Neurology Flashcards

1
Q

Describe the management of epilepsy

A

Most neurologists now start antiepileptics following a second epileptic seizure.

NICE guidelines suggest starting antiepileptics after the first seizure if:
> neurological deficit
> brain imaging: structural abnormality
> EEG: unequivocal epileptic activity
> patient / family / carers seizure risk unacceptable

Drug treatment

  • Generalised tonic-clonic seizures
    > males: sodium valproate
    > females: lamotrigine or levetiracetam
    » sodium valproate if under 10 or women unable to have children
    » sodium valproate causes weight gain
  • Focal seizures
    > first line: lamotrigine or levetiracetam
    > second line: carbamazepine, oxcarbazepine or zonisamide
  • Absence seizures (Petit mal)
    > first line: ethosuximide
    > second line:
    male: sodium valproate
    female: lamotrigine or levetiracetam
    carbamazepine may exacerbate absence seizures
  • Myoclonic seizures
    > males: sodium valproate
    > females: levetiracetam
  • Tonic or atonic seizures
    > males: sodium valproate
    > females: lamotrigine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe autonomic dysreflexia

A

caused by excessive sympathetic response below level of injury without coordinated parasympathetic counter response

can only occur if spinal cord injury is above T6

features
- severe hypertension
- flushing and sweating above level of injury
- reflex bradycardia

causes
- urinary retention / catheter blockage
- faecal impaction / loading

complications: stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe Guillain-Barré syndrome

A

immune-mediated demyelination of peripheral nervous system usually post-diarrhoeal illness e.g. Campylobacter jejuni

clinical features
- back/leg pain
- progressive symmetrical ascending weakness (starting in legs)
- reflexes are reduced or absent
- sensory symptoms usually mild

other features
- respiratory muscle weakness
- cranial nerve involvement: diplopia, bilateral facial nerve palsy, oropharyngeal weakness
- autonomic involvement: urinary retention, diarrhoea

investigations
- LP: rise in CSF protein with normal WCC
> gold-standard investigation
- anti-ganglioside antibodies
- Nerve conduction studies: decreased motor nerve conduction velocity

treatment - plasma exchange, IV immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which medications can be given for the following problems in MS?

  • fatigue
  • spasticity
  • oscillopsia
  • bladder dysfunction
A

fatigue: amantadine

spasticity: baclofen, gabapentin

oscillopsia: gabapentin

bladder dysfunction: anticholinergics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which medications can be given to reduce the risk of relapse in MS?

A

indications
> relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

medications
- natalizumab: first-line

  • ocrelizumab: another first-line option
  • fingolimod
  • beta-interferon: less effective
  • glatiramer acetate: less effective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe hereditary sensorimotor neuropathy (HSMN) aka Charcot-Marie-Tooth

A

encompasses Charcot-Marie-Tooth disease (aka peroneal muscular atrophy)

2 common types in clinical practice
- type I: demyelinating
- type II: axonal pathology

HSMN type I
- Autosomal dominant
- due to defect in myelin-coding gene
- features start at puberty
- motor symptoms predominate
- distal muscle wasting, pes cavus, clawed toes
- foot drop and leg weakness often first features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when can anti-epileptic drugs (AED) be stopped?

A

can be considered if seizure free for >2 years with AEDs being stopped over 2-3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe localising features of focal seizures

A

temporal lobe
- with/without impairment of consciousness or awareness

  • aura
    > rising epigastric sensation
    > psychic/experiential phenomena e.g. deja vu, jamais vu
  • less commonly hallucinations (auditory/gustatory/olfactory)
  • seizures typically last around one minute
  • automatisms (lip smacking/grabbing/plucking of clothes)
  • post-ictal dysphasia
  • Todd’s paralysis

frontal lobe (motor)
- head/leg movements
- posturing
- post-ictal weakness
- Jacksonian march

parietal lobe (sensory)
- paraesthesia

occipital lobe (visual)
- floaters/flashes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe subacute combined degeneration of the cord

A

SCD: spinocerebellar tract, corticospinal tract, dorsal columns

causes
- vitamin B12 & E deficiency
- can result from replacing folate before b12 if b12 deficient (BeFore)
- nitrous oxide inhalation

features
- bilateral spastic paresis: weakness, spasticity
- bilateral loss of proprioception and vibration
- distal tingling, burning and/or sensory loss
- bilateral limb ataxia
- hyperreflexia
- positive Babinski sign

positive Romberg’s test due to sensory ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

list driving restrictions for individuals with epilepsy

A

first unprovoked/isolated seizure: 6 months off if no structural brain abnormalities on imaging or epileptiform activity on EEG

established epilepsy / multiple unprovoked seizures:
> qualify for driving license if they have been seizure free for 12 months
> if no seizures for 5 years, a til 70 license is restored

withdrawal of epilepsy medication: cannot drive whilst being withdrawn and for 6 months after

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe spinal muscular atrophy (SMA)

A

rare autosomal recessive condition which causes a progressive loss of lower motor neurones leading to progressive muscular weakness

features
- fasciculations
- reduced muscle bulk
- reduced tone
- reduced power
- reduced / absent reflexes

management: supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe myotonic dystrophy

A

genetic disorder usually presenting in adulthood

features
- progressive muscle weakness
- prolonged muscle contractions
- cataracts
- cardiac arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe the features, investigations and management of a TIA

A

brief period of neurological deficit due to a vascular cause, typically lasting less than an hour (always <24h)

Clinical features
- unilateral weakness or sensory loss
- aphasia or dysarthria
- ataxia, vertigo, or loss of balance
- visual problems
- sudden transient loss of vision in one eye (amaurosis fugax)
- diplopia
- homonymous hemianopia

ABCD2: prognostic score to risk stratify patients

Management
- immediate antithrombotic therapy: > aspirin 300 mg immediately

unless:
1. bleeding disorder / anticoagulated (needs immediate admission for imaging to exclude a haemorrhage)
2. already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
3. Aspirin is contraindicated: discuss management urgently with the specialist team

Advise the person not to drive until they have been seen by a specialist

Investigations
- diffusion-weighted MRI first-line

  • Carotid imaging
    > all patients should have an urgent carotid doppler unless they are not a candidate for carotid endarterectomy

Further management
> Secondary prevention
- clopidogrel is recommended first-line (as for patients who’ve had a stroke)
- aspirin + dipyridamole should be given to patients who cannot tolerate clopidogrel
- lipid modification
- high-intensity statin (such as atorvastatin 20–80 mg daily)

carotid artery endarterectomy if carotid stenosis > 70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the symptoms of stroke depending on the affected vessel

A

ACA
> contralateral hemiparesis and sensory loss
> lower extremity > upper

MCA
> contralateral hemiparesis and sensory loss
> upper extremity > lower extremity
> aphasia
> contralateral homonymous hemianopia

PCA
> Contralateral homonymous hemianopia with macular sparing
> Visual agnosia

Weber’s syndrome (branches of PCA supplying midbrain)
> contralateral upper and lower limb weakness
> ipsilateral CN III palsy

PICA (lateral medullary syndrome, Wallenberg syndrome)
> ipsilateral facial pain and temperature loss
> contralateral limb/torso pain and temperature loss
> ataxia, nystagmus
> ipsilateral Horner’s syndrome

AICA (lateral pontine syndrome)
> similar to Wallenberg’s but ipsilateral facial paralysis and deafness also
> reduced GCS, paralysis, bilateral pinpoint pupils

Retinal/ophthalmic artery: amaurosis fugax

Basilar artery: locked in syndrome

Lacunar strokes present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
> strong association with hypertension
> common sites include the basal ganglia, thalamus and internal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe bacterial meningitis and its management

A

Clinical features
- meningism: neck stiffness, photophobia
- nausea / vomiting
- reduced GCS
- non-blanching rash
- fever
- tachycardia, tachypnoea, hypotension
- Brudzinski / kernig’s sign +ve

attempt LP unless
- severe sepsis / rapidly evolving rash
- severe respiratory / cardiac compromise
- significant bleeding risk
- signs of raised ICP (focal neurological signs, papilloedema, continuous/uncontrolled seizures)

CT head prior to LP ONLY if risk of evolving SOL / signs of increased ICP

Management
- IV antibiotics
> <3 months: IV cefotaxime + amoxicillin
> 3 months-50 years: cefotaxime or ceftriaxone
> >50 years: cefotaxime (or ceftriaxone) + amoxicillin (increased risk of Listeria meningitis)

  • IV dexamethasone 0.15mg/kg QDS for 4 days
    > avoid in septic shock, meningococcal septicaemia, immunocompromised or meningitis following surgery
  • if allergic to penicillin / cephalosporins, use chloramphenicol
  • if Listeria monocytogenes: IV amoxicillin + gentamicin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe a post-LP headache and its management

A

Low pressure headache

can occur up to a week later from when the LP was taken

alleviated by lying down
> if headache lasts more than 3 days, consider subdural haematoma

management
- supportive analgesia - analgesia, rest
- consider blood patch, epidural saline and IV caffeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the diagnostic criteria for migraine

A
  • headache attacks lasting 4-72h
  • at least 2 of the following characteristics
    > unilateral location but may be bilateral
    > pulsating quality
    > moderate or severe pain
    > aggravation by routine physical activity
  • during headache at least one of the following
    > nausea or vomiting
    > photophobia, phonophobia
  • not attributed to another disorder

in children, attacks may be shorter-lasting, headache is bilateral and GI disturbance is more prominent

migraine with aura
> aura is progressive in nature and occurs hours prior to headache
> typical aura: transient hemianopic disturbance / spreading scintillating scotoma (jagged crescent)
> sensory symptom

auras may occur with/without headache and are fully reversible, develop over at least 5 minutes and last 5-60 minutes

atypical symptoms
> motor weakness
> double vision
> visual symptoms affecting only one eye
> poor balance / decreased GCS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name the most common cause of
- bacterial meningitis <60
- viral meningitis
- viral encephalitis

A

bacterial meningitis <60: Neisseria meningitidis, streptococcus pneumoniae

Viral meningitis: enterovirus
> Coxsackie, Echovirus

Viral encephalitis: HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe viral meningitis and its management

A

Presents similarly to bacterial meningitis
> less likely to have a non-blanching purpuric rash
> less severe than bacterial meningitis

management
- supportive, usually self-limiting course of 7-14 days
- aciclovir if thought to be caused by HSV
- IV aciclovir if concern regarding encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

in the context of meningitis, under which circumstances should LP be delayed?

A
  • signs of severe sepsis
  • rapidly evolving rash
  • severe respiratory / cardiac compromise
  • significant bleeding risk
  • signs of increased ICP
    > focal neurology
    > GCS <=12
    > Papilloedema
    > seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

describe CSF results depending on the cause of meningitis

A

bacterial
- appearance: cloudy
- glucose: low (<1/2 plasma)
- protein: high (>1g/l)
- WCC: 10-5000 polymorphs/mm3

viral
- appearance: clear/cloudy
- glucose: 60-80% of plasma glucose
- protein: normal/raised
- WCC: 15-1000 lymphocytes/mm3

TB
- appearance: slight cloudy, fibrin web
- glucose: low (<1/2 plasma)
- protein: high (>1 g/l)
- WCC: 30-300 lymphocytes/mm3

fungal
- appearance: cloudy
- glucose: low
- protein: high
- WCC: 20-200 lymphocytes/mm3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

describe the management of status epilepticus

A
  • ABCDE assessment
  • airway: lateral decubitus, nasal trumpets, O2, suction
  • IV access

0-5 mins (give benzos at 5 mins)
> lorazepam 0.1mg/kg IV, max 4mg, repeat once in 4min
> OR midazolam 10mg IM once

10-15 mins
> levetiracetam 60mg/kg IV
> OR fosphenytoin or phenytoin 20mg/kg IV
> OR valproate 40mg/kg IV

> advanced airway management
> RSI
> Preoxygenation
> Induction: propofol or ketofol
> paralytics: rocuronium, succinylcholine

15-20 mins: refractory medications
- propofol
- midazolam
- ketamine
- lacosamide
- phenobarbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe herpes simplex encephalitis

A

infection of brain parenchyma

features
- fever
- headache
- psychiatric symptoms
- seizures
- vomiting
- focal features e.g. aphasia, weakness, limping

investigations
- LP
> elevated protein
> lymphocytosis
> PCR for HSV, VZV, enterovirus

  • CT head: temporal lobe changes e.g. asymmetrical low density areas
  • EEG

management
- start aciclovir promptly in all suspected cases of viral encephalitis
> treats HSV and VZV
> ganciclovir is needed for CMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how would you check if fluid is truly CSF?

A

check a glucose level: bedside test

beta-2-transferrin level: gold standard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe the different types of aphasia

A

Wernicke’s (receptive) aphasia
> lesion of superior temporal gyrus
> usually supplied by inferior division of left MCA

> features
- sentences that make no sense
- word substitution
- neologism
- speech remains fluent
- “word salad”
- comprehension is impaired

Broca’s (expressive) aphasia
> lesion of inferior frontal gyrus
> usually supplied by superior division of left MCA
> speech is non-fluent, laboured and halting
> repetition is impaired
> comprehension is normal

Conduction aphasia
> usually due to stroke affecting arcuate fasciculus
> speech is fluent but repetition is poor
> aware of errors being made
> comprehension is normal

Global aphasia
> severe expressive and receptive aphasia
> may still be able to communicate using gestures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

describe chronic fatigue syndrome

A

aka myalgic encephalomyelitis (ME)

diagnosed after at least 3 months of disabling fatigue affecting mental and physical function >50% of the time in the absence of other disease which can explain symptoms

features
- fatigue
- sleep problems
- muscle/joint pains
- headaches
- painful lymph nodes
- cognitive dysfunction
- physical or mental exertion makes symptoms worse

management
- energy management
- CBT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the mechanism of controlled hyperventilation in raised ICP?

A

Reduced blood carbon dioxide to induce cerebral vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

describe the Barthel index

A

measure of disability or dependence in activities of daily living in stroke patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

describe neurogenic shock

A

causes
- trauma e.g. spinal cord transection

features
- bradycardia
- hypotension

management
- vasopressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the management of migraines

A

Acute:

  • analgesia
    NSAIDs or paracetamol + triptans
    > avoid opioids
  • antiemetic: metoclopramide
    > prokinetic agent that helps to relieve gastric stasis that occurs during acute migraine attack
    > consider even in cases without nausea

Prophylaxis:
- topiramate (teratogenic) or propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the antibiotics of choice for contacts of patients with meningococcal meningitis

A

PO ciprofloxacin or rifampicin

> one dose for close contacts within last 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe idiopathic intracranial hypertension

A

classically seen in young overweight females

features
- headache
- blurred vision
- papilloedema
- enlarged blind spot
- sixth nerve palsy
- high pressure features: worse on coughing/sneezing/lying flat/leaning forwards

associated with tetracycline antibiotics

investigations
- lumbar puncture: opening pressure values >25 cmH2O
- CT brain: enlarged arachnoid outpouchings, prominent perivascular spaces

management
- weight loss - semaglutide and topiramate
- carbonic anhydrase inhibitors e.g. acetazolamide
- repeated LP - temporary measure
- surgery:
> optic nerve sheath decompression and fenestration
> lumboperitoneal / ventriculoperitoneal shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe an Arnold-Chiari malformation

A

downward displacement or herniation of cerebellar tonsils through foramen magnum

malformation may be congenital or acquired through trauma

features
- non-communicating hydrocephalus may occur as a result of obstruction of CSF flow
- headache
- syringomyelia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

describe essential tremor

A

autosomal dominant condition which usually affects both upper limbs

Features
- postural tremor: worse if arms outstretched
- improved by alcohol and rest
- most common cause of titubation (head tremor)

Management
- propranolol is first-line
- primidone is sometimes used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

describe a myasthenic crisis and its management

A

myasthenic crisis
- acute respiratory failure characterised by FVC <1L
- accessory muscle use

Management
> plasmapheresis
> intravenous immunoglobulins
> ventilatory support: low threshold for intubation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe myasthenia gravis and its management (as well as exacerbating factors)

A

autoimmune disorder due to autoantibodies against ACh receptors

Features
- muscle fatiguability - muscles become progressively weaker during periods of activity and slowly improve after periods of rest
- extraocular muscle weakness: diplopia
- proximal muscle weakness: face, neck, limb girdle
- ptosis
- dysphagia

Associations
> thymomas in 15%
> autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
> thymic hyperplasia in 50-70%

Exacerbating factors
> penicillamine
> beta-blockers
> lithium
> phenytoin
> antibiotics: gentamicin, macrolides, quinolones, tetracyclines
> quinidine, procainamide

Investigations
> single fibre electromyography
> CT thorax - exclude thymoma
> antibodies to acetylcholine receptors

> Tensilon test: IV edrophonium reduces muscle weakness temporarily

Management
> long-acting acetylcholinesterase inhibitors: pyridostigmine is first-line
> immunosuppression: prednisolone initially
> azathioprine, cyclosporine, mycophenolate mofetil
> thymectomy

37
Q

Describe Wernicke’s encephalopathy and its management

A

Wernicke’s encephalopathy is a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics

Rarer causes; persistent vomiting, stomach cancer, and dietary deficiency

Classic triad: ophthalmoplegia/nystagmus, ataxia and encephalopathy

Features
> oculomotor dysfunction
> nystagmus (the most common ocular sign)
> ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy
> gait ataxia
> encephalopathy: confusion, disorientation, indifference, and inattentiveness
> peripheral sensory neuropathy

Investigations
> decreased red cell transketolase
> MRI

Treatment: urgent replacement of thiamine
> IV Pabrinex (vitamin B/C)

If not treated Korsakoff’s syndrome may develop
> antero- and retrograde amnesia
> confabulation

38
Q

Describe cluster headaches and their management

A

occur in clusters lasting 4-12 weeks
> clusters typically occur once a year

More common in men, smokers and alcohol drinkers

Features
-intense sharp, stabbing pain around one eye
- pain once or twice a day, each episode lasting 15 mins - 2 hours
- restless / agitatated during attack
- clusters typically last 4-12 weeks

  • ipsilateral autonomic features
    > conjunctival injection (redness)
    > orbital oedema
    > lacrimation
    > miosis and ptosis
    > nasal congestion
    > facial sweating

Investigations
- neuroimaging - underlying brain lesions are sometimes found
> MRI with gadolinium contrast: investigation of choice

Management
- acute:
> 100% oxygen
> subcutaneous triptan

  • prophylaxis: verapamil
39
Q

list the components of the Glasgow Coma Scale (GCS)

A

Eye-opening
> eyes open spontaneously (4)
> eyes open to voice (3)
> eyes open to pain (2)
> no eye-opening (1)

Verbal response
> orientated (5)
> confused (4)
> words (3)
> incomprehensible sounds (2)
> no verbal response (1)

Motor resopnse
> obeys commands (6)
> localises pain (5)
> normal flexion (4)
> abnormal flexion (3)
> abnormal extension (2)
> no motor response (1)

40
Q

describe cerebral venous sinus thrombosis (CVST)

A

clinical features
- headache (insidious or sudden onset)
- signs of increased ICP
> vomiting
> papilloedema
> focal / generalised seizures

risk factors: thrombophilia, female, pregnancy, COCP, infections (mastoiditis, otitis, sinusitis)

diagnosis: MR venogram

management
- anticoagulation: heparin or warfarin
- treat underlying cause if possible

41
Q

List contraindications to thrombolysis

A

Absolute
- Previous intracranial haemorrhage
- Seizure at onset of stroke
- Intracranial neoplasm
- Suspected subarachnoid haemorrhage
- Stroke / traumatic brain injury in preceding 3 months
- LP in preceding 7 days
- GI bleed in preceding 3 weeks
- Active bleeding
- Pregnancy
- Oesophageal varices
- Uncontrolled hypertension

Relative
- Concurrent anticoagulation
- Active diabetic haemorrhagic retinopathy
- Suspected intracardiac thrombus
- Major surgery / trauma in the preceding 2 weeks

42
Q

Describe the secondary prevention of stroke

A

clopidogrel 75mg daily lifelong (first-line)

aspirin plus MR dipyridamole (if clopidogrel is contraindicated)

Carotid artery endarterectomy if patient has suffered stroke / TIA in the carotid territory and is not severely disabled

43
Q

Describe the management of ischaemic stroke

A

aspirin 300mg orally or rectally - once haemorrhagic stroke has been excluded
> continue aspirin 300mg daily for 2 weeks then clopidogrel 75mg daily long-term

If AF - anticoagulants should not be started until 14 days have passed from the onset of an ischaemic stroke

if cholesterol is > 3.5 mmol/l - commence statin
> delay treatment until after 48 hours due to risk of haemorrhagic transformation

Thrombolysis with alteplase for acute ischaemic stroke
> if within 4.5 hours of onset of stroke symptoms and
haemorrhage definitively excluded

Thrombectomy for acute ischaemic stroke
> within 6 hours of symptom onset, PLUS intravenous thrombolysis (if within 4.5 hours)
> consider extended 6-24h if potential to salvage tissue as shown by CT perfusion or diffusion-weighted MRI showing limited infarct core volume

44
Q

List causes of subarachnoid haemorrhage and describe its diagnosis and management

A

Clinical features
- thunderclap headache
> maximal intensity <5mins
> sudden onset severe occipital headache
- meningism (photophobia, neck stiffness)
- nausea and vomiting
- coma
- seizures
- neurological symptoms: visual changes, dysphasia, focal weakness, reduced consciousness
- ECG changes - ST elevation

risk factors: female sex, smoker, hypertension, black ethnic origin, excessive alcohol

Diagnosis
- Non-contrast CT head <6h after onset: if negative, consider alternative diagnosis
- if CT >6h after onset is negative do LP after 12h (confirm xanthochromia)

  • after spontaneous SAH is confirmed
    > CT intracranial angiogram +/- digital subtraction angiogram

Management
> supportive: bed rest, analgesia, VTE prophylaxis, discontinuation of antithrombotics
> nimodipine for prevention of vasospasm

  • neurosurgical referral due to risk of aneurysm rebleeding
    > endovascular coiling by interventional neuroradiologist
    > if severe, neurosurgical clipping or craniotomy
45
Q

list complications of subarachnoid haemorrhage

A
  • Re-bleeding
  • hydrocephalus (treat with LP, external ventricular drain or long-term ventriculoperitoneal shunt)
  • vasopasm
    > prevention with nimodipine
  • hyponatraemia (due to SIADH)
  • Seizures
    > treat with anti-epileptics
  • Torsades de Pointes
46
Q

describe the management of Parkinson’s disease

A
  • Levodopa (co-careldopa contains levodopa and carbidopa)
    > reduced effectiveness with time
  • Carbidopa: DOPA decarboxylase inhibitor
  • dopamine receptor agonists e.g. bromocriptine, cabergoline, apomorphine
    > highest chance of inhibition disorders
  • COMT inhibitors e.g. entacapone
  • MAO-B inhibitors e.g. selegiline
  • amantadine
47
Q

List side-effects of levodopa

A
  • dry mouth
  • anorexia
  • CVS: palpitations, postural hypotension, arrhythmias
  • psychosis, hallucinations
  • on-off phenomenon
  • end-of-dose dyskinesia
48
Q

describe the features of Parkinson’s disease

A

clinical features
- Bradykinesia
> test with finger-tap test and pronation-supination test

  • Unilateral pill-rolling tremor
    > asymmetrical, 4-6 Hz, enhanced by anxiety
  • shuffling gait with reduced arm swing
  • Postural instability
  • Leadpipe rigidity or cogwheeling

Neuropsychiatric
- Anxiety, depression
- Hallucinations
- REM sleep disorders
- Cognitive impairment (Parkinson’s disease dementia)
> motor symptoms ongoing at least a year before the emergence of dementia

Autonomic
- Altered sense of smell (hyposmia)
- Constipation

Genitourinary
- Incontinence
- Nocturia, frequency
- Erectile dysfunction

Myalgia
Hyperhidrosis (sweating)
Hypomimia
Infrequency of eye blinking
Hypophonia

49
Q

List lower motor neurone signs

A
  • Reduced tone
  • Hyporeflexia
  • Fasciculations
  • Paresis
  • Weakness in a root innervated pattern
  • muscle atrophy
50
Q

Describe medication overuse headaches and their treatment

A

Features
- present for 15 days or more per month
- developed or worsened whilst taking regular symptomatic medication
- patients using opioids and triptans are at most risk
- may be psychiatric co-morbidity

Management
- simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
- opioid analgesics should be gradually withdrawn

51
Q

which medications can lead to drug-induced parkinsonism?

A

typical antipsychotics e.g. haloperidol

antiemetics e.g. metoclopramide, prochlorperazine

> symptoms are likely to be bilateral in drug-induced parkinsonism

52
Q

describe the management of acute confusional state

A

treat the underlying cause and modify environment

if not working then haloperidol / olanzapine can be used

if Parkinson’s use atypical antipsychotics like quetiapine or clozapine

53
Q

describe vertebrobasilar ischaemia

A

features
- vertigo upon neck extension (looking up)
- exacerbated by changes in head position
- falls in elderly patients

risk factors - CVD, atherosclerosis

54
Q

in a painful third nerve palsy where would the lesion be located?

A

posterior communicating artery aneurysm

after trauma an oculomotor nerve palsy + hemiparesis can be a sign of transtentorial / uncal herniation (medial aspect of temporal lobe compressing CN III and cerebral peduncle)

55
Q

describe the following conditions affecting the spinal cord

  • Brown-Sequard syndrome
  • friedrich’s ataxia
  • anterior spinal artery occlusion
  • neurosyphilis
A

Brown-Sequard syndrome
- aka spinal cord hemisection
- ipsilateral spastic paresis below lesion
- ipsilateral loss of proprioception and vibration sensatoin
- contralateral loss of pain and temperatures sensation

friedrich’s ataxia
- same as above + cerebellar ataxia, intention tremor

anterior spinal artery occlusion
- bilateral spastic paresis
- bilateral loss of pain and temperature sensation

neurosyphilis (tabes dorsalis)
- loss of proprioception and vibration sense as dorsal columns are affected

56
Q

which diet is used in children with epilepsy which is unresponsive to treatment?

A

ketogenic diet

57
Q

describe the diagnosis of multiple sclerosis

A

diagnosis requires dissemination of demyelinating lesions in time and space

  • MRI brain + spinal cord with contrast
    > high signal T2 lesions
    > periventricular plaques
    > Dawson fingers
  • +ve Hoffman’s sign
  • CSF
    > oligoclonal bands
    > increased intrathecal synthesis of IgG
  • Visual evoked potentials
    > delayed but well-preserved waveform

risk factors: EBV infection, multiple genes, low vitamin D, smoking, obesity

58
Q

Describe the symptoms of stroke depending on the affected vessel

A

ACA
> contralateral hemiparesis and sensory loss
> lower extremity > upper

MCA
> contralateral hemiparesis and sensory loss
> upper extremity > lower extremity
> aphasia
> contralateral homonymous hemianopia

PCA
> Contralateral homonymous hemianopia with macular sparing
> Visual agnosia

Weber’s syndrome (branches of PCA supplying midbrain)
> contralateral upper and lower limb weakness
> ipsilateral CN III palsy

PICA (lateral medullary syndrome, Wallenberg syndrome)
> ipsilateral facial pain and temperature loss
> contralateral limb/torso pain and temperature loss
> ataxia, nystagmus
> ipsilateral Horner’s syndrome

AICA (lateral pontine syndrome)
> similar to Wallenberg’s but ipsilateral facial paralysis and deafness also
> reduced GCS, paralysis, bilateral pinpoint pupils

Retinal/ophthalmic artery: amaurosis fugax

Basilar artery: locked in syndrome

Lacunar strokes present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
> strong association with hypertension
> common sites include the basal ganglia, thalamus and internal capsule

59
Q

describe multiple sclerosis and its clinical features

A

Idiopathic inflammatory demyelinating disease of the CNS

Acute episodes of inflammation are associated with focal neurological deficits

visual symptoms
- optic neuritis
- optic atrophy
- Uhthoff’s phenomenon: worsening of vision following rise in body temperature
- internuclear ophthalmoplegia

sensory symptoms
- pins/needles
- numbness
- trigeminal neuralgia
- Lhermitte’s syndrome: paraesthesiae in limbs on neck flexion

motor symptoms
- spastic weakness (most commonly in legs)

cerebellar symptoms
- ataxia
- tremor

others symptoms
- urinary incontinence
- sexual dysfunction
- intellectual deterioration

60
Q

describe Miller Fisher syndrome

A

subtype of Guillain-Barré syndrome (GBS)

characterised by areflexia, ataxia and ophthalmoplegia

descending weakness is a classic features as opposed to ascending weakness in more common forms of GBS

anti-GQ1b antibodies present in most cases

61
Q

describe osmotic demyelination syndrome

A

aka central pontine myelinolysis

  • can occur due to overcorrection of severe hyponatraemia
  • Na levels should only be raised by 4-6 mmol/l in 24h

symptoms usually occur after 2 days and are irreversible
- dysarthria
- dysphagia
- paraparesis or quadriparesis
- seizures
- confusion
- coma

patients are awake but unable to move or verbally communicate - locked-in syndrome

from high to low your brain will blow - cerebral oedema
from low to high your pons will die - central pontine myelinolysis

62
Q

Describe the subtypes of multiple sclerosis

A
  • Relapsing remitting Multiple Sclerosis (RRMS)
    > Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission
  • Primary progressive multiple sclerosis (PPMS)
    > At least 1 year of disease progression
    > Steady increase in disability without attacks
  • Secondary progressive multiple sclerosis (SPMS)
    > Initial relapsing-remitting multiple sclerosis
    > Suddenly begins to decline without periods of remission
  • Benign multiple sclerosis (BMS)
63
Q

describe the management of multiple sclerosis

A
  • disease-modifying therapies e.g. natalizumab for RRMS or ocrelizumab for PPMS
  • relapses: high dose steroids e.g. IV methylprednisolone
  • symptomatic
    > strength: exercise
    > fatigue: amantadine, modafinil, SSRIs
    > neuropathic pain: amitriptyline, gabapentin
    > depression: SSRIs
    > urge incontinence: solifenacin
    > spasticity: baclofen, gabapentin
    > oscillopsia: gabapentin, memantine
64
Q

describe the diagnosis of motor neurone disease (MND)

A

diagnosis is clinical

  • features
    > asymmetric limb weakness
    > mixture of LMN and UMN signs
    > wasting of small hand muscles / tibialis anterior
    > fasciculations
    > emotional lability
    > absence of sensory signs/symptoms
    > sparing of eye movements

> nerve conduction studies: normal motor conduction, exclude neuropathy

> electromyography: reduced number of action potentials with increased amplitude

> MRI - exclude cervical cord compression and myelopathy

usually pathological TDP-43 proteins

65
Q

describe the different types of motor neurone disease (MND) and their management

A
  • amyotrophic lateral sclerosis (ALS)
    > most common
  • progressive bulbar palsy
    > second most common
    > affects talking/swallowing
    > causes tongue wasting and fasciculations
  • progressive muscular atrophy
  • primary lateral sclerosis

management
- riluzole: slow progression of disease
- symptomatic
> spasticity: baclofen
> antimuscarinics: excessive salivation
> NIV to support breathing
- advanced directives, end-of-life care

66
Q

describe Lambert-Eaton myasthenic syndrome

A

usually a paraneoplastic syndrome occurring alongside small-cell lung cancer (SCLC)
> can occur as a primary autoimmune disorder

caused by antibodies against voltage-gated calcium channels

clinical features
- proximal muscle weakness (difficulty climbing stairs/rising from chair)
- autonomic dysfunction (dry mouth, blurred vision, impotence, dizziness)
- reduced / absent tendon reflexes

symptoms IMPROVE after periods of muscle contraction, as opposed to myasthenia gravis (fatiguability)

management
- exclude malignancy
- amifampridine: voltage-gated potassium channel blocker
- pyridostigmine, immunosuppressants
- IV immunoglobulins, plasmapheresis

67
Q

describe Huntington’s disease

A

aka Huntington’s chorea

AD trinucleotide repeat disorder
> demonstrates anticipation: successive generations have earlier age of onset / increased severity of disease

clinical features
- chorea: involuntary, random, irregular and abnormal body movements
- dystonia: abnormal muscle tone leading to abnormal postures
- rigidity
- eye movement disorders
- dysarthria, dysphagia
- cognitive, psychiatric or mood problems

investigations
> genetic testing
> MRI: caudate atrophy

management
- genetic counselling
- SSRIs if depressed
- tetrabenazine for chorea
- supportive: physio, SALT, advanced directives, end-of-life care

68
Q

describe tuberous sclerosis

A

AD condition

cutaneous features
- depigmented ash-leaf spots which fluoresce under UV light
- roughened patches of skin over lumbar spine (Shagreen patches)
- adenoma sebaceum (angiofibromas): butterfly distribution over nose
- subungal fibromata
- cafe-au-lait spots may be seen
- angiomyolipomas

neuro features
- developmental delay
- epilepsy (infantile spasms or partial)
- intellectual impairment

also: retinal hamartomas, rhabdomyomas of the heart, gliomatous changes in brain lesions, polycystic kidneys, lymphangioleiomyomatosis

69
Q

describe neurofibromatosis

A

2 types: neurofibromatosis type 1 is more common
> NF2 is associated with BILATERAL acoustic neuromas

AD inheritance

clinical features: CRABBING
- cafe au lait spots
- relative with NF1
- axillary or inguinal freckling
- bony dysplasia e.g. bowing of a long bone
- iris hamartomas (Lisch nodules)
- neurofibromas: skin-coloured raised nodules
- glioma of optic pathway

management: monitor for complications

complications
- migraines
- epilepsy
- renal artery stenosis
- multiple tumours (e.g. spinal cord, GIST…)
- vision loss due to optic nerve glioma

70
Q

describe a generalised tonic clonic seizure

A

clinical features
- body stiff, rigid, crashes to the ground
- from rigid to rhythmical jerking (not tremor)
- may have urinary incontinence / lateral tongue biting
- cyanotic
- eyes often open (rolled back)

usually last 1-2 minutes

post-seizure
- non-responsive
- heavy breathing/snoring
- post-ictal confusion
- patient may: not remember events, have headache, myalgia, and go to sleep it off

71
Q

describe seizure classification

A

generalised
- tonic
- clonic
- atonic
- tonic-clonic
- myoclonic
- absence

focal
- depends on origin of seizure
- +/- impaired consciousness
- +/- becoming generalised

72
Q

Describe spontaneous intracranial hypotension

A

Low CSF headaches caused by spontaneous intracranial hypotension

> worse on standing, improved lying flat

more common in connective tissue disorder e.g. Marfan’s syndrome

Conservative management. Epidural blood patch if this fails.

73
Q

Describe trigeminal neuralgia

A

Trigeminal neuralgia: pain syndrome characterised by severe unilateral pain in trigeminal distribution

> brief electric shock-like pains, abrupt in onset and termination with a refractory period

triggers
> light touch, washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously

idiopathic but compression of trigeminal roots by tumours or vascular problems may occur

Management
- carbamazepine is first-line

  • failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
    > surgery: microvascular decompression
74
Q

Describe the diagnosis of creutzfeldt jakob disease

A

Rapidly progressive neurodegenerative prion disorder, usually sporadic but can be inherited

clinical features
- rapid cognitive decline
- myoclonic jerks
- behavioural change
- visual disturbance
- ataxia

Key investigations
- MRI
- lumbar puncture
- EEG
> bi- or tri-phasic periodic sharp wave complexes appearing with a frequency of around 1-2 per second.

Definitive diagnosis: post-mortem biopsy

75
Q

describe the investigations used in stroke

A
  • ROSIER score: asymmetric weakness, speech disturbance, visual disturbance
  • Non-contrast CT head:
    > acute ischaemic strokes
    » areas of low density in the grey and white matter; changes may take time to develop

> > other signs include the ‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately

> acute haemorrhagic strokes
>hyperdense material (blood) surrounded by low density (oedema)

76
Q

describe chronic traumatic encephalopathy (CTE)

A

sequelae of chronic repeated head injury

usually in athletes e.g. rugby / boxing

clinical features
- behavioural change
- cognitive difficulties
- mood disturbance

77
Q

explain the use of prolactin in seizures

A

Rise in serum prolactin can help to differentiate a seizure from a pseudoseizure

pseudoseizures also tend to have a gradual onset while true seizures have sudden onset

Other features suggestive of seizure
> Tongue biting
> Urinary incontinence
> Post-ictal phase
> Memory loss
> Todd’s paresis (post-ictal weakness)

78
Q

Describe the clinical presentation of subdural haemorrhage

A

caused by rupture of bridging veins

risk factors: elderly, alcoholism, anticoagulation

Clinical presentation
- fluctuating consciousness
- altered mental state
- focal neurology
- falls
- can be triggered by alcohol excess

management
- acute subdural haematoma: neurosurgical referral for evacuation of haematoma e.g. decompressive craniectomy

  • chronic subdural haematoma:
    > asymptomatic: conservative
    > symptomatic: burr hole drainage
79
Q

describe Wilson’s disease

A

AR disorder characterised by excessive copper deposition in tissues

Features
- Liver: hepatitis, cirrhosis
- Neurological: speech, behavioural and psychiatric problems
- Kayser-Fleischer rings: green-brown rings in the periphery of the iris
- Renal tubular acidosis
- Haemolysis
- Blue nails

Lab
- Reduced serum caeruloplasmin
- Reduced total serum copper
- Increased 24h urinary copper excretion

Management
- penicillamine (chelates copper)

80
Q

describe an extradural haematoma

A

pathophysiology
> mostly trauma, low-impact head injury
> especially over temporal region due to the pterion overlying the middle meningeal artery

patients may experience a lucid interval
> briefly regain consciousness after injury before progressing into coma

imaging
- biconvex or lentiform hyperdense collection limited by suture lines of skull

management
- no neurological deficit: cautious clinical and radiological observation
- definitive treatment: craniotomy and evacuation of haematoma

81
Q

describe Bell’s palsy and its management

A

acute, unilateral, idiopathic, facial nerve paralysis.

risk factors
- age 20-40 years
- pregnant women

Features
> lower motor neuron facial nerve palsy → forehead affected
> post-auricular pain (may precede paralysis)
> altered taste
> dry eyes
> hyperacusis

Management
- oral prednisolone within 72 hours of onset of Bell’s palsy
- eye care to prevent exposure keratopathy: prescribe artificial tears and eye lubricants, taping at night

82
Q

describe syringomyelia

A

due to development of syrinx (CSF-filled cyst) in the anterior white commisure of the spinal cord

Presentation
- cape-like loss of pain and temperature sensation due to compression of spinothalamic tract fibres decussating in centre of spinal cord
- preserved light touch, proprioception and vibration
- spastic weakness
- neuropathic pain
- upgoing plantars
- autonomic features
> Horner’s syndrome due to compression of sympathetic chain
> scoliosis can develop if untreated

causes
- congenital e.g. Arnold-Chiari malformation
- acquired: trauma e.g haemorrhage, tumour
- idiopathic

investigations
- full spine MRI with contrast - exclude tumour / tethered cord
- brain MRI - exclude Chiari malformation

Treatment
- manage underlying cause
- shunt into syrinx

83
Q

describe a brain abscess and its management

A

causes
- extension of sepsis from middle ear or sinuses
- trauma or surgery to the scalp
- penetrating head injuries
- embolic events from endocarditis

clinical features
- depends on the site of the abscess
- headache (dull, persistent)
- fever
- focal neurology e.g. oculomotor nerve palsy
- other features of raised ICP: nausea, papilloedema, seizures

investigations
- CT head

management
- surgery
> craniotomy and debridement of abscess cavity
- IV Abx: IV 3rd generation cephalosporin + metronidazole
- Intracranial pressure management: e.g. dexamethasone

84
Q

describe Cheyne Stokes breathing

A

abnormal breathing pattern characterised by periods of hyperventilation alternating with apnoea

occurs due to compression of brainstem

85
Q

describe juvenile myoclonic epilepsy

A

typically affects teenage girls

  • infrequent generalised seizures often in the morning / following sleep deprivation
  • daytime absences
  • sudden shock-like myoclonic seizure
86
Q

describe the management of haemorrhagic transformation in ischaemic stroke

A
  • stop antiplatelets / anticoagulants
  • control BP (target 140 mmHg)
87
Q

describe cavernous sinus syndrome

A

usually caused by cavernous sinus tumours

features
- pain
- ophthalmoplegia
- proptosis
- trigeminal nerve lesion (ophthalmic branch)
- Horner’s syndrome

88
Q

describe degenerative cervical myelopathy

A

presentation
- pain (neck, upper or lower limbs)

  • loss of motor function (loss of digital dexterity, arm or leg weakness/stiffness leading to impaired gait and balance)
  • loss of sensory function causing numbness
  • loss of autonomic function (urinary or faecal incontinence / impotence)
  • Hoffman’s sign: exaggerated flexion of terminal phalanx of thumb after flicking DIP joint of middle finger
    > UMN sign

MRI - gold standard

management
- urgent referral for assessment by specialist spinal services
- decompressive surgery

89
Q
A