Title: Neurology

Q: DDx of acute weakness
A: Cerebral - Stroke
Brainstem - Locked-in
Spinal cord - Transverse myelitis
Peripheral nerve - GBS
NMJ - Myaesthenic crisis, tick paralysis
Muscle - Hypokalaemic, myopathy, dermatomyositis, polymyositis

Q: NMJ disorder DDx
A: Myaesthenia gravis
Lambert-Eaton
Botulism
Pesticide poisoning

Q: Acute peripheral neuropathy DDx
A: GBS
Bell's palsy
Ramsay Hunt
Acute neuropathies of Lyme disease

Q: Most common type of GBS
A: Acute inflammatory demyelinating polyneuropathy 85%

Q: When do GBS symptoms peak?
A: 2-4 weeks

Q: Classic presentation of GBS
A: Ascending paralysis with hyporeflexia following viral illness/dysentery

Q: What proportion of GBS have distal paraesthesia?
A: 50%

Q: What are the four variants of GBS?
A: AIDP - Acute inflammatory demyelinating polyneuropathy
Miller-Fisher variant
AMAN - Acute motor axonal neuropathy
AMSAN - Acute motor and sensory axonal neuropathy

Q: How is Miller-Fisher variant different?
A: Predominant CN involvement
C. jejuni related
Milder course
Strongly correlated to GQ1b antibodies

Q: Associated infectious with GBS
A: CMV, influenza, parainfluenza, mycoplasma, VZV, EBV
Campylobacter jejuni

Q: What proportion of GBS is related to C. jejuni?
A: ~30%

Q: What proportion of GBS follow URTI and GI illness?
A: 40% and 20%

Q: CSF findings in GBS
A: Albuminocytologic dissociation
 - Protein >450mg/L, WCC <10; predominent mononuclear

Q: Management of GBS
A: Monitor respiratory function/swallow
Avoid sux
Manage pain and autonomic dysfunction
IVIG 0.4g/kg IV for 5 days
Consider plasmapharesis and plasma exchange

Q: What proportion of GBS is fully recovered at 12 months?
A: 70%

Q: Mortality of GBS
A: 5-8%

Q: Poor prognostic factors in GBS
A: Age >60
Rapidly progressive to quadriparesis within 7 days
Mechanical ventilation
Preceding diarrhoeal illness

Q: How common is Bell's palsy?
A: 25/100 000 annually

Q: Clinical presentation of Bell's
A: Pain behind ear
Unilateral facial palsy with forehead involvement
Can get hyperaesthesia also (proprioceptive facial nerve fibres)
Decreased taste
Hyperacusis (nerve to stapedius)

Q: Mimic of Bell's palsy
A: Pontine lacunar stroke with infranuclear CN VII deficit + CN VI involvement - therefore check abduction of eyes in all Bell's

Q: Treatment of Bell's
A: Prednisone 1mg/kg per day for 7 days
Eye protection
QID eye lubricant drops and ointment at night
Tape at night if incomplete closure
Ophthal f/u
ENT/GP f/u within 7 days

Q: Prognosis of Bell's
A: Most begin to recover by 3 weeks
15% permanent paralysis

Q: What is Ramsay Hunt
A: Herpes zoster of geniculate ganglion

Q: Treatment of Ramsay Hunt
A: Prednisone 1mg/kg/day for 7 days
Acyclovir 200mg five times a day for 7 days

Q: Causes of carpal tunnel
A: Hypothyroidism
Pregnancy
Amyloidosis
Repetitive use
Obesity
Renal failure
Trauma
Oedema

Q: How does botulism cause weakness?
A: Toxins irreversibly bind presynaptic membranes preventing ACh release

Q: Why are infants at risk of botulism?
A: Spores in honey germinate in high pH infantile GI tract

Q: How can botulism present?
A: GI symptoms
Descending paralysis
No sensory changes
Anticholinergic syndrome
Fixed dilated pupils
Afebrile

Q: How is botulism confirmed?
A: Stool and serum toxin

Q: Treatment of botulism
A: Supportive therapy +- ventilation
Botulinum equine antitoxin
Human botulism immunoglobulin

Q: Do ticks cause sensory disturbance?
A: No

Q: Prognosis of tick paralysis
A: Complete recovery within hours to days if tick removed

Q: Treatment of painful diabetic neuropathy
A: Duloxetine 30mg daily
Pregabalin
Capsaicin

Q: How does diabetic amyotrophy present?
A: Back pain, progressive leg weakness due to lumbosacral plexopathy

Q: What is locked in syndrome?
A: Complete paralysis below third nerve nuclei with normal mental function

Q: What is persistent vegetative state?
A: Coma >1 month

Q: How common is delirium in the hospitalised elderly?
A: 10-25%

Q: What proportion of patients over 70 in ED will have delirium?
A: 1/4

Q: Four major differentials of delirium
A: Primary neurological disease
Extracranial illness
Toxins
Withdrawal

Q: Quick confusion scale?
A: What year?
What month?
Repeat a memory phrase
What time is it?
Count backwards from 20
Say months in reverse
Repeat memory phrase again

Q: Coma with focal signs
A: Traumatic
ICH
Ischaemic stroke
Brain abscess

Q: Coma withn meningeal irritation
A: Meningoencephalitis
SAH

Q: How does pontine haemorrhage present?
A: Coma with pinpoint pupils (mimics opioids)

Q: What part of the brain controls conjugate eye movement?
A: Median longitudinal fasciculus

Q: Hypothermic coma DDx
A: Exposure
Alcohol
Barbiturate
Opioid
Sepsis with shock
Hypoglycaemia
Myxoedema
Addison's

Q: Hyperthermic coma DDx
A: Sepsis with shock
Hypothalamic stroke
Intracranial infection
Stroke
Anticholinergic toxidrome
Serotonin syndrome
Malignant hyperthermia
Sympathomimetic toxidrome
Neuroleptic malignant syndrome
Acute lethal malignant catatonia

Q: Unilateral miosis
A: Horner's

Q: Bilateral miosis
A: Opioids
Pontine stroke
Thalamic haemorrhage
Metabolic encephalopathy
Organophosphate poisoning
Barbiturates

Q: Unilateral mydriasis
A: Uncal herniation
Midbrain stroke

Q: Bilateral mydriasis
A: Sympathetic overdrive
Anticholinergic
Massive midbrain haemorrhage (bilateral 3rd nerve nuclei)
Hypoxic cerebral injury
Atropine
TCA

Q: Central herniation
A: Progressive obtundation
Cheyne-STokes
Initial small pupils then -->
Extensor posturing
Fixed mid-size pupils

Q: Uncal herniation
A: Early blown pupil

Q: Systemic causes of ataxia
A: Intoxication with reduced alertness - Opioids, sedatives, ethanol
Intoxication without reduced alertness - Phenytoin, valproate, CBZ, heavy metals
Hyponatraemia
Wernicke's

Q: Neurological causes of ataxia
A: Cerebellar stroke/infection/abscess/tumor
Cortex - Frontal pathology, hydrocephalus
Subcortical - Thalamic lesion, Parkinson's
Spinal cord - Compression/dorsal column disease
Peripheral neuropathy
Vestibular

Q: How do lateral and midline cerebellar lesions present differently?
A: Lateral - Ipsilateral cerebellar limb signs
Midline - Axial incoordination

Q: Cerebellar gait?
A: Wide-based unsteady

Q: Sensory ataxia gait
A: Slapping feet, abrupt

Q: Circumduction gait
A: Outward swinging leg due to mild hemiparesis and proximal weakness

Q: Waddling gait
A: Bilateral weakness of pelvic girdle musculature

Q: Heel-shin testing: Cerebellar vs. posterior column
A: Cerebellar overshoot knee and then jerky movement
Posterior column have difficulty finding knee and then waver down shin

Q: How is Romberg's performed?
A: Stand with feet shoulder width apart
Arms outstretched
If cannot stand = ataxia of some cause
If on closing eyes, worsens = Romberg's positive = Sensory ataxia made worse by lack of visual input
If no change = Motor ataxia

Q: Normal range of cerebral autoregulation
A: 50-150mmHg

Q: How does PaCO2 correlate to cerebral blood flow?
A: Directly proportional

Q: How much CSF made per day?
A: 500mL

Q: Indications for ICP monitoring (non-traumatic)
A: Suspected raised ICP in the setting of:
Stroke
Cerebral oedema
Hydrocephalus
Hepatic encephalopathy
EVD for SAH at risk of obstructive hydrocephalus

Q: Indications for ICP monitor in trauma (BTF)
A: Moderate to severe head injury (GCS <=13) who cannot be serially neurologically assessed
GCS <8 with abnormal CT scan
GCS <8 with normal CT if 2 or more of:
 - Age >40
 - BP <90
 - Abnormal posturing

Q: Infection rate with ICP monitors
A: 1% per day

Q: Issues with intraparenchymal Codman bolts?
A: Cannot be recalibrated
Cannot drain CSF
Only measures local pressure (not global)

Q: Which cerebral artery is most at risk with raised ICP?
A: Posterior cerebral artery due to pressure effect - occipital infarcts

Q: What is amyotrophic lateral sclerosis?
A: Motor neurone disease
Lou Gehrig's

Q: Pathology of Motor neurone disease
A: Rapidly progressive muscle atrophy with upper and lower motor neuron degeneration

Q: How does motor neuron disease usually present?
A: Initially peripheral motor nerve degeneration with asymmetric hand muscle wasting/fasciculations
Then UMN degeneration leads to spasticity/hypertonia/hyperreflexia
Emotional lability due to frontal lobe degeneration
Cognitive fx, sensory and autonomic neurons usually spared

Q: What facets of neurological function are usually spared in motor neuron disease?
A: Cognition (in 85%), facial/ocular muscles, sensory, autonomic

Q: Best indicator of impending respiratory failure in motor neuron disease?
A: FVC <25mL/kg or <50% of predicted

Q: What proportion of myaesthenia gravis patients are positive for anti-AChR?
A: 80%

Q: Pathophysiology of myaesthenia gravis?
A: Autoimmune destruction of AChR thought to derive from dysfunction of thymus or molecular mimicry

Q: How does myaesthenia gravis present?
A: Fatiguable weakness in proximal limbs, neck extensors and facial muscles

Q: What is myaesthenic crisis
A: Acute respiratory failure in undiagnosed disease or inadequate drug therapy

Q: DDx of myaesthenia gravis
A: Congenital MG
Lambert-Eaton
Drug-induced myaesthenia (aminoglycosides)
Botulism
Thyroid
CVA

Q: Treatment of myaesthenia gravis
A: Acetylcholinesterase inhibitors e.g. neostigmine
Thymectomy
Chronic immunosuppression
IVIG/plasma exchange if severe

Q: Drugs to avoid in myaesthenia gravis
A: Steroids (unless treating MG)
Aminoglycosides, quinolones, macrolides, metronidazole
Paralytic agents
Quinine
Phenytoin

Q: Management of missed acetylcholinesterase inhibitor dosing?
A: Double the next dose
If NBM, give 1/30 of PO dose of physostigmine under Neurology guidance

Q: Causes of myaesthenic crisis
A: Infection
Surgery
Rapid tapering of immunosuppression
Non-compliance

Q: Intubation of myaesthenic crisis?
A: Avoid paralytics if possible
DO NOT USE SUX
Try sedation and intubation, gaseous induction if possible
If need paralysis - 1/2 dose non-depolarising

Q: Main differential of myaesthenic crisis?
A: Cholinergic crisis
 - salivation, lacrimation, urinary incontinence, diarrhoea, miosis

Q: Management of myaesthenic crisis
A: ABCDE
Treat underlying precipitant e.g. infection
Normal K, Ca, Mg
Steroids/plasma exchange
Edrophonium 1mg IV aliquots up to 10mg
SC neostigmine 0.5mg

Q: What proportion of MS is relapsing/remitting?
A: 90%

Q: Three subtypes of MS
A: Relapsing/remitting
Relapsing and progressive
Chronic progressive

Q: What proportion of MS first presents with optic neuritis?
A: 30%

Q: How does MS optic neuritis present?
A: Central vision loss + colour desaturation + painful eye mivement +- nystagus/diplopia/INO

Q: Do MS patients suffer autonomic dysfunction?
A: Yes. Urinary incontinence, urgency, frequency, constipation, faecal incontinence or sexual dysfunction

Q: Diagnostic criteria for MS
A: 2 or more prolonged or worsening episodes of neurological dysfunction that suggest white matter/spinal cord disorders in 2 or more distinct locations

Q: CSF findings in MS
A: High protein
Oligoclonal bands (80-95%)

Q: Treatment of MS
A: Mitoxantrone
Glucocorticoids
Natalizumab
IFN-beta
Glatiramer
IVIG

Q: Management of MS exacerbation
A: Screen for UTI/fever/infection
D/W Neurology re: steroids

Q: What is Lambert-Eaton syndrome
A: Anti-vg Ca channel antibodies in small cell lung cancer with non-fatiguable weakness

Q: What proportion of Lambert Eaton have concurrent small cell lung cancer?
A: 50% and can precede diagnosis by years

Q: Lambert sign?
A: Progressive strengthening in hand grip over minutes

Q: Classic Parkinson's presentation
A: Bradykinesia, resting tremor and rigidity

Q: Pathophysiology of parkinsons
A: Destruction of dopaminergic neurons in basal ganglia
Excessive cholinergic input vs. dopaminergic

Q: What is Parkinson's tremor like?
A: Resting, pill-rolling, 5x/min in upper extremity
Unilateral then bilateral

Q: DDx of Parkinsonism
A: Parkinson's disease
Antipsychotic agents
Metoclopramide
Lithium
MDMA
Boxer's dementia (pugilistic encephalopathy)
Vascular dementia
Lewy body dementia
Corticobasal degeneration
Huntington's
Multiple systems atrophy (Shy-Drager syndrome)
Olivopontocerebellar atrophy
Progressive supranuclear palsy
Wilson's syndrome

Q: What is carbidopa?
A: Peripheral decarboxylase inhibitor to prevent peripheral conversion of levodopa to dopamine

Q: What are on-off phenomenon with levodopa?
A: Usually morning akinesia before dosing
Remedied by long-acting levodopa/carbidopa combinations

Q: Most common cause of death in Parkinson's
A: Respiratory failure due to off period +- aspiration

Q: Drugs to avoid in parkinson's
A: Dopamine antagonists e.g. haloperidol

Q: What proportion of acute poliomyositis are symptomatic?
A: 10%

Q: How does severe polio present?
A: Flaccid paralysis with areflexia, often unilateral, lower limb, large muscle groups

Q: DDx of periodic paralysis
A: Electrolyte disturbances
Myaesthenia gravis
Lambert-Eaton
TIA

Q: When do symptoms of period paralysis usually occur?
A: After rest/sleep (vs. exertion)

Q: Does hypokalaemic periodic paralysis usually involve respiratory muscles?
A: Rarely

Q: Management of hypokalaemic period paralysis?
A: Rule out thyrotoxicosis
Treat thyrotoxicosis if present - Propranolol
Acetazolamide prevents episodes
DO NOT start on oral potassium supplementation

Q: Treatment of hyperkalaemic period paralysis
A: Carbohydrates
Thiazides/acetazolamide are preventive

Q: How common is bacterial meningitis?
A: 1.8/100 000

Q: Case fatality rate of bacterial meningitis?
A: 14%

Q: Most common causes of bacterial meningitis?
A: S. pneumoniae (58%), GBS (18%), N. meningitidis (14%), H. influenzae (7%), listeria (3%)

Q: Immunocompromised meningitis organisms
A: Usual + Fungal, cryptococcus, viral, HIV, TB

Q: Meningitis following neurosurgery?
A: S. aureus
S. epidermidis

Q: Risk factors for bacterial meningitis
A: Immunosuppression
Otitis media
Sinusitis
Alcoholism
Diabetes
CSF leak
Endocarditis
Neurosurgical procedure
Head injury
Cochlear implant
Unvaccinated

Q: Most common symptom of bacterial meningitis?
A: Headache (85%)

Q: What proportion of bacterial meningitis suffer seizures or focal signs?
A: 30%

Q: Common early symptoms of bacterial meningitis?
A: Leg pain, cold hands

Q: Which patients are at risk of Listeria meningitis?
A: Alcoholics and older patients

Q: Which patients need CT before LP?
A: ALOC
Focal neuro deficit
Seizures
Papilloedema
Immunocompromised
Malignancy
Age >60
Concern for CNS mass lesino

Q: Acceptable INR and platelets for LP
A: INR <1.5 and Plt >50

Q: Can LP be done on aspirin?
A: Unclear. Probably best to avoid until 7 days and treat empirically

Q: What proportion of CSF gram stain are positive before Ab in bacterial meningitis?
A: 70%

Q: Usual WCC in bacterial meningitis
A: >1000/mm3 with PMN >80%

Q: Usual WCC of viral meningitis
A: <300/mm3 with <20% PMN

Q: Usual WCC in fungal meningitis?
A: <500

Q: Glucose in CSF bacterial meningitis
A: CSF:serum <0.4

Q: Which types of meningitis have protein >2 in CSF?
A: Bacterial, fungal, neoplastic

Q: How quickly does CSF get sterilised by antibiotics in N. meningitidis?
A: 2 hours

Q: How quickly does CSF get sterilised in S. pneumoniae meningitis?
A: 6 hours

Q: PCR tests on CSF
A: N. meningitidis
S. pneumoniae
GBS
H. influenzae
L. monocytogenes
M. tuberculosis

Q: Empirical meningitis treatment
A: Dexamethasone 10mg IV before or within 1 hour of first dose then 10mg q6h for 4 days
Ceftriaxone 2g BD IV
Add BenPen 2.4g IV q4h if Listeria possible (alcoholics, >50yo, pregnant)
Add Vanc if Gram-pos diplococci, pneumococcal antigen positive in CSF, suspected otitis media/sinusitis origin, recent beta-lactam therapy, Staph on Gram stain or unable to perform LP
Add metronidazole if suspected otitis media/sinusitis origin
Add acyclovir if Herpes simplex suspected

Q: Which patients need BenPen added to bacterial meningitis regime?
A: If immunocompromised, alcoholic, >50yo or pregnant

Q: Which patients need Vanc added to empirical bacterial meningitis regime?
A: Gram-pos diplococci on Gram, positive pneumococcal antigen, resembling Staph on Gram, otitis media/sinusitis origin, recent beta-lactam therapy or unable to perform LP

Q: Antibiotics for neurosurgery-related bacterial meningitis
A: Cefepime + vancomycin

Q: Benefits of dexamethasone in bacterial meningitis
A: Reduces hearing loss and neurological sequelae
No reduction in death rate overall
Reduces death rate in S. pneumoniae
Reduces hearing loss only in H. influenzae
No evidence for benefit in N. meningitidis

Q: Which patients need metronidazole added to regime for bacterial meningitis?
A: Otitis media/sinusitis origin

Q: How effective is chemoprophylaxis for bacterial meningitis?
A: 90%

Q: Who needs chemoprophylaxis for bacterial meningitis?
A: Close contacts
 - Housemates or overnight stays in last 7 days before illness
 - Secretion exposure (sexual/intimate kissing)
 - Childcare attendees in same room for 4 hours
 - Dormitory
 - Travel contacts adjacent to patient for >8 hours
 - Intubated without mask

Q: Drugs for bacterial meningitis chemoprophylaxis
A: Rifampicin 600mg BD for four doses OR
Cipro 500mg PO once OR
Ceftriaxone 250mg IM once

Q: Most common causes of viral meningitis
A: Enteroviruses (Echovirus, Coxsackie)
HSV
VZV
CMV
Adenovirus
HIV

Q: Management of viral meningitis
A: If toxic looking - treat as for bacterial until LP results back
If encephalopathic - Suspect HSV-2 encephalitis --> Acyclovir 10mg/kg q8h IV

Q: Which HSV infection causes encephalitis?
A: HSV-1
HSV-2 is the predominant cause of aseptic meningitis but can lead to necrotising encephalitis and still warrants IV acyclovir

Q: Most common fungal meningitidies
A: Cryptococcal
Aspergillus
Coccidioidomycosis
Candida
Mucormycosis (diabetic sinusitis)

Q: Testing for suspected fungal meningitis?
A: India ink stain
Fungal culture
Cryptococcal antigen testing
Cytology
Histopathology

Q: Treatment of fungal meningitis
A: Cryptococcus - Amphotericin
Coccidioides - Fluconazole
Candida - Amphotericin B and flucytosine

Q: How is viral encephalitis differentiated from meningitis?
A: Focal neurology
Seizures
ALOC

Q: Which HSV causes meningitis and which encephalitis?
A: HSV-1 causes encephalitis
HSV-2 causes meningitis (with small risk of necrotising encephalitis --> hence acyclovir therapy)

Q: PCR CSF for aseptic meningitis?
A: HSV and enteroviruses

Q: MRI findings in HSV encephalitis
A: Medial temporal lobe gray matter and inferior frontal lobe involvement

Q: Treatment of viral encephalitis
A: Acyclovir 10mg/kg IV TDS

Q: Mortality of HSV encephalitis?
A: 25% (75% untreated)

Q: What proportion of brain abscesses are:
Haematogenous
Direct spread
Trauma
A: 50%
30%
20%

Q: Causes of sinogenic brain abscesses
A: Anerobes and streptococcus pneumoniae in frontal lobes

Q: Causes of brain abscesses in direct traumatic injuries?
A: Staph aureus

Q: Why might diagnosis of brain abscess be delayed?
A: Only 25% present with classic headache, fever, focal neurology
Signs/symptoms of origin of infection e.g. otitis media may dominate

Q: Treatment of otogenic brain abscess
A: Ceftriaxone 2g BD + Metronidazole 500mg BD IV

Q: Treatment of odontogenic brain abscess
A: Pen G 4 million U q4h

Q: Treatment of sinogenic brain abscess
A: Ceftriaxone 2g BD + Metronidazole 500mg BD

Q: Treatment of post-neurosurgical brain abscess
A: Ceftazidime 2g IV TDS + Vancomycin 30mg/kg load then 15mg/kg BD

Q: Do aminoglycosides penetrate brain abscesses?
A: No

Q: Which brain abscesses can be conservatively managed with antibiotics?
A: <2.5cm, GCS >12 and known aetiology

Q: Mortality of epidural abscess
A: 2-20%

Q: Most common cause of epidural abscess?
A: S.aureus

Q: Origins of epidural abscess
A: Haematogenous spread (25-50%)
 - Soft tissue, GI, GU, respiratory infection
 - Usually posterior
Direct extension
 - Psoas abscess, vertebral discitis, vertebral osteomyelitis (10-30%)
 - Usually anterior
Neurosurgical iatrogenic (20%)

Q: What proportion of epidural abscess have classic presentation?
A: 30% have back pain, fever, neuro deficit

Q: Keys to diagnosis of epidural abscess?
A: Bladder/bowel assessment
Recent infections
Indwelling lines
IVDU
Red flag assessment

Q: Most sensitive marker of epidural abscess?
A: ESR

Q: Antibiotic therapy for epidural abscess
A: Ceftazidime 2g IV TDS + Vanc 30mg/kg load then 15mg/kg BD

Q: What is Mollaret's meningitis
A: Recurrent aseptic meningitis usually due to HSV-2
>3 episodes lasting 2-5 days with spontaneous resolution in between
No benefit to suppressive valacyclovir

Q: When does post-LP headache usually arise?
A: 24-48 hours after procedure

Q: Treatment of post-LP headache
A: Supination
IV fluids
Antiemetics
Analgesia
IV caffeine 500mg (not proven)
If >24 hours duration --> Blood patch via anaesthetics

Q: Order in which CSF shunts block
A: Proximal tubing, distal tubing, valve chamber

Q: How does CSF shunt overdrainage present?
A: Cyclical episodic headache with focal neurology, ataxia and lethargy
Cyclical as get shrinkage from overdrainage, obstructs, then pressure builds again and it drains again

Q: How is CSF shunt evaluated clinically?
A: Compress chamber and see if refills
 - If empties easily = distal open
 - If failure to empty = distal obstruction
 - If fills quickly = proximal open
 - If fills slowly (>3 seconds) = proximal obstruction

Q: How accurate is chamber emptying for evaluation of CSF shunt?
A: 40% of obstructed shunts show normal refill

Q: Can CT rule out CSF shunt malfunction?
A: No. Can assess size of ventricles compared to baseline but if high clinical suspicion, only 83% sensitive for obstruction.

Q: How do you perform a shunt tap?
A: Aseptic
23G needle or butterfly attached to manometer
If pressure >20cmH20, slowly (to prevent choroid plexus bleeding) remove some CSF until <20cmH20

Q: When do most shunt infections occur?
A: First 2 weeks

Q: Usual organisms to cause shunt infection?
A: S. epidermidis (50%), S. aureus and Proprionibacterium acnes

Q: Presentation of shunt infection
A: Obstruction
Meningitis (1/3)
Abdominal pain if VP

Q: Treatment of suspected shunt infection
A: Ceftriaxone 2g BD + Vancomycin

Q: What proportion of halo pin-site infections are deep?
A: <1%

Q: What to do if halo patient needs CPR?
A: Removed front part of halo and perform CPR with rest of halo in place

Q: Mortality of halo-devices in the elderly?
A: 21% if >79yo
Respiratory failure and dysphagia

Q: Complications of intrathecal baclofen pumps
A: Mechanical disruption
Hypotension, bradycardia, apnoea, oversedation
Local infection/meningitis
Withdrawal if fails can be fatal with hypertonicity and spasms with rhabdo

Q: Management of intrathecal baclofen pump failure?
A: Oral baclofen, dantrole and benzodiazepines

Q: What is the cooling regime for comatose cardiac arrest?
A: 36 degrees for 28 hours with fever actively managed until 72 hours

Q: What is the cooling regime for TBI?
A: For first 48 hours - Don't warm if cool, otherwise keep at 36
After 48 hours - Can cool if struggling to control ICP
Aggressively cool if >39 throughout

Q: What did the DECRA trial show?
A: Bifrontotemporoparietal craniectomy for refractory (to stage 1 interventions) raised ICP in severe TBI
Worse functional outcome with no mortality benefit
Reduced ICP and ICU length of stay

Q: What did RESCUEicp show?
A: Decompressive craniectomy (uni- or bilateral) for refractory ICP to both Stage 1 and 2 interventions reduced mortality but higher proportion of disability in survivors

Q: 4 mechanisms of headache
A: Tension
Traction
Vascular
Inflammatory

Q: What proportion of headaches are dangerous?
A: 4%

Q: What proportion of thunderclap headaches are dangerous?
A: 10%

Q: Red flags in headache
A: Age >50 with new or worsening headache
Sudden onset
Onset during exertion
Onset with valsalva
Change in severity, pattern, frequency, quality or intensity
Fever
Anticoagulation/antiplatelets/immunosuppression
Chronic analgesic use
FHx of aneurysms/PCKD
Pregnant
Cancer
Cocaine/amphetamines

Q: How much does FHx in first-degree relative of SAH increase risk?
A: 3-5x

Q: Thunderclap headache differential
A: SAH
Spontaneous intracranial haemorrhage
Cervical/vertebral dissection
Cerebral venous thrombosis
PRES
Coital headache
Acute hydrocephalus
Pituitary apoplexy

Q: Features suggestive of migraine
A: Unilateral (adults)
Throbbing
Parieto-occipital (adults)
Younger
Previous Hx
FHx of migraine
Nausea/vomiting
Phonophobia/photophobia

Q: Diagnosis of cluster headache
A: 5 attacks that are:
 - Severe
 - Unilateral
 - 15-180 min
 - Associated ipsilateral autonomic signs

Q: Mortality of SAH from aneurysm?
A: 50% at 30 days

Q: What proportion of SAH survivors have neurological impairment?
A: 50%

Q: What proportion of ED presentations have SAH?
A: 1%

Q: What proportion of thunderclap headaches presenting to ED have SAH?
A: 15% (Cameron 25% of sudden severe)

Q: What proportion of SAH have sentinel bleed?
A: 50%

Q: What proportion of SAH present after exercise/valsalva/intercourse?
A: Up to 1/3

Q: What proportion of SAH are aneurysmal?
A: 85%

Q: What proportion of SAH are not aneurysmal?
A: 10% perimesencephalic and 5% rarer causes

Q: What proportion of patients with one cerebral aneurysm have another one?
A: 20%

Q: Are cerebral aneurysms congenital?
A: No. Develop over lifetime

Q: What proportion of the population have cerebral aneurysms?
A: 2.3%

Q: Risk factors for SAH
A: Previous aneurysmal SAH
FHx of first-degree relative with SAH
PCKD
Connective tissue disorder
Neurofibromatosis
Sickle cell disease
Alpha-1 AT disease
Smoking
HTN
Sympathomimetic use
Alcohol

Q: What is Terson syndrome?
A: Subhyaline retinal haemorrhage in SAH

Q: What proportion of SAH present in coma?
A: 50%

Q: What proportion of SAH present with impaired LOC?
A: 2/3

Q: Systemic features of SAH
A: STEMI pattern, neurogenic pulmonary oedema, severe hypertension

Q: Sensitivity of non-con CT for SAH within 6 hours?
A: 98%

Q: Probability of excluding SAH after negative CT and CTA?
A: 99.4%

Q: Problem with performing CTA instead of LP?
A: Detects incidental aneurysms with subsequent further Ix that may not be clinically required

Q: What do you do if negative CT, negative xanthochromia but CSF RBC >5x10^6/L?
A: Need CT-A as cannot rule out SAH

Q: Hunt and Hess grading scale
A: Predicts outcomes
1 - Mild headache, normal mental status, no cranial nerve or motor signs
2 - Severe headache, normal mental status, may have cranial nerve sign
3 - Somnolent, confused, may have cranial nerve or mild motor deficit
4 - Stupor, moderate to severe motor deficit, may have intermittent reflex posturing
5 - Coma, reflex posturing

Q: WFNS scale
A: Predicts outcome
1 - GCS 15, no motor deficit
2 - GCS 13 or 14, no motor deficit
3 - GCS 13 or 14, motor deficit
4 - GCS 7-12
5 - GCS <7

Q: Fisher scale
A: Predicts vasospasm
I - No blood
II - Diffuse blood without clots or layers >1mm
III - Localised clots/vertical layers >1mm
IV - Intracerebral or intraventricular clot

Q: How common is re-bleeding post-SAH?
A: 15% within hours
40% within 4 weeks

Q: How can SAH re-bleeding be prevented?
A: Good BP control
Early clipping/coiling

Q: What proportion of SAH have clinically significant vasospasm?
A: 20%

Q: When does vasospasm occur in SAH?
A: Days 3-15 (peak day 6-8)

Q: What proportion of SAH suffer hydrocephalus?
A: 20%

Q: Early complications of SAH
A: Re-bleeding
Large intracerebral haematoma
Global ischaemia
Cerebral vasopasm
Hydrocephalus
Seizures
SIADH
Cerebral salt wasting
Neurogenic pulmonary oedema
ECG changes
Systemic HTN
VTE

Q: Late complications of SAH
A: Late re-bleeding from new aneurysm or re-growth
Anosmia
Epilepsy
Cognitive defects
Personality change

Q: BP target in SAH
A: Controversial
SBP <160 probably sufficient
<140 if conscious

Q: Prevention of vasospasm in SAH
A: Nimodipine 60mg PO q4h

Q: How common are seizures after SAH?
A: 5-20% of patients

Q: Relative risk reduction of cerebral vasospasm post-SAH with nimodipine?
A: 18% (absolute RR 5.1%)

Q: Survival rates as per WFNS score SAH?
A: I - 70%
II - 60%
III - 50%
IV - 40%
V - 10%

Q: What proportion of strokes are haemorrhagic?
A: 10%

Q: Mortality of haemorrhagic stroke?
A: 30% at 1 week
50% at 1 year
80% at 10 years

Q: What proportion of survivors of haemorrhagic stroke have disability?
A: 80%

Q: Risk factors for haemorrhagic stroke?
A: Long-term HTN
AV malformations
Anticoagulant therapy
Sympathomimetic abuse
Intracranial tumors
Amyloid angiopathy
Current smoking

Q: What proportion of haemorrhagic stroke is due to hypertensive vascular disease?
A: 85%

Q: Where do hypertensive bleeds occur?
A: Penetrating vessels in putamen, thalamus, upper brainstem and cerebellum

Q: Where do amyloid angiopathy bleeds occur?
A: Lobar haemorrhages in the elderly

Q: Poor prognostic factors for haemorrhagic stroke
A: Age >80
High NIHSS
GCS 3-4
Volume >30mL
Infratentorial
Intraventricular extension

Q: Treatment of haemorrhagic stroke
A: Neuroprotective measures
Anticonvulsants if seizures occur
Reversal of coagulopathy
 - No platelets for antiplatelets unless undergoing neurosurgical procedure
 - Consider desmopressin
BP control
 - If >180 or MAP >130: Drop by 15% within 1 hour (Cameron)
 - Consider maintaining <140mmHg as per INTERACT2
EVD for hydrocephalus
Consider surgical drainage

Q: What did INTERACT show?
A: Intensive BP reduction within 6 hours showed reduction in haematoma growth

Q: What did INTERACT2 show?
A: Intensive lowering to <140mmHg within 1 hour did not alter mortality but did improve functional outcome in ordinal analysis

Q: What did ATACH2 show?
A: Target SBP 110-140 vs. 140-179 in ICH showed no difference in functional outcome

Q: Which BP lowering agents are preferred in ICH?
A: Labetalol and hydralazine
*SNP and GTN increase cerebral blood volume and may worsen ICP

Q: Which patients with supratentorial ICH benefit most from drainage?
A: Lobar clots within 1cm of surface
Refractory ICP
Non-dominant hemisphere
Deteriorating
Not obtunded

Q: Which patients are at risk of cerebral venous sinus thrombosis?
A: New headache +
Women
Peripartum
Recent surgery
Thrombophilia
COCP

Q: What is the sensitivity of CT venogram for cerebral venous thrombosis?
A: 95%

Q: What is PRES?
A: Posterior reversible encephalopathy syndrome
 - Related to severe hypertension

Q: What is RCVS?
A: Reversible cerebral vasoconstriction syndrome
 - Widespread vasoconstriction with subsequent focal neurology seen in perimenopausal women

Q: What is the most common vasculitis in patients over 50?
A: Temporal arteritis

Q: Diagnostic criteria for temporal arteritis?
A: 3 out of 5 of:
 - Age >50
 - New headache
 - Temporal artery tenderness/reduced pulsation
 - ESR >50
 - Abnormal biopsy

Q: Treatment of temporal arteritis?
A: Do not wait for biopsy results
 - Methylprednisolone 1g daily for 3 days then oral prednisolone 60mg daily

Q: What is chronic migraine?
A: 5 or more migraine headache days per month for 3 months

Q: Above what age is first migraine rare?
A: 55yo

Q: Prevalence of migraine in males?
A: 5%

Q: Prevalence of migraine in females?
A: 15%

Q: How long do migraines last?
A: 4-72hours

Q: What are the different types of migraine with aura?
A: Typical aura with migraine
Typical aura with non-migraine headache
Typical aura without headache
Familial hemiplegic migraine
Sporadic hemiplegic migraine
Basilar-type migraine

Q: How long does aura last?
A: <60 minutes

Q: How soon after aura does migraine start?
A: Usually within 60 minutes

Q: How does basilar-type migraine present?
A: Dysarthria
Vertigo
Tinnitus
Hyperacusis
Diplopia
Visual symptoms in both temporal and nasal visual fields in both eyes
Ataxia
Reduced LOC
Simultaneous bilateral paraesthesia

Q: Common triggers of migraine?
A: Missing meals
Sleep deprivation
Prior to or during menses
Stress
SSRI
COCP
PPI

Q: Typical migraine prodrome?
A: Different to aura
Occurs in up to 80%
Up to 24 hours prior
Yawning, osmophobia, photophobia/phonophobia, irritability

Q: What proportion of migraines have aura?
A: 15%

Q: What proportion of migraines are unilateral?
A: 60%

Q: What proportion of migraines are throbbing?
A: 50%

Q: Management of mild migraine
A: Aspirin 900mg + Metoclopramide 10mg PO

Q: Management of moderate migraine
A: Aspirin 900mg +
Metoclopramide 10mg IM or
Prochlorperazine 10mg IM or
Sumatriptan 6mg SC

Q: Management of severe migraine or with vomiting
A: Chlorpromazine 12.5-25mg IV in 1L saline over 1 hour

Q: What proportion of migraine sufferers still have headache on discharge from ED?
A: >50%

Q: How can migraine recurrence be prevented from the ED?
A: IV dexamethasone 10mg (26% reduction) + script for abortive agent e.g. sumatriptan

Q: How does prochlorperazine compare to chlorpromazine for migraine?
A: Less effective but also less hypotensive and less sedating

Q: What is the success rate of chlorpromazine?
A: 85%

Q: In which patients should triptans be avoided?
A: Concomitant ergot use
Hemiplegic migraine
Basilar migraine
ischaemic stroke
Ischaemic heart disease
Prinzmetal's angina
Uncontrolled HTN
Pregnancy

Q: Treatment of trigeminal neuralgia?
A: Carbamazepine 200mg BD increased by 200mg/day up to 1200mg/day
Refer to neurology

Q: What is the treatment for occipital neuralgia?
A: Occipital nerve block
1mL 0.5% bupivicaine without adrenaline each side of midpoint between occipital protuberance and mastoid process

Q: How does idiopathic intracranial hypertension present?
A: Obese women
Headache + visual disturbance + back pain + pulsatile tinnitus

Q: Treatment of idiopathic intracranial hypertension
A: Remove CSF to pressure 15-20cmH20
Oral acetazolamide 250mg BD to start
Ophthalmology f/u for vision monitoring
Neurology f/u

Q: How do cluster headaches present?
A: Mostly middle aged men with clusters of severe headache and then weeks of reprieve

Q: Cluster headache Rx
A: 100% O2
Sumatriptan 6mg SC
Steroid bridging then verapamil

Q: What is pituitary apoplexy?
A: Spontaneous haemorrhage or infarct of pre-existing pituitary adenoma

Q: How does pituitary apoplexy present?
A: Sudden severe headache, ophthalmoplegia, reduced VA, ALOC, meningismus, nausea, vomiting

Q: Treatment of pituitary apoplexy?
A: Hydrocortisone 100mg QID, Neurosurgical consult + Endocrine/Ophthal/Neuro/ICU consults

Q: Treatment of tension headache
A: Ibuprofen 400mg > Aspirin 900mg > Paracetamol 1g

Q: Order of full neuro examination
A: Mental status testing
Higher cerebral functions
Cranial nerves
Limbs

Q: How can higher cerebral functions be screened?
A: Dominant cortex - Free speech, comprehension, repetition
Dominant parietal - AALF - Acalculia, agraphia, left-right disorientation, finger agnosia
Non-dominant parietal - Sensory/visual inattention, spatial neglect, tactile agnosia
Temporal - Short and long-term memory
Frontal lobe - Interpret a proverb

Q: How is receptive aphasia detected?
A: Fluent but peculiar words
Repeat 'no ifs ands or buts'

Q: How is productive aphasia detected?
A: Non-fluent speech

Q: How do dominant and non-dominant parietal lesions present?
A: Dominant - AALF - Acalculia, agraphia, left-right disorientation, finger agnosia
Non-dominant - Spatial neglect, tactile agnosia

Q: How are EOM supplied?
A: SO4LR6AO3
 - Superior oblique supplied by CN IV
 - Lateral rectus supplied by CN VI
 - All others by CN III

Q: How does CN IV palsy present?
A: Failure to depress eye in adduction

Q: How does CN VI palsy present?
A: Failure to abduct eye

Q: How does CN III palsy present?
A: Down and out with dilated pupil and partial ptosis (levator palpebrae)
 - If pupil spared, suggests ischaemia or diabetic vs. traumatic

Q: What does tunnel vision suggest?
A: Glaucoma, papilloedema, syphilis

Q: In diplopia, if the lateral image disappears with eye closure, what does this mean?
A: The closed eye is the pathological eye

Q: What does a positive head impulse test suggest?
A: Peripheral lesion i.e. loss of ability to maintain visual fixation

Q: Which types of nystagmus suggest a central lesion?
A: Direction changing
Spontaneous vertical
Multidirectional

Q: What type of skew deviation suggests a central aetiology?
A: Vertical skew deviation

Q: In which patients is HINTS testing useful?
A: Acute vestibular syndrome (not paroxysms)

Q: How is nystagmus described?
A: The fast direction (corrective saccade) is the direction of the nystagmus

Q: How does vestibular nystagmus present?
A: Acute fast phase away from side of lesion
Chronic fast phase towards side of lesion
Usually mixed horizontal-torsional
Alexander's law - Nystagmus more pronounced with gaze toward side of fast-beating component

Q: In which direction does fast phase of nystagmus go in cerebellar lesions?
A: Towards side of lesion

Q: DDx of jerky horizontal nystagmus
A: Vestibular
Cerebellar
Toxic
INO

Q: DDx of jerky vertical nystagmus
A: Brainstem lesion
Alcohol
Phenytoin

Q: Three branches of CN V
A: Ophthalmic
Maxillary
Mandibular

Q: 5 divisions of facial nerve
A: Temporal
Zygomatic
Buccal
Mandibular
Cervical

Q: How is Dix-Hallpike performed?
A: 30 degrees neck extension and 30 degrees towards examiner
Positive is latency then nystagmus fast phase towards down ear and then gradual improvement
If no latent period or no fatiguability suggests brainstem or cerebellar lesion

Q: Pseudobulbar =
A: UMN IX, X, XII

Q: Bulbar =
A: LMN CN IX, X, XII

Q: How to different pseudobulbar from bulbar palsy?
A: Pseudobulbar has spastic tongue, hyperreflexic jaw jerk and gag reflex and labile emotions vs.
Bulbar has wasted/fasciculating tongue, absent gag/jaw jerk, normal emotions

Q: DDx of pseudobulbar palsy
A: Bilateral internal capsule
MS
Motor neurone disease

Q: DDx of bulbar palsy
A: Motor neurone disease
GBS
Brainstem infarction affecting lower motor neurons of CN IX, X, XI, XII

Q: What is pronator drift?
A: Subtle sign of weakness where arms outstretched start to turn in or fall down

Q: What does motor strength of 3 =
A: Full range against gravity only

Q: What does motor strength 2=
A: Active movement with gravity eliminated

Q: What does motor strength 1=
A: Flicker only

Q: What does motor strength 0 =
A: Complete paresis

Q: Pathological post-void residual
A: >100mL (>200mL definitely)

Q: Normal reflex score
A: 2

Q: Define status epilepticus?
A: Seizure activity >= 5 minutes
2 or more seizures without regaining full consciousness in between

Q: Define refractory status epilepticus
A: Ongoing seizures despite IV anticonvulsant or two anticonvulsant drugs

Q: Lifetime prevalence of seizures
A: 10% of general population

Q: How common is epilepsy?
A: 1-3% of population

Q: How are first seizures classified?
A: Acute symptomatic
Remote symptomatic - CNS insult >1 week ago
Progressive encephalopathy
Febrile
Cryptogenic (no known CNS insult)

Q: DDx of acute symptomatic seizures
A: Hypoxia
Hypotension
Hypoglycaemia
Hypo/hypernatraemia
Hypocalcaemia
Head trauma
Meningitis/encephalitis
Eclampsia
Drugs
Drug withdrawal
Cerebral tumor
Bleed
Stroke

Q: Do absence seizures alter tone?
A: No

Q: Do absence seizures have post-ictal phase?
A: Usually not

Q: Do absence seizures occur in adults?
A: Very rarely. More likely partial complex

Q: What are complex partial seizures?
A: Focal seizures with loss of consciousness
AKA temporal lobe epilepsy

Q: What is Todd's paresis
A: Transient (<48 hours) focal deficit following simple or complex focal seizure

Q: First seizure investigative plan
A: Glucose, VBG, Chem20, pregnancy test, tox studies as indicated
Consider anticonvulsant levels if unknown epilepsy status
Non-contrast CT (<1% yield if no focal signs and complete recovery)
 - Urgent MRI preferred in children
Contrast CT or MRI in follow-up or in ED if risk of tumor
 - 25% will have pathology on MRI (50% if focal seizure)

Q: Status epilepticus management
A: IV midazolam 5mg x 2 q5min
IV phenytoin 20mg/kg over 30 min OR IV keppra 20mg/kg OR Phenobarbitone 10mg/kg IV
IV sodium valproate 40mg/kg over 10 min
IV midazolam infusion up to 5-10mg/hr + I&V
Phenobarbitone coma 0.2mg/kg/min
Treat underlying cause if known

Q: When is clobazam recommended in seizure therapy?
A: 2 or more seizure episodes with full regaining of consciousness
 - 2mg PO

Q: Management of seizure in known epilepsy
A: Check anticonvulsant level/compliance
Load and regular dose usual agent if known
Keppra load and regular if not known
If single seizure and falls within usual pattern - discharge
If not within usual pattern or recurrent - Liaise with neurology

Q: Discharge criteria for first unprovoked seizure
A: Normal mental status
Normal neuro exam
Normal non-contrast CT head
No significant comorbidities
Not alone at home
Normal labs
Discussed with Neurology re: initiating anticonvulsant (rarely)
Educated re: not driving, swimming, heavy machinery, working at heights

Q: Management of seizure in HIV
A: Needs extensive workup
Contrast CT +- MRI for all
LP for all

Q: Most common causes of status epilepticus
A: Subtherapeutic anticonvulsant levels
Pre-existing neurological condition e.g. CNS infection/trauma/lesion
Acute stroke
Anoxia/hypoxia
metabolic disturbance
Alcohol or drug intoxication or withdrawal

Q: Mortality of status epilepticus <1 hr and >1 hr?
A: <1 hour = 3%
>1 hour = 30%

Q: What proportion of status epilepticus is non-convulsive?
A: 25%

Q: Why is IV lorazepam preferred over midaz/diaz in seizure management
A: Longer acting

Q: Why is phenytoin CI in heart block?
A: Sodium channel blocker

Q: How much does pregnancy increase risk of seizures in known epilepsy?
A: 17%

Q: Risk of teratogenicity with epileptic mothers on treatment and off?
A: 3.7% with treatment vs. 3.4% without treatment
BUT risk of uncontrolled seizures greatly outweighs risk of teratogenicity

Q: What proportion of pre-eclamptic women suffer eclampsia?
A: 1/300

Q: What does the artery of Adamkiewicz supply?
A: Anterior spinal cord from T8 to conus medullaris
Anastamoses with anterior spinal artery off vertebrals

Q: What proportion of strokes are ischaemic and haemorrhagic?
A: 87% vs. 13%

Q: What proportion of ischaemic strokes are embolic?
A: 30%

Q: Major causes of thrombotic stroke?
A: Atherosclerosis
Vasculitis
Arterial dissection
Polycythaemia
Hypercoagulable state
Syphilis

Q: Major causes of embolic ischaemic stroke
A: AF
Mural thrombus
IE vegetation
Sterile vegetation (Libman-Sacks)
Paradoxical emboli
Atrial myxoma
Carotid emboli
Fat emboli
IVDU particulate
Septic emboli

Q: What is the most common symptom of posterior stroke?
A: Sudden onset headaceh

Q: What is the NIHSS score biased towards?
A: Anterior strokes
Dominant hemisphere strokes

Q: How do anterior cerebral artery strokes present?
A: Rarely
Contralateral sensory and motor symptoms in lower limb with hand/face sparing

Q: How does MCA syndrome present?
A: Contralateral motor and sensory loss
Hand/face > legs
Dominant hemisphere - Aphasia + AALF
Non-dominant - Spatial neglect, dysarthria without aphasia
Hononymous hemianopia with gaze preference towards side of infarct

Q: What do crossed signs suggest in stroke?
A: Brainstem stroke (e.g. ipsilateral CN with contralateral limb signs = Wallenberg lateral medullary syndrome)

Q: For which stroke syndromes is CT least sensitive?
A: Cerebellar stroke

Q: How do lacunar infarcts present?
A: Pure motor or sensory deficits due to small penetrating artery infarction

Q: How do carotid/vertebral artery dissections present?
A: Usually minor trauma and subsequent neurology within 14 days
Often neck pain/headache/facial pain preceding neurology

Q: Best investigation for carotid dissection?
A: CTA with f/u MRA to confirm

Q: Best investigation for vertebral dissection
A: CTA

Q: What is partial Horner's?
A: Miosis and ptosis without anhidrosis associated with carotid artery dissection

Q: What proportion of ischaemic stroke are visible on CT at 24 hours?
A: 50%

Q: Early signs on CT of ischaemic stroke?
A: Loss of grey-white
Hyperdense clot (MCA/basilar)

Q: Which acute stroke patients warrant early MRI?
A: Posterior fossa and brainstem strokes with negative CT (as not sensitive enough)

Q: BP management in ischaemic stroke
A: If for thrombolysis - Target <185/110 with labetalol/hydralazine
If not for thrombolysis - Treat if >220/>120 and then aim for reduction by 15% over first 24 hours

Q: What did ECASS-III show?
A: Functional improvement up to 4.5 hours from onset (vs. 3 in NINDS)

Q: What did IST-3 show?
A: Thrombolysis up to 6 hours showed no difference in functional outcome or mortality at 6 months

Q: Dosing of stroke thrombolysis
A: Alteplase 0.9mg/kg (10% in 1 minute and 90% over 60min)

Q: Absolute exclusion criteria for stroke thrombolysis
A: Brain tumor/vascular abnormality
Previous ICH
Ischaemic stroke in last 3 months
Head trauma in last 3 months
Symptoms suggestive of SAH
Non-compressible arterial puncture in last 7 days
Seizure with post-ictal residual neurology
Recent intracranial or spinal surgery
BP >185/110 despite therapy
Active internal bleeding
Plt <100
Heparin in last 48 hours and APTT >ULN
INR >1.7
NOAC use
BSL <2.7
>1/3 cerebral hemisphere infarction on non-con CT

Q: Relative contraindications to stroke thrombolysis
A: Minor or rapidly improving symptoms
Pregnancy
Seizure at onset
Major surgery or trauma in last 14 days
Previous GU or GI haemorrhage in 3 weeks
Previous MI in last 3 months

Q: When should aspirin be initiated after an ischaemic stroke?
A: Within 48 hours but not within 24 hours of lysis

Q: Management of post-stroke lysis bleeding?
A: Cease infusion
FBC/Coags
X-match
Urgent imaging of bleeding site
Haematology/neurology/neurosurgery/radiology consultation
Reverse fibrinolysis
 - FFP 2U q6h for 24 hours
 - Cryo 10U
 - TXA 1g IV
Reverse any antiplatelets - Plt 1 bag, DDAVP 0.3mcg/kg
Reverse heparin - Protamine 1mg / 100IU heparin

Q: Excellent outcome on mRS
A: 0 or 1

Q: Functional independence on mRS
A: 0-2

Q: What did MR CLEAN show?
A: ECR within 6 hours showed improved mRS at 90 days with no increase in mortality

Q: What did DAWN show?
A: ECR within 24 hours for <1/3 MCA territory, M1, intracranial MCA showed improved functional outcome

Q: Risk factors for subsequent stroke in TIA
A: HTN
DM
Symptoms >10 min
weakness
Speech impairment
Male
>60yo
Dyslipidaemia
CT or MRI changes of infarction

Q: ABCD2 score criteria
A: Age >60
BP >140/90
Clinical
 - 0 = absent
 - 1 = Speech impairment without unilateral weakness
 - 2 = Unilateral weakness
Duration
 - 0 = Absent
 - 1 = 10-59 min
 - 2 = >60 minutes
Diabetes

Q: Which TIA patients need admission for MRI with DWI and risk profiling?
A: ABCD >=3
AF
Crescendo
Carotid territory symptoms

Q: Should all suspected TIA's have neuroimaging?
A: Yes. All should get CT and CTA +- CT perfusion scan if clot found

Q: Should anticoagulation be initiated for TIA patients in AF?
A: Not acutely. Need inpatient initiation once further imaging performed as risk of haemorrhage is > benefit in acute stroke

Q: Most common causes of stroke in young people?
A: Carotid/vertebral artery dissection (20%)
Cardioembolic (20%)

Q: Complications of stroke
A: Cerebral oedema
Raised ICP
Haemorrhagic transformation
Aspiration
DVT/PE
Seizures
Pressure areas

Q: What proportion of cerebral aneurysms are in anterior circ?
A: 90%

Q: Where are most cerebral aneurysms?
A: ACA/AComA (30-40%)

Q: What type of aneurysms predominate?
A: 90% saccular

Q: Positive LP for SAH rate after negative CT?
A: 0.4% overall BUT if CT within 6 hours --> 1/2000

Q: Who needs LP after negative CT within 6 hours?
A: Multiple relatives with SAH
Previous SAH
PCKD
Anaemic

Q: NPV of CT + CT-A for SAH?
A: 99.5%

Q: If CT performed >6 hours from onset of headache --> Plan?
A: LP (or CT-A if refuses or prefers with explanation of risk of perimesencephalic/further testing)

Q: Target BP in SAH?
A: <160mmHg until secured
<140mmHg if conscious (as obviously has adequate CPP)
If unconscious -- Only treat if >180mmHg as may be due to inadequate CPP

Q: NNT for nimodipine in SAH
A: 20
Reduces risk of ischaemic stroke by 1/3

Q: Which Fisher score has highest risk of vasospasm?
A: III (23-96%)

Q: Rate of rebleed in SAH?
A: 20% in first 2 weeks then 1.5% per day for next 2 weeks

Q: What proportion of SAH suffer vasospasm?
A: 70% but ~20% symptomatic

Q: Complications of SAH
A: Arrhythmias (35%)
Hydrocephalus
DVT/PE
Aspiration
Neurogenic pulmonary oedema (23%)
SIADH
Cerebral salt wasting
Diabetes insipidus if raised ICP

Q: Which anticonvulsant is CI in SAH?
A: Phenytoin shows poorer outcomes

Q: Should SAH be given seizure prophylaxis?
A: Only if has one. Otherwise avoid as unclear benefit and possible risk of worse outcomes e.g. phenytoin

Q: What is acute vestibular syndrome?
A: Vertigo, nausea, vomiting > 24hours

Q: What proportion of acute vestibular syndrome is due to stroke?
A: 25%

Q: Peripheral vertigo DDx
A: BPPV
Vestibular neuritis
Meniere's
Ramsay Hunt
Schwannoma
Aminoglycosides
Loop diuretics

Q: Central vertigo DDx
A: Vertebrobasilar insufficiency
Cerebellar stroke
Lateral medullary syndrome
Cerebellopontine tumors
MS
Phenytoin/alcohol

Q: What does vertical nystagmus suggest?
A: Central vertigo

Q: How long do episodes of Meniere's last?
A: Hours (therefore not Acute vestibular syndrome)

Q: Recent head/neck trauma + vertigo =
A: Vertebral artery dissection until proven otherwise

Q: What proportion of AVS patients with stroke have neurological findings?
A: 80%

Q: Vertigo + gait unsteadiness/truncal ataxia =
A: Central until proven otherwise

Q: Positive Romberg test with vertigo =
A: More likely central

Q: What proportion of patients with positive Dix-Hallpike are resistant to Epley manoeuvre?
A: 5%

Q: How often should Epley be repeated?
A: Every few days

Q: Main differential of true vertigo in the elderly?
A: Disequilibrium in the elderly due to postural hypotension/anaemia/arrhythmia

Q: Hearing loss + Vertigo + No tinnitus =
A: Acoustic neuroma

Q: Peripheral vertigo + no hearing loss + no tinnitus
A: Vestibular neuronitis or BPPV

Q: Hearing loss + Tinnitus + Aural fullness + No recent infection
A: Meniere's

Q: hearing loss, tinnitus and recent otitis media/URTI?
A: Bacterial labyrinthitis

Q: Treatment of peripheral vertigo
A: Initial control with prochlorperazine (stemetil) 5-10mg PO TDS but then withdraw to allow central compensation

Q: What is the most common cause of acute vertigo?
A: BPPV

Q: How long do episodes of BPPV usually last?
A: 2 weeks

Q: Majority of BPPV is from which semicircular canal?
A: Posterior (85%)

Q: What is the Pagnini-McClure test?
A: Supine head turn test for horizontal semi-circular canal BPPV

Q: Most common cause of acute vestibular syndrome?
A: Vestibular neuronitis

Q: Deafness, vertigo, facial nerve palsy + vesicles
A: Ramsay Hunt

Q: Profound gait ataxia =
A: Cerebellar stroke until proven otherwise

Q: When would central vertigo have hearing loss?
A: vertebrobasilar ischaemia affecting auditory nerve nuclei

Q: Criteria for imaging in vertigo?
A: Vertigo +
 New onset occipital headache
 Focal neurological signs
 Intact head impulse test
 Acute deafness
 Risk factors for stroke
 Pure vertical/horizontal nystagmus
 Direction-changing nystagmus
 Severe gait ataxia
 Positive Rombergs
Truncal ataxia

Q: Ototoxic agents
A: Aminoglycosides
Erythromycin
Frusemide
Fluoroquinolones
NSAID's

Q: Drugs that cause central vertigo
A: TCA
Anticonvulsants
Alcohol
Opiates

Q: How do cerebellopontine angle tumors present?
A: Deafness
Ataxia
Ipsilateral facial nerve palsy
Loss of corneal reflex
Cerebellar signs

Q: DDx of acute vertigo with deafness
A: Meniere's disease
Cogan’s
Vertebrobasilar ischaemia
Acoustic neuroma
Labryinth haemorrhage
Bacterial labyrinthitis

Q: What is the most common cause of acute vertigo with deafness?
A: Meniere's

Q: How often does Meniere's episodes occur?
A: Usually a few hours, several times a week to month

Q: Treatment of Meniere's
A: Prochlorperazine 5-10mg PO TDS or 12.5mg IM

Q: Acute vertigo while flying/straining/coughing/diving?
A: Perilymph fistula
Prochlorperazine and refer ENT

Q: How does Wallenberg/lateral medullary syndrome present?
A: Classic vertigo +
Ipsilateral facial numbness, loss of corneal reflex, Horner's, dysphagia/dysponia
Contralateral loss of pain and temperature sensation in trunk and limbs

Q: What is disequilibrium of ageing?
A: Ill-defined dizziness and gait disturbance due to combination reduced visual input, reduced proprioception, orthostatic changes, reduced balance, proximal strength, reactional hypertonia and fear of falling

Q: What is the most common systemic vasculitis?
A: Temporal arteritis

Q: What proportion of GCA are over 70?
A: 80%

Q: What proportion of GCA have PMR?
A: 50%

Q: What proportion of PMR have GCA?
A: 15%

Q: How often is the aorta involved in GCA?
A: Up to 50%

Q: Most specific finding on physical examination for temporal arteritis?
A: Enlarged temporal artery

Q: What proportion of GCA suffer permanent visual loss?
A: 20%

Q: How common is aortic aneurysm in GCA?
A: 10-20%

Q: How common is aortic dissection/rupture in GCA?
A: 1-6%

Q: What is the 90 day stroke risk after TIA?
A: 9.5%

Q: What proportion of strokes within 90 days occur in first 2 days after TIA?
A: 50%

Q: What is the Rosier score?
A: Used to identify stroke in ED

Q: What proportion of strokes can be prevented by early Ix and intervention of TIA?
A: 80%

Q: Admission criteria for TIA?
A: Recurrent
Crescendo
High-grade carotid stenosis
Presumed cardiac source i.e. AF
Embolic despite anticoagulation
ABCD2 >= 3

Q: Which TIA warrant CT-A?
A: All anterior TIA
NOT recommended for syncope or non-focal neurology

Q: Which patients with TIA can be discharged for follow-up appointment within 1 week?
A: ABCD <4 without crescendo TIA, AF, carotid stenosis or carotid territory symptoms

Q: Antiplatelet regime after TIA?
A: Aspirin 300mg PO stat
Aspirin/dipyramidole 25/200 SR OD + Aspirin 150mg OD for 1 week
Aspirin/dipyramidole 25/200 SR BD onwards
Aspirin 150mg BD if asasantin not tolerated
Clopidogrel if aspirin CI or not tolerated

Q: What proportion of TIA patients started on aspirin will suffer disabling or fatal stroke within 2 weeks?
A: 1/3000

Q: How much does aspirin reduce 2 week stroke risk following TIA?
A: From 2.5% to 1%

Q: Indications for carotid endarterectomy?
A: Carotid territory TIA/stroke in last 6 months with >70% stenosis on CT-A or >50% on catheter angiography +
Perioperative mortality/stroke risk <6%

Q: How do you test for direction-changing nystagmus?
A: Ask patient to look left and right for at least 15-30 seconds each (as need to make sure not just transient physiological)
Do NOT ask to fixate on finger as may suppress nystagmus

Q: How does lateral medullary syndrome present?
A: Nystagmus and vertigo
Ipsilateral Horner's
Ipsilateral facial hemisensory loss with contralateral pain and temp limb loss
Bulbar weakness

Q: How does medial medullary syndrome present?
A: Ipsilateral tongue weakness and deviation
Contralateral hemiparesis
Contralateral hemisensory loss to touch and proprioception

Q: How does pontine ischaemia present?
A: Hemiparesis or hemisensory loss
Ataxia
Dysarthria
Gaze palsy
Locked in syndrome

Q: How does tip of the basilar syndrome present?
A: Somnolence
Confusion
Bilateral loss of vision with denial of blindness
Coma

Q: How does posterior cerebral artery syndrome present?
A: Contralateral homonymous hemianopia
Hemisensory loss
Hemi-body pain

Q: Poor prognostic factors in ICH
A: Blood in ventricles
Low GCS (3-4)
Haematoma volume >30mL
Age >80
High NIHSS score
Infratentorial

Q: Define syncope
A: Transient, self-limited loss of consciousness with inability to maintain posture followed by spontaneous recovery

Q: What causes anterior cord syndrome?
A: Anterior spinal artery infarction

Q: Sensory symptoms in central cord syndrome
A: Variable
Burning dysaesthesia

Q: Post-partum seizure DDx
A: Eclampsia
Cerebral venous thrombosis
Meningoencephalitis secondary to epidural
Hypoxia secondary to PE
Primary epilepsy

Q: Seizure mimics
A: Hypoglycaemia
Hyponatraemia
Todd's paresis/seizure
Conversion
Syncope
Mass lesion
MS
Bell's palsy
Hemiplegic migraine

Q: Indications for stroke lysis
A: NIHSS 5-22 or significant for this patient
>18yo
Onset within 4.5 hours
Consent
No haemorrhage on non-con CT