term
tension-type headache is a misnomer because there is no evidence that muscle tension is the
underlying cause of this headache subtype.

Treatment:
 Treatment of tension-type headache may be either pharmacological or nonpharmacological,
depending on the frequency and severity of headaches.
 Nonpharmacological approaches such as biofeedback, massage, relaxation, cervical traction,
chiropractic manipulation, hot packs, and cold packs have all been reported to be effective,
although there are no convincing guidelines to suggest one modality over another.
 Similar to the short-term treatment of migraine, analgesics and the NSAIDs are the first-line
treatment for tension-type headache.
 It is important to note that symptoms of tension-type headache may arise iatrogenically from drugs
such as ergotamine used to treat migraine, often as a result of overuse of the drug. Up to 40 percent
of chronic headache cases are associated with overuse of drugs intended to alleviate headache.
 The treatment of chronic tension-type headache is similar to that of migraine; the most commonly
used drug treatment for chronic tension-type headache is the tricyclic drug amitriptyline (100 to
150 mg per day).

CLUSTER HEADACHE:

 Cluster headache is a distinct syndrome characterized by frequent attacks (often several per day)
over a 1- to 2-month period, separated by headache-free intervals for as long as 1 or 2 years.
 Cluster refers to a “clustering in time,” with the headache bouts occurring every day to several
times a day over a period of days to weeks, followed by a lengthy headache-free interval.
 Cluster headache is generally retro-orbital in location and is accompanied by autonomic changes
such as lacrimation, rhinorrhea, erythema of the eye, and agitation.
 Patients with cluster headache do not retire to dark rooms and lie down to avoid the stimulation;
they may do quite the opposite, appearing almost manic in their agitation.
 The pain can be so intense that the sufferer may appear to be psychotic because of the screaming
and thrashing that may be associated with the pain.
 Chronic paroxysmal hemicrania is a type of cluster headache that is specifically responsive to
treatment with indomethacin and characterized by many daily focal attacks of pain, each lasting for
about 15 or 20 minutes.

Epidemiology:

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  Cluster headache has a very low population prevalence (less than 1 percent of the general
population) and occurs nearly exclusively in males.
 The age at onset of cluster headache is somewhat later than that of migraine and tension-type
headache; the first attack of cluster usually begins in the late 20s or 30s and may recur
intermittently throughout life; risk factors include smoking and heavy alcohol use.

Diagnostic criteria:
A. At least 5 attacks fulfilling criteria B – D.
B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15 – 180 minutes
if untreated.
C. Headache is accompanied by at least one of the following:
1. ipsilateral conjunctival injection and/or lacrimation
2. ipsilateral nasal congestion and/or rhinorrhoea
3. ipsilateral eyelid edema
4. ipsilateral forehead and facial sweating
5. ipsilateral miosis and/or ptosis
6. a sense of restlessness or agiatation.
D. Attacks have a frequency from one every other day to eight per day
E. Not attributed to another disorder.

Etiology:
 Current theory of the cause of cluster headache holds that hypothalamic and central pain control
regions trigger a cascade of events in the brainstem comprising afferent pain and efferent
parasympathetic pathways.

Treatment:
 Prophylactic medicine is almost always indicated for treating cluster headache because of the
extreme severity of pain induced by an acute attack, which often occurs at night.
 Inhaled oxygen, narcotics, and self-injected dihydroergotamine and sumatriptan are the most
commonly used agents for the treatment of acute attacks.
 Medications that have been shown to be effective in preventing attacks of cluster headache are
lithium, the corticosteroids, methysergide, the calcium channel inhibitors and valproic acid,
combinations of these agents are often necessary to achieve success.
 Histamine desensitization and surgical intervention are options on exhaustion of traditional agents.

POSTTRAUMATIC HEADACHE:
 Posttraumatic headache is variable in symptom presentation, severity, and duration.
 The key symptoms include a headache following head trauma and accompanied by a loss of
consciousness, posttraumatic amnesia, and abnormal laboratory tests.
 Although headache following a traumatic head injury has often been attributed to emotional
factors, empirical evidence suggests that emotional factors are more likely to be sequelae rather
than causes of posttraumatic headache.

Etiology:
 Nevertheless, the etiology of posttraumatic headache is unknown.
 The major hypotheses of the pathogenesis of posttraumatic headache include cerebral edema,
cortical spreading depression, innate vulnerability to cerebral vasospasm, and transient elevation of
intracranial pressure.

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  There is no direct relationship between the prevalence or chronicity of posttraumatic headache and
several indicators of severity of head injury including duration of unconsciousness, posttraumatic
amnesia, electroencephalographic abnormalities, presence of skull fracture, or the presence of
blood in the cerebrospinal fluid. There appears to be an inverse relationship between the severity of
the head injury and the development of postinjury headache.

Epidemiology:
 Although posttraumatic headache is quite rare in the general population, it is not uncommon among
those with a history of a concussion or head injury.
 Children and young adults appear to be particularly susceptible to developing headache after head
trauma.
 Persistence of headache has been related to female sex; age over 45; the presence of dizziness; lack
of skull fracture; intracranial hematoma; disorders of smell, hearing, or vision; depression; and
impaired concentration.

Diagnostic criteria:
A. Headache, no typical characteristics known, fulfill criteria C and D.
B. Head trauma with at least one of the following:
1. loss of consciousness for > 30 minutes
2. Glasgow Coma Scale score <13
3. posttraumatic amnesia for more than 48 hours.
4. imaging demonstration of a traumatic brain lesion (cerebral hematoma, intracerebral and/or
subarachnoid hemorrhage, brain contusion and/or skull fracture)
C. Headache develops within 7 days after head trauma or after regaining consciousness after head
trauma.
D. Headache persists for more than 3 months after head trauma

Treatment:
 Posttraumatic headache is often treated on an emergency basis but long-term posttraumatic
headache is commonly encountered in psychiatry.
 Steroids are often given immediately subsequent to the acute injury, and diagnostic imaging will
reveal the presence of skull fracture or subdural hematoma.
 NSAIDS are the most commonly prescribed agents for headache that persists beyond the acute
injury; thereafter, the prophylactic treatment approaches to migraine can be implemented.