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Headache

This document summarizes different types of headaches, migraines, and facial pains. It describes tension headaches, migraines (including classical, common, basilar, hemiparetic, ophthalmoplegic, and facioplegic migraines), cluster headaches, episodic paroxysmal hemicrania, atypical facial pain, and giant cell arteritis. For each type, it discusses mechanisms, clinical patterns, management, and differential diagnosis. Migraines are the most common and have unclear genetic and vascular mechanisms, while cluster headaches cause excruciating unilateral pain and giant cell arteritis causes facial pain worse with eating due to external carotid artery inflammation.

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Marwan M.
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217 views4 pages

Headache

This document summarizes different types of headaches, migraines, and facial pains. It describes tension headaches, migraines (including classical, common, basilar, hemiparetic, ophthalmoplegic, and facioplegic migraines), cluster headaches, episodic paroxysmal hemicrania, atypical facial pain, and giant cell arteritis. For each type, it discusses mechanisms, clinical patterns, management, and differential diagnosis. Migraines are the most common and have unclear genetic and vascular mechanisms, while cluster headaches cause excruciating unilateral pain and giant cell arteritis causes facial pain worse with eating due to external carotid artery inflammation.

Uploaded by

Marwan M.
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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HEADACHE, MIGRAINE AND FACIAL PAIN

1. Tension headache
Is generated by neurovascular irritation and referred to scalp muscles and soft
tissues, although the exact pathogenesis remains unclear. Tight band sensations,
pressure behind the eyes, throbbing and bursting sensations are common. What is
clear is that almost all headaches with these features are benign.
Precipitating factors such as worry, noise, concentrated visual effort or fumes.
Depression is also a frequent co-morbid feature. Tension headaches are often
attributed to cervical spondylosis, refractive errors or high blood pressure:
evidence for such associations is poor. Headaches also follow even minor head
injuries. Tenderness and tension in neck and scalp muscles are the only physical
signs. Analgesic overuse is a prominent cause of headache.
Management

 explanation (imaging is often needed)


 avoiding evident causes, e.g. bright lights
 analgesic withdrawal
 physical treatments - massage, ice packs, relaxation
 antidepressants - when indicated
 Drugs for recurrent headache/migraine.

2. Migraine
Migraine is recurrent headache associated with visual and gastrointestinal
disturbance. Over 20% of any population report migrainous symptoms; in 90%,
these began before 40 years of age.
Mechanisms
Remain unclear. Genetic factors play some part - a rare form of familial migraine
is associated with mutation in the voltage-gated calcium channel on chromosome
19.
The pathophysiology is thought to involve changes in the brainstem blood flow
which have been found on PET scanning during migraine attacks →unstable
trigeminal nerve nucleus and nuclei in the basal thalamus → release of calcitonin-
related peptide (CGR8), substance P and other vasoactive peptides → neurogenic
inflammation →pain, and vasodilation of cerebral and dural vessels → headache.
Cortical spreading depression is also proposed as a mechanism for the aura.
Some patients recognize precipitating factors:

1. weekend migraine (a time of relaxation)


2. chocolate (high in phenyl ethylamine)
3. cheese (high in tyramine)
4. noise and irritating lights
5. Association with premenstrual symptoms.

Migraine is common around puberty, at the menopause and sometimes increases


in severity or frequency with hormonal contraceptives, in pregnancy and
occasionally with the onset of hypertension or following minor head trauma.
Migraine is not suggestive of any serious intracranial lesion. However, since
migraine is so common, an intracranial mass and migraine sometimes occur
together by coincidence.
Clinical patterns
Migraine attacks vary from intermittent headaches to discrete episodes. Distinction
between variants is somewhat artificial. Migraine can be separated into phases:

 well-being before an attack (occasional)


 prodromal symptoms
 the main attack - headache, nausea, vomiting
 Sleep and feeling drained afterwards.

1. Migraine with aura (classical migraine)


Prodromal symptoms: usually visual and related to depression of visual cortical
function or retinal function. Unilateral patchy scotomata (retina), hemianopic
symptoms (cortex), teichopsia (flashes) and fortification spectra are common.
Transient aphasia sometimes occurs, with tingling, numbness, vague weakness of
one side and nausea. The prodrome persists for a few minutes to about an hour.
Headache then follows. This is occasionally hemicranial (i.e. splitting the head)
but often begins locally and becomes generalized. Nausea increases and
vomiting follows. The patient is irritable and prefers the dark. Superficial scalp
arteries are engorged and pulsating. After several hours the migraine settles,
sometimes with a diuresis. Deep sleep often ensues.
2. Migraine without aura (common migraine)
This is the usual variety. Prodromal visual symptoms are vague. There is a
similar headache often accompanied by nausea and malaise.
3. Basilar migraine
Prodromal symptoms: circumoral and tongue tingling, vertigo, diplopia, transient
visual disturbance (even blindness), syncope, dysarthria and ataxia. These occur
alone or progress to a typical migraine.
4. Hemiparetic migraine
This rarity is classical migraine with hemiparetic features, i.e. resembling a stroke,
but with recovery within 24 hours. Exceptionally, cerebral infarction occurs.
5. Ophthalmoplegic and facioplegic migraine
These rarities are 3rd, 6th or 7th nerve palsy with a migraine.
Differential diagnosis
May resemble SAH or the onset of meningitis. Hemiplegic, visual and
hemisensory symptoms must be distinguished from thromboembolic TIAs. In
TIAs maximum deficit is present immediately and headache is unusual.
Unilateral tingling or numbness may resemble sensory epilepsy (partial seizures).
In epilepsy, distinct march (progression) of symptoms is usual.
Management
General measures include: explanation and avoidance of dietary factors-rarely
helpful
Patients taking hormonal contraceptives may benefit from a brand change, or
trying without. Depot oestrogens are sometimes used. Severe hemiparetic
symptoms are a potential reason to stop hormonal contraceptives. Premenstrual
migraine sometimes responds to diuretics. At the start of the attack give
Paracetamol or other analgesics with an antiemetic if necessary. Repeated use of
analgesics leads to further headaches. Triptans (5HT1 agonists) sometimes
aborting an attack effectively. Triptans should be avoided when there is vascular
disease, and not overused.
Prophylaxis.
The following are used continuously when attacks are frequent:

 pizotifen (5HT antagonist) 0.5 mg at night for several days, increasing to


1.5 mg (common S.Es are weight gain and drowsiness)
 propranolol 10 mg three times daily, increasing to 40-80 mg three times
daily
 Amitriptyline 10 mg (or more) at night.

Sodium valproate, methysergide, SSRIs, verapamil, topiramate, nifedipine and


naproxen are also used. Gap junction blockers are being used in trials.
Other benign headaches: Often resolve spontaneously.

 Ice-cream headache. Retropharyngeal head pain lasting for a few seconds


or minutes following very cold foods.
 Primary cough headache. No underlying cause is found but intracranial
pathology should be excluded. For severe headache, A L.P with removal of
CSF can help.
 Primary low CSF volume headaches, seen typically on standing up. The
patient may give a history of a vigorous Valsalva (straining or orgasm).
May arise spontaneously. Secondary low CSF volume can follow L.P.
 Primary sex headache typically rise to a crescendo at orgasm, largely in
males. Exceptionally occur with an unruptured intracranial aneurysm.
 Post-traumatic headache is also a common problem.

Facial pain
The face has many pain-sensitive structures: teeth, gums, sinuses,
temporomandibular joints, jaw and eyes. Facial pain is also caused by specific
neurological conditions.
Cluster headache
Describes recurrent bouts of excruciating unilateral pain that typically wake the
patient. Attacks cluster around one eye. Cluster headache affects adults, mostly
males aged between 30 and 40. Alcohol sometimes provokes an attack. During an
attack, changes in the hypothalamus appear on MRI and PET. Presumed to be
due to activation of the trigeminal-vascular and autonomic systems. Severe
pain rises to an even worse crescendo over some minutes, lasting for several hours.
Vomiting can occur. One cheek and nostril become congested. Transient
ipsilateral Horner's syndrome is common. One bout of cluster attacks, with pain
every few nights, usually lasts one to two months. Despite excruciating pain there
are no sequelae. Bouts recur at intervals over several years but tend to disappear
after the age of 55.
Management.
Analgesics are unhelpful. Subcutaneous sumatriptan is the drug of choice.
Oxygen inhalation sometimes aborts an attack. Most prophylactic migraine
drugs are unhelpful. Verapamil, topiramate, lithium carbonate and/or a short
course of steroids sometimes help bring to an end a bout of cluster headaches.
Episodic Paroxysmal hemicrania(trigeminal autonomic cephalalgia type II)
Is a rare condition describing unilateral sudden, brief (<20 min) pains with some
characteristics of cluster headache. Paroxysms can occur many times each day;
typically they respond to Indometacin.
Atypical facial pain
Is seen in the elderly, mainly in women.TCAs are sometimes helpful.
Other causes of facial pain
Giant cell arteritis (temporal arteritis; cranial arteritis)
These are granulomatous arteritides seen almost exclusively in people over 50.

1. Headache is almost invariable in (GCA). Pain develops over inflamed


superficial temporal and/or occipital arteries. Arterial pulsation is soon lost;
the artery becomes hard, tortuous and thickened. The scalp over inflamed
vessels may become red. Rarely, gangrenous patches appear.
2. Facial pain. In the face, jaw and mouth due to inflammation of facial,
maxillary and lingual branches of the external carotid artery. Pain is
characteristically worse on eating (jaw claudication). Mouth opening and
protruding the tongue become difficult. A painful, ischaemic tongue occurs
rarely.
3. Visual problems. Visual loss occurs in 25% of untreated cases. Posterior
Ciliary artery occlusion causes anterior ischaemic optic neuropathy in
75%of these (the disc becomes swollen and pale; retinal branch vessels
usually remain normal). Other mechanisms are central retinal artery
occlusion (sudden permanent unilateral blindness, disc pallor and visible
retinal ischaemia), cilioretinal artery occlusion and posterior ischaemic
optic neuropathy. There is sudden monocular visual loss (partial or
complete), usually painless. Amaurosis fugax may precede permanent
blindness. Bilateral blindness may develop, with the second eye being
affected in 1-2 weeks.
4. Rare complications. Brainstem ischaemia, cortical blindness, ischaemic
microangiopathic neuropathy of peripheral or cranial nerves, and
involvement of the aorta, coronary, renal and mesenteric arteries
sometimes occurs.

Management
The ESR is greatly elevated. The diagnosis should be established immediately by
superficial temporal artery biopsy, because of the risk of blindness. Immediate
high doses of steroids (prednisolone, initially 60-100 mg daily) should be started
in a patient with typical features, even before biopsy. Since the risk of visual loss
persists, long-term treatment is recommended, for some years at least.

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