Neuro Flashcards
Causes of bilateral cerebellar signs with spasticity
Demyelination
Friedrichs
Spinocerebellar ataxia
Arnold chiari malformation
Syringomyelia
Unilateral cerebellar syndrome
Demyelination
Stroke
SOL
Lateral medullary syndrome
Bilateral cerebellar syndrome
Most common:
Demyelination
Paraneoplastic condition
Bilateral posterior circulation stroke or bilateral SOL
Multisystems atrophy
Drugs- phenytoin, lithium, carbamazepine
Metabolic- thyroid disease, Wilson’s, coeliac, b12 deficiency
Infective- HIV, syphyllis, toxoplasmosis
Inflammatory- MF variant
Hereditary - friedrichs ataxia. Ataxic telangiectasia, spinocerebellar ataxia
Bilateral cerebellar pontine angle lesion eg neurofibromatosis
Other signs to look for in a cerebellar exam
INO/ RAPD for MS
Cachexia, clubbing, tar staining- paraneoplastic syndromes
Visual field defect- stroke, SOL
CN involvement- cerebellar pontine lesion
Parkinsonism- MSA
Gum hypertrophy- phenytoin use
Dupuytrens or CLD signs- Alcohol
Opthalmoplegia- MF variant
Pes cavus- friedrichs
Weakness- Stroke
Horners- lateral medullary syndrome
Causes of spastic paraparesis
Ideally want history for onset and progression and FH
Most likely spinal cord pathology:
Demyelination- MS, NMO, transverse myelitis (HIV, HSV, VZV, paraneoplastic)
Vascular- acute infarction, AVM
SOL- tumour (benign or malignant), disc prolapse, abscess
Hereditary- HSP, Friedrichs (cerebellar signs also)
Other infection - tropical spastic paraparesis
Brain - parasagittal menigioma
Investigating spastic paraparesis
DRE- anal tone
Check for catheters
Bloods- FBC, CRP/ESR, UE LFT, b12 and folate, viral screen inc HIV, bone profile, immunoglobulins,
MRI- brain and spinal cord
Nerve conduction studies and EMG
NCS- axonal vs demyelination
Demyelination shows reduction in conduction velocity
Axonal- reduction in amplitude
Wheelchair
Pseudoathetosis -worse on eye closing
Reduced reflexes
Weakness inc proximal weakness
low tone
Asymmetric sensory Sx
Lower motor neurone
Peripheral neuropathy
However given element of proximal weakness does not follow usual peripheral neuropathy pattern which is usually length dependent (eg alcohol, diabetes).
Likely more inflammatory in nature eg GBS or CIDP
Management of GBS
Usually supportive
Close monitoring of FVC as patient may require resp / ventilatory support
May need to escalate to ITU/crit care teams due to risk of ventilatory failure
Plasma exchange / IV immunoglobulins may be required
Management of CIDP
MDT approach
Neurology team - neuropathic pain agents
PT/OT
SALT
Orthotics
