Neurology Flashcards
Indications for thrombectomy in aute ischaemic stroke?
- location of lesion
- timing
Location: large vessel occlusion -> ICA, M1, proximal M2, basilar
Timing: less than 6 hours from symptom onset. Can perform up to 24 hours from last seen well if there is a large penumbra/core mismatch as identified by CT Perfusion (DAWN trial)
Still need to thrombolyse prior if eligible
Cranial nerve distribution - rule of 4s
4 above pons -> 1-4
4 in pons -> 5-8
4 in medulla -> 9-12 (bulbar)
4 medial structures in Brainstem
Start with M
Motor pathway
Medial lemniscus (part of dorsal column)
Medial longitudinal fasciculus
Motor nucleus (of CN 3,4,6,12)
4 side structures of brainstem
Starting with S
Spinocerebellar pathways
Spinothalamic pathways
Sensory nucleus of CN 5 (large, from pons to medulla)
Sympathetic tract
3rd nerve palsy
Manifestations?
Common causes?
3rd CN -> oculomotor nerve
Supplies:
- levator muscle of eyelid
- 4 extraocular muscles: medial rectus, superior rectus, inferior rectus, and inferior oblique
- contricts pupil through parasympathetic fibres
Clinical presentation:
- diplopia
- ptosis
- “down and out” position
Lesions:
- PCA aneurysms compressing pathway
- ischaemia (diabetes)
- trauma
4th nerve palsy
Manifestations?
Common causes?
4th CN -> Trochlear
Supplies superior oblique muscle -> intorts, depresses in adducted position
Clinical features:
- blurred vision / diplopia
- eye is deviated upwards and outwards
Causes:
- congenital
- trauma
- microvascular
6th cranial nerve palsy
Clinical features?
Causes?
6th CN -> abducens
Supplies lateral rectus -> abducts eye
Clinical features:
- horizontal diplopia
- horizontal gaze palsy
- strabismus
Causes:
- raised ICP causing compression
- tumours
- vascular disease
- inflammation
- trauma
What is Broca’s aphasia?
Other names for it
Where is the lesion?
Non-fluent / Expressive issue
Can’t repeat
Can comprehend perfectly, leading to intense frustration
Lesion -> dominant frontal lobe
What is Wernicke’s aphasia?
Where is the lesion?
Fluent aphasia. Receptive issue, cannot comprehend
Cannot repeat
Lesion -> Dominant temporal lobe
What is conduction aphasia?
Where is the lesion?
Mixture between Broca’s and Wernicke’s
Able to comprehend, fluent but paraphasic errors common
Not able to repeat
Lesion -> Arcute fasciculus (connection between Broca’s and Wernicke’s area)
What is transcortical motor / sensory aphasia?
What type of lesion?
Transcortical motor aphasia -> expressive aphasia but CAN repeat
Transcortical sensory aphasia -> receptive aphasia but CAN repeat
Lesion -> Classically watershed infarcts that spare main language centres of Broca’s and Wernicke’s but affect other areas
What is Horner’s syndrome?
Where is the lesion?
Triad:
Ptosis
Miosis
Anhydrosis
Lesion = in sympathetic tract. Runs with lower brachial plexus around lung apex up to brainstem
Internucleur ophthalmoplegia
What is the clinical finding?
Where is the lesion?
Causes?
INO = impaired horizontal eye movements with weak adduction of the affected eye, and abduction nystagmus of the contralateral eye
Convergence is NORMAL.
Lesion = in medial longitudinal fasciculus (usually in pons, can be midbrain). MLF connects 6th CN on one side to 3rd CN on contralateral side so eyes move in same direction horizontally
Eye that cannot adduct = side of the lesion
Causes: MS (particularly if bilateral), stroke
Corticospinal tract:
What does it do?
Where does it travel?
-> where do the fibres cross?
Key motor pathway
Long tract that descends from primary motor cortex in frontal lobe
- through internal capsule
- crux cerebri
- basis pontis
- cross over at level of pyramids in lower medulla
- meet lower motor neurons in anterior horn

Spinothalamic tract
Major function?
Where does it run?
Responsible for pain and temperature sensation
Receives input at posterior horn
- decussates over 2-3 spinal segments while ascending
- through brainstem to thalamus
- primary sensory cortex in parietal lobe

Dorsal Column
What is it’s main function?
Where does it run?
Responsible for proprioception and vibration sensation
Input through dorsal root ganglion
- ascends entire spinal cord
- crosses over to contralateral medial lemniscus in lower medulla
- ascends to thalamus
- primary sensory cortex in parietal lobe

What is Brown-Sequard Syndrome?
Where is the lesion?
Cord hemisection
- Ipsilateral UMN weakness below level of lesion (corticospinal)
- ipsilateral proprioception/vibration loss below level of lesion (dorsal column)
- contralateral pain and temprature loss 1-2 levels below lesion (spinothalamic)
- ipsilateral LMN and sensory loss AT level of lesion
What is Central Cord Syndrome?
Where is the lesion?
Central cord lesion, usually syrinx
- suspended sensory level = loss of pain/temperature in adjacent dermatomes at level of lesion
Larger lesions -> will involve LMNs, then corticospinal tract and spinothalamic tract
What is Anterior Cord Syndrome?
Where is the lesion?
Loss of all function, except dorsal column preserved (proprioception / vibration)
Caused by occlusion of anterior spinal artery
Lacunar syndromes:
Name 5 classic lacunar syndromes
- Pure motor (internal capsule or basis pontis)
- Pure sensory (thalamic)
- Ataxic hemiparesis (internal capsule, basis pontis and corona radiata)
- Dysarthria/clumsy hand (basis pontis)
- Mixed sensorimotor (thalamus + internal capsule)
What are the absolute contraindications to thrombolysis?
Contraindications:
- extensive hypoattenuation on CT
- current or previous ICH
- intracranial tumour
- severe head trauma last 3 months
- intracranial / intraspinal surgery
- plts <100
- INR >1.7
- APTT >40
- Clexane last 24 hours
- possible endocarditis
- active GI / other bleed
- aortic arch dissection
What medication do we use for thrombolysis?
Within what time frame can it be given?
Alteplase 0.9mg/kg
Current guidelines -> within 4.5 hours of symptom onset
What should BP be before giving thrombolysis?
< 180 / 105
Thalamus =
Blood supply from which artery?
4 nuclei -> function of each?
Blood supply = PCA
Centre of all sensory input. Pure sensory loss-> classically thalamic injury
Anterior nuclei = language and memory
Lateral nuclei = motor and sensory
Medial nuclei = arousal and memory
Posterior nuclei = visual
2012 A6
63 year old man with atrial fibrillation presents with sudden onset visual changes where he is unable to recognize objects in the right lower quadrant of his visual field bilaterally. Where is the deficit?
A. Occipital lobe
B. Optic chiasm
C. Parietal lobe
D. Superior colliculus
E. Temporal Lobe
Optic Pathways =
Optic nerves from retina
Optic chiasm -> cross over
Lateral geniculate nucleus
Optic radiations -> upper = parietal (lower visual field) and lower = temporal (upper visual field)
Primary visual cortex in occipital lobe (upper and lower banks)
Answers =
A. Occipital lobe -> CORRECT (quadrantanopia usually results from lesions (especially infarcts) that damage either the inferior or superior banks of the occipital cortex. Less commonly, a quadrantanopia represents a lesion in the optic radiations in the temporal or parietal lobe
B. Optic chiasm
C. Parietal lobe
D. Superior colliculus (this is an area involved with spatial attention and eye movements)
E. Temporal Lobe

What is the indication for a hemicraniectomy in stroke?
Malignant MCA infarct
- very large infarct, which will cause significant swelling and oedema, leading to brainstem compression/herniation
Improves mortality, but patients will have significant disability
What is the drug of choice for getting BP into target prior to thrombolysis?
IV labetalol 10mg
What is the most significant risk factor for stroke?
Hypertension (both for ischaemic and haemorrhagic)
What is the BP aim post stroke for secondary prevention?
BP < 130 (120-140) / 90
Antiplatelets for secondary stroke prevention:
What are the short-term and long-term regimes?
Short-term -
Minor strokes or TIAs = DAPT with Aspirin + Clopidogrel for first 3 weeks
Intracranial large vessel atherosclerosis = DAPT for 90 days
Long-term = single antiplatelet (clopidogrel OR aspirin/dipyridamole OR aspirin alone)
What are the indications for a carotid entarterectomy?
Symptomatic carotid stenosis:
- 70-99% in everyone
- 50-99% in males
Should be done within 2 weeks of stroke/TIA
Post stroke/TIA, what would be indication for carotid stenting over CEA?
- Unfavourable anatomy
- Re-stenosis after CEA
- previous radiotherapy
- younger patients (<70)
What is the management of symptomatic intracranial atherosclerosis?
Aggressive medical management:
- DAPT for 90 days
- single APT lifelong thereafter
- statin
- BP control
No role for intracranial stenting
Which imaging modality are MS lesions best seen on?
White matter lesions -> best seen on T2 flair
What is the treatment approach for acute MS attack?
Steroids -> methylpred pulse
Plasmapheresis if severe
Following ischaemic stroke in AF, when can anticoagulation be restarted?
Warfarin - within 24 hours
NOACs - a few days
When is PFO closure indicated in the post stroke setting?
In patients <60 years, with no other cause found for stroke, who have associated atrial septal aneurysm or moderate-large R to L shunt
What is the definition of a TIA?
How do you stratify risk?
Brief episode of neurological dysfunction, resulting from focal cerebral ischaemia not associated with permanent cerebral infarction. Usually less than 1 hour in duration
Risk stratified by ABCD3 score
What is amaurosis fugax?
Where is the lesion?
Transient monocular vision loss, descending curtain
Due to hypoperfusion / blockage of ophthalmic artery from ICA
What is the classical presentation of cerebral amyloid angiopathy?
- lobar haemorrhages
- cortical microhaemorrhages
- cortical superficial siderosis (may present with positive TIA symptoms)
What is the management of ICH due to cerebral amyloid angiopathy?
Avoid anticoagulation / antiplatelets
Treat HTN
What is the treatment of cerebral venous thrombosis?
Anticoagulation
- heparin initially
- transition to warfarin (3-6 months provoked, 6-12 months unprovoked)
What may prolonged or absent F waves indicate in NCS?
Early sign of Guillian-Barre
How should patients with GBS be monitored for respiratory failure?
2 hourly FVC on ward
What are some typical nerve biopsy findings in CIDP?
Segmental demyelination + remyelination, clusters of macrophages
What is the approach to treatment of CIDP?
1st line -> IVIG, plasma exchange, steroids.
2nd line -> immunosuppressive drugs (eg mycophenolate mofetil, cyclosporin, cyclophosphamide, rituximab) may be used.
What are the favoured medical therapies for painful diabetic neuropathy?
TCAs
Duloxetine
Pregabalin
Nitrous oxide as a recreational drug can have what link with peripheral neuropathy?
Functional inactivation of B12, causing peripheral neuropathy
What are the classic histopathologic findings in MND?
Cytoplasmic eosinophilic intracellular inclusions, positive for TDP 43
What is the mode of genetic transmission in most forms of Charcot-Marie-Tooth?
Autosomal dominant
What are the 2 antibodies involved in immune-mediated necrotising myopathy?
HMG-CoA reductase Ab
Anti-SRP
What is the approach to managing a statin-associated immune-mediated myopathy?
Cease the statin
Commence immunosuppression -> stopping the medication is not enough
What is the classic histopath finding in dermatomyositis?
Perivascular inflammatory infiltrate
Which muscles are classically involved in inclusion-body myositis?
Long finger flexors
Also involves quads, ankle dorsiflexors, can involve bulbar
What antibodies are involved in myasthenia gravis?
80-90% have IgG autoantibodies against the acetyl choline receptor (AChR)
Where are the antibodies in myasthenia gravis thought to originate?
Thought to originate in hyperplastic germinal centres in the thymus
What is the key to treatment of Bell’s palsy?
Steroid treatment within 72 hours
What are the indications for thymectomy in myasthenia gravis?
Indicated if thymoma, or if <60 with AChR antibodies
What is the classic triad of Wernicke’s encephalopathy?
Encephalopathy
Oculomotor dysfunction
Gait ataxia
What is the cause of Wernicke’s encephalopathy?
Thiamine (Vitamine B1) deficiency
What are Anti-Yo ab associated with?
A paraneoplastic cerebellar syndrome
Cancers = breast, ovarian, SCLC
What malignancy is KELCH-11 ab encephalitis associated with?
Testicular seminoma
What malignancy is commonly found in NMDA encephalitis?
Ovarian teratomas
What do positive sharp waves and fibrillation potentials on EMG indicate?
Spontaneous electrical activity - active denervation/ imflammatory myopathy
What may be the earliest abnormality on NCS in GBS?
Prolonged F wave latency
What is the role of steroids in AIDP?
NO ROLE - worse outcomes
What is the classic LP finding in AIDP / CIDP ?
Albuminocytologic dissociation
What is the key ab in AIDP (Miller-Fisher)?
What is the key ab in CIDP?
AIDP - GQ1b
CIDP - NF-155
What condition is classically associated with dorsal root ganglionopathy?
Sjogren’s Syndrome
Which anti-epileptic drug has highest association with birth defects?
What can occur?
Sodium valproate
Increases the risk of spina bifida up to ten-fold, associated with other serious malformations.
Can cause lower intelligence and greater risk of learning difficulties
What is the commonest identifiable cause of epilepsy in older adults?
Previous strokes
What are the EEG findings in juvenile myoclonic epilepsy?
4 to 6 Hz bilateral polyspike and slow wave discharges with frontal predominance
What is the gold standard treatment of juvenile myoclonic epilepsy?
What are alternatives?
Sodium valproate
Lamotrigine, Keppra (these are options in pregnancy / young females of childbearing age)
Which anti-epileptic can cause neurocognitive SEs?
Topiramate
Are fasciculations present in UMN or LMN lesions?
LMN
On NCS what is indicated by slowed conduction velocity?
Demyelination
On NCS what is indicated by decreased amplitude?
Axon loss
What is the usual pattern seen on NCS with nerve entrapment?
Focal demyelination ->
- delayed or absent F waves
- slowed conduction velocity
- conduction block
What is Wallerian degeneration?
When does this happen for
- motor nerves?
- sensory nerves?
Active process of degeneration that results when a nerve fiber is cut or crushed and the part of the axon distal to the injury (i.e. farther from the neuron’s cell body) degenerates.
Motor - Day 3-7
Sensory - Day 6-10
What is Saturday Night Palsy?
Radial neuropathy, classically at spiral groove
Clinical features = wrist drop, finger extensor and brachioradialis weakness
What is the key way to differentiate between radial neuropathy and central lesion?
Brachioradialis will be spared in Stroke
On EMG, what do fibrillations and positive sharp waves indicate?
How long do they take to develop?
Abnormal spontaneous activity -> active denervation, can be present in inflammatory myopathies
Over 10-42 days
In Myopathy, what pattern is seen on EMG?
Recruitment -> early
Amplitude -> reduced
In chronic denervation, what pattern is seen on EMG?
Recruitment -> reduced
Amplitude -> increased
What is the earliest finding usually seen in GBS on NCS?
Loss of F waves
What HLA allelle is associated with SJS/TENs with carbamazepine use?
HLA-B*1502
What is split hand syndrome?
What is it found in?
Thenar and 1st dorsal interosseous wasting
MND
Multifocal motor neuropathy with conduction block
- classical features?
- How is it treated?
Features: progressive LMN signs, peripheral weaknes
Unusual sites of demyelination
Rx: IVIG
What is the most common gene associated with CMT?
PMP22
(CMT1A - most common type)
What is the classic phenotype of Anti-MuSK ab positive myasthenia gravis?
Bulbar involvement, respiratory crises, less ocular involvement
What is the classic finding seen on single fibre EMG in myasthenia gravis?
Increased jitter
What is the initial treatment for mild to moderate myasthenia gravis?
Pyridostigmine
What anti-epileptic medication is preferred in pure absence seizures?
Ethosuximide
What is the anti-epileptic agent of choice in focal epilepsies?
Carbamazepine
What is the treatment of choice in myasthenic crisis?
PLEX or IVIG (equal)
Usually need to add glucocorticoids for lasting effect
How does fingolimod work?
What is the classic SE to be aware of?
Sphingosine-1-phosphate receptor modulator
Inhibits migration of T cells from lymphoid tissue into CNS
AE -> first dose bradycardia
Which MS drugs are contraindicated in pregnancy?
Fingolimod
Dimethyl fumerate
Teroflunomide
What is area postrema syndrome?
Episode of unexplained hiccups or nausea and vomiting
What are the auto antibodies found in NMOSD?
AQP4 ab
MOG ab
In which Parkinsons Plus syndrome is hummmingbird sign and Mickey Mouse appearance seen on MRI?
PSP
In which Parkinson’s Plus syndrome is alien hand found?
Corticobasal degenration
Where in the brain does HSV encephalitis tend to affect?
Mesial temporal lobe
What is the most common cause of rhomboencephalitis?
LIsteria
What is seen in Myasthenia Gravis on repetitive nerve stimulation?
ON single fibre EMG?
Decrementing amplitudes
sfEMG -> “Jitter”
Neuropathic Root lesions
L5 vs Common Peroneal drop ?
Common peroneal
- inversion preserved
L5 -
INVERSION also affected
Sciatic -
issues ABOVE the knee
Neurogenic vs vascular claudication
Neurogenic
- better with sitting down and going up hills
Brachial neuritis features?
Unil shoulder pain then weakness
Winging of scapular
What are F waves on NCS trying to detect?
Proximal demyelination
What is the finding on CSF of GBS?
Albumino-cytological dissociation
- high protein, but no inflammatory cells
Split hand sign?
What condition?
Wasting of thenar eminence + FDI with preservation of hypothenar
MND
When can you thrombolyse a stroke (time frame)?
What agent do you use?
- Within 4.5hrs of onset
- Within 9 hours of onset / midpoint of sleep if wake-up stroke -> pending CT perfusion with large penumbra
Alteplase
When can you do thrombectomy for stroke?
Defs within 6 hours in large vessel stroke
Within 24 hours -> pending CT perfusion findings
Classic features of Menieres?
Episodic Vertigo
Tinnitus
Aural fullness
Sensorineural hearing loss
How to differentiate between posterior stroke and vestibular neuronitis?
What is the initial management of IIH?
What is the treatment for IIH with visual compromise?
Weight loss, acetazolamide, topiramate
Optic nerve sheath fenestrations
Most SPECIFIC sign of Bell’s palsy vs central cause?
Loss of taste (chorda tympani)
CADASIL? What is it?
MRI findings?
Gene?
Cerebral Autosomal Dominant Arteriopathy Subcortical Infarcts & Leucoencephalopathy
Features:
- Migraine with aura (20-40%, 5x population)
- Stroke (60-85%, mean age~50)
- Dementia
Anterior temporal white matter changes on MRI
Notch 3 gene mutation
Recurrent thunderclap headaches?
Reversible cerebral vasoconstriction
DDx SAH
Key classes of chemoTx which cause peripheral neuropathy?
Platinums
Taxanes
Vincristine
Bortezomib
Which MS drugs are contraindicated in pregnancy? (3)
Teriflunamide
Dimethyl Fumarate
Fingolimod
In migraine, what vasoactive substance is thought to be central to vasodilation and inflammation?
Calcitonin Gene Related Peptide (CGRP) - from trigeminal fibres
What is the key area of the brain involved in trigeminal autonomic cephalgias?
Why must an MRI be performed?`
Hypothalamus
To assess for pituitary and posterior fossa lesions
What is the recommended 1st line agent for prevention in cluster headaches?
Verapamil IR TDS
Which of the trigeminal autonomic cephalgias are exquisitely responsive to indomethacin?
Paroxysmal hemicrania
Hemicrania continua
What makes up the lentiform nucleus?
What is its clinical relevance?
Globus pallidus + putamen
Part of basal ganglia
What is the preferred treatment option for SUNCT?
Lamotrigine
What is the usual pathophysiology of trigeminal neuralgia?
What is the 1st line agent?
Neurovascular compression
Carbamazepine
Which side do eyes deviate in cortical infarcts?
Towards lesion
Where is the lesion in locked-in syndrome?
What function is spared?
Bilateral ventral pons (basilar artery)
Paralysis of all movements except vertical gaze and eyelid opening
Fully conscious
What innervates posterior 1/3 of tongue?
Glossopharyngeal nerve (CN 9)
In tongue weakness, what side does the tongue deviate to in
- UMN lesion?
- LMN lesion?
UMN - away from side of lesion
LMN - towards side of lesion
At what level does the spinal cord end?
L1/L2
What part of CNS does polio affect?
Anterio horn cells
What is the lesion / where?
- Loss of elbow extension
- weakness of supination
- loss of hand/finger extension, wrist drop
- loss of sensation to lateral arm, and lateral dorsum of hand
Radial nerve
Proximal, at GH joint, can occur in crutch injury
What is the lesion / where?
- normal triceps
- weakness of supination
- loss of hand/finger extension, wrist drop
- loss of sensation to lateral arm, and lateral dorsum of hand
Radial nerve
- humeral fracture at radial groove
What is the lesion?
- weakness in extension of hand and fingers
- finger drop, partial wrist drop
- no sensory deficit
Radial nerve
Entrapment in arcade of Frohse
What is the lesion?
- no motor deficit
- Numbness and tingling in radial half of hand dorsum
Radial nerve
Laceration of forearm
What are the LOAF muscles?
What are they innervated by?
Lumbricals (1st and 2nd)
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
Median nerve
What is the deficit in ‘hand of Benediction’?
Median nerve
When attempting to form a fist, cannot flex 1st two fingers
What is the lesion?
- loss of pronation, weak wrist flexion, loss of thumb opposition
- Benediction sign
- loss of sensation lateral 3.5 digits and thenar area
Median nerve
Pronator teres syndrome or supracondylar fracture
What is the lesion?
- weakness in flexion of lateral digits and thumb flexion/opposition
- numbness lateral 3.5 digits, sparing thenar eminence
Median nerve
Carpal tunnel
What is the lesion?
- no sensory deficit
- loss of pronation
- loss of flexion of lateral digits and thumb
Median nerve -> anterior interosseous branch
Why is there paradoxical worsening of claw hand with more peripheral ulnar lesions?
The extent of clawing of digits four and five can be worse with lesions at the wrist than at the elbow as a result of sparing of the flexor digitorum profundus and weakness of the third and fourth lumbricals, resulting in greater muscle imbalance.
In what lesion will there be foot drop but preserved eversion?
Deep branch of peroneal nerve
What does a positive head impulse test suggest?
Vertigo - peripheral cause
What are the findings on HINTS screen that would suggest a central cause of vertigo?
Negative head impulse
Direction-changing nystagmus
Positive test of skew
**also new hearing loss
What condition is vestibular neuritis commonly associated with?
What is the treatment, if required?
Herpes SImplex 1 reactivation
Rx: Pred 1mg/kg for 5 days, then taper over 2 weeks
What is the recommended prophylactic treatment for episodic vertigo of Meniere’s DIsease?
Thiazide diuretic -> to lower endolymphatic pressure
Can be combined with potassium-sparing diuretic e.g. amiloride
Low salt diet, avoid caffeine
What is the Semont manoeuvre?
Manoeuvre for BPPV.
Equally effective to Epley’s.
However, the Semont manoeuvre is usually easier to perform on patients with limited neck movement or a prominent cervical kyphosis.
Management of Status Epilepticus
At what time frame is medication given?
What options?
After 5 minutes of continuous seizing / repeated activity with incomplete recovery
- Midazolam 10 mg IV OR Diazepam 10 mg IV OR Clonazepam 1 mg IV
- Unless cause easily reversed, start an anti-epileptic:
- Phenytoin 20 mg/kg IV
OR
- Sodium valproate 40 mg/kg IV
Consider need for HDU/ICU