01

HEADACHE

2
Definition:
It is discomfort or pain in the head, it is the commonest complaint in
medicine, and it is a symptom and not a disease.
Pain Sensitive Structures in Head:
• All the tissues covering the cranium.
• The intracranial structures:
a. Vascular channels: arteries and
venous sinuses.
b. Parts of the dura, covering the
base skull.
• Nerves carrying pain fibers: 5th, 9th &
10th cranial nerves and the upper 3
cervical sensory roots.
Mechanism Through Which Headache Can Be Produced:
1. Vascular: vasodilatation and stretching of arteries and veins.
2. Muscular: spasm of occipito-frontalis and neck muscles.
3. Pressure traction of intracranial pain sensitive structures.
4. Inflammation of pain sensitive structures.
5. Referred pain
Causes of Headache:
1. Psychogenic: In anxiety, depression and hysteria.
2. Organic:
A. Local causes:
- Extracranial or Intracranial
B. General causes:
- Hypotension
- Infections and toxemias
- Miscellaneous group
Local Causes
Extracranial Intracranial
- Temporal arteritis. - Space-occupying lesion.
- Migraine

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- Referred pain from eyes, teeth,
sinuses and ears
- Neuritis and neuralgia
- Vascular as intracerebral and
subarachnoid hemorrhage.
- Post-traumatic.
- Meningeal.
- Altered CSF pressure.

Types of Headache:
Primary Headache Secondary Headache
1. Migraine: 1. Chronic post-traumatic
a. Migraine without aura headache.
(Common migraine). 2. Headache due to subarachnoid
b. Migraine with aura (Classic hemorrhage and giant cell
migraine). arteritis.
2. Tension-type headache. 3. Headache due to idiopathic
3. Cluster headache. intracranial hypertension.
4. Other primary headaches as 4. Headache due to low CSF
cough, exertion, and sexual pressure.
activity headaches. 5. Headache due to intracranial
neoplasm.
6. Headache due to substance
abuse and drug-induced
headache.
7. Headache due to intracranial
infection.
8. Headache due to acute glaucoma.
9. Headache due to eyes, ears, nose,
sinuses, teeth, mouth and neck
causes.

Diagnosis:
A. Description of the pain:
1. Time setting.
2. Site or distribution of pain.
3. Character of pain: throbbing, aching, stabbing, or bursting.
4. Severity of pain.

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 5. The factors which provocate or aggravate the headache.
6. The symptoms associated with headache.
B. History: Including past history and family history.
C. Examination: Mental state, head, fundus, blood pressure, and other
methods of investigations e.g. urine analysis, X-ray skull, EEG and CAT.
Treatment of Headache:
1. Treatment of the cause
2. Symptomatic relief: acetyl salicylic acid (Aspirin) 0.3 gm and it can be
repeated.

MIGRAINE
Definition:
Paroxysmal headache, commonly unilateral "hemicrania" preceded by an
aura, usually associated with nausea, and may be vomiting.
Etiology & Pathology:
- Cortical spreading depression
- Vascular theory

Triggers:
1. Environment or diet e.g. Weather,
Altitude, diet, alcoholic beverages,
smoking, some medications and bright
light.
2. Mental e.g. Anxiety, depression, fear
and anger.
Clinical Picture of classic migraine:
1. Aura: 15-30 minutes before the onset, relatively constant character,
usually visual (irregular and scintillating scotomata). It may be sensory
and rarely, transient dysphasia or hemiparesis.
2. Headache:
- Typical pain is unilateral in localized area and gradually spreads.

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 - Its duration is usually several hours: more than 4 hours if not
treated.
- Throbbing in character.
- Moderate to severe.
- Intensified by stooping, exertion and by bright light.
- Usually associated with nausea, may be vomiting, photophobia and
phonophobia.
Differential Diagnosis:
1. Tension-type headache.
2. Frontal sinusitis.
3. Intracranial aneurysm and angioma.
4. Trigeminal neuralgia.
5. Temporal arteritis.
6. Supraorbital neuralgia.
7. Psychogenic pain (Atypical facial pain).

Treatment:
Treatment of the Individual Attack Prevention of the Recurrence of
Attacks
1. Simple analgesics and NSAIDs 1. Precipitating factors should be
2. Dihydroergotamine (DHE) and dealt with e.g. refractive errors.
Ergotamine 2. Calcium channel blockers
3. Triptans 3. Antidepressant drugs
4. GABA ergic drugs 4. Adrenergic B-receptor blocking
5. Narcotic-based analgesics agents
6. Non-medical treatment of 5. GABA ergic Drugs
migraine 6. ACE inhibitors may be used

6
02

EPILEPSY

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Definition:
Epilepsy is a disease of recurrent unprovoked seizures.
Seizures are transient events that include symptoms and/or signs of abnormal
excessive hypersynchronous activity in the brain.
Epilepsy is diagnosed when an individual has:
✓ At least two unprovoked or reflex seizures >24 h apart.
✓ One unprovoked or reflex seizure and a probability of having another
seizure over the next 10 years,
✓ An epilepsy syndrome

Etiology
1. Idiopathic (no cause).
2. Cryptogenic (hidden cause).
3. Symptomatic (25%) (secondary):
- Local
- Systemic
Local Systemic (outside the brain)
• Congenital: cortical dysgenesis and • Hypoxia.
arteriovenous malformation. • Hypoglycemia.
• Trauma • Hypocalcemia.
• Infections • Alkalosis.
• Vascular • Drugs
• Brain tumors: e.g. meningiomas and
gliomas.
• Degenerative: e.g. Alzheimer's
disease
Origin Of Epileptic Discharge

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Classification
A. Partial.
B. Primary generalized.
C. Secondary generalized

A. Partial:
1. Simple partial (conscious is preserved):
• Motor: either tonic (spasm) or clonic (twitching).
• Sensory: sensory symptoms like tingling or pain
• Autonomic: epigastric sensations, sense of defecation or micturition and
pallor.
• Psychic: fear or atypical psychosis.
2. Complex partial (CPS) (consciousness is clouded).
Clinical picture of complex partial
The epileptic focus is present commonly in the temporal lobe and sometimes in the
frontal lobe. It is characterized by:
• Clouded consciousness
• Amnesia.
• Illusions or hallucination (gustatory or olfactory).
• Automatisms: abnormal motor activity with confusion and amnesia e.g. lip
smacking, bicycling.
• Persist for few minutes
B. Primary Generalized:
• Petit-mal (absence)
• Myoclonic.
• Generalized tonic-clonic seizure (GTCS).
• Tonic.
• Clonic.
• Atonic
Clinical Picture of GTCS:
• Tonic phase lasts several seconds. All the muscles are in tonic spasm leading
to stop of respiration and sometimes epileptic cry.
• Clonic phase lasts 1-2 minutes.
• Confusion phase may persist for seconds, minutes or hours.
Clinical picture of Absence seizures:

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 • It is generalized seizure which occurs commonly in children.
• It is frequent and may reach one hundred of times a day.
• Each attack lasts 15-30 seconds during which the child is unresponsive and
staring followed by immediate recovery

Diagnosis
Epilepsy or not?
a. Clinical:
- Description of the attacks (eye witness) e.g. circumstances, timing,
precipitating factors, symptoms preceding the attacks, during the attack
and after the attack.
- Medical history, neurological history, psychiatric history, and family
history.
b. EEG (confirmatory).

Causes of epilepsy?
- Brain MRI is indicated in chronic cases while CT of the brain is indicated in
acute conditions e.g. trauma and stroke.
- Other investigations are done according to the suspected etiology e.g. blood
sugar, serum calcium and so on.

Differential Diagnosis
Item GTCS Psychogenic Seizures
Precipitants None Psychogenic stress
Circumstances In sleep Occur Not
When Occur Not
alone
Motor phenomena Typical Bizarre
(Tonic then clonic)

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Vocalization Absent Present
Injury Common Absent
Tongue biting Common Absent
Urine or fecal incontinence Common Absent
Consciousness Lost Preserved
Duration Usually short Prolonged
EEG Usually positive Negative
Serum prolactin level Elevated Not Elevated

Item GTCS Syncope

Precipitants None Usual (emotional or pain)
Circumstances Any Special as crowded hot
places, upright posture,
dentist chair, stress
situations
Onset Abrupt Gradual (graying of vision)
Respiration Sertorius, foaming Shallow & slow
Skin color Usually flushed Usually pale
Motor phenomena Major, typical None or minor
phases
Duration Minutes Few seconds
Injury Common Rare
Tongue biting Common Rare
Urine or fecal incontinence Common Rare
Postictal confusion Present Absent (rapid recovery)

Treatment
A. General measures:
1. Avoid dangers e.g. driving, machines, swimming, heights and so on.
2. Good sleep.
3. Teaching the family& the patient
B. Specific measures:
1. Pharmacotherapy (antiepileptic drugs "AEDs"):
2. Vagal nerve stimulation:
3. Surgery:
4. Ketogenic diet

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Pharmacotherapy (antiepileptic drugs "AEDs"):
• Start AEDs with recurrent seizures.
• Monotherapy is better than polytherapy.
• Start low and go slow (building up of the dose).
• Titration to reach the minimal therapeutic dose (lowest dose to control
seizures).
• Always check compliance of the patient and serum drug level.
Partial with or without secondary GTCS Primary GTCS Petit mal epilepsy
Carbamazepine Valproate Valproate
Phenytoin Lamotrigine Ethosuximide
Oxcarbazepine Phenytoin
Lamotrigine
Topiramate
− Carbamazepine (Tegretol) 400-1200 mg/day; (20-30 mg/kg/day).
− Oxcarbazepine (Trileptal) 600-1800mg/day
− Phenytoin (Epanutin) 200-400 mg /day; (5-8 mg/kg/day).
− Lamotrigine (Lamictal) 100-200 mg/day.
− Topiramate (Topamax) 100-200 mg /day.
− Valproate (Depakine) 600-1400 mg/day, (30-50 mg/kg/day).
STATUS EPILEPTICUS
✓ Continuous seizure activity for 5 minutes or more without return of
consciousness.
✓ Recurrent seizures (2 or more) without regaining conscious level in
between.
Treatment:
• General measures:
- In neurocritical care.
- ABC.
- Oxygen: through nasal cannula or mask
- ECG monitoring.
- Glucose iv infusion
- Take samples of blood for investigations: electrolytes, toxicology
screen, blood profile.
• Abort the seizures:
1. Midazolam: iv or IM

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 2. Lorazepam: iv
3. Phenobarbital: iv 15mg/kg/dose
4. Diazepam: rectal
• 2nd line therapy:
- Fosphenytoin: iv
- Valproic acid: iv
- Levitiracetam: iv
- If seizures continue, repeat 2nd line or anesthetic doses of thiopental
or propofol
INTRACTABLE EPILEPSY
Seizures persist despite treatment with at least 2 antiepileptic drugs
tolerated at reasonable dosage.
Treatment:
- Optimize correct diagnosis, treatment and avoid seizures triggers
- Ketogentic diet and high dose vit. B6 in children,
- Polytherapy (another one or two drugs).
- Vagal nerve stimulation.
- Surgery usually resective.

EPILEPSY AND PREGNANCY

Effect of pregnancy on epilepsy:
- One third show increase in frequency of seizures, one third show
decrease and one third show no change.
Effect of AEDs on pregnancy:
- Risk of teratogenicity of AEDs is much lower than the risk of epilepsy
on both mother and baby.

- AEDs during pregnancy are better monotherapy, minimal therapeutic

doses, and use of folic acid 1mg or more per day in order to lower the
risk of teratogenicity.

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03
INFECTIONS OF CNS

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 Meningitis
Definition:
− It is the inflammation of the meninges which are the membranes covering
the CNS, including the dura, arachnoid and pia maters.
− Inflammation of the dura is rare and is known as pachymeningitis, while
inflammation of
− The pia-arachnoid is more common and is known as leptomeningitis.

Leptomeningitis can be classified into:

1. Bacterial meningitis:
a. Pyogenic: Meningococcal (most common), pneumococcal,
streptococcal, H-influenza.
b. Tuberculous meningitis.
2. Viral meningitis.
3. Spirochetal (syphilitic) meningitis.
Meningococcal Meningitis (Most common form):
Causative organism: gram negative cocci
Mode of transmission: Droplet

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Clinical Picture:
The disease usually shows 2 stages:
1. The septicemic stage
2. The meningitic stage
The septicemic stage
Symptoms: Onset is acute with a
triad of fever, headache and
vomiting
Signs: The temperature is 39-40°C
with drowsiness and a skin rash
(petechiae) may appear
The meningitic stage
Symptoms: The headache becomes
severer with generalized pain,
irritability, photophobia and
hypersensitivity.
The patient tends to lie in an
attitude of flexion, away from the
light, and resists any manipulation
Signs:
- Fever with tachycardia.
- Disturbed consciousness
- Meningeal irritation sings
- Cranial nerves

Course:
- In untreated cases: the picture remains for 1-3 weeks. The patient
either recovers gradually or gets worse and dies.
- With adequate therapy, recovery usually occurs in few days.
- In complicated cases: Waterhouse-Frederickson's syndrome

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Investigations
1. Blood examination shows leukocytosis of about 20.000/mm3.
2. CSF examination shows:
- High pressure.
- Turbid.
- Polymorphonuclear pleocytosis (about 1000/mm3).
- Meningococci by gram stain.
- High protein.
- Low sugar and chlorides.
Differential Diagnosis
• Meningism
• Subarachnoid hemorrhage
• Other types of meningitis:
a. other causes of pyogenic meningitis:
- A primary source of infection can be discovered.
- The skin rash is absent.
- Demonstration of the causative organism in CSF.
b. Causes of lymphocytic meningitis
Treatment
1. Specific Treatment:
Ampicillin sulbactam (200 mg/kg/day) IV in divided
doses every 4 hours.
OR
In neonates Third generation cephalosporin (e.g. cefotaxime 200
mg/kg/day) IV in divided doses every 4 hours.
PLUS
Aminoglycoside (e.g. amikacin 15 mg/kg//day) IV in
divided doses every 12 hours.
In children up to Ampicillin + 3rd generation cephalosporin (as before)
6 years PLUS
Imipenem 500 mg IV q6h or 1 gm q8h.
For all other age Third generation cephalosporin (ceftriaxone or
groups cefepime 1-2 gm/12h IV )
OR cefotaxime 2gm/4-6h IV

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 OR ceftazidime 2 gm/8h IV
PLUS
Vancomycin (1 gm/12h IV OR penicillin-G 4 million
units/4 h IV.

2. General Treatment: proper nursing, feeding and analgesics.

3. Prophylaxis:
1. Rifampicin 600 mg twice daily orally for 2 days to all exposed
persons.
2. Meningococcal vaccine (live attenuated) is given esp. to children 0.5
ml S.C it gives immunity for 2-3 years.
Tuberculous Meningitis
• The onset is insidious, usually preceded by prodromal symptoms
of malaise, night fever, and sweating and weight loss.
• Signs of meningeal irritation are mild but headache and vomiting
are pronounced.
CSF findings in TB meningitis:
- The pressure is raised.
- The appearance is cloudy or ground glass a cob-web clot may appear on
standing.
- Cells are mainly lymphocytes are increased up to 500/mm3.
- Proteins are increased.
- Sugar is decreased to 20-40 mg%.
- Chlorides are markedly decreased and may reach below 600mg%.
- No organisms can be demonstrated by the usual staining methods, but
may be shown by the Ziel- Nelson stain
Treatment of TB meningitis:
Antituberculous Drugs:
1. Pyrazinamide: 1.2-1.5 Gm orally daily.
2. Ethambutol: 800 mg orally daily.
3. Isoniazid (INH): 300-600mg orally daily.
4. Rifampicin: 450 mg orally daily.

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 5. Vitamin B6: 40-50 mg orally daily

Encephalitis
Definition:
It is inflammation of the brain substance, when the spinal cord is involved the
term encephalomyelitis is used.
Types
The following are the main types:
1. Virus encephalitis and encephalomyelitis.
2. Non-viral encephalitis:
a. Bacterial: as a part of bacterial meningo-encephalitis, typhoid and
others.
b. Parasites: malaria, toxoplasmosis, leishmaniasis, and others.
3. Suppurative encephalitis (Brain abscess).
4. Acute disseminating encephalomyelitis (ADEM)

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Viral Encephalitis
- Adult patients with encephalitis present with acute onset of flu-like
symptoms as fever, or severe headache, confusion, and sometimes
seizures.
- Personality or mood changes may precede onset.
- Younger children or infants may present with irritability, poor appetite
and fever.
- Neurological examinations usually reveal a drowsy or confused patient.
- Stiff neck, due to the irritation of the meninges covering the brain,
indicates that the patient has either meningitis or meningoencephalitis
Treatment of Virus Encephalitis:
1. Proper nursing.
2. Antibiotics, vitamins and tonics.
3. In herpes simplex encephalitis acyclovir is given in a dose of 10mg/kg
by IV infusion over 1hr. / 8hrs for 10-14 days.
4. Gancyclovir in CMV.
Brain abscess
Etiology
1. Direct spread from vicinity e.g. middle ear or nasal sinuses.
2. Hematogenous spread particularly from chest e.g. lung abscess.

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Clinical Picture
• Onset may be acute, subacute or insidious.
• In addition to those of the original disease (e.g. otitis media or lung
abscess)
There are 3 groups of manifestations:
- General manifestations of infection as pyrexia and leukocytosis.
- Manifestations of increased intracranial pressure as those of a tumor.
- Focal depending upon the site and are similar to those of a tumor
Prognosis
• Untreated cases usually end fatally.
• Treated cases usually recover, though epileptic fits or residual
neurological deficits e.g. hemiparesis may occur depending upon the
site of the abscess.
Treatment
1. Acute cases should receive preoperative treatment for at least 2 weeks
to allow for capsule formation. Such treatment consists of penicillin I.V.
in doses similar to that of meningitis then surgical removal of the
abscess.
2. Chronic cases need excision straightforward.

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04

STROKE

22
Cerebrovascular Stroke
Cerebro-vascular stroke "CVS" is a rapidly developing clinical signs of focal
or global disturbance of cerebral function, with symptoms lasting 24 hours or
longer or leading to death, with no apparent cause other than of vascular
origin.
Stroke is divided into:
• Ischemic.
• Hemorrhagic:
1. Intracerebral
2. Subarachnoid strokes.
Ischemic Stroke
Etiology
1. Thrombosis of the arteries in the CNS may be due to
a) Abnormalities of the vessel wall (atherosclerosis- vasculitis-dissection).
b) Abnormalities of the blood e.g. polycythemia, sickle cell anemia.
c) Disturbances of the blood flow.
2. Embolism
• may complicate degenerative disease of the arteries to the CNS
• it may arise from the heart as a result of:
a) valvular disease. b) Atrial fibrillation. c) Recent myocardial infarction.
Clinical Picture
Carotid ischemia Vertebrobasilar ischemia
1. Hemiparesis or hemipleia. 1. Double vision or manifestation
2. Hemi-hypoesthesia. of other cranial nerve affection
3. Language and speech as Dysphagia and Dysarthria.
4. disturbances if dominant 2. Disturbed conscious level.
5. hemisphere is affected. 3. Blindness or visual field defect.

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 6. Poor vision or blindness. 4. Ataxia & vertigo (Dizziness).
7. Seizures may occur. 5. Hemiparesis or quadriparesis.
8. Sometimes headache

Transient ischemic attacks

These are episodes of focal neurological deficits due to brain ischemia which
resolve completely in less than 1 hour.
Investigations
1. Brain non-contrast CT (NCCT). It is done initially to exclude intracerebral
hemorrhage.
2. Brain MRI and/or MRA; can show the infarction in the first hour.
3. Carotid duplex.
4. Trans-cranial Doppler.
5. Laboratory: CBC, ESR, hematocrite value, lipid profile, Blood sugar, renal
and liver functions.
6. ECG / Echocardiogram.
7. Others according to the possible etiology.
Treatment
1-Fibrinolytic therapy (recombinant tissue plasminogen activator; r-TPA).
2-Endovascular Procedures: Mechanical thrombectomy,
Prevention:
A. Control of risk factors: for example, hypertension DM, dyslipidemia,
treating heart diseases, stop smoking, reducing body weight and regular
physical exercise.
B. Anticoagulants.
C. Antiplatelet Therapy: 1. Aspirin (Acetylsalicylic acid) 75-300 mg/day
orally. 2. Clopidogrel 75 mg/day orally. 3. Cilostazole 100 mg twice daily
orally.

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D. Anti-edema measures (In massive edema): mannitol, diuretics,
dexamethasone.
E. Neuro-protective agents.
F. Anti-convulsant: in case of seizures.
G. Surgery: 1. Carotid endarterectomy if carotid stenosis more than 75%.
2. Decompression for massive infarction.

Hemorrhagic stroke
Types:
1- Intra-cerebral hemorrhage.
2- Subarachnoid hemorrhage.
Intra-cerebral hemorrhage.
• Presentation is maximal at the start "sudden onset".
• It occurs during activities rather than during rest.
• Headache and vomiting are common.
• Conscious level is usually disturbed.
• Focal neurological signs depend on the site of the bleed
• Seizures and features of raised intracranial pressure may occur.
• Poorly controlled hypertension is the most common risk factor.
• Other causes include: bleeding into tumors, trauma, blood disorders,
blood vessel disorders e.g. arteriovenous mal-formations, vasculitis..
• Complications include
- hydrocephalus and brain herniation.
- Large hematomas have poor prognosis.
• Investigation: CT is diagnostic, CT angiography may be needed.

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Risk factors
Modifiable Non-Modifiable
- Hypertension. - Age.
- TIAS. - Male gender.
- Heart diseases (AF). - Black races.
- Asymptomatic carotid - Genetic factors.
stenosis. - Positive family history of
- Diabetes mellitus. stroke.
- Sedentary lifestyle. - A prior stroke.
- Dyslipidemia.
- Obesity.
- Cigarette smoking.
- Alcohol consumption.
Treatment
1. Rapid admission in stroke unit.
2. Control of blood pressure.
3. Care of the comatose patient and ventilatory support if needed.
4. Anti-edema measures.
5. Anti-epileptics in cases of seizures.
6. Surgical evacuation in superficially located and cerebellar hematomas
or ventricular drainage for acute hydrocephalus.

Subarachnoid Hemorrhage
Etiology:
The patient is usually young age, and is most commonly from:
1. Rupture of an aneurysm typically at junctions in the circle of Willis.
2. Arteriovenous malformations.
3. Other rare causes:
A) Trauma. B) Mycotic aneurysm. C) Coagulopathies.

26
Clinical picture:
1. Sudden (seconds) very severe headache (worst headache) with
photophobia, nausea, vomiting and signs of meningism (neck stiffness and
kernig’s sign).
2. With more severe hemorrhage, intracranial pressure may rise, and the
level of consciousness deteriorates.
3. . Focal neurological signs may develop as a result of:
a. False localizing effect of raised intracranial pressure.
b. Coexistent intracerebral hemorrhage.
c. Spasm of the vessels, as a result of the irritant effect of blood →
ischemia.
Investigations:
CT brain and CT angiography are indicated.
Treatment:
- Admission of the patient to ICU.
- Control of blood pressure.
- Control of headache up to morphia.
- Care of comatose
- Calcium channel blocker (Nimodipine) to prevent arterial vasospasms.
- Neurological intervention to coil the aneurysm.
- Surgical clamping of the aneurysm.
Hemiplegia
• Hemiplegia is paralysis of one half of the body-which includes arm, leg and
often face. Hemiparesis means weakness of one side of the body.
• Results from pyramidal tract lesion (upper motor neuron lesion)

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Clinical Manifestations of pyramidal tract lesion:
1. Selective weakness or paralysis; affecting fine skilled movements,
being more distal and being greater in the extensors of the arms and
flexors of the legs i.e., selective pyramidal weakness.
2. Superficial reflexes e.g., abdominal and cremasteric reflexes are lost or
diminished.
3. Positive Babinski sign: dorsiflexion of big toe and fanning of the other
toes.
4. Increased muscle tone i.e., hypertonia (clasp-knife spasticity).
5. Increased deep tendon reflexes with or without clonus.
6. No involuntary movement.
7. Mild Disuse atrophy.

28