Neurology

Updated: March 2023

NEUROLOGY (NERVOUS SYSTEM & DISEASES) FINAL EXAM TOPIC CHECKLIST

1. Headache & Facial Pain 4. Multiple Sclerosis & Differentials

2. Disorders of Equilibrium 5. Stroke

Vertigo 6. Seizures & Syncope

Ataxia 7. Coma & Confusion States

Peripheral Vestibular Disorders 8. Myasthenia

3. Polyneuropathy 9.

Acute (GBS) 10.Brain Injuries

Chronic 11.Brain Tumors

Neurology
Updated: March 2023
HEADHACE & FACIAL PAIN

RED FLAGS:
1. Symptoms of systemic
disease e.g. fever, bleeding,
weight loss, stiff neck, rash
2. Older age of onset (>50yrs)
3. Acute onset
4. Atypical onset
5. Neoplastic history
6. Continuous intensifying
headache
7. New-onset headache in
immunocompromised
patient (eg, HIV, cancer)
8. Autoimmune disease
9. Focal neurological symptoms
10. Precipitated by sneezing,
exercise.
11. Post traumatic onset
12. Painkiller overdose
13. Headache with aura
14. Papilledema
15. Pregnancy
 Neurology
Updated: March 2023

MIGRAINE TENSION CLUSTER

Localisation

Character Unilateral; pulsating; moderate-severe - Unilateral ; piercing/stabbing/burning ;

intensity; limits physical activity -moderate severe intensity
intensity; no effect of physical activity
Course W/O Aura WITH AURA Initially episodic lasting mins to days. Could occur from once every other day to
Recurrent, o infrequent = <1d/m; 8x/d and attacks last 15-180 mins.
slow progressing symptoms (flashes o but <15d/m for Clustering of attacks could last 3-16 weeks
and attacks may of light) develop 3m) followed by periods of remission
last from 4-72 gradually over 5- But may progress to chronic (daily; o Episodic - g 7 - 365
hours 20 mins and last >15d/m for >3mo.) days, at least 1 month apart (remission)
<60 mins Chronic lasts longer than a year with no
remission (or remission <1 month)
Additional Nausea/vomiting ; No nausea/vomiting ; (autonomic symptoms):
symptoms Phono/photophobia, eye-bulge feeling Phono/photophobia may occur ; lacrimation, nasal congestion, rhinorrhoea,
Reversible focal neurologic (visual, pericranial muscle tenderness ; No sweating (face/ forehead), miosis, ptosis,
paraesthesia) autonomic symptoms conjunctival infection
Pathogenesis Role of serotonin: Theories: Psychological actions, pain Activation of trigeminal-autonomic reflex ;
o constriction of big arteries/veins control deficit, genetic predisposition arachnoid vessels & neurogenic
o dilation of capillaries/arterioles and decreasing of grey brain matter inflammation = pain sensation; ipsilateral
 Neurology
Updated: March 2023
hypothalamus dysfunction = neurovascular
headache
Risk Factors Hormones: Sensoric-visual: Food: Idiopathic Often occurs at night
/ Triggers Menstruation Light, sound Alcohol F>M M>F
Contraceptives Odour Cheese 30-39y 27-31y
Pregnancy Temp Chinese
Menopause Stress
travelling
Tests Exclusion Tests: CBC, Thyroid hormones, MRI/CT, LP to rule out neurological cause
Complication W/O Aura WITH AURA Medication-overuse headache!
Attack duration Persistent aura
>72hrs Stroke
Chronic migraine Seizures
(>15d/month)
Medication-overuse headache!
Treatment Attack (staircase) Prophylaxis (if >3-4x/ Episodic: Chronic: Attack Prophylaxis:
1. Paracetamol (1g) month) 1. NSAIDs 1. TCA 1. O2 (7-15L 1. CCB-Verapamil
2. Paracetamol + 1. Beta blockers 2. Paracetamol 2. Anti-epileptics 100%) 2. Corticosteroids
caffeine / (propranolol) 3. Relaxation 2. Serotonin 3. Lithium carbonate
metoclopramide 2. Anti-epileptics - methods receptor 4. Methysergide
/ codeine Topiramate 4. Psychotherapy agonists 5. Anti-epileptics
3. Effective NSAIDS 3. CCB- Verapamil 5. Correct Triptans Topiramate
Serotonin receptor 4. TCA ergonomics 3. Lidocaine Surgery- deep
agonists - Triptans (amitriptyline) 6. Reflexotherapy i/n stimulation of post.inf.
5. NSAIDs 4. Octreotide hypothalamus
Botulinum toxin
injection (near
trigeminal)
 Neurology
Updated: March 2023 HEADACHE & FACIAL PAIN DIFFERENTIALS:

Typically >50y Headache usually worse URT signs rhinorrhea, History of regular (and Sharp shooting pain / electric shock
Temporal artery swelling in mornings congestion combined) medication in the jaw, teeth or gums
Temporal pain, vision Visual disturbances Sinus pain (maxillary, use Short, unpredictable attacks that last
disturbed, jaw pain (diplopia, hemianopia, ethmoidal sinus area) Constant pain (for few seconds to 2 mins
Night sweats loss) 15+d/m) Usually unilateral (except in MS)
Focal neurologic deficits No other explanation
Ischaemic chest pain, Tx: Carbamazepine (anti-convulsant)
maybe back pain
Renal symptoms
(poly/noct / hematuria)

*If chronic pain - ALSO consider: Hemicrania continua (continuous headache)-

sharp, stabbing) 3-5x/d
 Neurology
Updated: March 2023 VERTIGO
TRUE VERTIGO PSEUDO-VERTIGO
Objective vertigo: an illusion of movement of the Possible accompanying symptoms: This is just Dizziness
environment o Autonomic (nausea, vomiting, blush or pallor,
Subjective vertigo: sense of turning of one’s body angst) o Sway/swing
o Nystagmus or impairment of vision o Dizziness before syncope
o Most often benign, but could be a symptom of o Imbalance o Feeling of swimming
serious neurological disorder o Feeling of instability
o Weakness
o Strange feeling in head
Acute Chronic o Fatigue
Hours-days, months months
Causes: Causes: Causes:
Vertebrobasilar ischaemia, labyrinthitis, vestibular Cerebral ischaemia, Hypertension, Chronic otitis, 1. Hyperventilation
neuronitis, cerebellar stroke, bilateral vestibular Head trauma,
deficiency, cochlear nerve neurinoma, labyrinth 2. Cardiovascular
apoplexy, Multiple sclerosis (arrhythmia, aortic
Peripheral Vertigo Central Vertigo stenosis, hypotension)

Area Affect the labyrinth of the inner ear / Affects brainstem vestibular nuclei or their 3. Orthostatic hypotension
affected vestibular part of CN 8 connections or cerebral cortical lesion (medications,
(labyrinthitis, vestibular neuronitis, (Vertebrobasilar ischaemia, Siringobulbia, hypotension)
Meniere’s disease, BPPV, trauma, toxicity, Vestibular epilepsy, Multiply sclerosis, Brain stem
pontocerebellar angle tumor) tumours, Intoxication, Cerebellar disorders,) 4. Psycogenic disorders
Sudden onset, intermittent, lasts for brief Gradual onset, continuous and is mild. usually (anxiety, hysteria)
Duration
periods and more severe than central chronic
vertigo 5. Hematological disorders
(anemia)
Nystagmus Nystagmus is always present with Can be with or without nystagmus (if present-
peripheral vertigo (unidirectional vertical, unidirectional or multidirectional)
(horizontal/rotary but never vertical)) 6. Pulmonary emphysema
Gaze Visual fixation decreases nystagmus Visual fixation causes no change in nystagmus
7. Hypoglycemia
fixation
Additional CN8 dysfunction (hearing loss, tinnitus), If due to central lesion- motor/sensory defects,
8. Thyroid diseases
symptoms severe nausea hyperreflexia, extensor plantar responses,
dysarthria, limb ataxia
Medicamental intoxication
Neurology
Updated: March 2023
DIAGNOSIS OF VERTIGO TREATMENT OF VERTIGO
1. Detailed anamnesis Vestibular origin Vertigo:
2. Detail neurological and Otolaryngologic examination • Antihistamines (Betahistine)
a. Examination of cranial nerves • Benzodiazepines (Diazepam, Alprazolam)
b. Gait, coordination, balance examination • Meniere’s- diuretics
c. Electronistagmography • Rehabilitation of vestibular disorders
i. quantative evaluation of nystagmus, it’s type, direction, o Physical exercises (e.g. Canalith repositioning
frequency, duration manoeuvres for BPPV)
ii. audiometrical investigation
iii. tonic, lingual audiometry Vascular origin Vertigo:
d. BERA (brain evoked auditory potentials investigation) • Nicergoline
• Vinpocetine
3. Vertigo provocative tests • Nootrops Egb 761 (Ginko)
a. Ortostatic hypotension test
b. Rapid eyes movements
c. Intensive breathing exercises
d. Test for benign positional vertigo evaluation (Hallpike test)
e. Perilimfal fistula test

4. Otoneurological tests

5. Radiological investigations in case of suspicion of brain disorder

a. CT
b. MRT
c. Ultrasound brain vessels investigations
d. Angiography

6. Blood analysis

7. ECG
 Neurology
Updated: March 2023 PERIPHERAL VESTIBULAR DISORDERS THAT CAUSE VERTIGO

BPPV (benign paroxysmal positional vertigo) Meniere Disease Vestibular neuronitis

Duration Seconds Minutes to hours Hours (>24) to weeks
Symptom Brought on when turning in bed or tilting the Attack remissions and exacerbations Decrease during a few days,
Progression head backward to look up Symptoms increase during attack worsen due to rapid head
Different attack frequency movements and
Vertigo Brief rotational dizziness episodes Severe, rotational repeating attacks Rapid onset of severe, persistent
(fatiguing)
Additional 1. Possible nausea 1. Burr in ear (tinnitus) 1. Nausea, vomiting
Symptoms No neurological findings 2. Loss of hearing 2. Gait instability
3. Ear fullness 3. No neurological findings
4. Nausea, vomiting + unilateral hearing loss =
5. Disabling imbalance labyrinthitis

Nystagmus Peripheral (Horizontal, jerk) positional Peripheral (Horizontal-rotational, jerk) Peripheral (horizontal, jerk)
positional spontaneous = vestibular
nystagmus ; (+) head thrust sign
Epidemiology >60y 30-50y <30y
Etiology o Canalithiasis (calcium debris within the Excess endolymphatic fluid pressure - Viral / post-viral inflammatory
posterior semi-circular canal) > episodic inner ear dysfunction disorder, affecting the vestibular
o Head and neck trauma o ↑ Volume of endolymph portion of the eighth cranial nerve.
o Otitis o Disturbed resorption of
o Stapedotomy endolymph
o Brain stem disorders (eg. MS) o Labyrinth rupture
o Intoxication
 Neurology
Updated: March 2023
NYSTAGMUS
Involuntary, repetitive, rhythmic movement of the eyes

Peripheral Nystagmus Central Nystagmus

Cause labyrinth of the inner ear / vestibular part of CN 8 Brainstem or cerebellar cause
(labyrinthitis, vestibular neuronitis, Meniere’s disease, (Vertebrobasilar ischaemia, Siringobulbia, Vestibular
BPPV, trauma, toxicity, pontocerebellar angle tumor) epilepsy, Multiply sclerosis, Brain stem tumours,
Intoxication, Cerebellar disorders)

Direction Horizontal-rotational and jerk (unidirectional) Vertical, pendular (horizontal) (unidirectional or

multidirectional)
Fast-beat Fast beat away from side of lesion Fast beat towards side of lesion
Gaze fixation Relieved/inhibited by gaze fixation Not relieved by gaze fixation,
Direction Does not change direction during the change of eyes Change direction during eye position changes
change movement direction (Gaze evoked nystagmus)
Cerebellar signs No cerebella signs Cerebella signs
Grades 1. Head-shaking - induced only by vigorous shaking of head
2. I - only with gaze in direction of nystagmus
3. II - visible with gaze straight ahead OR in direction of nystagmus
4. III - present in all directions of gaze
 Neurology
Updated: March 2023
JERK PENDULAR
Has slow and fast phase (Slow (reflexic) conjugate deviation (pathologic) Equal speed phases (oscillation like pendulum)
occurs in one direction, followed by a rapid conjugate movement
returning the eyes to the original position (normal))

Convergence- retraction `Horizontal (pendular)

Midbrain tegmental Congenital loss of
damage visual acuity /
multiple sclerosis

Upward jerking of eyes back into the orbit during upward gaze Oscillation of equal velocity around a centre point

Vertical (see-saw)
Downbeat nystagmus
Optic chiasm lesion
Lower medullary damage

One eye appears to rise while the other appears to fall

Irregular downward jerking of the eyes during downward gaze

Vestibular nystagmus
Vestibular disease or
cochlear dysfunction

Horizontal or rotary movements of eye

Neurology
Updated: March 2023

LESIONS AND THEIR RELATION TO VERTIGO & NYSTAGMUS

 Neurology
Updated: March 2023 ATAXIA
Lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements.

Hemiplegic gait (Circumduction) Parkinsonian gait (Hypokinetic) Wide based gait High Steppage gait
(Ataxic, Cerebellar)
the leg is held stiffly and Slow gait, stiff bent posture, small Uncoordinated stomping, Advancing leg is raised high then
abducted with each step and steps. Lack of accessory arm unsteady, deviating irregularly placed on the ground toe first.
swung around to the ground in movements. Turning requires from a straight line. Heel-to-toe Often with an audible slap. Due to
front, forming a semicircle. multipole small steps walking impossible foot drop caused by peroneal
nerve palsy
 Neurology
Updated: March 2023 VERTIGO
TRUE VERTIGO PSEUDO-VERTIGO
Objective vertigo: an illusion of movement of the Possible accompanying symptoms: This is just Dizziness
environment o Autonomic (nausea, vomiting, blush or pallor, angst)
Subjective vertigo: o Nystagmus or impairment of vision o Sway/swing
o Imbalance o Dizziness before syncope
o Most often benign, but could be a symptom of o Feeling of swimming
serious neurological disorder o Feeling of instability
o Weakness
o Strange feeling in head
Acute Chronic o Fatigue
Hours-days, months months
Causes: Causes: Causes:
Vertebrobasilar ischaemia, labyrinthitis, vestibular Cerebral ischaemia, Hypertension, Chronic otitis, Head 1. Hyperventilation
neuronitis, cerebellar stroke, bilateral vestibular trauma,
deficiency, cochlear nerve neurinoma, labyrinth 2. Cardiovascular (arrhythmia,
apoplexy, Multiple sclerosis aortic stenosis, hypotension)
Peripheral Vertigo Central Vertigo
3. Orthostatic hypotension
Affect the labyrinth of the inner ear / Affects brainstem vestibular nuclei or their connections (medications, hypotension)
Area
affected vestibular part of CN 8 or cerebral cortical lesion
(labyrinthitis, vestibular neuronitis, (Vertebrobasilar ischaemia, Siringobulbia, Vestibular 4. Psycogenic disorders (anxiety,
epilepsy, Multiply sclerosis, Brain stem tumours, hysteria)
pontocerebellar angle tumor) Intoxication, Cerebellar disorders,)
Sudden onset, intermittent, lasts for brief Gradual onset, continuous and is mild. usually chronic 5. Hematological disorders
Duration
periods and more severe than central (anemia)
vertigo
Nystagmus is always present with Can be with or without nystagmus (if present- vertical, 6. Pulmonary emphysema
Nystagmus
peripheral vertigo (unidirectional unidirectional or multidirectional)
(horizontal/rotary but never vertical)) 7. Hypoglycemia
Gaze Visual fixation decreases nystagmus Visual fixation causes no change in nystagmus
8. Thyroid diseases
fixation
CN8 dysfunction (hearing loss, tinnitus), If due to central lesion- motor/sensory defects,
Additional
Medicamental intoxication
symptoms severe nausea hyperreflexia, extensor plantar responses, dysarthria,
limb ataxia
Neurology
Updated: March 2023
DIAGNOSIS OF VERTIGO TREATMENT OF VERTIGO
1. Detailed anamnesis Vestibular origin Vertigo:
2. Detail neurological and Otolaryngologic examination Antihistamines (Betahistine)
a. Examination of cranial nerves Benzodiazepines (Diazepam, Alprazolam)
b. Gait, coordination, balance examination - diuretics
c. Electronistagmography Rehabilitation of vestibular disorders
i. quantative o Physical exercises (e.g. Canalith repositioning
frequency, duration manoeuvres for BPPV)
ii. audiometrical investigation
iii. tonic, lingual audiometry Vascular origin Vertigo:
d. BERA (brain evoked auditory potentials investigation) Nicergoline
Vinpocetine
3. Vertigo provocative tests Nootrops Egb 761 (Ginko)
a. Ortostatic hypotension test
b. Rapid eyes movements
c. Intensive breathing exercises
d. Test for benign positional vertigo evaluation (Hallpike test)
e. Perilimfal fistula test

4. Otoneurological tests

5. Radiological investigations in case of suspicion of brain disorder

a. CT
b. MRT
c. Ultrasound brain vessels investigations
d. Angiography

6. Blood analysis

7. ECG
 Neurology
Updated: March 2023

PERIPHERAL VESTIBULAR DISORDERS THAT CAUSE VERTIGO

BPPV (benign paroxysmal positional vertigo) Meniere Disease Vestibular neuronitis

Duration Seconds Minutes to hours Hours (>24) to weeks
Symptom Brought on when turning in bed or tilting the Attack remissions and exacerbations Decrease during a few days,
Progression head backward to look up Symptoms increase during attack worsen due to rapid head
Different attack frequency movements and
Vertigo Brief rotational dizziness episodes Severe, rotational repeating attacks Rapid onset of severe, persistent
(fatiguing)
Additional 1. Possible nausea 1. Burr in ear (tinnitus) 1. Nausea, vomiting
Symptoms No neurological findings 2. Loss of hearing 2. Gait instability
3. Ear fullness 3. No neurological findings
4. Nausea, vomiting + unilateral hearing loss =
5. Disabling imbalance labyrinthitis

Nystagmus Peripheral (Horizontal, jerk) positional Peripheral (Horizontal-rotational, jerk) Peripheral (horizontal, jerk)
positional spontaneous = vestibular
nystagmus ; (+) head thrust sign
Epidemiology >60y 30-50y <30y
Etiology o Canalithiasis (calcium debris within the Excess endolymphatic fluid pressure - Viral / post-viral inflammatory
posterior semi-circular canal) > episodic inner ear dysfunction disorder, affecting the vestibular
o Head and neck trauma o Volume of endolymph portion of the eighth cranial nerve.
o Otitis o Disturbed resorption of
o Stapedotomy endolymph
o Brain stem disorders (eg. MS) o Labyrinth rupture
o Intoxication
 Neurology
Updated: March 2023 NYSTAGMUS
Involuntary, repetitive, rhythmic movement of the eyes

Peripheral Nystagmus Central Nystagmus

Cause labyrinth of the inner ear / vestibular part of CN 8 Brainstem or cerebellar cause
(Vertebrobasilar ischaemia, Siringobulbia, Vestibular
BPPV, trauma, toxicity, pontocerebellar angle tumor) epilepsy, Multiply sclerosis, Brain stem tumours,
Intoxication, Cerebellar disorders)

Direction Horizontal-rotational and jerk (unidirectional) Vertical, pendular (horizontal) (unidirectional or

multidirectional)
Fast-beat Fast beat away from side of lesion Fast beat towards side of lesion
Gaze fixation Relieved/inhibited by gaze fixation Not relieved by gaze fixation,
Direction Does not change direction during the change of eyes Change direction during eye position changes
change movement direction (Gaze evoked nystagmus)
Cerebellar signs No cerebella signs Cerebella signs
Grades 1. Head-shaking - induced only by vigorous shaking of head
2. I - only with gaze in direction of nystagmus
3. II - visible with gaze straight ahead OR in direction of nystagmus
4. III - present in all directions of gaze
 Neurology
Updated: March 2023
JERK PENDULAR
Has slow and fast phase (Slow (reflexic) conjugate deviation (pathologic) Equal speed phases (oscillation like pendulum)
occurs in one direction, followed by a rapid conjugate movement
returning the eyes to the original position (normal))

Convergence- retraction `Horizontal (pendular)

Midbrain tegmental Congenital loss of
damage visual acuity /
multiple sclerosis

Upward jerking of eyes back into the orbit during upward gaze Oscillation of equal velocity around a centre point

Downbeat nystagmus Vertical (see-saw)

Optic chiasm lesion
Lower medullary damage

One eye appears to rise while the other appears to fall

Irregular downward jerking of the eyes during downward gaze

Vestibular nystagmus
Vestibular disease or
cochlear dysfunction

Horizontal or rotary movements of eye

Neurology
Updated: March 2023 LESIONS AND THEIR RELATION TO VERTIGO & NYSTAGMUS
 Neurology
Updated: March 2023 ATAXIA
Lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements.

Hemiplegic gait (Circumduction) Parkinsonian gait (Hypokinetic) Wide based gait (Ataxic, Cerebellar) High Steppage gait
the leg is held stiffly and Slow gait, stiff bent posture, small Uncoordinated stomping, unsteady, Advancing leg is raised high then placed on
abducted with each step and steps. Lack of accessory arm deviating irregularly from a straight the ground toe first. Often with an audible
swung around to the ground in movements. Turning requires line. Heel-to-toe walking impossible slap. Due to foot drop caused by peroneal
front, forming a semicircle. multipole small steps nerve palsy
 Neurology
Updated: March 2023
ACUTE INFLAMMATORY POLYRADICULONEUROPATHY: GUILLIAN BARRE SYNDROME (GBS)

ETIOPATHOGENESIS CLINICAL DIAGNOSIS TREATMENT/ MANAGEMENT

1. Infection 1-4 weeks Initially: Parasthesia in the toes and Clinical Supportive care
before the onset of fingertips Must include: Management of respiratory
GBS. Advanced disease: progressive weakness of more than 1 failure and autonomic
1. Symmetric lower extremity weakness limb (legs and arms) (minimal dysfunction;
Most common: ascending weakness over hours to weakness) paralysis Prophylaxis for DVT;
C. Jejuni days (stocking sign) hands become Distal areflexia with proximal ECG monitoring for
CMV affected areflexia or hyporeflexia arrhythmias;
Assess bulbar function
Supporting features:
2. Post-infectious 2. Neuropathic pain in limbs/ back (can be
involvement of cranial nerves
autoimmune reaction severe) Medications:
(especially VII)
due to cross-reactive High dose of Intravenous
antibodies against 3. Ascending paralysis; severe respiratory Immunoglobulins 400mg/kg/d
CSF fluid sample:
schwann muscle weakness respiratory failure for 5 days
elevated protein levels
cells/gangliosides
4. Reduced/abscent reflexes of arms/legs normal white blood cell counts
Plasmapheresis To remove
(albuminocytologic dissociation)
3. Segmental circulating antibodies,
5. Cranial nerve involvement: bilateral Oligoclonal bands
demyelination
facial nerve palsy; occulomotor Plasma exchange in very
weakness Nerve conduction studies and EMG
4. Axonal degeneration severe cases may be useful/ if
(Optic nerve not affected as it is part of Abnormalities related to motor nerve
IVIG is contraindicated
the CNS) conduction
Most common form:
Acute inflammatory Repeat treatment after 2 weeks if
6. Dysautonomia: Serology
demyelinating no effect!
polyradiculopathy (AIDP) diarrhoea/constipation, Anti- GM1 antibodies (against
brady/tachycardia, urinary retention gangliosides) and detection of other
(Glucocorticoids not useful!)
autoantibodies;
confirmation of previous infection
 Neurology
Updated: March 2023
CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY
CLINICAL DIAGNOSIS TREATMENT/ MANAGEMENT
similar to Guillain Barré syndrome except Clinical Supportive care
that: Must include: Management of respiratory failure
it follows a chronic progressive course, Chronically progressive, stepwise, or recurrent and autonomic dysfunction;
or a course character- ized by relapses, and symmetric proximal and distal weakness and sensory Prophylaxis for DVT;
no improvement is apparent within the 6 dysfunction of all extremities, developing over at ECG monitoring for arrhythmias;
months after onset. least two months; cranial nerves may be affected Assess bulbar function
Absent or reduced tendon reflexes in all extremities
Advanced disease: Medications:
1. Symmetric lower extremity weakness Supporting features Corticosteroids: prednisone 60-100
ascending weakness over hours to days CSF fluid sample: mg/d for 2-4 weeks, then gradually
(stocking sign) hands become affected elevated protein levels tapered to 5-20 mg every other
normal white blood cell counts (albuminocytologic day
2. Neuropathic pain in limbs/ back (can be dissociation) High dose of Intravenous
severe) Oligoclonal bands Immunoglobulins: 1 g/kg daily for 2
Nerve conduction studies and EMG days
3. Ascending paralysis; severe respiratory Partial conduction block Plasma exchange
muscle weakness respiratory failure Conduction velocity slowing In non-responsive patients:
Prolonged distal motor latencies methotrexate, azathioprine, or
4. Reduced/abscent reflexes of arms/legs cyclophosphamide
Imaging
5. Dysautonomia: Dysarthria, dysphagia, MRI showing gadolinium enhancement and/or
impotence, incontinence. hypertrophy of the cauda equina, lumbosacral or
cervical nerve roots, or the brachial or lumbosacral
plexuses
 Neurology
Updated: March 2023 MULTIPLE SLEROSIS

WHEN TO SUSPECT TYPES OF DISEASE COURSE

Young patient (15-60) avg.30, especially women Clinically isolated syndrome (CIS) a first episode of
On and off symptoms (especially if vison is affected) neurologic symptoms that lasts at least 24 hours and is caused by
inflammation or demyelination in the CNS.
Multiple CNS lesions
ALL OTHER DISEASES EXCLUDED (INFECTION) Relaxing or relapse-emitting type characterized by the episodic
ETIOLOGY & PATHOGENESIS appearance of new neurologic deficits, which can then remit completely or
almost completely, leaving residual deficits of greater or lesser severity,
Viruses- EBV ( in >99% of pts.), HSV Ab travel centrally and cause
without any progression of disease between the episodes.
inflammation
Secondary progressive type episodic worsening at first, followed by
Bacteria e.g. Chlamydia Reactive Ag stimulates the release of steady progression (possibly punctuated by further episodes)
cytokines
Primary progressive type steady progression from the beginning, most
commonly seen in older patients with spastic-paraparetic MS
Vit D hypovitaminosis Disbalance of inflammatory/protective
factors. Progressive relapsing type steady progression with interspersed
episodes of acute worsening, from the onset of the disease onward
Autoimmune Myelin reactive T helper cells, activated in periphery
and travel centrally and cross reactivity against myelin antigen
occurs.

Genetic: HLA DR15/DQ

PATHOGENESIS

Inflammation

Demyelination formation of MS plaques

Axon degeneration

MS occurs only affects CNS!

Neurology
Updated: March 2023
CLINICAL SYMPTOMS DIAGNOSIS
Functional Systems: MS is diagnosed on the basis of MRI findings and CSF
evaluation
Optic Sensory
To detect involvement of visual and spinal cord dorsal column
o Optic neuritis blurry o
pathways when imaging studies and clinical findings are negative
vision, dark spots in vison
clinically silent lesions Evoked
o Lhermitte symptom( when
Potentials:
Pyramidal you ask the patient to move
Visual Evoked Potentials (70-90%)
o Motor symptoms, neck down, electric shock
Somatosensory Evoked Potentials (40-60%)
monoparesis, paraparesis, travels down body),
Motor Evoked Potentials (70%)
spasticity o Trigeminal Neuralgia
(bilateral in the case of MS) Brain stem auditory Evoked Potentials (20%)
Cerebellar
o Ataxia of gait and limb Bladder and bowel, sexual
MCDONALDS CRITERIA: (GENERAL, FOR DIAGNOSIS)
dyscoordination, intention dysfunction
o Urinary Urgency , Dissemination in space (DIS)
tremor, nystagmus,
dysarthria, dysmetria +ve frequency, hesitancy and >/= 1 T2 oval lesion >3mm transverse diameter in at
Romberg sign incontinence least 2/4 areas of the CNS: Periventricular,
o Chronic constipation or Juxtacortical/Cortical, Infratentorial, Spinal cord.
Brain Stem incontinence
o Diplopia vertigo dizziness Dissemination in Time (DIT)
eye movement Uhthoff Phenomenon: the Detection of gadolinium enhancement at least
abnormalities dysphagia worsening of neurologic symptoms 3months after onset of the initial clinical event, not at
dysarthria in MS when the body gets the site corresponding initial event.
overheated from hot weather, Detection of a new T2 lesion at any time 30 days after
Cognitive dysfunction, pain, exercise, fever, stress or saunas and onset of initial clinical event.
fatigue, paroxysmal symptoms hot tubs
No better explanation of symptoms.
 Neurology
Updated: March 2023
MCDONALDS CRITERIA: (SPECIFIC)
RRMS (Relapsing-Remitting MS) PPMS (Primary Progressive MS) RELAPSE ATTACK
A history of TWO or more clinical MS attacks who 1 year of disability progression Appearance of new neurological symptoms,
have objective clinical evidence of two or more (retrospectively / prospectively caused by new MS plaques formation
lesions OR Objective clinical evidence of one lesion determined) independent of clinical Duration >24h
with reasonable historical evidence of prior attack relapse + 2 of the following:
Not related with infection and/or fever
(anatomical location)
For patients with a history of two or more attacks Minimal period between two relapses 30
1. 1 or more T2 hyperintense lesions in
who have objective clinical evidence of only ONE days (remission)
1 or more of 4 DIS typical regions
lesion, the criteria require one of the following:
2. 2 or more T2 hyperintense lesions in
the spinal cord Differentiate with pseudo relapse:
1. Additional evidence of DIS on MRI (2 of 4 typical 3. Presence of CSF-specific oligoclonal o Uhthoff phenomenon (the worsening of
regions) OR bands neurologic symptoms in MS when the body gets
2. Development of an additional clinical attack, overheated from hot weather, exercise, fever,
supported by objective clinical evidence stress or saunas and hot tubs)
o and/or paroxysmal disorders

SYMPTOMATIC TREATMENT
Spasticity - baclofen (intrathecal pump if severe) Bowel symptoms -
Tremor - proanolol, orthopaedic devices o if constipation: laxative (lactulose)
Bladder dysfunction - o if incontinence: loperamide Sexual dysfunction - for
o if hyperactivity: anticholinergic (oxybutynin) or TCA (amitriptyline) erectile dysfunction: sildenafil

o if retention: alfa-blockers (Tamsulosin) Depression - psychotherapy, SSRI (fluoxetine), TCA (amitriptyline)

Pain - TCA (amitriptyline), Anti-convulsant (gabapentin, carbamazepine), Opioids Fatigue - amantadine, SSRI, physical therapy
(tramadol)
Neurology
Updated: March 2023
TREATMENT BASED ON TYPE
CIS, RRMS Disease Modifying drugs (INF-Beta)

GA: Glatiramerum acetate ; Terl: Teriflunomide ; Fingo: Fingolimode ; Clad: Cladribine ; Nz: Natalizumab ; Az: Alemtuzumab ; Ocr:
Ocroelizumab

PPMS or SPMS DMD/ Immunosuppressants

RELAPSE

Glucocorticoids (IV methylprednisolone 1g/d for 3-5d followed by: Oral prednisone 1-1.5mg/kg and then taper dose) Must do in hospital
setting at first due to side effects.
Plasmapheresis If GC resistant
 Neurology
Updated:NEUROMYELITIS
March 2023 OPTICA (NMO) PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML)
Inflammation and demyelination of optic nerve and spinal Opportunistic JC virus infection, as a result of immune-suppression or drug such as
cord. Natalizumab that is used for MS

Diagnostic Criteria:
Definite Criteria Additional 2015 Criteria
1. Optic Neuritis Area postrema
2. Acute Myelitis syndrome (nausea,
3. At least 2 or 3 of: vomiting, hiccup)
a. Contiguous spinal cord
Brainstem syndromes
MRI lesion extending
(cranial nerve palsies)
over 3 vertebral
segments Symptomatic
narcolepsy (excessive
b. Brain MRI not meeting
daytime sleep)
diagnostic criteria for MS
c. NMO-IgG seropositive Symptomatic cerebral
syndrome + MRI
status
findings
ACUTE DISSEMINATED ENCEPHALOMYELITIS (ADEM)
A sudden widespread attack of inflammation in the brain and spinal cord often triggered
by viral infections
Characteristics ADEM MS
Age Younger (5-8y) Young Adults (15-40y)
Infections Frequent Rare
Onset Fever, Headache, Behaviour, Mental Frequently
Status, Seizure monosymptomatic
Relapse Rare Frequent
Optic Neuritis Bilateral Unilateral
Transverse Myelitis Frequent, complete Relatively rare, partial
Progressive Symptoms No Frequent
CSF Lymphocytes, OB+ (<50%) OB+ (95%)
Brain MRI Fuzzy, large multifocal, asymmetrical Dawson Fingers
lesions
GM Involvement Thalamus Juxtacortical
Gadolinium Patchy / absent Focal
SC Lesions Long, swollen Multiple, small
Follow-up Resolution New lesions
 Neurology
Updated: March 2023 DEFINITIONS & EXPLANATIONS

LESION INFARCTION / STROKE INTRACRANIAL HEMORRHAGE

Brain lesions are areas of brain tissue that A cerebral infarction (or stroke) is a brain lesion in which a Hemorrhage = Bleeding. This can be divided into:
show damage from injury or disease. They cluster of brain cells die when they
1. Hemorrhagic Stroke ruptured blood vessel
can be from: blood (and oxygen). They can be divided into:
2. Hematoma clotting of blood due to a
Tumors 1. Ischemic stroke artery supplying blood to an area of
bleed.
Infarction / Stroke the brain becomes blocked by thrombus or embolus
Main issue in hemorrhage is the loss of blood
Hemorrhage 2. Hemorrhagic stroke itself or due to the
Infection (Abscess) ruptures and so blood flow is stopped or reduced
collection of blood in the brain/skull

INFARCTION

CLASSIFICATION GENERAL SYMPTOMS RISK FACTORS DIFFERENTIAL DIAGNOSIS

Total anterior circulation infarction, TACI How to suspect: Hypertension: MOST Tumour
Unilateral motor and sensory deficit, 1. Sudden Onset IMPORTANT. subdural hematoma
hemianopia, 2. Anamnesis: Cigarette smoking acute hydrocephalus
disturbance of higher cerebral a. High BP Diabetes Migraine
function b. Atrial fibrillation Heart disease (AF, MI, CHF) Slow progression of positive
c. Diabetes Mellitus Transient Ischemic Attack (TIA)- symptoms (flashing lights
Partial anterior circulation infarction, d. Sitting for long time (DVT) Stroke produces neurologic (photopsia), tingling)
PACI e. Congenital (e.g. ASD) deficits that resolve completely together with headache
Any two of above usually within 1 hour) without Seizures
Isolated disturbance of higher 3. Neurological signs: evidence of cerebral infarction Positive symptoms
cerebral function a. Weakness (monoparesis, hemiparesis, (Red flag for complete stroke predominate (twitches)
paraparesis, hemiplegia) within 24hrs) impairment of consciousness
Posterior circulation infarction, POCI b. Sensory loss (hemihypoesthesia, Elevated cholesterol Usually common only to
Signs of brainstem dysfunction hypoesthesia) Obesity venous strokes, not arterial
Isolated hemianopia c. Incoordination (ataxia) Inactivity Hyponatremia
d. Hemianopia Narcotics Hypoglycaemia
Lacunar infarction, LACI e. Aphasia, dysphasia Age, sex, race, genetic Hyponatremia
f. Apraxia, hemi-inattention, anosognosia, predisposition
graphesthesia, stereognosis, etc.
 Neurology
Updated: March 2023 LESION SYNDROMES

SYNDROME & ARTERIES AFFECTED SYMPTOMS

ICA/Anterior circulation syndrome Contralateral hemiparesis and/or hemihypesthesia

Contralateral homonymous hemianopia
Internal carotid a. (ICA)
Cortical dysfunction (graphesthesia, stereognosis, aphasia, apraxia, hemi-inattention, anosognosia (unawareness
Middle cerebral a. (MCA) 90%
of illness), etc.)
of all strokes
Anterior cerebral a. (ACA) A forced deviation of eyes and head towards the side of the infarct (away from the paretic side, in case of large MCA
Anterior choroidal a. infarcts)

Brainstem symptoms Cranial nerve palsy AND Contralateral hemiparesis/ hemihypesthesia

o Diplopia Hemianopia with sparing of central vision(macular sparing) (can be the
Posterior circulation syndrome o Dizziness isolated symptom)
o Dysarthria A forced deviation of eyes and head away from the side of the infarct
Vertebral a. o Dysphagia (towards the paretic side, in case of pons infarcts)
Basilar a. o Dysmetria-dyssynergia Vertigo, Nystagmus
Posterior cerebral a. (PCA) (with involvement of
cerebellar pathways) Hemisensory loss+ hemianopia without paralysis is pathognomic
A red flag for BA syndromes is impairment of the level of consciousness, which can include coma

Vertigo, nausea and vomiting (VIII) Ipsilateral cerebellar signs and symptoms
Lateral medullary Syndrome/ Dysphagia, dysarthria (IX, X n. ambiguus) o Asynergia (pedunculus cerebellaris inferior)
Wallenberg Syndrome (if PICA o Muscle hypotonia, ataxia (tr. spinocerebellaris anterior)
Dissociated sensory loss (pain, temperature):
affected) o Face ipsilaterally (n.tr.spinalis, n. trigeminus)
Vertebral a. o Trunk & extremities contralaterally (tr.
Posterior inferior cerebellar a. spinothalamicus lateralis)
(PICA)
The motor system, tongue movements, and vibration & position sense are typically spared
 Neurology
Updated: March 2023
SYNDROME & ARTERIES AFFECTED SYMPTOMS

Ipsilateral flaccid paresis, atrophy, and fibrillation of the tongue (XII).

Medial medullary syndrome The protruded tongue deviates toward the lesion (away from hemiplegia)
Vertebral a. Non-spastic contralateral hemiplegia (pyramidal system)
Anterior spinal a. (paramedian Contralateral loss of position and vibratory sensation (lemniscus medialis)
branch) Vertical nystagmus (FLM)
Pain and temperature sensation are spared

Complete motor paralysis below the level of the lesion due to interruption of the corticospinal tract
Loss of pain and temperature sensation at and below the level of the lesion due to interruption of
Anterior Spinal artery syndrome/ the spinothalamic tract
Anterior spinal cord syndrome Retained proprioception and vibratory sensation due to intact dorsal columns
Autonomic dysfunction may be present and can manifest as hypotension (either orthostatic or frank
Anterior spinal artery hypotension), sexual dysfunction, and/or bowel and bladder dysfunction
Areflexia, flaccid internal and external anal sphincter, urinary retention and intestinal obstruction may also be
present in individuals with anterior cord syndrome
 Neurology
Updated: March 2023 STROKE VS. HEMORRHAGE
INTRACRANIAL HAEMORRHAGE
STROKE
ISCHEMIC HAEMORRHAGIC HEMATOMA
THROMBOTIC EMBOLIC INTRACEREBRAL SUBARACHNOID SUBDURAL EPIDURAL / EXTRADURAL
Thrombus Embolus 1. Hypertension 1. Head Trauma 1. Brain atrophy 1. Head trauma (+ skull
endothelial cell arteriolosclerosis, 2. Aneurysm (eg. 2. Alcohol abuse (vein wall fracture)
dysfunction causes 1. Heart disease microaneurysms saccular) damage) 2. Bleeding disorder
atherosclerosis (AFib/MI) that 2. AVM 3. AVM 3. Head trauma (incl. 3. Blood vessel
results in blood 3. Vasculitis shaken baby syndrome) malformation
Cause

1. smoking stasis 4. Vascular tumours 4. Acceleration-

2. hypertension 5. Ischemic stroke deceleration injury
3. vascular disease ** lenticulostriate
vessels often affected
(basal ganglia)
Gradual (mins, hrs); Rapid; Sudden Sudden Delayed Acute -> lucid interval ->
during night sleep no warnings acute: 2d rapidly progressing
Onset

subacute: 3-14 d
chronic: > 15d

Focal neurologic deficits (sensory, motor) depending on location of damage/lesion

F A S T (facial drooping, arm weakness, speech disturbances, time urgent)
No headache (or Headache Severe headache Severe headache / loss consciousness 1. Transient loss of
only mild) Neurologic Consciousness (thunderclap, Pupils abnormal consciousness
Depending on deficits may Nausea/vomiting ( occipital) Headache (concussion)
Clinical

where the infarct resolve as due to ICP) Consciousness Nausea/vomiting ( ICP) 2. Awaken (lucid interval
is, can have embolus breaks Nausea/vomiting ( Affected RR, HR blood accumulates
different ICP) slowly)
neurologic deficits Epileptic seizures 3. Then loses
Meningeal irritation consciousness again
(neck stiffness) Ongoing severe
**vasospasm could lead headache
to ischaemia Nausea/vomiting ( ICP)
 Neurology
Updated:
Can occur March
in any 2023artery, but most
cerebral Brain parenchyma Between pia and Between internal dura & Between external dura
commonly Middle Cerebral Artery arachnoid mater arachnoid mater mater & skull bone
Location

Cytotoxic edema vasogenic edema Hyperdensity in brain Hyperdensity in basal - If large hematoma = Midline shift
herniations (cingulate, uncal, cerebellar parenchyma cisterns, fissures, sulci, - ICP = Herniation (supra, infratentorial)
tonsil) ventricles, tentorium

Hypodense infarct ; hyperdense vessel

- Crescent shaped, - Lens shaped
- Density varies according - Hyperdense
to age of hematoma - Does NOT cross suture
Imaging

** If -ve CT do lumbar
puncture after 12 hrs =
can show Xanthochromia
- Crosses suture lines
(breakdown of RBC
yellow) = evidence of lines
hemorrhage

< 4.5hrs - Thrombolysis (Alteplase) Anti-hypertensives Craniotomy - removal

< 6 hrs / large artery Thrombectomy and mannitol of hematoma / repair If large / acute - Craniotomy
Anti-aggregative - Aspirin Surgery craniotomy of vessel If small / chronic Burr-hole catheter drainage
Aneurysm = clipping or
Treatment

Stereotactic
ICP Osmotherapy (glycerol + mannitol) aspiration aspirate coiling Blood is jelly-like in acute cases but becomes more
/ surgical decompression off blood & relieve Vasospasm = HHH, liquid/CSF like chronically.
pressure CCB
Hydrocephalus =
extra-ventricular drain
/ shunt
 Neurology
Updated: March 2023 ISCHAEMIC STROKE
ONSET LAB/INSTRUMENTAL. TREATMENT
Thrombotic: CBC, glucose, electrolytes, ECG, clotting panel 1. Stabilize general condition:
Relatively slow (over In emergency case- always do CT fist to find cause/ location BP,02, Temperature monitoring
minutes, hours) progression Oxygen (if Sp02 <95%)
If symptoms but no lesion seen, treat for ischaemic stroke
of focal neurological Paracetamol and fanning (if T >37.5)
and do a repeat CT after a day/2 to give time for defect to
symptoms and signs; Correct glycaemia if >10/<2.8
show
onset during night sleep is ACE I (Captopril) to lower BP if >220/120mmHg
MRI if symptoms laxst >24hrs and no lesions seen (e.g. in
common Fluid & electrolytes
small arteries in vertebrobasilar a.)
Embolic: Angiography 2. Specific therapy:
Rapid, with no warnings Carotid &Transcranial US If within 4.5hours Thrombolysis (tissue
plasminogen activator- Alteplase) (if criteria fits)
CT MRI ANGIOGRAPHY If within 6hrs Thrombectomy
Symptoms Hypodense infarct Aspirin (160-325 loading within 48hrs of attack)
Focal neurological deficit o If thrombolytic therapy is given, antiplatelet
depending on region of brain therapy(asprin) should not be given for 24hrs
affected (scroll down) ICP /oedema head elevation at 300 &
Osmotherapy(mannitol, glycerol) OR surgical
Headache more common to decompression
embolic type. Later rehab from day 1

PREVENTION
Primary: Secondary:
Reduce modifiable risks (diet, exercise, Management of risk factors(statins)
smoking, alcohol), Treat chronic conditions Aspirin, Oral anticoagulant (if A fib associated)
(AH, Cholesterol, DM), Aspirin Carotid artery endartectomy (CAE) 77-99% stenosis
Angioplasty/stenting: severe stenosis
Prevent complications: Abx, rehydration, anticoagulants (venous thromboembolism)
Neurology
Updated: March 2023 INCLUSION CRITERIA EXCLUSION CRITERIA
1. Ischemic stroke with: 1. Stroke or serious head trauma within the previous 3 months OR
a. Clearly defined onset time (within 4.5hrs) active bleeding
b. Measurable deficit on the NIH Stroke Scale 2. BP of >185/110 or aggressive means to lower the BP below this
goal
2. CT scan without evidence of intracranial haemorrhage
3. Seizure at onset of the stroke
3. Patient older than 18yr 4. History/symptoms of haemorrhagic stroke
4. On MRI/CT: <33% of blood supply area is ischaemic 5. GI or genitourinary haemorrhage in the past 21 days
6. Aneurysms
5. mRs (Modified Rankin Scale) 0-2 7. Novel anticoagulants within 48 hrs
8. Endocarditis
9. Oncology (due to high bleeding risk)
10. Surgery within the past 3 months
11. Liver failure

Lab test:
12. INR >1.7 on aspirin OR PT> 15s without aspirin
13. Platelets <100
14. Glucose >22.3 or <2.8 mmol/l

ARTERIAL SUPPLY TO THE BRAIN

Anterior Cerebral Artery Middle Cerebral Artery Posterior Cerebral Artery

 Neurology
Updated: March 2023 HEMORRHAGIC STROKE
TYPE ONSET ETIOLOGY SYMPTOMS DIAGNOSTICS TREATMENT
Spontaneous Sudden, during Rupture of small vessels Severe headache CT Close BP control
intracerebral physical activity affected by Arterial Decreased Hyperdensity in brain Mannitol
haemorrhage Hypertension(AH) or consciousness parenchyma Fluid balance and
(ICH) amyloidosis (80%) Increased ICP CT with contrast for electrolytes
(nausea, vomiting) ddx with tumour. Anticonvulsants if
AH locations: seizures
Basal ganglia Nasogastric feeding
Thalamus within 48hrs
Cerebellum Surgical treatment only
Pons if large cerebellar
Amyloidosis location hematoma
Lobar, multifocal (Craniotomy)

Subarachnoid Severe Intracranial aneurysms Headache CT

haemorrhage headache with 85 % (80%-anterior Transient or Hyper density in basal 1. Hypertensive therapy
(SAH) instant onset circulation, 25%- prolonged loss of cistens, fissures, sulci, 2. Hypervolemia
multiplex) consciousness ventricles, tentorium 3. Haemodilution
head- Peri mesencephalic Epileptic seizures
thunderclap (interpeduncular r.) SAH Nausea and vomiting ischemia due to arterial
Nausea/ 10 % spasm
Vomiting A-V malformations Clinical findings o Calcium antagonists
Meningeal 5% (Nimodipine)
irritation(neck Signs of meningeal
stifness) RISK FACTORS: irritation: neck Surgery (Craniotomy,
Cigarette smoking x 10 removal of hematoma)
AH Lumbar puncture
Alcohol (binge drinking) Focal neurological Clipping/Coiling of
Family history signs may be present aneurysm
Angiography
 Neurology
Updated: March 2023 EPILEPSY

ETIOLOGY PATHOGENESIS SYMPTOMS DIAGNOSIS

Structural: 1. Altered neurotransmitter Sudden and transitory abnormal Diagnostic Criteria
Structural brain changes that balance stereotyped phenomena which
may be exogenic (eg. stroke, may include: At least two unprovoked seizures
trauma, infection) or Increased glutamate alterations of consciousness occurring greater than 24 hours apart
Due to a genetic defect which (excitatory) motor
Decreased GABA (inhibitory) sensory or
is responsible for structural
abnormalities (cortical Altered neuro modular Autonomic
activity One unprovoked seizure and an
malformation) psychic events
increased probability of further
Infectious: Which are perceived by the patient
2. Altered ionic homeostasis seizures:
Chronic brain infections - or an observer
Obvious epileptiform activity on EEG
congenital CMV or
Potassium, calcium, chloride Structural brain damage:
toxoplasmosis
o Clinically relevant findings on
AIDS 3. Rearranged neuronal circuits Symptoms following seizures:
CT/MRI
Neurocysticercosis Post-ictal confusion: usually lasts
o Obvious neurologic/cognitive
Brain abscess Loss of inhibitory synapses minutes
dysfunction
Immune: Overgrowth of excitatory Prolonged post ictal confusion
Family history of epilepsy
Auto immune limbic synapses Todds paralysis: Paralysis in arms
Very young age at onset
encephalitis Simplified circuits that improve and legs, lasts around 15hrs,
MS neuronal synchronization subsides completely in 2 days. or
Genetic:
Primary consequence of 40% just seizures, no Diagnosis of a specific epilepsy
genetic defect The duration and behavioural concomitant abnormalities syndrome
Metabolic: involvement of induced seizures 60% have concomitant
increases after seizures are disorders: Tests:
Inherited metabolic condition,
induced repeatedly. intellectual If Urgent Urgent brain CT, ECG,
genetically determined in
motor metabolic lab test
most cases (eg. aminoaciduria,
depression If not Urgent Planned CT/MRI
porphyria, GLUT1 deficiency)
Neurology
Updated: March 2023 SEIZURE TYPES / CLASSIFICATION

Motor Onset: Non-Motor Onset:

Automatism
Autonomic
Atonic
Behavioural arrest
Tonic
Cognitive
Clonic
Emotional
Epileptic spasm Sensory
Hyperkinetic
Myoclonic
 Neurology
Updated: March 2023
FOCAL GENERAL
The onset can be Motor or Non-motor. It will present as either Motor or Non-motor Onset.
-
Can have different symptoms depending on which area is affected:
-motor
Tonic-Clonic (Grand Mal): Absence (Petit
Mal):
Tonic: Stiffening. Arching of neck and back A blank stare,
Clonic: Rhythmic jerking of limbs beginning and
Loss of consciousness before onset of ending abruptly,
seizure usually lasting a
Cyanosis commonly occurs during few seconds
seizure due to slowing down/stopping Person is
of breating unaware
Patient can be aware they are having a seizure, or lose consciousness: May be
Aware (Simple partial seizure) Impaired awareness (Complex partial accompanied by
seizure/Temporal lobe seizure) rapid blinking or
Full awareness maintained Can be a simple partial seizure chewing
Multiple daily
Usually manifested by speech followed by a loss of consciousness OR
Provoked by
disturbances Impaired consciousness from onset. hyperventilation
Motor/parasympathetic symptoms: Preceded by an aura EEG:
focal twitching of extremity, begins Inadequate reaction to external stimuli generalized 3Hz
on one side of body e.g. clonic during the seizure discharges
jerking of left thumb Inability to recall the events after the
Sensory symptoms: tingling, seizure is over Myoclonus
brief shock-like jerks of a muscle or group of muscles. e.g.
weakness, sound, smell, taste, visual, Automatism Repeated jerking
hiccups, abrupt jerking of shoulder muscles, falling feeling
speech disturbances, salivation, movements e.g. lip smacking, chewing, when falling asleep
upset stomach picking at clothes, walking around Person is awake and able to think clearly
Psychic symptoms: deja-vu, aimlessly
hallucinations, fear, anxiety, joy Screaming, crying out loud or
Automatic symptoms: Sweating, repeating words/phrases.
flushing, pupil dilation

Focal Seizures can progress to generalised (usually tonic clonic!)

Neurology
Updated: March 2023 TREATMENT OF SEIZURES (EPILEPSY)

FIRST AID DRUGS

1. Loosen the clothes Given for 2-5yrs after last seizure

2. Turn on side Start with 1 drug, go slow, slowly wean off
3. Remove sharp objects, glasses, put something soft under head
4. Hold gently, sweep saliva Medication depends on type of seizure:
5. Observe time and events
Focal Focal or Generalized Generalized
6. Call for medical help if seizures last >5mins
Carbamazepin Valproic acid * Ethosuximide

DO NOT RESTRAIN Gabapentin Lamotrigin Valproic acid

DO NOT PUT ON BACK Oxcarbazepin Topiramate
DO NOT PUT ANYTHING IN THEIR MOUTH * Not used on women (because it is teratogenic) or in heart/liver
failure

NON-MEDICAMENTAL

1. Ketogenic Diet
2. Vagus Nerve Stimulation
3. Surgery Drug-resistant focal epilepsy if the seizures emanate from a region that can be removed with minimal risk of disabling
neurologic or cognitive dysfunction (Refractory epilepsy caused by mesial temporal sclerosis)
a. Resection
b. Corpus callosotomy (pathway is cut)
 Neurology
Updated: March 2023 CONFUSIONAL STATE

MOST COMMON CAUSES NEUROLOGIC EXAMINATION GENERAL PHYSICAL EXAMINATION

1. Hypoglycaemia/Hyperglycaemia
2. Subarachnoid haemorrhage
3. Traumatic intracranial
haemorrhage
4. Drug intoxication/ withdrawal
(benzodiazepines, opiates,
anticholinergics)
5. Alcohol intoxication/Withdrawal
6. Hypo/Hyperthyroidism
7. Electrolyte disorders-
hyponatremia,
hyper/hypocalcaemia
8. Vit. B12 deficiency
9. Hepatic encephalopathy
10. Acute bacterial meningitis
11. Wernicke encephalopathy
Neurology
Updated: March 2023 COMA
Coma is a state of unresponsiveness in which a patient is unaware of himself and the environment, lies with eyes closed, and
cannot be aroused to respond appropriately to stimuli even with strong stimulation

MECHANISM
1. Dysfunction of ascending reticular formation in the thalamus or brainstem, and/or
2. Dysfunction of both cerebral hemispheres
CLASSIFICATION CAUSES
1. Coma without focal or lateralizing neurological signs or Intoxications (sedative drugs, ethanol, opioids)
meningeal irritation symptoms Metabolic disturbances (hyperosmolar states-hyperglycaemia,
Usually normal brainstem functions, CT & CSF hypothermia)
Severe systemic infections
Circulatory collapse
Post-seizure states, status epilepticus
Hypertensive encephalopathy and eclampsia
Hyperthermia and hypothermia
Concussion
Acute hydrocephalus

2. Coma with meningeal irritation symptoms Subarachnoid haemorrhage (SAH)

With or without fever, excess of WBC or RBC in CSF, CT Acute bacterial meningitis
normal or abnormal Some forms of viral meningitis
Neoplastic and parasitic meningitides

3. Coma with focal brainstem or localizing cerebral signs Brainstem infarction

With or without changes of CSF, CT abnormal Brain abscess, subdural empyema, Herpes encephalitis
Epidural and subdural haemorrhage
Brain contusion
Brain tumor
Cerebellar and pontine haemorrhage
Miscellaneous
 Neurology
Updated: March 2023 COMA: DIFFERENTIAL DIAGNOSIS

Brain death Vegetative state Minimally conscious state Locked-in syndrome Akinetic mutism
Vital structures of the brain Evidence of limited but clearly Conscious of their environment Patients tend neither to
necessary to maintain visible self or environmental but cannot move any speak (mutism) nor
consciousness and independent Complete unawareness awareness on a reproducible or extremities, cannot talk, or do move (akinesia) due to
vegetative survival must be of self and environment sustained basis, as not have horizontal eye severe frontal lobe
damaged beyond all possible accompanied by regular demonstrated by one or more movements The only damage.
recovery: sleep-wake cycles, with of the following behaviours: communication may be through
Damage to known structural either complete/partial vertical eye movements and Causes:
injury preservation of 1. Simple command following blinking o An olfactory groove
Irreversible metabolic injury hypothalamic and brain 2. Gestural or meningioma
e.g. prolonged asphyxia stem autonomic responses Lesion location: brainstem and o Creutzfeldt-Jakob
functions 3. Intelligible verbalization involves the motor pathway, the disease (late stages)
CRITERIA 4. Purposeful behaviours in efferent abducent nerve fibres, o Lethargic encephalitis
All must be present for 12 and 1. No evidence of contingent relation to and the corticobulbar fibres o A stroke that affects
24hrs after their first awareness of self relevant stimuli (i.e. both anterior cerebral
assessment to confirm brain 2. No evidence of appropriate smiling or Major causes: a pontine infarct arteries territories
death awareness of crying; etc.) or haemorrhage and central o Ablation of the
environment pontine myelinolysis cingulate gyrus
1. Absence of pupillary 3. Retained brainstem
responses regulation of
2. Absence of corneal cardiopulmonary
responses function and visceral
3. Absence of caloric vestibulo- autonomic
ocular reflexes regulation
4. Absence of oculo-cephalic
reflexes Persistent vegetative
5. Absence of gag reflex state from the 31st
6. Absence of motor responses day of vegetative state
to painful stimuli
7. Absence of respiratory drive
 Neurology
Updated: March 2023 DIAGNOSIS / EXAMINATION OF A COMATOSED PATIENT

ORDER OF EVALUATION: NEUROLOGICAL EXAMINATION: GLASGOW COMA SCALE:

A. ABCs (airway, breathing, circulation) 1. Verbal responses
B. oxygen, glucose, naloxone 2. Eye opening
C. 3. Optic fundi
4. Pupillary reactions
D. other electrolytes, renal, hepatic,
temperature 5. Spontaneous eye movements
6. Oculocephalic responses (assuming
E. everything else
cervical trauma has been excluded)
7. Doll's manoeuvre
(After addressing the most urgent
8. Oculovestibular responses
conditions that can affect mental status:
9. Corneal responses
systemic derangements like hypotension
10. Respiratory pattern
and hypoglycaemia, the possibility of
structural brain damage must be 11. Motor responses
considered most urgent cause is cerebral 12. Deep tendon reflexes
herniation!) 13. Skeletal muscle tone

EYE REACTIONS

PUPILARY RESPONSE
Pupillary light reflex: Equality in size Eyelids and corneal responses
The single most important physical sign in Unilateral dilated & unreactive
differentiating metabolic from structural pupil indicates temporal Eyelids are closed
coma (absent in cerebral herniation) The lobe herniation or posterior
pupillary pathways are among the most communicating artery Corneal reflex:
resistant to metabolic insult aneurism with a wisp of cotton or with a
drop of sterile saline reflex
ie. if the pupils are Both unreactive and fixed at closure of both eyelids and
eyes response is not, the coma is not due to the intermediate size pupils
herniation a systemic metabolic Cerebral herniation phenomenon)
abnormality is more likely
Neurology
Updated: March 2023 OCULOMOTOR RESPONSES (EYE MOVEMENTS)
Asymmetric oculomotor function structural rather than metabolic cause of coma

Oculocephalic reflex (Dolls eye) Caloric vestibulo-ocular responses

Normal: When the head is rotated, the eyes turn together to the side
opposite to the head movement 1. The head of the bed should be raised to about 30
2. A large syringe of ice water is used to stimulate tympanic
membrane
3. Infusion rate: 10 ml/min or until response is obtained
4. Wait at least 5 min for the response to dissipate before testing
the opposite ear

Results
Tonic deviation toward the ear that is irrigated: intact brainstem
Absence of the response: braistem dysfunction, phenytoin or
tricyclic antidepresant toxicity

Abnormal: When the head is rotated, the eyes do not turn in a

conjugate manner
 Neurology
Updated: March 2023 MOTOR RESPONSES
MOTOR TONE MOTOR REFLEXES MOTOR RESPONSES
Is of greatest value in pts who Deep tendon reflexes The best motor response is to sensory stimulation:
are drowsy but responsive to Brisk or hyperactive in drowsy or confused pts Voice Gentle shaking Painful stimuli
voice! Unobtainable in deeply comatose pts
Spastic rigidity (clasp-knife)
Cutaneous reflexes
Parkinsonian is usually
The abdominal or cremaster reflex become
diminished in unconscious pt.
depressed as the level of consciousness wanes
Paratonic rigidity- irregular Bilateral Babinski sign not significant
resistance to passive Unilateral Babinski sign injury to the
movement that increase in corticospinal tract
intensity as the speed of
movement increases Prefrontal cutaneous reflexes GRADING OF MOTOR RESPONSE:
(especially in case of The grasp reflex reflects bilateral prefrontal Appropriate: Inappropriate
metabolic encephalopathies) impairment Attempts to escape the stimulus (i.e.
Pushing the stimulus away or attempting No response
to avoid the stimulus)
 Neurology
Updated: March 2023 POSTURING RESPONSES
DECORDICATE RIGIDITY DECEREBATE RIGIDITY
Flexor posturing of the upper extremities & extension of the lower extremities Extensor posturing of both the upper and lower extremities

Reflects dysfunction of the forebrain down to the level of the rostral Reflects dysfunction extending into the upper brainstem
midbrain Reflects the release of vesibulospinal postural reflexes
Causes: a variety of metabolic disorders or intoxications. from forebrain control
The presence of DR in cases of brain injury is ominous!!
Disturbances of ocular mobility
Often fragmentary or asymmetric Is the more severe finding than decorticate posturing
Usually normal ocular mobility

On rare occasions where posture is

neither Decorticate nor
Decerebrate it can be:

Extensor posturing of the arms

with flaccid or weak flexor
responses in the leg

This is typical for injury to the

lower brainstem at the level of the
vestibular nuclei
 Neurology
Updated: March 2023 MYASTHENIA GRAVIS
PATHOGENESIS SYMPTOMS INVESTIGATIONS TREATMENT
Autoimmune disorder of the Fluctuating weakness is increased Clinical testing targeted at muscle fatigability 1. Acetylcholinesterase
neuromuscular junction by exertion during the day and upward gaze inhibitors
characterized by fatigable improves with rest. strong repeated eye closure (blink 20 times) o Pyridostigmine bromide
weakness of voluntary muscles. holding arms up, etc. o Neostigmine
Ocular form: Give weights to lift and measure power with +/-
Antibodies (AB) are directed Extraocular and eyelid muscle dynamometer before and after. 2. Corticosteroids (prednisone) are
toward the acetylcholine weakness is present initially in reflexes normal added on to cholinesterase
receptors (AChRs) at the 50% of patients. No sensation abnormalities inhibitors gradually
postsynaptic membrane of Ptosis OR
neuromuscular junction. diplopia ENMG Other immune suppressants:
asymmetric Repetitive nerve stimulation produces abnormal o Azathioprine
Binding of AB results in decrement in the amplitude over 10%. o Cyclosporine
destruction of junctional folds Single fibre EMG most sensitive
of the postsynaptic Plasmapheresis / Intravenous
membrane with resultant Pharmacological testing immunoglobulin for exacerbations/
decreased availability and short-acting cholinesterase inhibitor (Endrophonium) severe cases
number of AChRs and Positive if muscle strength improves subjectively and
blocking the binding of ACh to Generalized form: objectively for 4-5 min. (in 90% pts with MG) Thymectomy if combined with
AChR. limbs and axial muscles (esp. neck) prednisone will result in a
and respiratory muscles ICE Pack Test decreased need for
Performed by keeping icepack over eyes for 2-5mins and immunosuppressants/
Oropharyngeal muscles weakness looking at improvement in ptosis hospitalization and lowers dose of
produces regurgitation of food Cooling improves neuromuscular transmission GC needed
and liquids, chocking, aspiration,
nasal voice (dysphagia, dysphonia) Drugs to avoid:
o Antispasmodics
Bilateral facial and jaw muscle o Abx (e.g. Aminoglycosides)
weakness: mask-like face, o B-blockers
difficulty chewing Seropositive: in 80-90% of generalized from, 50% in o Muscle relaxants
Thymus is the central organ in ocular myasthenia o BDZ
T cell mediated immunity Seronegative: search for other antibodies, e.g., MuSK As they Induce myasthenia like
o Thymic hyperplasia found (muscle-specific tyrosin kinase), LRP4 (lipoprotein symptoms and exaggerate
in most young-onset receptor related protein 4) weakness
patients Test for Anti-Ro, Anti-Yo AB for ddx with paraneoplastic.
Thymomas occur in 10-15% of MG
patients (seropositive cases) CT/ Chest X-ray:
Thymoma/Thymic hyperplasia
 Neurology
Updated: March
Myasthenic Crisis2023 Cholinergic Crisis
Respiratory failure due to the weakness of respiratory muscles requiring Too high doses of cholinesterase inhibitors and overstimulation of
ventilation neuromuscular junction due to an excess of Ach

May be provoked by Leads to flaccid paralysis,

Intercurrent illness Respiratory failure,
Some medications (benzodiazepines, aminoglycosides, chinin) Increased salivation and bronchial secretion,
Insufficient treatment Miosis
Bradycardia
Management: Hypotonia
Immediate intubation and ventilation
Plasmapheresis or (I/V Ig If very unstable and plasmapheresis not Management:
possible) Immediate ventilation
Prednisone 60-100mg/d Atropine (anti-cholinergic)
Anticholinesterase medications i/v with atropine (after extubation) Stop of cholinesterase inhibitors (slow reintroduction later)

MYASTHENIC SYNDROME (Lambert Eaton Syndrome)

variable weakness due to defective release of acetylcholine at the neuromuscular junctions.
PATHOGENESIS CLINICAL DIAGNOSIS TREATMENT
1. Underlying neoplasm Weakness: especially of the ENMG Treat underlying cause.
(paraneoplastic syndrome): proximal muscles of the limbs. Incremental response to repetitive
antibodies directed against nerve stimulation. Short-term symptomatic treatment:
tumor antigens cross-react with Unlike myasthenia gravis, the Plasmapheresis
voltage-gated calcium channels extraocular muscles are Antibodies: Intravenous immunoglobulin
involved in acetylcholine spared, Autoantibodies to the P/Q subtype treatment must be repeated to sustain effect.
release, leading to a of voltage-gated calcium channels :
presynaptic disturbance of power steadily increases if a found on the presynaptic membrane Long term:
neuromuscular transmission contraction is maintained. of the neuromuscular junction Immunosuppressive drug therapy
(corticosteroids, mycophenolate, and
2. Autoimmune diseases e.g. Autonomic disturbances: e.g. Detection of underlying neoplasm azathioprine)- may lead to improved muscle
pernicious anemia (usually small cell lung cancer) strength.
dry mouth, constipation, and
repeat after 3-6months if negative
impotence, may occur. Guanidine hydrochloride - enhancing the
3. Occasionally no cause is found. initially
release of acetylcholine in seriously disabled
patients,
 Neurology
Updated: March 2023 DISEASE
Severe loss of pigmented dopaminergic cells of the substantia nigra pars compacta (SNc, ventrolateral tier)
and the dopamine deficit in the corpus striatum in the brain.

RISK FACTORS PATHOPHYSIOLOGY

Genetic factors (Familial forms <10-15% of all cases) In Parkinson disease, there is degeneration of the pars compacta of the substantia
Age (50-60y.o. Early onset <40y.o.) nigra, leading to overactivity in the indirect pathway (red) and increased
Environmental factors (herbicides, pesticides, CO, heavy glutamatergic output from the subthalamic nucleus.
metals. disrupting voluntary motor control and causing the characteristic symptoms of PD.
Gender ( Men: Women 1.35-1.5:1, or 3:2 M:F predominance)
Head trauma

o Personality or affective disorders (OCD, severe depression)

o Intestine microflora disbalance

DIAGNOSTIC TESTING
1. To elicit bradykinesia (motor 2. To detect tremors
tasks) a. Writing task
a. Dysdiadokinesia i. Micrography
b. Touch finger to thumb b. spiral
c. Tight fist and open hand drawing
fully
3. Gait 4. Tone
a. Physiological dyskinesia a. Cog-wheel rigidity
b. Small steps while turning
c. No arm swinging 5. Postural instability
d. Shuffling Push patient back while
e. Hard to stop and start they stand firm
(severe)
 Neurology
Updated: March 2023 DIAGNOSTIC CRITERIA PATHOLOGICAL CRITERA
STEP 1: PARKINSONIAN STEP 2: Exclusion Criteria. e.g. STEP 3: Additional Positive Criteria (post mortem)
SYNDROME (TRAP) (>/=3 needed +STEP 1) to 1. Significant degeneration of the
1. history of repeated strokes with stepwise diagnoses PARKINSONS DISEASE substantia nigra neurones,
1. Akinesia/ Bradykinesia
progression of parkinsonian features e.g. associated with gliosis
e.g. Hypomimia (e.g.
2. history of repeated head injury 1. Unilateral onset 2. At least 1 Lewy body in the
blinking rate reduced)
3. history of definite encephalitis 2. Rest tremor present substantia nigra or locus coeruleus
AND At least 1: 4. More than 1 affected relative 3. Progressive disorder 3. Absent evidence of other diseases,
2. muscular rigidity 5. Oculogyric crises (dystonic reaction to 4. Persistent asymmetry affecting which can cause parkinsonism
3. 4-6 Hz rest tremor drugs) side of onset most
4. postural instability (NOT 6. neuroleptic treatment at onset of 5. Excellent response (70-100%) IMAGING
caused by primary symptoms to levodopa MRI: thinning of the substantia nigra
visual, vestibular, 7. Signs of dementia before symptoms onset 6. Severe levodopa-induced pars compacta (>/=1.5 T)
cerebellar, or 8. L-Dopa does not help symptoms chorea PET/SPECT: reduced binding in
proprioceptive 9. Strictly unilateral features after 3 years 7. Levodopa response for 5 years striatum region (especially in posterior
dysfunction) 10. Babinski sign or more part of the putamen)
8. Clinical course of 10 years or
more

DISEASE TREATMENT INDICATIONS

 Neurology
Updated: March 2023
PARKINSONS TREATMENT
1. Dopaminergic medications 1.2. Dopamine agonists (1st line alternative to 2. COMT inhibitors (Onicapone,
1.1. Levodopa preparations (Gold standard) levodopa) Entacapone) Prolong levodopa
Levodopa + carbidopa - co-careldopa Pramipexole can be standard effect and reduce
Levodopa + benserazide - co-beneldopa or extended/prolonged formulations Can be prescribed only with
o Carbidopa prevents breakdown of levodopa before it Ropinirole levodopa (Give with each dose
reaches the brain Apomorphine - inject. or continuous of levodopa)
o High potency drugs inf. SC, short half life Levodopa+ carbidopa+
o If young pt., usually try to hold off on using levodopa or Rotigotine - plaster (transdermal entacapone can be in a single
give low doses system) 24 hours/d tab. (e.g., Stalevo)
o Before treatment: Chronic levodopa test can be Pergolide Added in late course of disease
prescribed for patients with suspected PD, to assess if Adverse effects: ICD (gambling, with motor
treatment helps symptoms and confirm diagnosis. hypersexuality, hypomanic states), peripheral fluctuations/dyskinesia
Adverse reactions: nausea, hypotension, dyskinesia, motor oedema Needs liver function (LFT)
fluctuations monitoring

3. MAO-B inhibitors (Rasagiline 1mg/d, 4. Anticholinergics (Trihexyphenidyl: 5. NMDA rec. antagonist 6. If disease progresses still
Selegiline, Safinamide) Reduce 2-15 mg/p, Biperiden, Benztropine, (amantadine) Reduce Deep Brain
dopamine metabolism ( Ethopropazine) Reduce tremor dyskinesias/motor Stimulation (DBS)
dopa breakdown in CNS) Mild potency drugs fluctuations due to levodopa a. Only for Pure
Mild potency drugs Dopamine deficit cholinergic Mild potency drug
May increase effectiveness (and side hyperactivity Weakly effective
effects) of levodopa Use limited by confusion and monotherapy responsive to
Can give as initial monotherapy if other anticholinergic side effects Daily dose 200-300 mg/d levodopa
there are no/little debilitating (especially in patients >70y.o.) PO
symptoms Contraindicated in patients with Adverse reactions: ANS
prostatic hyperplasia, narrow-
RESCUE THERAPY
Adverse effects: insomnia, headache, nausea. dysfunction, psychiatric
Avoid with SSRI, TCA or MAO-B inhibitors that angle glaucoma, or obstructive symptoms
Apomorphine (IV dopamine),
can cause serotonin syndrome! gastrointestinal disease Amantadine
 Neurology
Updated: March 2023 BRAIN INJURY
Can be diffuse (concussion & diffuse axonal injury) or focal (contusion & compression)
CONCUSSION CONTUSION COMPRESSION
Loss of consciousness for a brief time, without Microhaemorrhages into the brain substance, It is not an independent syndrome, but a
spontaneous motion or response to verbal or resulting from cortical tissue damage, produced by complication of:
painful stimuli. the absorbed energy of the impact. o Intracranial hematomas
o without stable neurological symptoms Causes: (Extradural/epidural, subdural,
o no evident morphological changes in CT scans falls, motor vehicle accidents, violence. Intracerebral, ventricular)
o Extensive brain swelling
o complaints of headache, nausea, vomiting;
Clinical: o Depressed skull fractures
initial mental clouding, impaired judgement,
o Focal neurological signs (>4days)
unsteadiness of gait, motor dyspraxia. -nystagmus-
reflex movements of eyelids due to increased o Disorders of consciousness (not always) Clinical:
activity of vestibular centres. o Meningeal signs due to subarachnoid General symptoms:
haemorrhage Irritation Depression
DIFFUSE AXONAL INJURY Dynamic disorders Progressive
Imaging: CT of consciousness disorders of
primary lesion of rotational acceleration
deceleration head injury with damage of deep o Focal collection of high-density blood. After some (after consciousness
midline structures: white matter, corpus callosum, time low density surroundings (edema) appears. coma;
midbrain and pons. o The maximum mass effect occurs at 48 to 72 hours without it) Tachycardia;
after injury. Bradycardia Arterial
o Contusions may be in all cortical lobes, basal Arterial hypotension;
Causes: Clinical:
ganglia, brainstem and cerebellum, but mostly in hypertension Disorders of
High speed motor Prolonged coma with
temporal lobe tips and inferior frontal lobes, as Frequent respiration
vehicle accidents, decorticate or
they strike the sphenoid ridge or scrape the floor of respiration (cheyne-stokes
contact sport, violence. decerebrate posturing.
the anterior fossa Hyperthermia type, even apnea)
Imaging:
Management: Focal neurological symptoms:
o There are no space occupying lesions on CT
Surgery only if: According to compressed structures: speech,
o Only small haemorrhages may be seen in
o In case of cerebral shift threatening with sensation disorders, paresis, etc.
mentioned midline structures.
herniation local debulking
o Some lesions may be detected by MRI.
o Decompressive craniotomy is necessary. Signs of brain herniation: paresis, coma, etc.
Neurology
Updated: March 2023 BRAIN TUMORS CLASSIFICATION
 Neurology
Updated: March 2023 GLIOMA
CLASSIFICATION DIAGNOSIS TREATMENT
Grade I benign MRI Surgery
Grade II semi benign no distinct borders, tumor cells gradually infiltrate the normal open surgery is recommended when:
Grade III semi malignant brain tissue. o Tumor is located in superficial, functionally
Grade IV malignant (Glioblastoma) insignificant parts of the brain
Glioblastoma: heterogenic ring enhancement, perifocal o Benign pilocytic astrocytoma is suspected
SIGNS edema & necrosis within. o Gross total resection of glioma can be
Constant increasing neurological deficit such (e.g. performed.
cognitive dysfunction, weakness, sensory loss, MRA assess relationship of tumours and brain vessels Radiotherapy
aphasia and visual disturbances) Chemotherapy
Mental disorders Biopsy: Biological therapy
Epileptic seizures (most common sign) Glioblastoma: Nuclear atypia and mitotic activity, endothelial Immunotherapy
Increased ICP can cause herniation proliferation, necrosis Gene therapy

ACOUSTIC NEURINOMA (VESTIBULAR SCHWANNOMA)

ORIGINS SIGNS DIAGNOSIS TREATMENT
Schwann cells derived Early symptoms: Clinical picture of cochlear Surgical:
tumors that commonly Non-pulsating tinnitus (unilateral) deficit, non-pulsating tinnitus and 1 grade - middle fossa / retrosigmoid approach
arise from the vestibular Unilateral hearing loss vertigo. 2 grade - translabirinthine / retrosigmoid approach
portion CN 8th. Vertigo Audiometry, Weber/Rinne test 3 grade - translabirinthine / retrosigmoid approach
Unsteady gait and disequilibrium Vestibular function test 4 grade - retrosigmoid / transpetrosal approach
Origins location: CT and MRI- enhancing esion in
Inferior part of Late symptoms: internal auditory canal Post-op follow up is done to assess 7th nerve function:
vestibular nerve (70%) 5th CN damage paresthesia, hypoesthesia 1 grade 96-100% normal
Superior part of and/or unilateral facial pain facial weakness Staging: 2 grade - 96 % slight dysfunction
vestibular nerve (20%) 7th CN damage peripheral, unilateral facial 1 grade-up to 1cm 3 grade 77 % moderate dysfunction
Cochlear nerve origin weakness that can progress to paralysis 2 grade-up to 2cm 4 grade - about 60 % severe dysfunction
(10%) Compression of posterior fossa structures 3 grade-up to 3cm 5 grade complete paralysis
o Cerebellum: ataxia 4 grade-more than 3cm
Usually unilateral o 4th ventricle: hydrocephalus Complications of surgery
VII (facial nerve) neuropathy!
 Neurology
Updated: March 2023 MENINGIOMA

ETIOLOGY SIGNS DIAGNOSIS

Set of tumours that arise contiguously to the Convexital: MRI-
meninges deficit Round, sharply
Arise from arachnoidal cells demarcated space-
Usually benign, rarely malignant Parasagittal (and falcine / falx cerebri): occupying lesion; with
Anterior part of sagittal sinus radiological features of an
Female gender, age >65, cranial epileptic seizures extra-axial tumor
irradiation to head/neck, trauma,
neurofibromatosis type 2 Middle part (most frequent) or sensory seizures in lower Dural tail sign
Most common primary brain tumor in adulta! extremities
Histology Psammoma
Tumor possible location: Posterior part bodies
Convex visual field disturbances
Parasagittal (anterior, middle, posterior
part) Intraventricular: headaches, mental disorders and hemianopsia TREATMENT
Sphenoid ring Surgical resection
Intraventricular Skull base:
If inoperative-
Tentorial Anterior fossa (olfactory groove, optic sheath
Radiotherapy
Skull base: disorders , olfactory disorders , seizures and visual disturbances
o Anterior,
o middle, Middle fossa (sphenoid wing)
o posterior temporal seizures , dysphasia and II/III verve deficit
fossa
Posterior fossa (tentorial, posterior fossa)
vertigo , depression of corneal reflex , headaches , cerebellar dysfunction

Tentorium cerebelli Depends on direction of growth hemianopsia,

seizures, increased intracranial pressure, cerebellar dysfunction
 Neurology
Updated: March 2023 CRANIOPHARYNGIOMA

ETIOLOGY SIGNS DIAGNOSIS

rare solid or mixed solid-cystic tumor The tumor arises in the suprasellar region and can extend into the CT and MRI- suprasellar calcified cyst
that arise from remnants of Rathke's intrasellar region. with a lobulated contour
pouch (ectoderm)
along a line from the nasopharynx to Compression of the pituitary gland Biopsy- cholesterol crystals found in a
the diencephalon hypopituitarism motor oil-like fluid
Hypogonadotropic hypogonadism
Most common childhood Failure to thrive TREATMENT
supratentorial tumor Central diabetes insipidus Radical surgery (densely adhere to the
Slow growing, extra axial, epithelial- optic chiasm, pituitary stalk, ACI)
squamous, cystic, calcified tumor Compression of the ventromedial hypothalamic nucleus
Transsphenoidal and endonasal
and obesity
Usually arise in the pituitary stalk in endoscopic approach resection
the suprasellar region, adjacent to the Compression of the infundibular stalk Adjuvant radiotherapy
optic chiasm.
Low-grade malignancies Compression of the optic chiasm Complications of surgery: nasal CSF leak