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Headache
Dr Mohamed Rizk Khodair
Lecturer of neurology
October 6 Universirty
Mohamedrizk.med@o6u.edu.eg
Approach to patient with headache & facial pain
Headache or cephalalgia: it is the pain in the head from the orbit back to the sub
occipital region.
Facial pain: pain elsewhere in the face .
Pathophysiology of headache & facial pain: Headache is caused by traction, compression,
inflammation, or distention of the pain-sensitive structures in the head or neck.
NB: The brain itself is insensitive to the pain.
Brain sensitive structures
Extracranial
Within cranial vault
Skin and Periosteum of skull
Arteries of circle of wills
SC (tissue, muscles , arteries )
Arteries of meninges (dura ,
arachnoid , pia )
Upper 3 cervical A.
Brainstem periaqueductal grey
matter and sensory nuclei of
thalamus
Eye, ear, teeth , TMJ , sinuses
Cranial Ns 1 ,2 ,5 ,9, 10
Dura (especially at the base)
Venous sinuses
Headache classification
Secondary headache
Primary headache
- Related to underlying medical condition
- Represent about 10% of cases
- Life threating
-Not related to underlying medical conditions
- Represent about 90% of cases
- Not a life threating
Types:
-Headache attributed to head trauma
- Headache attributed to systemic disorder (HTN)
-Headache attributed to cranial or cervical disorders
-Headache attributed to a substance or its withdrawal
-Headache attributed to disorders of eyes, ears, tooth, sinuses (referred
headache )
-Headache attributed to inflammation (trigeminal neuralgia)
Types:
-Migraine and its subtypes
-Tension headache (most common)
-Cluster headache
Red flags
Criteria of serious headache: (red flags) (SNOOP)
-Systemic signs and disorders.
-Neurological symptoms (focal or global neurological symptoms).
-Onset new , sudden, or changed & patient > 50 years old.
-Onset in thunderclap presentation.
-Papilledema, pulsatile tinnitus, positional provocation, precipitated by
exercise.
Migraine
• Paroxysmal disorder characterized by throbbing headache (usually unilateral)
associated with autonomous manifestations (e.g., nausea, vomiting…) and may be
proceeded by visual, sensory, or motor manifestations.
• Migraine is extremely common, affecting 12% of the population: 18% of women
and 6% of men (more common in females due to hormonal changes ).
Migraine Theories & pathophysiology
1. Trigmeno-vascualr theory
• The trigeminovascular system (TVS) is thought to comprise neurons
located in the trigeminal ganglion that innervate the cerebral vasculature
including the dura mater.
• Afferent fibers, mainly from the first or ophthalmic division of the
trigeminal nerve, project from these areas to the ganglion neurons and
these neurons have centrally projecting axons to the trigeminal nucleus.
• Several neurotransmitters and neuropeptides [e.g., calcitonin gene-
related peptide (CGRP) and neurokinin-1] are produced in the ganglion
neurons that may modulate pain transmission and vascular tone.
• In migraine, releasing of CGRP at vascular terminals of trigeminal nerve
and trigeminal nucleus causes blood vessels in head to swell and it
produces inflammation around the brain leading to activation of
trigeminal pain pathway.
2.Neurovascular theory:
Migraine triggers → over excitation of trigeminal N. axons → release of vasoactive neuropeptides → VD
and sterile inflammation
3.Serotonin theory (5-HT ) :
 Initially: increasing of plasma serotonin → VC of cerebral B.Vs Aura
 Later: subsequent drop in plasma serotonin → VD of B. Vs headache of migraine
NB: serotonin drugs play an important role in treatment of
migraine:
- During attack (headache = VD): use serotonin agonist
drugs (to induce VC and relive the pain)
- In between the attacks (prophylaxis): use serotonin
antagonist (to prevent VC)
4. Dopamine theory:
Abnormal dopaminergic stimulation (increasing of dopamine or hypersensitivity of dopamine
receptors) → headache and associated manifestations (nausea, vomiting)
5.Ca+2 uptake theory (Hypoxic Theory):
Focal cerebral hypoxia associated with rapid entry of Ca into brain cells and smooth muscle of
Blood Vessel → VC followed by reactive VD.
Migraine triggers
 Hormonal changes (period, pregnancy,
menopause)
 Diet (chocolate, cheese, caffeine, nuts,
smoking, alcohol)
 Drugs (vasodilators as nitrates)
 Sensory (flickering light, strong smells as
perfume, noise)
 Change in lifestyle (dehydration, stress,
sleep pattern, exertion, weather changes)
Types of migraine
Classic Migraine: migraine with aura (15 %)
Common Migraine: migraine without aura (85 %)
Hemiplegic Migraine: headache associated with temporary unilateral hemiparesis or hemiplegia
Basilar Migraine: patient presented with vertebrobasilar symptoms as: vertigo, ataxia, confusion, dysarthria, incoordination.
Ophthalmoplegic Migraine: associated with transient paralysis of extraocular MS and ophthalmoplegia.
Facial Migraine: associated with transient facial paralysis
Variants
Clinical picture: (for classic migraine)
A. Prodroma:
 From 12 to 36 hours before Aura and headache.
 Symptoms include constipation, mood change, food craving, neck stiffness, thirst, frequent yawing
B. Aura:
 Immediately before attack
 Develop over 5 -20 min and last less than 60 min
 Include visual symptoms as scotomas, flashes of light (most common)
 Sensory and motor disturbance as weakness (hemiparesis), dysphasia, parathesia, olfactory, visual, or gustatory hallucinations.
C. Headache:
 Site: usually unilateral (start in the temple or around the eye)
 Type: pulsatile or throbbing pain (moderate to severe)
 Duration: 4 to 72 hours
 Increased by exercise, light, movement
 Decreased by sleep and rest
 Associated by nausea, vomiting, photophobia, phonophobia
D. Post headache:
 After headache Patient may have fatigue, polyuria, weakness, confusion
Clinical criteria of migraine
Diagnosis
A) Medical history
B) Headache diary
C) Migraine triggers
D) Investigations (for 2ry causes): as
EEG, CT brain, MRI, CRP, ESR …
Treatment of Migraine
During attack:
Acute treatment aims to stop or prevent the progression of a headache or reverse
a headache that has started ask patient to relax in a dark quit room and try to
sleep.
Goals of acute treatment:
1. Rapid treatment.
2. Minimize recurrence.
3. Restore ability to function.
4. Minimize use rescue medications.
5. Optimize self-care.
6. Reduce use of resources.
7. Cost effectiveness.
8. Minimal or no adverse events
a. Analgesics:
 Paracetamol (1 gm), aspirin (900-1200 mg ), Ibuprofen (400-800mg ), diclofenac (25-50mg)
b. Triptans:
 Mechanism of action:
- Triptans are Serotonin receptor agonists, Stimulation of the 5-HT1B receptors on smooth muscle cells of blood vessels causes cranial
vasoconstriction
- Blocks effects of Calcitonin Gene-Related Peptide (CGRP).
 Side effects:
-Chest discomfort, throat heaviness.
-Paraesthesias in UL, LL, head, or neck.
-Anxiety, mild difficulty breathing.
-Sumatriptan, zolmitriptan, and rizatriptan are primarily metabolized by monoamine oxidase (MAO) and should be avoided in patients
taking MAO-A inhibitors.
 Contraindications:
- ICD, CV disease, Uncontrolled HTN, PVD , liver disease, pregnancy
 Triptans oral doses:
- Sumatriptan (Imitrex) 50 -100 mg
- Almotriptan (Axert) 12.5 mg
- Frovatriptan (Frova) 12.5 mg
- Zolmitriptan (Zomig) 2.5 -5 mg
C. Ergots:
 Used in migraine specially in patient intolerant to triptans.
 Mechanism of action: The ergot alkaloids are nonspecific 5-HT
agonists and vasoconstrictors (partial agonists or antagonists at
adrenergic, dopaminergic and tryptaminergic receptors).
 Used for migraine are related to the effects on smooth muscle. The
drugs constrict arteries and veins by direct stimulation of cerebral
vascular smooth muscle.
 Orally: Ergotamine, 1 mg, 2 tablets once.
 Ergotamine 1 mg + Caffeine 100 mg (added caffeine will enhance
absorption of ergotamine & potentiate its VC effect)
D.Dopamine Antagonists:
 METOCLOPRAMIDE (orally, IV)
 Adjunctive therapy in an acute attack of migraine.
 Relieves associated nausea & vomiting (antiemetic effect).
In between attack (prophylaxis):
Indication of prophylactic therapy
A. Avoid Migraine triggers:
 As diet (e.g., alcohol, Caffeine overuse or caffeine withdrawal, Chocolate, aged cheese, Aspartame (NutraSweet), bananas, and
nuts); drugs (oral contraceptives, vasodilators).
B. Beta-Blockers:
 Most widely used preventive medication class.
 50% effective in producing> 50% reduction in attack frequency.
 As Propranolol 80- 240 mg/d (atenolol, metoprolol, timolol, nadolol also effective).
 Inhibit nitric oxide production (propranolol).
 It decreases effect of adrenaline lead to decrease VD of cerebral vessels
C. Serotonin Antagonists:
 Pizotifen 0.5 mg tds.
 Methysergide: 1 mg tds.
 Amitriptine
D. Calcium Channel Antagonists:
 Mechanism of Action:
- Block 5-HT release.
- Block calcium dependent "enzymes involved in prostaglandin formation.
- Interfere with propagation of spreading depression.
 Verapamil most useful, flunarizine.
 Nicardipine and nifedipine are not recommended.
E. Antiepileptic drugs
 Topiramate, valproic acid.
Status Migrainous
It’s a migraine attacks that persist for longer than 72 hours despite treatment.
Clinical picture
 Headache-free periods for less than 4 hours may occur
 Usually associated with prolonged use of analgesics.
Treatment
 Hospitalization, fluid replacement, electrolytes imbalance correction
 Suppression of vomiting (metoclopramide, chlorpromazine)
 IV dihydroergotamine
 Dexamethasone or prednisolone, IV Na valproate, or levetiracetam.
Cluster headache
Definition
Neurological disorder characterized by recurrent severe headaches on one side of the head, typically around the eye, then extends back on the same
side to sub-occipital area and upper neck.
Attacks are accompanied by ipsilateral autonomic symptoms (conjunctival injection, lacrimation, rhinorrhea, miosis, ptosis, flushing, and sweating
of the face on the affected side).
 More common in males usually in the 3rd decade.
 abrupt onset and cessation and last from 15 min to 3 hours.
 The attacks are characterized by their regularity and occurrence in clusters i.e., every 24 hours for a few weeks or months.
The clusters are followed by long periods (up to 6 months or 1 year), where the patients are completely free.
The attacks are precipitated by alcoholic beverages and injection of histamine. They are aggravated by the application of heat and relieved by cold.
Clinical picture
A) At least 5 attacks fulfilling criteria B - D
B) Severe or very severe unilateral orbital, supraorbital and / or
temporal pain lasting 15 minutes to 3 hours ( when
untreated )
C) Either or both of the following:
1- At least one of the following symptoms or signs, ipsilateral
to the headache
 Nasal congestion and / or lacrimation
 Nasal congestion and /or rhinorrhea
 Eyelid edema
 Forehead and facial sweating
 Miosis and / or ptosis
2- A sense of restlessness or agitation
D) Occurring with a frequency between one every other day and
8 per day
E) Not better accounted for by another ICHD - 3 diagnosis.
Differential diagnosis
 Unilateral headache & facial pain.
 Glaucoma.
 Migraine
 Temporal arteritis
 Trigeminal autonomic cephalalgia
Treatment
A. Pharmacological treatment:
1) Acute treatment:
A. 100% high flow oxygen 6-12 L/min Oxygen (for 15 minutes).
B. Subcutaneous sumatriptan 6 mg, or nasal spray 20 mg.
C. Zolmitriptan nasal spray 5 mg and 10. mg, or oral
D. DH Ergotamine: given IV, IM, SC.
E. Others as: intranasal lidocaine.
F. Sphenopalatine ganglion stimulation
2) Preventive treatment
1) Transitional prophylaxis: short-term aiming to rapid suppression of attacks.
A) Short course steroids: Prednisolone 60 mg I day for 3-4 days then decrease dose by 10 mg every 3-4 days or Methyl prednisolone 80-120 mg
IM.
B) Ergotamine tartrate: oral or rectal at night to prevent nocturnal attacks- regular dose of 2 mg I day.
C) DH Ergotamine: 0.5-1 mg / 6-8 hr only for few days to avoid ergotism.
D) Occipital nerve block: result in temporary relief if medical treatment is contraindicated or poorly tolerated.
2) Maintenance prophylaxis:
A) Verapamil (isopten): first line treatment- dose at 80-160 mg / 8 hrs.
B) Lithium: 400 mg tab aiming at serum Level 1 meq/liter.
C) Methysergide: 4-10 mg/day, effective in 60% of patients.
D) For resistant cases:
1) Combination of verapamil with lithium or topiramate
or
2) Combination of verapamil, lithium and topiramate, or
3) Methysergide, or addition of indomethacin or
clonidine.
Tension headache
Definition
Tension-type headache (TTH) is also known as Muscle Contraction Headache, Stress Headache.
It is generally a mild to moderate pain that's often described as feeling like a tight band around the head.
- The most common type of primary headache.
- occurring in about three-quarters of the general population.
- Occur at any age, more in females.
- Trigger factors of tension headache: Anxiety, Emotional Stress, Depression, And Lack of Sleep, Physical
Exhaustion, Certain Smells, And Poor Posture.
Types of TTH
Infrequent episodic TTH: one or fewer episodes per month.
Frequent episodic TTH: more than one, but fewer than 15 episodes per month for three or more months.
Chronic TTH: more than 15 episodes per month for three or more months. There may be mild nausea with this type of
tension-type headache.
Clinical Picture
Site: Bilateral, Commonly Occpito-Nuchal, Bitemporal or Frontal.
Characteristics:
 Pressing or tightening (non-pulsatile)
 Pressure or bursting sensation
 No Sleep disturbance
 Wax and wane or steady
 A duration of between 30 minutes to 7 days
 Not associate with nausea, vomiting, photophobia or phonophobia.
 May associate with neck pain or spasm.
Pathogenesis
The potential pathophysiological mechanisms of tension-type headache involve possible genetic factors, peripheral and
central mechanisms.
Peripheral mechanisms: including myofascial and to a lesser degree vascular factors, may lead to peripheral sensitization
of nociceptors.
Central mechanisms: involve central sensitization of nociceptive pathways and altered descending pain modulation. 5-
HTTLPR,
5-hydroxytryptamine (serotonin)-transporter-linked-gene-linked polymorphic region; APOE, apolipoprotein; COMT
(catechol-O-methyltransferase).
Diagnostic criteria of Tension headache
A) Headaches lasting from 30 minutes to 7 days.
A) At least two of the following pain characteristics:
 Pressing or tightening (non - pulsating ) quality
 Mild to moderate intensity
 Bilateral location
 No aggravation from walking stairs or similar routine activities
A) Both of the following:
 No nausea or vomiting
 No Photophobia and phonophobia.
Treatment
Nonmedical treatment:
 Reassurance, sympathy with the patient.
 Improve the posture
 Relaxation exercises of neck, scalp, and
head muscles.
 Massage of neck,
 Apply a heating pad or ice pack to head for
5 to 10 minutes several times a day.
Medical treatment:
In acute attack:
a. Simple analgesics as Aspirin, Acetaminophen, NSAIDs (Ibuprofen,
Ketoprofen …)
b. Analgesics in combination with caffeine are more effective as Excedrin
c. Muscle relaxant can be used to relief muscle tension, but it has sedating
effect so it should be taken at bedtime as Tizanidine.
Prophylactic:
If tension headaches are frequent, long-lasting, or associated with a
significant amount of disability.
As: amitriptyline 50-150 mg/d.
Treatment of Chronic TTH:
Amitriptyline, Relaxation Therapy.
Comparison between different type of primary headaches
Features Migraine Tension Cluster
Age of onset 25-55 30-50 y 20-40
sex F > M F>M M>F
location 60-70% unilateral Bilateral Unilateral, orbital supraorbital,
temporal
Duration of episode 4-72 hours 30 minutes to 7
days
15-190 minutes
Severity Moderate to
severe
Mild to moderate Extremely severe
Type of pain Pulsating,
throbbing
Pressing,
tightening, but
not pulsating
Boring, searing
Pattern 1-2 attacks per
month
<180 attacks per
year or <15
attacks per month
1-8 attacks per day separated
by pain free period
Associated symptoms Nausea, vomiting,
photophobia,
phonophobia
no nausea or
vomiting,
may associated
with neck muscle
spasm
Conjunctival injection, lacrimal,
facial / forehead swelling, nasal
congestion, rhinorrhea, ptosis,
miosis, eyelid edema
Acute management oral triptam and NSAIDs Aspirin
Paracetamol
NSAIDs
Oxygen 100%
Trigemial neuralgia
Trigeminal neuralgia (TN) is characterized by recurrent brief episodes of unilateral
electric shock-like pains, abrupt in onset and termination, in the distribution of one
or more divisions of the fifth cranial (trigeminal) nerve that typically are triggered by
innocuous stimuli
ANATOMY
The trigeminal nerve is the sensory
supply to the face and the sensory
and motor supply to themuscles of
mastication. The nerve starts at the
midlateral surface of the pons, and
its sensory ganglion (gasserian
ganglion) resides in Meckel cave in
the floor of the middle cranial fossa.
EPIDEMIOLOGY
TN is a rare condition that affects women more than men.
The annual incidence of TN is 4 to 13 per 100,000
The incidence increases gradually with age; most idiopathic cases begin after age 50,
althoughonset may occur in the second and third decades or, rarely, in children.
Etiology
● Secondary TN, defined as TN caused by an underlying disease. Recognized causes
include multiple
sclerosis, cerebellopontine angle tumor, and arteriovenous malformation.
●Idiopathic TN, defined as TN with neither electrophysiological tests nor MRI showing
significant
abnormalities.
PATHOGENESIS
Most cases of TN are caused by compression of the trigeminal nerve root, usually within a few millimeters of
entry into the pons (the root entry zone)
Other causes of TN via nerve compression include vestibular schwannoma (acoustic neuroma), meningioma,
epidermoid or other cyst, or, rarely, a saccular aneurysm or arteriovenous malformation
The mechanism by which compression of the nerve leads to symptoms appears to be related to demyelination in
a circumscribed area around the compression
Demyelinated lesions may set up ectopic impulse generation, possibly causing ephaptic
transmission.
Ephaptic cross-talk between fibers mediating light touch and those involved in pain generation
could account for the precipitation of painful attacks by light tactile stimulation of facial trigger zones .
Furthermore, alteration of afferent input may disinhibit pain pathways in the spinal trigeminal nucleus.Evidence for a role of central pain
mechanisms includes the presence of refractory periods after a triggered
episode, trains of painful sensations after a single stimulus, and latency from the time of stimulation to the onset
of pain .
In addition, electrophysiologic evidence of central sensitization of trigeminal nociceptive processing
has been observed in patients with atypical TN who have concomitant chronic facial pain .
Demyelination of one or more of the trigeminal nerve nuclei may also be caused by multiple sclerosis or other
structural lesions of the brainstem. In multiple sclerosis, a plaque of demyelination typically occurs in the root
entry zone of the trigeminal nerve although vascular compression also has been noted in these patients.
CLINICAL FEATURES
TN is defined clinically by paroxysmal, stereotyped attacks of
usually intense, sharp, superficial, or stabbing painin the
distribution of one or more branches of the fifth cranial
(trigeminal) nerve (described as electric, shock-like, or stabbing.
It usually lasts from one to several seconds, but may
occurrepetitively.
A refractory period of several minutes during which a paroxysm
cannot be provoked is common.
TN is typically unilateral. The distribution of pain most often involves the V2 and/or V3
subdivisions of the trigeminal nerve.
triggers of TN paroxysms include chewing, talking, brushing teeth, cold air, smiling, and/or
grimacing
Autonomic symptoms, usually mild or moderate, can occur in association with attacks of
TN in the V1 trigeminal distribution, including lacrimation, conjunctival injection, and
rhinorrhea
DIAGNOSIS
The International Classification of Headache Disorders, Third Edition (ICHD-3) diagnostic
criteria for TN are as follows :
A) Recurrent paroxysms of unilateral facial pain in the distribution(s) of one or more
divisions of the trigeminal nerve, with no radiation beyond, and fulfilling criteria B and C
● B) Pain has all of the following characteristics:
• Lasting from a fraction of a second to two minutes
• Severe intensity
• Electric shock-like, shooting, stabbing or sharp in quality
● C) Precipitated by innocuous stimuli within the affected trigeminal distribution
● D) Not better accounted for by another ICHD-3 diagnosis
The ICHD-3 further defines several subtypes of TN
1. Classic , which develops without apparent cause other than neurovascular compression,
fulfilling the criteria above and requiring demonstration on MRI or during surgery of
neurovascular compression (not simply contact), with morphological changes in the
trigeminal nerve root. Most patients with classic TN will have a purely paroxysmal form
without persistent background facial pain (ie, they are pain-free between attacks in the
affected trigeminal distribution).
2. Secondary , defined as TN caused by an underlying disease. Recognized causes include
multiple sclerosis, cerebellopontine angle tumor, and arteriovenous malformation.
3. Idiopathic , defined as TN with neither electrophysiological tests nor MRI showing
significant abnormalities.
1. Neuroimaging: MRI (or CT if MRI is not an option) is useful for identifying the small
proportion of patients who have a structural lesion (eg, tumor in the cerebellopontine
angle, demyelinating lesions including multiple sclerosis) as the cause of TN.
2. Electrophysiologic testing does not clearly distinguish classic TN from secondary TN
and has no established role in the diagnostic evaluation of TN.
MEDICAL THERAPY
Carbamazepine is the best studied treatment for classic TN and is established as effective.
Side effects can be a problem but are generally manageable, particularly if low doses are prescribed
initially with gradual titration.
The usual starting dose of carbamazepine is 100 to 200 mg twice daily.
A systematic review and practice parameter published in 2008 from the American Academy of
Neurology (AAN) and the European Federation of Neurological Societies (EFNS): concluded that
1-carbamazepine is effective for controlling pain in patients with TN
2- oxcarbazepine is probably effective
3-baclofen, lamotrigine, and pimozide are possibly effective .
4- botulinum toxin injections, clonazepam, gabapentin, phenytoin, tocainide, tizanidine, and
valproate are uncertain effectiveness
SURGICAL THERAPY
Patients with TN who are refractory to medical therapy are candidates for surgery.. The
major types of procedures are :
● Microvascular decompression for TN caused by compression of the trigeminal nerve root.
● Ablative procedures, including:
• Rhizotomy with radiofrequency thermocoagulation, mechanical balloon compression, or
chemical (glycerol) injection
• Radiosurgery
• Peripheral neurectomy and nerve block
Thank you
Mohamedrizk.med@o6u.edu.eg

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Primary headache and facial pain. (2024)

  • 1. Headache Dr Mohamed Rizk Khodair Lecturer of neurology October 6 Universirty Mohamedrizk.med@o6u.edu.eg
  • 2. Approach to patient with headache & facial pain Headache or cephalalgia: it is the pain in the head from the orbit back to the sub occipital region. Facial pain: pain elsewhere in the face . Pathophysiology of headache & facial pain: Headache is caused by traction, compression, inflammation, or distention of the pain-sensitive structures in the head or neck.
  • 3. NB: The brain itself is insensitive to the pain. Brain sensitive structures Extracranial Within cranial vault Skin and Periosteum of skull Arteries of circle of wills SC (tissue, muscles , arteries ) Arteries of meninges (dura , arachnoid , pia ) Upper 3 cervical A. Brainstem periaqueductal grey matter and sensory nuclei of thalamus Eye, ear, teeth , TMJ , sinuses Cranial Ns 1 ,2 ,5 ,9, 10 Dura (especially at the base) Venous sinuses
  • 4. Headache classification Secondary headache Primary headache - Related to underlying medical condition - Represent about 10% of cases - Life threating -Not related to underlying medical conditions - Represent about 90% of cases - Not a life threating Types: -Headache attributed to head trauma - Headache attributed to systemic disorder (HTN) -Headache attributed to cranial or cervical disorders -Headache attributed to a substance or its withdrawal -Headache attributed to disorders of eyes, ears, tooth, sinuses (referred headache ) -Headache attributed to inflammation (trigeminal neuralgia) Types: -Migraine and its subtypes -Tension headache (most common) -Cluster headache
  • 5. Red flags Criteria of serious headache: (red flags) (SNOOP) -Systemic signs and disorders. -Neurological symptoms (focal or global neurological symptoms). -Onset new , sudden, or changed & patient > 50 years old. -Onset in thunderclap presentation. -Papilledema, pulsatile tinnitus, positional provocation, precipitated by exercise.
  • 6. Migraine • Paroxysmal disorder characterized by throbbing headache (usually unilateral) associated with autonomous manifestations (e.g., nausea, vomiting…) and may be proceeded by visual, sensory, or motor manifestations. • Migraine is extremely common, affecting 12% of the population: 18% of women and 6% of men (more common in females due to hormonal changes ).
  • 7. Migraine Theories & pathophysiology 1. Trigmeno-vascualr theory • The trigeminovascular system (TVS) is thought to comprise neurons located in the trigeminal ganglion that innervate the cerebral vasculature including the dura mater. • Afferent fibers, mainly from the first or ophthalmic division of the trigeminal nerve, project from these areas to the ganglion neurons and these neurons have centrally projecting axons to the trigeminal nucleus. • Several neurotransmitters and neuropeptides [e.g., calcitonin gene- related peptide (CGRP) and neurokinin-1] are produced in the ganglion neurons that may modulate pain transmission and vascular tone. • In migraine, releasing of CGRP at vascular terminals of trigeminal nerve and trigeminal nucleus causes blood vessels in head to swell and it produces inflammation around the brain leading to activation of trigeminal pain pathway.
  • 8. 2.Neurovascular theory: Migraine triggers → over excitation of trigeminal N. axons → release of vasoactive neuropeptides → VD and sterile inflammation 3.Serotonin theory (5-HT ) :  Initially: increasing of plasma serotonin → VC of cerebral B.Vs Aura  Later: subsequent drop in plasma serotonin → VD of B. Vs headache of migraine NB: serotonin drugs play an important role in treatment of migraine: - During attack (headache = VD): use serotonin agonist drugs (to induce VC and relive the pain) - In between the attacks (prophylaxis): use serotonin antagonist (to prevent VC)
  • 9. 4. Dopamine theory: Abnormal dopaminergic stimulation (increasing of dopamine or hypersensitivity of dopamine receptors) → headache and associated manifestations (nausea, vomiting) 5.Ca+2 uptake theory (Hypoxic Theory): Focal cerebral hypoxia associated with rapid entry of Ca into brain cells and smooth muscle of Blood Vessel → VC followed by reactive VD.
  • 10. Migraine triggers  Hormonal changes (period, pregnancy, menopause)  Diet (chocolate, cheese, caffeine, nuts, smoking, alcohol)  Drugs (vasodilators as nitrates)  Sensory (flickering light, strong smells as perfume, noise)  Change in lifestyle (dehydration, stress, sleep pattern, exertion, weather changes)
  • 11. Types of migraine Classic Migraine: migraine with aura (15 %) Common Migraine: migraine without aura (85 %) Hemiplegic Migraine: headache associated with temporary unilateral hemiparesis or hemiplegia Basilar Migraine: patient presented with vertebrobasilar symptoms as: vertigo, ataxia, confusion, dysarthria, incoordination. Ophthalmoplegic Migraine: associated with transient paralysis of extraocular MS and ophthalmoplegia. Facial Migraine: associated with transient facial paralysis Variants
  • 12. Clinical picture: (for classic migraine) A. Prodroma:  From 12 to 36 hours before Aura and headache.  Symptoms include constipation, mood change, food craving, neck stiffness, thirst, frequent yawing B. Aura:  Immediately before attack  Develop over 5 -20 min and last less than 60 min  Include visual symptoms as scotomas, flashes of light (most common)  Sensory and motor disturbance as weakness (hemiparesis), dysphasia, parathesia, olfactory, visual, or gustatory hallucinations. C. Headache:  Site: usually unilateral (start in the temple or around the eye)  Type: pulsatile or throbbing pain (moderate to severe)  Duration: 4 to 72 hours  Increased by exercise, light, movement  Decreased by sleep and rest  Associated by nausea, vomiting, photophobia, phonophobia D. Post headache:  After headache Patient may have fatigue, polyuria, weakness, confusion
  • 14. Diagnosis A) Medical history B) Headache diary C) Migraine triggers D) Investigations (for 2ry causes): as EEG, CT brain, MRI, CRP, ESR …
  • 15. Treatment of Migraine During attack: Acute treatment aims to stop or prevent the progression of a headache or reverse a headache that has started ask patient to relax in a dark quit room and try to sleep. Goals of acute treatment: 1. Rapid treatment. 2. Minimize recurrence. 3. Restore ability to function. 4. Minimize use rescue medications. 5. Optimize self-care. 6. Reduce use of resources. 7. Cost effectiveness. 8. Minimal or no adverse events
  • 16. a. Analgesics:  Paracetamol (1 gm), aspirin (900-1200 mg ), Ibuprofen (400-800mg ), diclofenac (25-50mg) b. Triptans:  Mechanism of action: - Triptans are Serotonin receptor agonists, Stimulation of the 5-HT1B receptors on smooth muscle cells of blood vessels causes cranial vasoconstriction - Blocks effects of Calcitonin Gene-Related Peptide (CGRP).  Side effects: -Chest discomfort, throat heaviness. -Paraesthesias in UL, LL, head, or neck. -Anxiety, mild difficulty breathing. -Sumatriptan, zolmitriptan, and rizatriptan are primarily metabolized by monoamine oxidase (MAO) and should be avoided in patients taking MAO-A inhibitors.  Contraindications: - ICD, CV disease, Uncontrolled HTN, PVD , liver disease, pregnancy  Triptans oral doses: - Sumatriptan (Imitrex) 50 -100 mg - Almotriptan (Axert) 12.5 mg - Frovatriptan (Frova) 12.5 mg - Zolmitriptan (Zomig) 2.5 -5 mg
  • 17.
  • 18. C. Ergots:  Used in migraine specially in patient intolerant to triptans.  Mechanism of action: The ergot alkaloids are nonspecific 5-HT agonists and vasoconstrictors (partial agonists or antagonists at adrenergic, dopaminergic and tryptaminergic receptors).  Used for migraine are related to the effects on smooth muscle. The drugs constrict arteries and veins by direct stimulation of cerebral vascular smooth muscle.  Orally: Ergotamine, 1 mg, 2 tablets once.  Ergotamine 1 mg + Caffeine 100 mg (added caffeine will enhance absorption of ergotamine & potentiate its VC effect)
  • 19. D.Dopamine Antagonists:  METOCLOPRAMIDE (orally, IV)  Adjunctive therapy in an acute attack of migraine.  Relieves associated nausea & vomiting (antiemetic effect).
  • 20. In between attack (prophylaxis): Indication of prophylactic therapy
  • 21. A. Avoid Migraine triggers:  As diet (e.g., alcohol, Caffeine overuse or caffeine withdrawal, Chocolate, aged cheese, Aspartame (NutraSweet), bananas, and nuts); drugs (oral contraceptives, vasodilators). B. Beta-Blockers:  Most widely used preventive medication class.  50% effective in producing> 50% reduction in attack frequency.  As Propranolol 80- 240 mg/d (atenolol, metoprolol, timolol, nadolol also effective).  Inhibit nitric oxide production (propranolol).  It decreases effect of adrenaline lead to decrease VD of cerebral vessels C. Serotonin Antagonists:  Pizotifen 0.5 mg tds.  Methysergide: 1 mg tds.  Amitriptine
  • 22. D. Calcium Channel Antagonists:  Mechanism of Action: - Block 5-HT release. - Block calcium dependent "enzymes involved in prostaglandin formation. - Interfere with propagation of spreading depression.  Verapamil most useful, flunarizine.  Nicardipine and nifedipine are not recommended. E. Antiepileptic drugs  Topiramate, valproic acid.
  • 23. Status Migrainous It’s a migraine attacks that persist for longer than 72 hours despite treatment. Clinical picture  Headache-free periods for less than 4 hours may occur  Usually associated with prolonged use of analgesics. Treatment  Hospitalization, fluid replacement, electrolytes imbalance correction  Suppression of vomiting (metoclopramide, chlorpromazine)  IV dihydroergotamine  Dexamethasone or prednisolone, IV Na valproate, or levetiracetam.
  • 24.
  • 25. Cluster headache Definition Neurological disorder characterized by recurrent severe headaches on one side of the head, typically around the eye, then extends back on the same side to sub-occipital area and upper neck. Attacks are accompanied by ipsilateral autonomic symptoms (conjunctival injection, lacrimation, rhinorrhea, miosis, ptosis, flushing, and sweating of the face on the affected side).  More common in males usually in the 3rd decade.  abrupt onset and cessation and last from 15 min to 3 hours.  The attacks are characterized by their regularity and occurrence in clusters i.e., every 24 hours for a few weeks or months. The clusters are followed by long periods (up to 6 months or 1 year), where the patients are completely free. The attacks are precipitated by alcoholic beverages and injection of histamine. They are aggravated by the application of heat and relieved by cold.
  • 26. Clinical picture A) At least 5 attacks fulfilling criteria B - D B) Severe or very severe unilateral orbital, supraorbital and / or temporal pain lasting 15 minutes to 3 hours ( when untreated ) C) Either or both of the following: 1- At least one of the following symptoms or signs, ipsilateral to the headache  Nasal congestion and / or lacrimation  Nasal congestion and /or rhinorrhea  Eyelid edema  Forehead and facial sweating  Miosis and / or ptosis 2- A sense of restlessness or agitation D) Occurring with a frequency between one every other day and 8 per day E) Not better accounted for by another ICHD - 3 diagnosis.
  • 27. Differential diagnosis  Unilateral headache & facial pain.  Glaucoma.  Migraine  Temporal arteritis  Trigeminal autonomic cephalalgia
  • 28. Treatment A. Pharmacological treatment: 1) Acute treatment: A. 100% high flow oxygen 6-12 L/min Oxygen (for 15 minutes). B. Subcutaneous sumatriptan 6 mg, or nasal spray 20 mg. C. Zolmitriptan nasal spray 5 mg and 10. mg, or oral D. DH Ergotamine: given IV, IM, SC. E. Others as: intranasal lidocaine. F. Sphenopalatine ganglion stimulation
  • 29. 2) Preventive treatment 1) Transitional prophylaxis: short-term aiming to rapid suppression of attacks. A) Short course steroids: Prednisolone 60 mg I day for 3-4 days then decrease dose by 10 mg every 3-4 days or Methyl prednisolone 80-120 mg IM. B) Ergotamine tartrate: oral or rectal at night to prevent nocturnal attacks- regular dose of 2 mg I day. C) DH Ergotamine: 0.5-1 mg / 6-8 hr only for few days to avoid ergotism. D) Occipital nerve block: result in temporary relief if medical treatment is contraindicated or poorly tolerated. 2) Maintenance prophylaxis: A) Verapamil (isopten): first line treatment- dose at 80-160 mg / 8 hrs. B) Lithium: 400 mg tab aiming at serum Level 1 meq/liter. C) Methysergide: 4-10 mg/day, effective in 60% of patients. D) For resistant cases: 1) Combination of verapamil with lithium or topiramate or 2) Combination of verapamil, lithium and topiramate, or 3) Methysergide, or addition of indomethacin or clonidine.
  • 30. Tension headache Definition Tension-type headache (TTH) is also known as Muscle Contraction Headache, Stress Headache. It is generally a mild to moderate pain that's often described as feeling like a tight band around the head. - The most common type of primary headache. - occurring in about three-quarters of the general population. - Occur at any age, more in females. - Trigger factors of tension headache: Anxiety, Emotional Stress, Depression, And Lack of Sleep, Physical Exhaustion, Certain Smells, And Poor Posture. Types of TTH Infrequent episodic TTH: one or fewer episodes per month. Frequent episodic TTH: more than one, but fewer than 15 episodes per month for three or more months. Chronic TTH: more than 15 episodes per month for three or more months. There may be mild nausea with this type of tension-type headache.
  • 31. Clinical Picture Site: Bilateral, Commonly Occpito-Nuchal, Bitemporal or Frontal. Characteristics:  Pressing or tightening (non-pulsatile)  Pressure or bursting sensation  No Sleep disturbance  Wax and wane or steady  A duration of between 30 minutes to 7 days  Not associate with nausea, vomiting, photophobia or phonophobia.  May associate with neck pain or spasm.
  • 33. The potential pathophysiological mechanisms of tension-type headache involve possible genetic factors, peripheral and central mechanisms. Peripheral mechanisms: including myofascial and to a lesser degree vascular factors, may lead to peripheral sensitization of nociceptors. Central mechanisms: involve central sensitization of nociceptive pathways and altered descending pain modulation. 5- HTTLPR, 5-hydroxytryptamine (serotonin)-transporter-linked-gene-linked polymorphic region; APOE, apolipoprotein; COMT (catechol-O-methyltransferase).
  • 34. Diagnostic criteria of Tension headache A) Headaches lasting from 30 minutes to 7 days. A) At least two of the following pain characteristics:  Pressing or tightening (non - pulsating ) quality  Mild to moderate intensity  Bilateral location  No aggravation from walking stairs or similar routine activities A) Both of the following:  No nausea or vomiting  No Photophobia and phonophobia.
  • 35. Treatment Nonmedical treatment:  Reassurance, sympathy with the patient.  Improve the posture  Relaxation exercises of neck, scalp, and head muscles.  Massage of neck,  Apply a heating pad or ice pack to head for 5 to 10 minutes several times a day.
  • 36. Medical treatment: In acute attack: a. Simple analgesics as Aspirin, Acetaminophen, NSAIDs (Ibuprofen, Ketoprofen …) b. Analgesics in combination with caffeine are more effective as Excedrin c. Muscle relaxant can be used to relief muscle tension, but it has sedating effect so it should be taken at bedtime as Tizanidine. Prophylactic: If tension headaches are frequent, long-lasting, or associated with a significant amount of disability. As: amitriptyline 50-150 mg/d. Treatment of Chronic TTH: Amitriptyline, Relaxation Therapy.
  • 37.
  • 38. Comparison between different type of primary headaches Features Migraine Tension Cluster Age of onset 25-55 30-50 y 20-40 sex F > M F>M M>F location 60-70% unilateral Bilateral Unilateral, orbital supraorbital, temporal Duration of episode 4-72 hours 30 minutes to 7 days 15-190 minutes Severity Moderate to severe Mild to moderate Extremely severe Type of pain Pulsating, throbbing Pressing, tightening, but not pulsating Boring, searing Pattern 1-2 attacks per month <180 attacks per year or <15 attacks per month 1-8 attacks per day separated by pain free period Associated symptoms Nausea, vomiting, photophobia, phonophobia no nausea or vomiting, may associated with neck muscle spasm Conjunctival injection, lacrimal, facial / forehead swelling, nasal congestion, rhinorrhea, ptosis, miosis, eyelid edema Acute management oral triptam and NSAIDs Aspirin Paracetamol NSAIDs Oxygen 100%
  • 39. Trigemial neuralgia Trigeminal neuralgia (TN) is characterized by recurrent brief episodes of unilateral electric shock-like pains, abrupt in onset and termination, in the distribution of one or more divisions of the fifth cranial (trigeminal) nerve that typically are triggered by innocuous stimuli
  • 40. ANATOMY The trigeminal nerve is the sensory supply to the face and the sensory and motor supply to themuscles of mastication. The nerve starts at the midlateral surface of the pons, and its sensory ganglion (gasserian ganglion) resides in Meckel cave in the floor of the middle cranial fossa.
  • 41. EPIDEMIOLOGY TN is a rare condition that affects women more than men. The annual incidence of TN is 4 to 13 per 100,000 The incidence increases gradually with age; most idiopathic cases begin after age 50, althoughonset may occur in the second and third decades or, rarely, in children.
  • 42. Etiology ● Secondary TN, defined as TN caused by an underlying disease. Recognized causes include multiple sclerosis, cerebellopontine angle tumor, and arteriovenous malformation. ●Idiopathic TN, defined as TN with neither electrophysiological tests nor MRI showing significant abnormalities.
  • 43. PATHOGENESIS Most cases of TN are caused by compression of the trigeminal nerve root, usually within a few millimeters of entry into the pons (the root entry zone) Other causes of TN via nerve compression include vestibular schwannoma (acoustic neuroma), meningioma, epidermoid or other cyst, or, rarely, a saccular aneurysm or arteriovenous malformation The mechanism by which compression of the nerve leads to symptoms appears to be related to demyelination in a circumscribed area around the compression Demyelinated lesions may set up ectopic impulse generation, possibly causing ephaptic transmission. Ephaptic cross-talk between fibers mediating light touch and those involved in pain generation could account for the precipitation of painful attacks by light tactile stimulation of facial trigger zones . Furthermore, alteration of afferent input may disinhibit pain pathways in the spinal trigeminal nucleus.Evidence for a role of central pain mechanisms includes the presence of refractory periods after a triggered episode, trains of painful sensations after a single stimulus, and latency from the time of stimulation to the onset of pain . In addition, electrophysiologic evidence of central sensitization of trigeminal nociceptive processing has been observed in patients with atypical TN who have concomitant chronic facial pain . Demyelination of one or more of the trigeminal nerve nuclei may also be caused by multiple sclerosis or other structural lesions of the brainstem. In multiple sclerosis, a plaque of demyelination typically occurs in the root entry zone of the trigeminal nerve although vascular compression also has been noted in these patients.
  • 44. CLINICAL FEATURES TN is defined clinically by paroxysmal, stereotyped attacks of usually intense, sharp, superficial, or stabbing painin the distribution of one or more branches of the fifth cranial (trigeminal) nerve (described as electric, shock-like, or stabbing. It usually lasts from one to several seconds, but may occurrepetitively. A refractory period of several minutes during which a paroxysm cannot be provoked is common.
  • 45. TN is typically unilateral. The distribution of pain most often involves the V2 and/or V3 subdivisions of the trigeminal nerve. triggers of TN paroxysms include chewing, talking, brushing teeth, cold air, smiling, and/or grimacing Autonomic symptoms, usually mild or moderate, can occur in association with attacks of TN in the V1 trigeminal distribution, including lacrimation, conjunctival injection, and rhinorrhea
  • 46. DIAGNOSIS The International Classification of Headache Disorders, Third Edition (ICHD-3) diagnostic criteria for TN are as follows : A) Recurrent paroxysms of unilateral facial pain in the distribution(s) of one or more divisions of the trigeminal nerve, with no radiation beyond, and fulfilling criteria B and C ● B) Pain has all of the following characteristics: • Lasting from a fraction of a second to two minutes • Severe intensity • Electric shock-like, shooting, stabbing or sharp in quality ● C) Precipitated by innocuous stimuli within the affected trigeminal distribution ● D) Not better accounted for by another ICHD-3 diagnosis
  • 47. The ICHD-3 further defines several subtypes of TN 1. Classic , which develops without apparent cause other than neurovascular compression, fulfilling the criteria above and requiring demonstration on MRI or during surgery of neurovascular compression (not simply contact), with morphological changes in the trigeminal nerve root. Most patients with classic TN will have a purely paroxysmal form without persistent background facial pain (ie, they are pain-free between attacks in the affected trigeminal distribution). 2. Secondary , defined as TN caused by an underlying disease. Recognized causes include multiple sclerosis, cerebellopontine angle tumor, and arteriovenous malformation. 3. Idiopathic , defined as TN with neither electrophysiological tests nor MRI showing significant abnormalities.
  • 48. 1. Neuroimaging: MRI (or CT if MRI is not an option) is useful for identifying the small proportion of patients who have a structural lesion (eg, tumor in the cerebellopontine angle, demyelinating lesions including multiple sclerosis) as the cause of TN. 2. Electrophysiologic testing does not clearly distinguish classic TN from secondary TN and has no established role in the diagnostic evaluation of TN.
  • 49. MEDICAL THERAPY Carbamazepine is the best studied treatment for classic TN and is established as effective. Side effects can be a problem but are generally manageable, particularly if low doses are prescribed initially with gradual titration. The usual starting dose of carbamazepine is 100 to 200 mg twice daily. A systematic review and practice parameter published in 2008 from the American Academy of Neurology (AAN) and the European Federation of Neurological Societies (EFNS): concluded that 1-carbamazepine is effective for controlling pain in patients with TN 2- oxcarbazepine is probably effective 3-baclofen, lamotrigine, and pimozide are possibly effective . 4- botulinum toxin injections, clonazepam, gabapentin, phenytoin, tocainide, tizanidine, and valproate are uncertain effectiveness
  • 50. SURGICAL THERAPY Patients with TN who are refractory to medical therapy are candidates for surgery.. The major types of procedures are : ● Microvascular decompression for TN caused by compression of the trigeminal nerve root. ● Ablative procedures, including: • Rhizotomy with radiofrequency thermocoagulation, mechanical balloon compression, or chemical (glycerol) injection • Radiosurgery • Peripheral neurectomy and nerve block