deck_4244706 Flashcards
Guillian-Barre SyndromeHow does it classically present (history + examination)?
Post-infectious - classically following C. jejuni diarrhoeal illness Acute, symmetrical, ascending muscle weaknessUsually starts in limbs and progresses to involve proximal muscles, particularly muscles of respiration Pain is common (low back, limbs)Typically no or minimal sensory involvement AreflexiaMay be have autonomic dysfunction - difficulty controlling BP, urinary retention
Guillian-Barre SyndromeBriefly outline the pathophysiology
Acute autoimmune demyelinating neuropathy, commonly caused by cross-reaction of antibodies generated post-infectionClassically associated with C. jejuni infection, but also EBV, CMV, HIV, mycoplasmaTypically progresses over 4 weeks and then begins to recover
Guillian-Barre SyndromeWhat are the Ix and management?
- LP - increased protein, normal WCC2. Nerve conduction studies demonstrate slow conductionNo response to steroidsIV immunoglobulin for ~5 daysMay have plasma exchange (plasmapheresis)
Guillian-Barre SyndromeWhat is the main DDx?
Miller-Fischer variant syndrome Opthalmoplegia characteristic, usually first muscles affectedTypically a descending, rather ascending
SAH Briefly outline the pathophysiology/aetiology
Accumulation of blood in the space between the arachnoid and pia matter Most commonly due to rupture of berry saccular aneurysms in the COW but can also be due to AV-malformation and trauma
SAHWhat is the typical presentation?
Immediate onset of severe headache (thunder-clap), most commonly in the occipital regionTypically associated with vomiting Neck stiffness may occur sometime after onset of headache due to irritation from blood
SAHWhat initial Ix are performed?
CTB will detect the majority of SAH and will typically show loss of the lateral (sylvian) fissure, sulcal effacement, blood (hyperdense) following the fissures/sulci of the brain Lumbar puncture can confirm diagnosis if CTB negative but still clinically suspicious for SAHMust be performed later (~12 hours later) and will be yellow (xanthochromic) due to bilirubin from RBC breakdown
SAHWhat are some complications?
Hydrocephalus - blood obstructs the arachnoid granulations Cerebral ischaemia - vasospasm causing ischaemia Re-bleeding - most common cause of death
Stroke Outline the acute management
- Admission, preferably to a stroke unit 2. CTB - exclude haemorrphage and stroke mimics3. Glucose & electrolytes to exclude derangement’s as cause 4. If CTB negative for haemorrhage, patient >18 yo and symptom onset
StrokeOutline sub-acute management and secondary prevention
- Identify source of emboli ECHO, ECG - cardiac cause Carotid doppler U/S - carotid atherosclerosis2. If carotid stenosis >70%, and stroke/TIA which was not disabling then carotid endarterectomy is indicated within 2 weeks of episode3. Hypertension and hypercholesterolaemia management, glycaemic control, weight reduction, smoking cessation are important to reduce risk of further strokes
MNDKey features that point towards a diagnosis
FasciculationAbsence of sensory signs/symptoms*Lower motor neurone signs in arms and upper motor neurone signs in legsWasting of the small hand muscles/tibialis anterior is commonDoesn’t affect external ocular musclesNo cerebellar signsAbdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature
