Neurology Flashcards
define a TIA
transient neurological dysfunction secondary to ischaemia without infarction
what is a crescendo TIA?
2 or more TIAs within a week
features of stroke?
typically sudden onset:
- limb weakness
- facial weakness
- dysphasia
- visual / sensory loss
risk factors for stroke?
- pre-existing CVD
- AF
- carotid artery disease
- HTN
- DM
- smoking
- vasculitis
- thrombophilia
- COCP
what is the ROSIER tool for? what is a significant score?
- recognition of stroke in the emergency room
- anything above 0
what is the ABCD2 score used for?
to calculate risk of subsequent stroke in patients with suspected TIA
what are the components of ABCD2?
- Age
- BP
- Clinical features
- Duration of symptoms
- DM
immediate management steps for a suspected stroke?
- admit to specialist stroke unit
- exclude hypoglycaemia
- CT head to rule out haemorrhage
- aspirin 300mg to be continued for 2 weeks
what can be offered immediately after a CT head has ruled out an intracranial haemorrhage in suspected stroke? hint: within 4.5h
- thrombolysis
- done with alteplase
what is the window for thrombolysis?
4.5 hours
what is done following thrombolysis?
repeat CT heads to check for complications (e.g. haemorrhage)
should HTN be controlled at the time of a stroke?
- no
- the extra perfusion keeps brain tissue alive
management of TIA?
- aspirin 300mg daily for 2 weeks
- then lifelong clopidogrel
- start secondary prevention of CVD
- get ABCD2 score
- diffusion-weighted MRI (gold standard)
- carotid USS (look for stenosis, offer endarterectomy if present)
how is the ABCD2 score interpreted?
- 3 or less = specialist assessment within a week
- >3 = specialist assessment within 24h
secondary prevention of stroke?
- clopidogrel 75mg daily
- atorvastatin 80mg (after 2 weeks)
- endarterectomy for carotid stenosis
- treat modifiable RFs (e.g. DM)
- offer rehabilitation
what % of strokes are intracranial bleeds?
10-20%
risk factors for an intracranial bleed?
- head injury
- HTN
- aneurysms
- ischaemic stroke (progressing to haemorrhage)
- brain tumours
- anticoagulation (warfarin)
presentation of intracranial bleed?
- sudden onset headache
- seizures
- weakness
- vomiting
- reduced consciousness
- any other sudden onset neuro sign
how is GCS interpreted?
8 or less = consider intubation
motor scoring in GCS?
- 1 = none
- 2 = extends
- 3 = abnormal flexion
- 4 = normal flexion / withdraws from pain
- 5 = localises to pain
- 6 = obeys command
verbal scoring in GCS?
- 1 = none
- 2 = incomprehensible sounds
- 3 = inappropriate words
- 4 = confused conversation
- 5 = orientated
eye opening scoring in GCS?
- 1 = none
- 2 = open to pain
- 3 = open to speech
- 4 = open spontaneously
pathophysiology of subdural haemorrhage?
- rupture of bridging veins
- between dura mater and arachnoid mater
SDH appearance on CT?
- crescent (moon) shaped
- crosses suture lines
which patient demographics are more affected by SDH?
- elderly
- alcoholics
pathophysiology of an extradural haemorrhage?
- rupture of middle meningeal artery in temporo-parietal region
- between skull and dura mater
appearance of EDH on CT?
- biconvex (lens) shaped
- does not cross suture lines
typical history of EDH?
- young pt with traumatic head injury
- lucid interval first
- followed by rapid decline as haematoma grows and compresses things
where can an intracerebral bleed occur?
- lobes
- intraventricular
- basal ganglia
- cerebellar
management of intracranial bleeds?
- immediate CT head (diagnostic)
- check FBC and clotting
- admit to specialist stroke unit
- consider intubation and ventilation if low GCS
pathophysiology of a subarachnoid haemorrhage?
- bleed in the subarachnoid space, where the CSF is
- between pia mater and arachnoid membrane
- typically due to ruptured cerebral aneurysm
features of SAH?
- sudden onset occipital “thunderclap” headache
- neck stiffness
- photophobia
- neuro changes (vision, speech, weakness, seizures, LOC)
risk factors for SAH?
- HTN
- smoking
- excessive alcohol consumption
- cocaine use
- FHx
which other medical conditions are associated with SAH?
- HTN
- sickle cell anaemia
- marfan’s syndrome
- ehlers-danlos syndrome
- neurofibromatosis
appearance of SAH on CT?
- star-shaped hyperattenuation
- if normal, does NOT rule out SAH
investigations for SAH?
- CT
- LP
- CT / MRI angiography
findings on LP in SAH?
- raised RBC
- xanthochromia
management of SAH?
- admit to specialist neurosurgical unit
- intubate and ventilate if low GCS
- coiling / clipping of aneurysms
- nimodipine to prevent vasospasm
- LP / shunt insertion to treat hydrocephalus
- AEDs for seizures
typical demographic affected by MS?
white women <50
when might symptoms improve in MS?
- during pregnancy
- postpartum
describe the pathophysiology of MS
oligodendrocytes of the CNS end up demyelinated
how are the lesions in MS described?
- white matter plaques
- disseminated in space and time
how can MS be classified?
- relapsing-remitting
- secondary progressive (follows on from RRMS)
- primary progressive
when might symptoms worsen in MS? what is this called?
- heat
- exercise
- uhthoff’s phenomenon
presentation of MS?
lots of different presentations:
- unilateral vision loss (optic neuritis, most common)
- double vision (internuclear ophthalmoplegia, conjugate gaze disorder, CN6-related)
- focal weakness
- focal sensory symptoms
- ataxia (sensory or cerebellar)
examples of focal weakness seen in MS?
- bells palsy
- horner’s synrome
- limb paralysis
- incontinence
examples of focal sensory symptoms seen in MS?
- trigeminal neuralgia
- numbness
- parasthesia
- lhermitte’s sign
describe lhermitte’s sign. which condition is this seen in?
- flexion of the neck causes electric shock sensations in the trunk and limbs
- MS
sign O/E of sensory ataxia?
positive romberg’s test
after the first presentation of demyelination, what determines progression to MS?
- presence of lesions on MRI = high risk of MS
- if no further episodes, this is called “clinically isolated syndrome”
how is MS diagnosed?
- done by neurologist
- symptoms must have been progressive over a year for primary progressive MS diagnosis
- must exclude other causes
potential causes of MS?
true cause unknown but the following might contribute:
- certain genes
- EBV
- low vit D (lowest rates at equator)
- smoking
- obesity
causes of optic neuritis?
- MS (most likely)
- sarcoidosis
- SLE
- DM
- syphilis
- measles, mumps
- lyme disease
findings on LP in MS?
- raised protein
- oligoclonal bands
management of relapses in MS?
- 500mg methylprednisolone PO for 5 days
- given IV if severe
- DMARDs (natalizumab, ocrelizumab)
management of symptoms in MS?
- exercise (maintains strength)
- amitriptyline / gabapentin for neuropathic pain
- SSRIs for depression
- tolterodine / oxybutynin for urge incontinence
- baclofen / gabapentin / physio for spasticity
most common form of MND?
amyotrophic lateral sclerosis (ALS)
name some different types of MND
- ALS
- progressive bulbar palsy (second most common)
- progressive muscular atrophy
- primary lateral sclerosis
risk factors for MND?
- FHx of MND
- smoking
- heavy metal exposure (lead)
- pesticide exposure
typical patient affected by MND?
man in 60s with affected relative
presentation of MND?
- insidious, progressive weakness
- affects: limbs, trunk, face and speech (dysphasia)
- typically starts off in upper limbs
- Hx clumsiness, dropping things, tripping over
- mixed UMN and LMN signs
signs of LMN disease?
- muscle wasting
- reduced tone
- fasciculations
- reduced reflexes
signs of UMN disease?
- increased tone / rigidity
- spasticity (velocity-dependent)
- brisk reflexes
- upgoing plantar reflex
how is MND diagnosed?
- clinically O/E
- done by specialist
management of MND?
- riluzole slows disease progression
- NIV to support breathing at night
- advanced directives put in place
- end of life care planning
what are the 2 main causes of death in MND?
- respiratory failure
- pneumonia
pathophysiology of parkinson’s disease?
- progressive reduction of dopamine production from substantia nigra
- found in the basal ganglia
- leads to disordered movement
classic triad of parkinson’s disease?
asymmetrical, unilateral:
- resting tremor
- rigidity
- bradykinesia
presentation of parkinson’s disease? hint: there’s a LOT
- pill-rolling tremor
- cogwheel rigidity
- micrographia
- shuffling gait
- difficulty in initiating movement (chair to standing)
- difficulty in turning when walking
- hypomimia / masked facies
- depression
- sleep disturbance, insomnia
- anosmia
- postural instability
- cognitive impairment
typical demographic affected by parkinson’s disease?
man >70
what are the 4 parkinson’s plus syndromes to know?
- multiple system atrophy
- lewy body dementia
- progressive supranuclear palsy
- corticobasal degeneration
features of multiple system atrophy?
- parkinsonian presentation, but also:
- autonomic signs (postural hypotension, constipation, sweating, sexual dysfunction)
- cerebellar signs (ataxia)
features of lewy body dementia?
- parkinsonian presentation, but also:
- progressive cognitive decline
- visual hallucinations
- delusions
- REM sleep disorders
- fluctuating consciousness
management of parkinson’s disease?
- levodopa (co-benyldopa includes benserazide, co-careldopa includes carbidopa)
- COMT inhibitor (entacapone, taken with levodopa)
- DA agonists (bromocriptine, cabergoline)
- MAO-B inhibitors (selegiline, rasagiline)
what is a disadvantage of starting levodopa early in parkinson’s treatment?
- it becomes less effective over time
- best to reserve it for when other treatments have stopped working
adverse effects of levodopa?
dyskinesias:
- dystonia
- chorea
- athetosis
describe athetosis
involuntary twisting, writhing movements in hands and feet
describe dystonia
excessive muscle contractions causing abnormal postures / exaggerated movements
describe chorea
abnormal, involuntary, jerking movements
important benefit of COMT inhibitor?
extends effective duration of levodopa action
key adverse effect of DA agonists?
pulmonary fibrosis
key risk factor for benign essential tremor (BET)?
ageing
features of BET?
- fine tremor
- symmetrical
- worse on voluntary movement
- worse when tired / stressed / caffeinated
- improved by alcohol
- absent in sleep
what are the differential causes of tremor?
- BET
- parkinson’s
- MS
- huntington’s chorea
- hyperthyroidism
- fever
- antipsychotics
management of BET?
can try the following for symptomatic relief:
- propanolol
- primidone
define epilepsy
umbrella term for condition where there is a tendency to have seizures
what is a seizure?
a transient episode of abnormal electrical activity in the brain
investigations in epilepsy?
- EEG
- MRI brain
- ECG (exclude heart problems)
what are the different types of seizure?
- generalised tonic clonic
- focal / partial
- absence
- atonic
- myoclonic
- infantile spasms (west syndrome)
features of a generalised tonic clonic seizure?
- LOC
- muscle tensing (tonic)
- muscle jerking (clonic)
- tongue biting
- incontinence
- groaning
- irregular breathing
features of post-ictal period following a GTC seizure?
- confusion
- feeling drowsy
- irritability
- feeling depressed
management of tonic clonic seizures?
1st: valproate
2nd: lamotrigine or carbamazepine
where do focal seizures start in the brain?
temporal lobe
how could a focal seizure present?
- hallucinations
- memory flashbacks
- deja vu, jamais vu
- doing strange things on autopilot
management of focal seizures? hint: opp. to GTC
1st: carbamazepine or lamotrigine
2nd: valproate or levetiracetam
which demographic is typically affected by absence seizures? how might it present?
- children
- look blank, stare into space for 10-20 secs, then recover
prognosis for absence seizures?
> 90% of children stop getting them as they grow up
management of absence seizures?
valproate or ethosuximide
presentation of atonic seizure?
- “drop attack”
- brief drop in muscle tone
- typically lasts <3 mins
- seen in children
which condition is associated with having atonic seizures?
lennox-gastaut syndrome
management of atonic seizures?
1st: valproate
2nd: lamotrigine
presentation of myoclonic seizure?
sudden, brief muscle contraction
which condition is myoclonic seizures seen in?
juvenile myoclonic epilepsy
management of myoclonic seizures?
1st: valproate
2nd: lamotrigine, levetiracetam or topiramate
which age is west syndrome seen at?
6 months
prognosis of west syndrome?
- poor
- 1/3 die by age 25
- 1/3 go on to live seizure free
management of west syndrome
- prednisolone
- vigabatrin
important adverse effects of valproate?
- teratogenic (must be on contraception)
- liver damage, hepatitis
- hair loss
- tremor
important adverse effects of carbamazepine?
- agranulocytosis
- aplastic anaemia
important adverse effects of phenytoin?
- folate and vit D deficiency
- therefore: megaloblastic anaemia and osteomalacia
side effects of ethosuximide?
- night terrors
- rashes
important adverse effects of lamotrigine?
- stevens-johnson syndrome (DRESS syndrome)
- leukopenia
define status epilepticus
- seizures lasting > 5 minutes
- OR >3 seizures in 1 hour
management of status epilepticus in hospital?
- ABCDE
- high flow O2
- check glucose
- insert cannula
- IV lorazepam 4mg
- repeat after 10 mins if seizure continues
- then: IV phenobarbital or phenytoin
management of status epilepticus in community?
- buccal midazolam
- rectal diazepam
causes of neuropathic pain?
- post-herpetic neuralgia from shingles (dermatomal)
- nerve damage from surgery
- MS
- diabetic neuralgia (feet)
- trigeminal neuralgia
- complex regional pain syndrome
features of neuropathic pain?
- burning
- tingling
- pins and needles
- electric shocks
- loss of touch sensation in affected areas
what is the DN4 questionnaire used for?
to assess characteristics of pain to determine if it’s neuropathic
management of neuropathic pain? name the drug class for each one
pick one of the following and if it fails, try another instead:
- amitriptyline (TCA)
- duloxetine (SNRI)
- gabapentin (anticonvulsant)
- pregabalin (anticonvulsant)
what can be tried if all 4 neuropathic pain drugs fail?
- tramadol (short-term)
- capsaicin cream (chilli pepper)
- physio
- psychological input
which drug is used to manage trigeminal neuralgia?
- carbamazepine
- not a conventional neuropathic pain drug
typical presentation of complex regional pain syndrome?
- area of skin becomes hypersensitive to even simple clothing
- neuropathic pain and abnormal sensation
- usually restricted to 1 limb
- follows injury to area
what is syringomyelia?
a collection of CSF within the spinal cord itself
what is syringobulbia?
collection of fluid in medulla of brainstem
presentation of syringomyelia?
- cape-like distribution (neck, shoulders, arms)
- loss of temp sensation
- pt could accidentally burn hands
- spastic weakness of LLs
- upgoing plantars
- horner’s syndrome
- scoliosis
which demographic is most likely to get idiopathic intracranial hypertension?
young, obese women
features of idiopathic intracranial hypertension?
- headache
- associated vomiting
- visual disturbance
describe the headache caused by idiopathic intracranial hypertension
- non-pulsatile
- bilateral
- worse in the morning
describe the vision changes in idiopathic intracranial hypertension
transient visual darkening
findings on fundoscopy in idiopathic intracranial hypertension?
bilateral papilloedema
which drugs are associated with idiopathic intracranial hypertension?
- COCP
- steroids
- tetracycline
- vit A
- lithium
management of idiopathic intracranial hypertension?
weight loss
causes of spinal cord compression?
- trauma
- tumour
- infection (esp TB)
- disc prolapse
- epidural haematoma
