Neuro Flashcards
causes of unilateral visual loss
- vascular (amaurosis fugax, CRVO, anterior ischaemic optic neuropathy)
- optic neuritis
- retinal detachment
Optic neuropathy causes
- inflammatory (optic neuritis)
- demyelination associated with MS
- vascular (ischaemic optic neuropathy)
- space occupying lesion
- toxins/drugs (alcohol, methanol, tobacco)
- raised ICP
- trauma
Investigations to do in unilateral visual loss
VEP/MRI (optic neuritis)
Fluorescein angiography (CRVO)
tonometry (glaucoma)
USS (haemorrhage/detachment)
Optic Neuritis Ax
Inflam of optic nerve, associated with MS.
Other causes - infection (lyme, HIV), B12 deficiency, arteritis
Optic neuritis presentation
Reduced acuity over days, pain on moving eye, exacerbated by heat or exercise.
Afferent pupillary defect
total colour blindness (dyschromatopsia)
Recovery normally occurs around 6 weeks
Optic neuritis treatment
Steriods help pain and hasten recovery
MS typical presentation
Optic neuritis 1st presentation
spastic paraparesis
cerebellar (dysarthria, tremor, nystagmus)
Lhermittes (electric) Uhthoffs (bath)
UMN signs
afferent pupillary defect
MS investigations
MRI - multiple plaques disseminated in place and time
LP - oligoclonal bands
Electrophysiological tests - prolonged evoked potentials
MS Mx
Steroids (methylpred)
Disease modifying agents (natalizumab, alemtuzumab) (beta interferon)
Muscle relaxants (baclofen)
Difference between clincally isolated symptom and MS?
CIS - first attack of MS
MS Dx- multiple CNS lesions -> symptoms that >24h disseminated in place and time (>1 month)
Sites more likely to have demyelination plaque
- optic nerve
- cerival cord
- brainstem
- corpus callosum
- periventricular region of cerebral hemispheres
Diff diagnosis for recurrent black outs
- syncope
- epilespy
- non epileptic seizure
Features in Hx suggesting epilepsy or syncope
Epilepsy - aura, incontinence, post ictal recovery slow and confused, tongue bite
Syncope - rapid recovery, prodrome - hot, dizzy, feel faint
Pathophysiology of epileptic seizure
recurrent spontaneous intermittent abnormal electrical activity in part of the brain manifesting as seizures
Pathophysiology of syncope
abrupt and transient loss of consciousness associated with loss of postural tone that follows a sudden fall in cerebral perfusion
Role of EEG in recurrent blackouts
shows abnormalities in 70% cases if withint 24-48 hours after first seizure
only used to support clinical suspicion not in isolation
Role of Neuro imaging in recurrent blackout
identify structural abnormalities that cause certain epilepsies
MRI if focal onset on history, examination or EEG
CT if MRI not availble or CI
Complications of a stroke
Raised ICP
Aspiration
Pressure Sores
Depression
Cognitive impairment
Thrombolysis +ve -VE
+ improves chances of pt being depended on discharge
- need to give in 4.5 hours (time is brain)
- haemorrhage (1 in 20)
- ischamic strokes only
TACS symptoms and affected area
MCA/ACA
- unilat weakness (and or sensory) of AFL
- homonymous hemianopia
- higher cerebral dysfunction (dysphagia, visuospatial disorder)
POCS symptoms
- cerebellar or brainstem syndromes
- locked in syndrome
- isolated homonymous hemianopia
LACS symptoms
uni lat weakness of face and arm, arm and leg, or all 3
pure sensory loss
ataxic hemiparesis
