Headache

PowerPoint Presentation By Dr.P.L.John Israel



COMMON CAUSES

• Viral Rhinitis (Common Cold)• Sinusitis • Fevers• Hypertension• Refractive Error• Tension Headache• Hypoglycemia• Post ictal headache


SPECIFIC CAUSES

• Migraine Headache

• Cluster Headache

• Temporal Arteritis

• Post traumatic Headache

• Thunderclap Headache (Subarachnoid Haemorrhage)


Specific Causes Contd..

• Intracerebral Haemorrahage • Subdural Haematoma• Brain Abscess• Primary Brain Tumor• Metastatic Brain Tumor• Meningitis • Hydrocephalus• Glaucoma


BRAIN• Seat of intelligence• By itself is not sensitive to pain but the

adjacent structures protect the brain to make sure that the brain is safe.

• Headache is like an alerting signal• Face and scalp are richly supplied by pain

receptors than other parts of the body in order to protect the precious contents of the skull

• Also the nasal, oral passages , eye and ear all are delicate and highly sensitive structures which reside here and must be protected


CRANIAL STRUCTURES SENSITIVE TO PAIN

• The scalp• Scalp blood supply• Head and neck muscles• Great venous sinuses• Arteries of the meninges• Larger cerebral arteries • Pain –sensitive fibers of the fifth, ninth and tenth

cranial nerves• Parts of the dura mater at the base of the brain


• Migraine occurs commonly in – Females – 70% – Males – 30%

• Cluster Headache occurs almost entirely in men – 90%

• Tension Headache seen equally in both sexes


Location of Headache

• Hemicranial

• Bi-Temporal

• Occipital

• Frontal

• Peri-Orbital

• Vertex


Nature of Headache

• Constant

• Paroxysmal

• Lancinating

• Throbbing



MIGRAINE HEADACHE

• Familial Disorder characterised by periodic, Commonly unilateral , often pulsa tile headache.

• Age of onset– Begins in childhood , adolescents in early

adult life and diminishes in frequency and severity during advancing years. (Typically begins in teenage years and seldom begins after 40yeras of age)


TYPES

• Classic Migraine or Neurologic Migraine– Is characterised by aura

• Common Migraine– Migraine without aura

• Ratio – Classic Migraine : Common Migraine

1 : 5


CLASSIC MIGRAINE

• Prodrome :– Occurs hours to days before headache and consists

of change in mood, behavior, apetite and cognition.

• Aura :– Occurs within 1 hour of headache, and is most

commonly visual or sensory – Visual Aura

• Most Common• Consist of photopsias, bright flashing lights, scintillating

scotomas, field cuts and fortification spectra (zigzag lines / Teichopsia)


– Sensory Auras• Next most common feature • Characterized by numbness or paresthesiae in a limb

– Motor Weakness and aphasia are less common

• HEADACHE– Often unilateral (Hemicranial in 60% of ages) and

throbbing in nature– Follows aura with in 60minutes and lasts 4 – 72 hrs – Is associated with

• nausea,• vomiting • Photophobia (aversion to light)• Phonophobia (aversion to sound)


– Headache may be relieved after vomiting – Is aggravated by strain, routine physical

activity or rapid movement of the head– Some relief with pressure on temporal vessels– Strong Family History (80%)

• Migraine attacks come once or twice per month, or three tp four times per year

• There is a strong association with menstruation in females


• Common Migraine– Symptoms are similar to classic migraine but there

are no aura

• Precipitating factors– Foods rich in tyramine (Cheese, redwine)– Foods containing monosodium glutamine (Chinese

and Mexican foods)– Foods containing Nitrates (Cold cuts – bologna,

salami, smoked meats)– Pickled,fermented,marinated foods (pasta salads)– Alcoholic beverages (especially red wine)– Caffeinated beverages (soft drinks, tea and coffee)


ETIOPATHOGENESIS OF MIGRAINE

• VASCULAR THEORY– Vascular Theory of Migraine states that the

migraine aura is due to cerebral vaso constriction and that the migraine itself is caused by vasodilatation

– Cerebral blood flow is decreased during migraine with aura but there is no changes in blood flow during migraine without aura – Controversial


• ROLE OF SEROTONIN– 90% in GI Tract– 10% distributed in the brain and platelets– During Migraine attack, serotonin levels in the

blood may decrease where as urinary concentration may increase.

– This shift in serotonin level may trigger changes in blood vessels and blood flow and also alter pain perception in the brain.


• ROLE OF SEROTONIN– Serotonin may thus play a role in the cause of

migraine– Amtriptyline, nortryptyline & sumatriptan which

have an effect on serotonin metabolism are therefore useful in migraine headache.


• SUBSTANCE - P– The intra and extra cranial vessels are

innervated by small unmyelinated fibers derived from trigeminal nerve and subserve both pain and autonomic function.

– Activation of these fibers releases substance P and other peptides into the vessel valve.

– The peptides dilate the cerebral vessels and increase there permeability causing a throbbing headache.


Nitric Oxide

Nitric Oxide generated by endothelial cells has been

implicated as the cause of pain in migraine headache.


BASILAR MIGRAINE

• Basilar artery or vertebra basilar migraine – Less common form – Prominent brain symptoms – Seen usually in young women with a family history of

migraine– Have visual aura and may even develop temporary

cortical blindness– There may be associated vertigo, staggering, inco-

ordination of limbs, dysarthria and tingling both hands and feet and around the mouth


BASILAR MIGRAINE contd…..

– Exceptionally there can be period of coma or quadriplegia .

– The symptoms lost 10-30minutes followed by headache which may be occipital

– Some patients at the onset of headache may faint, or become confused or stuporous and this stage may persist for several hours or longer.


Ophthalmoplegic Migraine

• Characterised by recurrent unilateral headaches associated with weakness of extra ocular muscles

• Transient 3rd nerve palsy with ptosis with or without involvement of the pupil is the usual picture.

• 6th nerve is early effected common in children • Paresis may persist even after headache for

days to weeks.• Occasionally opthalmoparesis may remian

permanent.


Retinal Migraine or Ocular Migraine

• Characterised by retinal or optic nerve ischemia.• There may be retinal haemorrhages or

narrowing of retinal venules during and attack.• Mono ocular blindness, disc edema may occur

and vision recovers only partially after several months.

• The retinal or ciliary circulation may be involved.


Post Traumatic Migraine

• Occurs following trivial head injury there may be loss of sight, headache confusion for hours or days before recovering

• In others there may be hemiparesis or aphasia


Abdominal Migraine

• Seen in young children

• Instead of complaining of headache the child appears limp and pale and complains of abdominal pain.

• There may be vomiting and fever

• There may also be disturbances in mood along with abdominal pain.


Hemiplegic Migraine

• The infant, child or adult has episodes of hemiparesis that may outlast the headache.

• Has autosomal dominant trait with a family history (familial hemiplegic migraine).


Complicated Migraine Or

Migranous Infarction• Here the temporary nerologic symptom of

migraine headache may remain permanent • Ex : A Homonymous visual field defect • Platelet aggregation, edema of the arterial wall

increased coagulability of blood, intense prolonged spasm of vessels have all been implicated in the pathogenesis of arterial occlusion and strokes that complicate migraine


• In children with mitochondrial disease (MELAS- Mitochondrial Myopathy- Encephalopathy Lactic Acidosis and Stroke like Episodes)

• And in adults with rare vasculopathy

(CADASIL – Cerebral Autosomal Dominant Arteriopathy

with Subcortical Infarcts and Leuko Encephalopathy), Migraine is prominent feature


STATUS MIGRAINOSUS

• Continuous migraine with unilateral throbbing and disabling headache.

• May follow head injury or viral headache.


Premenstrual / Menstrual Migraine

• Is thought to be due to withdrawal of estrogens.

• Migraine attacks tend to cease during pregnancy in 75-80% of patients

• Oral contraceptive pills or associated with increased frequency and severity of migraine and may be even be associated with permanent neurologic deficit.


FOOTBALLERS MIGRAINE

• Sudden jarring of the head may precipitate the migraine attack in susceptible footballers


TREATMENT OF MIGRAINE

•Treatment of Acute Attack (Primary treatment)

•Prophylactic treatment


Treatment of Acute attack(Primary Treatment)

• Mild attack of migraine– Acetaminophen– NSAIDS

• Severe attack– Ergot alkaloids:

• Ergotamine /Dihydroergotamine (DHE)• Best given at the on set of attack

– Is an α adrenergic agonist with a strong serotonin receptor affinity and has a vasoconstrictor action.


– Available as oral, sublingual, injectable and inhalation forms

• 1 – 2mg every half an hour (Dose ) Sublingual or to be swallowed

• Maximum dose (8mg)

– A Single dose of promethazine (Phenergan) 50mg or Metaclopramide (Reglan) 20mg given along with ergotamine relaxes the patient and allays nausea and vomiting.

– Caffeine 100mg is thought on slim evidence to potentiate the effects of ergot and other medications for migraine

– Reduces headache in 70-75% of patients.


5HT Receptor Agonists

• Sumatriptan – Is effective at stopping acute attack of migraine

headache– Can be given subcutaneously 6mg– As intranasal spray 20mg– Or orally 50-100mg– Provide relieve in 70% patients.

• Side Effects– Chest tightness & flushing – Should not be used concomitantly with

ergotamines or inpatients with heart disease


Other 5HT Receptor Agonists

• Zolmitriptan 2.5 to 5mg

• Rizatriptan 10mg– Doses can be repeated if needed in 2hrs


MIDRIN

• Is a combination medication that consists of dichloralphenazone (a muscle relaxant), isometheptene (a vasospasm agent) and acetaminophen.

• May be used as abortive therapy (2tabs with onset of headache) and one tab every hour after that, up to 5 tabs total.

• As prophylaxis ( 1tab 2-3times per day)


Prophylactic Treatment

• When headache occur at frequency of 2-3 per month the following drugs have been effective of prophylactic agents– Beta –Blockers

• Inderal – 20mg TID can increase up to 240mg /day• Atenolol – 40 to 160mg/day • Timolol - 20 to 40 mg /day• Metoprolol – 100 to 200 mg /day


• Sodium valproate - 500mg/day (upto 1000mg /day)

• Calcium channel blockers– Verapamil - 180 to 240mg /day– Nifedepine - 30 mg /day

• Tricyclic Antidepressants (Amitriptyline,Imipramine) – Amitriptyline – 25mg HS – OD increase upto

200mg/day (increase 25mg /week)– Side effects

• Dry mouth• Constipation• Urinary hesitancy• Sedation• Weight gain,


• Methysergide– Serotonin agonist , vasoconstrictor. Highly effective

for primary treatment but has side effects on prolonged use (Retroperitoneal fibrosis, Pulmonary fibrosis)

– Dose : 2 to 6 mg/day

• Other Drugs– Clonidine – 0.5mg TID/day– Cyproheptadine – 4 to 16mg /day– Flunarazine – 5 to 10mg/day– Indomethacin – 150 to 200mg /day


CLUSTER HEADACHE

• Also known has – Paroxysmal nocturnal cephalalgia– Migrainous neuralgia– Histamine cephalalgia – Red Migraine– Erythromelalgia of the Head


CLUSTER HEADACHE

• So called because these headaches occur during a short time span.

• The cluster then recurs periodically.• A typical cluster of headaches may last 4-8weeks with 1-

2 headaches/day during the cluster.• Patient may be free 6months to 1year before another

cluster of headache occurs.• They may be distinctly seasonal.• Young adult Men (20-50 yrs age) are more affected then

women • Male to Female ratio 5:1


SYMPTOMS

• Abrupt onset of headache originating in the eye and spreading over the temporal area.

• Pain extremely severe and last 20-60minutes

• The headache associated with – Nasal stuffiness – Rhinorrhoea– Redness of the Eye– Flush and edema of the cheek


SYMPTOMS

– There may also be partial Horner’s Syndrome with ptosis and miosis on the side of The Head pain. These autonomic phenomena are similar to those elicited by local action of histamine and was therefore previously called Horton’s Histamine Headaches

– These headaches are usually nocturnal, between 1-2hrs after the onset of sleep are several times during the night and day not associated with aura or vomiting. The headache recurs with remarkable regularity each day for periods that last over 6-12weeks


CAUSE AND MECHANISM OF CLUSTER HEADACHE

• Not clear

• Probably due to paroxysmal parasympathetic discharge mediated through the greater superficial petrosal nerve and sphenopalatine ganglion


CLUSTER MIGRAINE

• These persons have characteristics of both migraine headache as well as cluster headache


TREATMENT

• Ergotamine 2mg at bedtime• Inhalation of 100% oxygen for 10 – 15min at

onset of the headache• Intranasal lidocaine or sumatriptan• Methysergide 2-8 mg/day• Prednisolone - 75mg / day for 3days and then

taper the dose• Verapamil – upto 480mg /day • Lithium – 600 to 900mg/day (blood level of

lithium must be between 0.7 to 1.2 meq/Lt)• Indomethacin – 75 to 200mg /day


PowerPoint Lecture Presented by Dr.P.L.John Israel

Prof & HOD , Department of Internal Medicine

Education

Headache