Download Headache - Shanyar

Dr. Hawar Adnan Mykhan
M.B.Ch.B., F.I.B.M.S
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 Headache is caused by traction, displacement, inflammation,
vascular spasm, or distention of the pain-sensitive structures in
the head or neck.
 Isolated involvement of the bony skull, most of the dura, or
most regions of the brain parenchyma does not produce pain.
 Patients can be divided into those with chronic headache (a
duration of several weeks or more) and those with more acute
headache.
 Serious acute neurological disease should always be considered
in patients with headaches of very sudden onset.
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Pain-Sensitive Structures Within the Cranial Vault
 Venous sinuses (eg, sagittal sinus).
 Anterior and middle meningeal arteries.
 Dura at the base of the skull.
 trigeminal (V), glossopharyngeal (IX), and vagus (X)
nerves.
 Proximal portions of the internal carotid artery and its
branches near the Circle of Willis.
 Brainstem periaqueductal gray matter.
 Sensory nuclei of the thalamus.
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Extracranial Pain-Sensitive Structures
 The skin; the subcutaneous tissues, muscles, and arteries.
 Neck muscles.
 Periosteum of the skull.
 Second and third cervical nerves.
 The eyes, ears, teeth, sinuses, and oropharynx.
 The mucous membranes of the nasal cavity.
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International Classification of Headache
 The Primary Headaches
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Migraine.
Tension-type headache.
Trigeminal autonomic cephalalgias.
Primary stabbing headache.
Primary cough headache.
Primary exertional headache.
Primary coital headache: preorgasmic and orgasmic headache.
Hypnic headache.
Primary thunderclap headache.
Hemicrania continua.
New daily-persistent headache.
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 The Secondary Headaches
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Headache attributed to head and/or neck trauma.
Headache attributed to cranial or cervical vascular disorder.
Headache attributed to nonvascular intracranial disorder.
Headache attributed to substance or its withdrawal.
Headache attributed to infection.
Headache attributed to disorder of homeostasis.
Headache or facial pain attributed to disorder of cranium, neck,
eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial
structures.
 Headache attributed to psychiatric disorder.
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Warning Signs Of Serious Conditions In Patients
With Headache
 Red Flags
 New onset or new type or worsening pattern of existing
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headache.
New level of pain (e.g., worst ever).
Abrupt onset.
Triggered by Valsalva maneuver, cough or exertion.
Triggered by sexual activity: preorgasmic or orgasmic.
Headache during pregnancy or puerperium.
Age > 50 years.
Neurological signs: Seizures, Confusion, Impaired alertness,
Weakness or Papilledema.
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 Pain associated with local tenderness, such as of the
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temporal artery.
Systemic illness: Fever, Nuchal rigidity, Weight loss or
Scalp artery tenderness.
Secondary risk factors: Cancer and Immunocompromised
host.
 Yellow Flags
Wakes patient from sleep at night.
Postural headaches.
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Thunderclap headache
 Severe hyperacute (<30 s) explosive headache, sudden and
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unexpected like a clap of thunder,
Very severe pain intensity.
Headache may occur spontaneously or be precipitated by
Valsalva maneuver, sexual activity, or exercise.
Investigation is always required to rule out secondary causes.
Neuroimaging: CT to exclude subarachnoid hemorrhage; if
negative, proceed to CSF examination to look for blood,
xanthochromia; opening pressure.
If CT, CSF are normal, then additional investigations to look
for an unruptured intracranial aneurysm are unwarranted.
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Causes
Primary
 Coital.
 Exersional.
 Cough.
Secondary
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Subarachnoid hemorrhage.
Cerebral venous sinus thrombosis.
Intracranial or subdural hematoma.
Cervical artery dissection.
Pituitary apoplexy.
Acute hypertensive crisis.
Colloid cyst of the third ventricle.
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Tension-type Headache
 This is the most common type of headache.
 The pain is usually constant and generalised but often radiates
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forward from the occipital region.
It is described as 'dull', 'tight' or like a 'pressure', and there may
be a sensation of a band round the head or pressure at the
vertex.
In contrast to migraine, the pain may continue for weeks or
months without interruption, although the severity may vary,
and there is no associated vomiting or photophobia.
The pain is characteristically less severe in the early part of the
day and becomes more troublesome as the day goes on.
Typically, the headache is reported to be poorly responsive to
ordinary analgesia.
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Management
 Excessive use of analgesics, particularly of codeine, may
actually worsen the headache (analgesic headache).
 Physiotherapy (with muscle relaxation and stress
management) is usually beneficial, but low-dose
amitriptyline (10 mg nocte increased gradually to 30-50
mg) may be necessary.
 There is evidence that patients benefit from a perception
that their problem has been taken seriously and rigorously
assessed, but over-investigation can worsen a patient's
anxiety.
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Tension-type Headache
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Migraine
 The second most common cause of headache; afflicts 15% of
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women and 6% of men.
Onset is usually in childhood, adolescence, or early adulthood;
however, initial attack may occur at any age.
Family history is often positive.
The classic triad of premonitory auras (visual scotoma or
scintillations), unilateral throbbing headache, nausea and
vomiting happens in “classical migraine” ……25%
Other auras include tinnitus, sensory change, weakness, ataxia
or dysphasia.
Most of the patients do not have visual aura and are therefore
referred to as having “common migraine.”
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 Photo- and phonophobia are common in migraine patients.
 Vertigo may occur.
 Focal neurologic disturbances without headache or vomiting
(migraine equivalents) may also occur.
 An attack lasting 4–72 h is typical, as is relief after sleep.
 Attacks may be triggered by wine, cheese, chocolate,
contraceptives, stress, exercise, hunger, lack of sleep or travel.
 The brain of the migraineur seems more sensitive to stimuli
and to change; and this is even more notably amplified in
females during their menstrual cycle.
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 The patient with migraine does not habituate to sensory stimuli
easily.
 They may have headache when they or their environment alters
the patterns of:
 Sleep too little or too much;
 Eating skipping meals, or alcohol in particular;
 Stress excess stress or in the relaxation phase;
 Physical activity such as exertion;
 Weather stormy or barometric pressure change;
 Hormonal environment such as the menstrual cycle;
 Afferent stimulation such as bright lights or loud sounds.
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Treatment
 Treatment of an acute attack consists of simple analgesia with
aspirin or paracetamol, often combined with an antiemetic such
as metoclopramide or domperidone.
 Long-term use of codeine-containing analgesic preparations
should be avoided.
 Severe attacks can be treated with one of the 'triptans' (e.g.
sumatriptan), 5-HT agonists that are potent vasoconstrictors of
the extracranial arteries and can be administered orally,
sublingually, by subcutaneous injection or by nasal spray.
 Drugs used for prophylaxis include beta blocker, tricyclics,
anticonvulsants, serotonergic drugs, and calcium channel
blockers .
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Migraine
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Cluster Headache
 This is less common than migraine with a 3:1 males predominance,
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and the onset is usually in the third decade.
The characteristic syndrome comprises periodic, severe, unilateral
periorbital pain accompanied by unilateral lacrimation, nasal
congestion and conjunctival injection, often with the other features
of Horner's syndrome.
The pain, whilst being very severe, is characteristically brief (30-120
minutes).
Typically, the patient develops these symptoms at a particular time of
day (often in the early hours of the morning).
The syndrome may occur repeatedly for 8–10 weeks, followed by a
respite for a number of months before another cluster occurs.
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Management
 Acute attacks are usually halted by subcutaneous injections of
sumatriptan and inhalation of 100% oxygen.
 Other migraine therapies are ineffective, probably because of
the brevity of the individual attacks.
 Preventative therapy with the agents used for migraine is often
ineffective but attacks can be prevented in some patients by
verapamil (80-120 mg 8-hourly), methysergide (4-10 mg daily,
for a maximum of 3 months only) or short courses of
corticosteroids.
 Patients with severe and debilitating clusters can be helped
with lithium therapy, although the usual precautions concerning
the use of this drug should be observed.
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Cluster Headache
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Trigeminal Neuralgia
 This condition causes lancinating pains in the second and
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third divisions of the trigeminal nerve territory, usually in
patients over age 50 years.
The pain is severe and very brief but repetitive, causing
the patient to flinch as if with a motor tic; hence the
French term for the condition, 'tic douloureux'.
The pain may be precipitated by touching trigger zones
within the trigeminal territory or by eating.
There are no other signs.
There is a tendency for the condition to remit and relapse
over many years.
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Management
 The pain usually responds to carbamazepine.
 In patients who cannot tolerate carbamazepine; gabapentin,
Lamotrigine, phenytoin or baclofen may be effective.
 Various surgical treatments are available; the simplest is the
injection of alcohol or phenol into a peripheral branch of the
nerve.
 Probably more effective is the percutaneous placing of a
radiofrequency lesion in the nerve near the Gasserian ganglion.
 Alternatively, the vascular compression of the trigeminal nerve
can be relieved through a small posterior craniotomy, often
with substantial success.
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Trigeminal Neuralgia
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Giant Cell Arteritis
 Is the most common primary vasculitis affecting those over 50
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years.
Typically, the extracranial branches of the aorta are involved,
with intracranial involvement much more rarely.
Headache is the most common symptom.
Other symptoms include jaw claudication and scalp tenderness.
Constitutional symptoms are present in at least one-third of
cases as this condition overlaps with polymyalgia rheumatica
(weight loss, fever and myalgia).
Blindness is the most common serious neurological sequel and
can present with either monocular (or bilateral) or
homonymous visual loss.
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 Stroke is another complication and is preferentially
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affecting posterior cerebral artery.
Affected arteries feel thickened, pulseless and cord-like,
commonly the superficial temporal artery.
The ESR is almost always raised as is the CRP; anaemia is
present in two-thirds of cases with a leucocytosis and
raised transaminases in one-third.
Temporal artery biopsy is the most specific tool of
diagnosis.
Treatment is with high dose steroid to prevent blindness.
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Giant Cell Arteritis
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