Neuro Flashcards
what is a migraine?
complex neurological condition causing episodes or attacks of headache and associated symptoms due to hypothesised inflammation, vasodilation etc
*triggers - stress, dehydration, menstruation, disrupted sleep, missed meals, bright lights
what is a hemiplegic migraine?
unilateral limb weakness, ataxia, impaired consciousness
- familial can be autosomal dominant can mimic stroke or TIA
what is the management of a migraine?
acute: NSAIDs, triptan, antiemetics
prophylaxis: propranolol, amitriptyline etc
other: CBT, meditation, acupunture etc
what is the mechanism of action of triptans in the management of migraines?
abort migraines when they start to develop - 5-HT receptor agonists which cause cranial vasoconstriction, inhibiting transmission of pain signals and release of inflammatory neuropeptides
what is the significance of migraines and the complications it may cause?
Migraines are associated with a slightly increased risk of stroke, particularly when associated with aura
- The risk of stroke is further increased with the combined contraceptive pill, making them a contraindication to the combined pill
what is Bell’s palsy?
idiopathic, unilateral lower motor neurone facial palsy
- most recover within several weeks-12m
how do you differentiate between a stroke and Bell’s palsy?
- forehead has only ipsilateral, unilateral innervation from LMN
- forehead NOT spared
what are some other features of Bell’s palsy?
- unilateral facial weakness
- post-auricular pain
- difficulty chewing
- incomplete eye closure
- drooling
- tingling
- hyperacusis
what are some differentials for bell’s presentation?
- Ramsay hunt
- infections: otitis media+externa+HIV+lyme
- systemic: DM, sarcoid, leukaemia, MS, GBS
- tumours: acoustic neuroma
- trauma
how is Bell’s palsy managed?
- prednisolone in those 72h from onset
- 50mg 10 days
- antivirals
- prognosis good - reassure patient
- eye care - lubricating drops, tape when sleeping etc
What is an essential tremor?
most common type of action tremor (during voluntary contraction) that typically involves the hands and is brought out by anti-gravity positions (out-stretched)
- associated with family history in autosomal dominant pattern
how does essential tremor present?
- b/L voluntary tremor seen when performing task
- typical nodding
- tremor in voice when holding note
*rarely affects legs
what differentials would you consider in essential tremor?
- parkinsonism
- anxiety
- thyrotoxicosis
- hepatic encephalopathy
- CO2 retention
- cerebellar disease
- alcohol or drug withdrawal
how is essential tremor managed?
- propranolol
- other: primidone, gabapentin
- neuromodulation, botulinum toxin, deep brain stimulation
what is Horner’s syndrome?
IPSILATERAL ptosis, anhidrosis, miosis
how do you differentiate the levels of lesions in Horner’s?
*location of anhidrosis
- face, arm and trunk: first order, spinal
- face only: post spinal cord exit, on decent down towards lung
- none: postganglionic lesions
how would you investigate horners?
- systemic
- CXR
- apraclonidine to rever pupillary constriction
- hydroxyamphetamine: dilated pupil if underlying preganglionic lesion
how is Horner’s managed?
- treat underlying - may restore nerve function
- neuro-imaging, discussion with hyperacute stroke unit
- thrombolysis
- anti-platelets or anticoag
what is the pathophysiology of Subacute combined degeneration of the spinal cord?
- classical metabolic disorder of the spinal cord - due to vitamin B12 or folate deficiency - over 40y/o
- posterior columns and cortico-spinal tracts are specifically damaged
- symmetrical dorsal column loss - joint position sense and vibration affected
how does subacute spinal degeneration present?
*impaired proprioception, vibration sensation, muscle weakness and hyperreflexia
- peripheral and CNS sings
- visual loss
- incontinence
- numbness
how is subacute degeneration investigated?
- FBC - Hb low high MCV
- serum B12
- methylmalonic acid and homocysteine levels
- blood film - megaloblasts, hypersegmented polymorphs
- pernicious anaemia - intrinsic factor antibodies, parietal cell antibodies, schilling test
- MRI
how is subacute degeneration managed?
- B12 replacement key! and treat cause
- most improve
- peripheral neuropathy improved within first 3-6m
- cord signs shows little improvement to treatment
- not using nitrous oxide in anaesthetising those with malnutrition or gastrectomy
what is the pathophysiology of wernicke’s encephalopathy?
- disorder that occurs as a result of inadequate levels of vitamin B1 (thiamine)
- degradation of thalamic nuclei, brainstem nuclei and cerebellum and other structures around 3rd and 4th ventricles and the aqueduct
- associated with eating disorders, GI malignant, alcoholics
What is the triad of wernickes?
- ataxia
- opthalmoplegia
- nystagmus - horizontal and vertical
- conjugate gaze problems
- confusion
how is Wernicke’s managed?
*to prevent Korsakoff’s
- high dose IV thiamine (500mg thiamine TDS, pabrinex)
- continue with oral thiamine
*be weary of hypoglycaemia
- continue with oral thiamine
How does Korsakoff’s present?
antero and retrograde amnesia, loss of orientation in time and space, apathy to that around him, confabulation
*thiamine and adequate hydration
