nero medicine

1. Headache
Dr. Ra’ed Ahmed
MBChB, FIBMS
Neurologist

2. Headache
 A headache or cephalagia is pain anywhere in
the region of head or neck
 Headache is defined as diffuse pain in various
parts of the head, with the pain not confined to
the area of distribution of a nerve
 Isolated involvement of the bony skull, most of
the dura, or most regions of brain parenchyma
does not produce pain.

3. Pain Sensitivity of CranialPain Sensitivity of Cranial
StructuresStructures
 Cranial venous sinuses with
afferent veins
 Arteries at base of brain and their
major branches
 Arteries of the dura
 Dura near base of brain and large
arteries
 Dural, Cranial and extracranial
nerves
 All extracranial structures
 Brain parenchyma
 Ependyma
 Choroid
 Pia
 Arachnoid
 Dura over convexity
 Skull
Pain-Sensitive Pain-Insensitive

4. General Mechanisms of Headache
1.Traction, tension, or displacement of pain-sensitive
structures
2. Distention or dilation of intracranial arteries
3. Inflammation of pain-sensitive structures
4. Obstruction of CSF pathways with consequent
increased intraventricular pressure
5. Primary central pain: involvement of pain-modulating
systems
6. Stimulation from disease of eye, ear, nose and sinuses
(referred pain)

5. Primary headache syndromes
• Migraine (with or without aura)
• Tension type headache
• Trigeminal autonomic cephalalgia (including
cluster headache)
• Primary coughing/exertional/sex- related
headache
• New daily persistent headache syndrome

6. Secondary causes of headache
• Medication overuse headache( chronic daily headache)
• Intracerebral bleeding (SDH, SAH or ICH)
• Raised ICP ( Brain tumour , IIH )
• Infetions (meningitis , encephalitis , brain abscess)
• Inflammatory disease ( temporal arteritis , other vasculitis ,
arthritis)
• Referred pain from other structures ( orbit , TM joint, neck).

7. Temporal distribution of different
types of headache with time
Migraine
Tension headache
Migraine + Tension
(combination)
Cluster headache
Raised intracranial
pressure

9. MIGRAINE
 Migraine, the second most common cause of
headache,
 Afflicts approximately 15% of women and 6% of
men over a 1-year period.
 Migraine is a benign and recurring syndrome of
headache associated with other symptoms of
neurologic dysfunction in varying admixtures.

10. Pathophysiology
 The cause of migraine is unknown.
 Intracranial vasoconstriction and extracranial
vasodilatation
 More recent studies “Spreading depression” in cerebral
blood flow
 Later in the headache phase, blood flow increases to
parts of the cortex (cingulate, auditory, and visual
association areas) and the contralateral brainstem
 Aggregation of migraine within families

11. Clinical features of Migraine
 Headache that is usually unilateral and frequently
pulsatile in quality;
 it is often associated with nausea, vomiting,
photophobia, phonophobia, and lassitude.
 Visual or other neurologic auras occur in about 20% of
patients.
 Two-thirds to three-fourths of cases of migraine occur in
women;
 Onset is early in life—more than 90% before age 40.
 A family history of migraine is present in most cases.

12. Clinical features of migraineClinical features of migraine
SleepySleepy
Anorexia
Anorexia nauseanausea Vomiting
Vomiting
yawning
yawning
Phonophobia
Phonophobia
Photophobia
Photophobia
Phonophobia
Phonophobia
Photophobia
Photophobia
Osmophobia
Osmophobia
Osmophobia
Osmophobia
Vomiting
Vomiting
Deep sleep
Deep sleep
HeadacheHeadache
IIIIII IVIV
Headache ResolutionHeadache Resolution
Blau (1992)Blau (1992)
II IIII
NormalNormal Prodromes AuraProdromes Aura
NormalNormal
AppetiteAppetite
Awake/sleepAwake/sleep
Light toleranceLight tolerance
SmellSmell
NoiseNoise
Fluid balanceFluid balance
CravingCraving
TiredTired yawning
yawning
Heightened
Heightened
perception
perception
FluidFluid retention
retention
VV
Postdromes NormalPostdromes Normal
Limited
Limited
Light toleranceLight tolerance
NoiseNoise
SmellSmell
Fluid balanceFluid balance
TiredTired
FeelingFeeling
high orhigh or
lowlow
DiuresisDiuresis
AppetiteAppetite
Awake/sleepAwake/sleep
food tolerancefood tolerance
NormalNormal

14. Fortification Spectrum

15. DIAGNOSIS
 The diagnosis of migraine is based on the history. If the
headache is typical of migraine and the findings on
neurologic examination are normal, no further studies
 A headache diary can often be helpful in making the
diagnosis;
 The ddx includes tension-type headache,but migraine at
its most basic level is headache with associated features,
and tension-type headache is headache that is
featureless.Most patients with disabling headache
probably have migraine.
 History suggestive of a secondary headache, further
evaluation with MRI should be considered.

16. STRATEGIES FOR MIGRAINESTRATEGIES FOR MIGRAINE
TREATMENTTREATMENT
Preemptive
treatment
Migraine trigger
time-limited and
predictable
Preventive
Treatment
Decrease in
migraine frequency
warranted
Acute
treatment
To stop pain
and prevent
progression
Silberstein SD. Cephalalgia. 1997.

17. MIGRAINE TRIGGERSMIGRAINE TRIGGERS
Diet
Hormonal changes
Stress and anxiety
Sleep deprivation or excess
Environmental factors
Physical exertion

18. ACUTE ATTACK THERAPIES FOR
MIGRAINE:
 Severity of the attack
 Mild migraine attacks can usually be managed by
oral agents; Severe migraine attacks may require
parenteral therapy
 For mild attacks = Acetaminophen or Aspirin
 For moderate to severe attacks, options include
-Dihydroergotamine ( intranasally);
-Oral, intranasal, or SC Sumatriptan
 For very severe attacks = Dihydroergotamine SC or
IV is usually effective but generally requires an
antiemetic(e.g., promethazine) before intravenous
use.

19.  Ergotamine and DHE are nonselective receptor
agonists and they are C/I in pregnancy ,coronary
,peripheral vascular diseases and hypertension.
 while the Triptans are selective 5-HT 1B/1D receptor
agonists. They have the same contraindications as
previous group and should never combined with them.
 Recurrence of headache is another important limitation
of triptan. Ergotamine appears to have a much higher
incidence of nausea than triptans, but less headache
recurrence.

20. Pevention
 1-β-adrenergic blockers: Propranolol tab. 40–120 mg
bid
 2- Anticonvulsants : Topiramate tab.( 25–200 mg/d),
Valproate tab( 400–600 mg bid)
 3-Tricyclic antidepressants : Amitriptyline, (10-25 mg
qhs) ;
 4-Calcium-channel antagonists: Verapamil (120 to
480 mg/day)
 5-Other alternatives include the serotonergic drug
Cyproheptadine(4 to 20 mg)
 6-OnabotulinumtoxinA injection is also effective for

21. Tension-type headache
 most common type of headache
 Experienced to some degree by the majority of the
population.
 It is a chronic disorder that begins after age 20.
 Women are more commonly affected than men.
 The headache may be episodic or chronic (present
>15 days per month).
 Pathophysiology of tension-type headache is less
well understood

22. Clinical features
 ‘dull’, ‘tight’ or like a ‘pressure’, and there may be a sensation of
a band round the head or pressure at the vertex.
 It is of constant character and generalised, but often radiates
forwards from the occipital region.
 In contrast to migraine, the pain can remain unabated for
weeks or months without interruption
 no associated vomiting or photophobia
 Activities are usually continued throughout, and the pain may
be less noticeable when the patient is occupied.
 The pain is usually less severe in the early part of the day,
becoming more troublesome as the day goes on.
 Tenderness may be present over the skull vault or in the
occiput.

23. Treatment
 Episodic tension-type headaches are generally
treated successfully with acetaminophen (650 to
1000 mg) or NSAIDs (aspirin, 900 to 1000 mg;
naproxen, 250 to 500 mg; ibuprofen.
 Chronic tension-type headaches may benefit from
prophylactic treatment with amitriptyline (starting with
10 mg at bedtime and increased slowly up to 100 mg
until the patient improves or intolerable side effects
develop).
 Muscle relaxants and physical therapy are also

24. TRIGEMINAL AUTONOMIC
CEPHALALGIAS (TACs(
1. Unifying features include pain in distribution of
trigeminal nerve and autonomic signs reflecting
activation of cranial parasympathetic system
2. Includes cluster, paroxysmal hemicrania, short-
lasting unilateral neuralgiform headache with
conjunctival injection and tearing (SUNCT) syndrome
3. Because many of these syndromes are unilateral
and associated with autonomic symptoms,
neuroimaging is often necessary to rule out structural
causes

25. Cluster headache
 A rare form of primary headache much less common than migraine.
 5 : 1 male predominance and onset is usually in the third decade
(migraine more common in female & has earlier onset typically start in
teenage and rarely after 40).
 Cluster headache lacks genetic predisposition (-ve family history).
 Cluster headache lack of provoking dietary factors , Alcohol
provokes the already ongoing attacks of cluster headache.
 Different drug effect: propranolol and amitriptyline used as
preventive treatment in migraine are ineffective in cluster
headache.
 Lithium is beneficial for cluster headache and ineffective in
migraine.

26. Clinical features
 Cluster headaches are almost always unilateral, and have
characteristic ipsilateral autonomic features
 Usually behind or above the eye (periorbital)
 Attacks occur 1-8 times a day and are usually described as
“boring” or “stabbing” pain, excruciating in intensity, constant
nonthrobbing ,that is characteristically brief (30–90 minutes)
 Highly agitated during the headache phase and are unable to sit or
lie down
 Patients are generally perfectly well between episodes.
 Onset is nocturnal in about 50% of patients and awaken the patient
from sleep.

27.  Episodes are often precipitated by the use of alcohol or
vasodilating drugs nitroglycerin , especially during a cluster
siege
 Striking periodicity of cluster attacks in at least 85% of patients
(a daily periodicity and may also have a seasonal periodicity).
 Cluster period is typically a few weeks (8 to 10 weeks a year),
followed by remission for months to years, but a small
proportion do not experience remission. (Chronic cluster
headache may occur without a remission).

28. ACUTE ATTACK TREATMENT of
Cluster headache
 The attacks peak rapidly, and thus a treatment with quick onset is required
 Oxygen inhalation should be given as 100% oxygen at 10–12 L/min for 15–
20 min. It appears that high flow and high oxygen content are important.
 Sumatriptan: (4 to 6 mg) S.C injection can be helpful.
 Dihydroergotamine: 1-2mg I.M. , or S.C or even intravenously.
Prevention
 Preventive medications should be started at the beginning of a cluster
bout.
 Verapamil, 240 to 480 mg, is the drug of choice.
 Lithium (300 mg twice daily) is another alternative. •
 Corticosteroids (e.g., prednisone, 40 mg/day, or dexamethasone, 4 mg twice daily
for 2 weeks) act rapidly to prevent cluster headache and can be used acutely while
other preventive medications are started

29. Exertion-Induced Headaches
 More common in men than women
 Typically occurs in middle age
 Overall prevalence: about 1%
 Benign cough headache , Primary sex headache & Benign
exertional headache
 Diagnostic approach: exclusion of structural causes with
neuroimaging and/or lumbar puncture if subarachnoid hemorrhage
is a consideration
 Treatment Trial of prophylactic indomethacin if headaches are
frequent; may require concurrent gastritis prophylaxis . Alternative:
naproxen, other NSAIDS

30. New Daily Persistent Headache
(NDPH(
 Headache on most if not all days
 Headache typically develops within 1 to 3 days and persists
(evolution over 3 days)
 It is generally bilateral, nonpulsating, mild to moderate, and
associated with no more than one of the following: photophobia,
phonophobia, or nausea ( headache characteristics similar to
those of tension headache)
 Diagnostically, it is first important to exclude secondary forms of
headache (SAH, raised CSF pressure headache , post-traumatic
headache & chronic meningitis)
 Treatment: strategies similar to those for transformed migraine and
chronic tension headache.

31. TRIGEMINAL NEURALGIA (TIC
DOULOUREUX(
 TN is a distinct, excruciatingly painful condition
provoked by sensory stimuli in the distribution of the
trigeminal nerve
 TN occurs in 4 per 100,000 individuals,
 Between 50 and 70 years of age and in women slightly
more than in men (1.5:1).
 Associated with multiple sclerosis may result from a
plaque of demyelination in the brainstem (affect younger
individuals, and bilateral involvement).

32.  Trigeminal neuralgia pain is characteristically sharp, shooting, and electric
shock–like in the distribution of the trigeminal nerve: cheek (V2), chin or
lower teeth (V3) and a combination of V2 and V3 is the most common.
 Involvement of the first division(V1) or bilateral disease occurs in less than
5% of cases.
 The paroxysms are brief—seconds to up to 2 minutes and abate
spontaneously. It may be triggered by touch, a cold wind ,eating or
brushing the teeth.
 Ocurrence during sleep is rare ( this suggest cluster headache rather than
TN).
 Pain free intervals may last from minutes to weeks but long-term
spontaneous remission is rare.
 Physical signs are usually absent.

33. Treatment Of Trigeminal neuralgia
A. Medications
Carbamazepine (400 to 1200 mg) is considered the first-line agent for the
neuralgia.
Intravenous administration of phenytoin, 250 mg, will abort an acute attack.
Phenytoin (200 to 300 mg), baclofen (40 to 80 mg), clonazepam (2 to 6 mg),
lamotrigine (100 to 400 mg), , and oxcarbazepine (300 to 1800 mg)are also
used.
B. Surgical treatments include
Microvascular decompression of the vascular loop encroaching on the
trigeminal root is said to have a 90% success rate and preserve sensory
function.
Otherwise, localised injection of alcohol or phenol into a peripheral branch of
the nerve may be effective.

34. WORRISOME HEADACHE REDWORRISOME HEADACHE RED
FLAGSFLAGS
“SNOOP”“SNOOP”
Older: new onset and progressive headache, especially
in middle-age >50 (giant cell arteritis)
Systemic symptoms (fever, weight loss) or
Secondary risk factors (HIV, systemic cancer)
Neurologic symptoms or abnormal signs (confusion,
impaired alertness, or consciousness)
Onset: sudden, abrupt, or split-second
Previous headache history: first headache or different
(change in attack frequency, severity, or clinical features)

35. Medication Overuse Headache
(rebound headache(
 Overuse of analgesic medication for headache can aggravate
headache frequency and induce a state of refractory daily or near-
daily headache
 Offending agents: many types, including narcotics, barbiturates or
barbiturate-containing combination medications, general
analgesics, triptans, ergotamine, caffeine
 Headache is generally described as
a constant, diffuse, dull headache
 Anxiety and depression are common

36. Management of medication
overuse
Out-patients
It is essential to reduce or eliminate analgesic use. Regimes vary
from reductions of 10% every week or two .A careful diary over a
month or two is very helpful
A small dose of an NSAID, as naproxen 500 mg twice daily if
tolerated
In-patients (Some patients will require admission for detoxification)
•When such patients are admitted, acute medications are withdrawn
completely on the first day, unless there is a contraindication.
•Antiemetics, such as domperidone orally or by suppository, and
fluids are administered as required,
•If the patient does not settle over 3–5 days a course of intravenous
(DHE)

37. Idiopathic intracranial
hypertension(IIH(
 IIH is a disorder of elevated ICP of unknown cause
which may lead to visual loss due to papilloedema.
 Occurs in obese women of childbearing age
The diagnosis depends on fulfilling the modified Dandy criteria:
1 Symptoms and signs of elevated ICP in an awake and alert patient.
2 No localizing symptoms or signs other than a VIth nerve palsy.
3 Normal neuroimaging (apart from changes due to the raised
pressure itself).
4 Lumbar puncture showing elevated opening pressure (>250
mm/H2O) but normal fluid analysis.

38. Clinically
 IIH presents with headache in >90% of patients, it is
characteristically severe, daily and pulsatile; unilateral or bilateral ,
frontal or occipital may be worse in morning .
Associated symptoms may include
 Transient (seconds) visual obscurations: present in up to 70% of
patients (temporary graying of vision, especially with straining).
 Bilateral pulsatile tinnitus, and some patients develop hearing loss.
 Diplopia (abducens palsy), usually horizontal is present in up to
40% of patients.
 Visual loss
 Nausea and vomiting.

39. Physical examination 1) Papilledema 2) Abducens palsy
3) Visual field abnormalities

41. Pathophysiology of IIH: unknown
cause
 Increased CSF formation
 Decreased CSF absorption
 Increased venous pressure
Disorders associated with IIH:
 Endocrine disorders thyroid disorders, Addison’s disease and
Cushing’s disease.
 Obstructive sleep apnoea,
 Medications including antibiotics (naladixic acid, ciprofloxacin,
tetracyclines, and nitrofurantoin),
 Hormonal medications including growth hormone,OCP &
corticosteroids. The strongest link of IIH is with
hypervitaminosis A

42. Investigations of IIH
 MRI and MR/CT venography brain to rule out secondary
causes of increased ICP (to exclude hydrocephalus,
mass lesions, meningeal infiltration, and venous
thrombosis).
 Radiographic signs of raised intracranial pressure in IIH
include flattening of the posterior globe (80%) and an
empty sella (70%).
 CSF examination to measure opening pressure and rule
out secondary causes (meningitis). Also to do
therapeutic (high-volume) lumbar puncture.

43. Treatment of IIH
A.Nonpharmacologic: weight loss with restriction of calorie, salt and
fluid intake
B.Pharmacologic
Diuretics:
Acetazolomide is a strong carbonic anhydrase inhibitor "drug of
choice" as that reduces CSF production and is highly effective in IIH.
The dose is gradually increased to 1-2 g/day.
Common side effects: weight loss, diarrhea, nausea and/or vomiting,
altered taste sensation, paresthesias, confusion, polyuria.
Other diuretics such as frusemide (40-60 mg twice daily) can be
used if acetazolomide not tolerated.
Close follow-up is required with assessment of visual acuity, visual
fields initially at one month and then 3-monthly.

44. C.Procedures (serial lumbar punctures).
D. Surgery includes:
Lumboperitoneal shunt or ventriculoperitoneal shunt (used to
reduce severe headaches or progressive visual loss despite
conservative treatment)
Optic nerve fenestration: incision of dural covering of intraorbital
optic nerve, used to prevent progressive visual loss.
Outcome of IIH :
Early treatment prevents visual loss
Blindness may occur in up to 10% of patients

45. Temporal (Giant Cell( Arteritis
 Temporal arteritis is an inflammatory process seen mainly in
elderly individuals
 Headache is one of the most common features
Epidemiology
 It affects women more often than men (3:1), is more common in
white individuals & almost all older than 50
Pathology
 Inflammatory vasculitis affecting medium and large extracranial
branches of aortic arch . Other intracranial vessels (vertebral
and carotid arteries) can be involved

46. Clinical presentation
 Constitutional symptoms (low-grade fever, fatigue, night
sweats, anorexia)
 Jaw claudication
 Temporal headaches with scalp tenderness
 The headache has no specific feature, but the pain is usually
continuous, generalized, and occasionally throbbing.
 Ischemic stroke is uncommon but may occur in anterior or
posterior circulation
 Transient monocular blindness and diplopia can occur.
 Half of the patients have polymyalgia rheumatica

47. GCA
Diagnosis
Elevation of ESR and CRP occurs almost invariably.
ESR more than 50 mm/h
Irregularities may be found on angiography of extracranial blood
vessels
Temporal artery biopsy
Treatment
High-dose prednisone
Immediate treatment with corticosteroids, Oral prednisone (doses
between 40 and 80 mg daily) should be started without awaiting
biopsy results because of risk of blindness
Treatment usually continued for 2 year