Routine if asked to examine upper limbs:
Inspect (walking aids etc)
Pronator drift
Rebound test
Tone
Power
Reflexes
Coordination (dysdiadochokinesis, finger-nose testing). When notice problem with coordination proceed to:
Eye movements (nystagmus, INO), pupils (RAPD), Visual fields, observe for Horner’s syndrome
CNs V + VII (and look at gums for hypertrophy and face for telangiectasia) + VIII
Speech (eg. “How did you get here today?”)
Sensation
Hands and arms (clubbing, tar staining, dupuytrens contracture, diabetic fingerprick marks telangiectasias, signs of chronic liver disease)
Foot tapping test if sitting and observe for pes cavus
If time allows proceed to:
Gait, Heel to toe walking, Rhombergs test
Lower limbs (heel shin testing, tone, power, reflexes, look for pes cavus)
Routine if told patient is “unsteady, proceed as appropriate”:
Inspect (walking aids etc)
Start with gait, heel to toe walking and Rhomberg’s test
Pronator drift and rebound test
Dysdiadochokinesis, finger-nose testing
Eye movements (nystagmus, INO), pupils (RAPD), visual fields, observe for Horner’s syndrome
CNs V+VII (and look at gums for hypertrophy and face for telangiectasia) +VIII
Speech (eg. “How did you get here today?”)
Foot tapping whilst sitting and observe for pes cavus
Upper limbs Tone, Power, Reflexes, Sensation
Hands and arms (clubbing, tar staining, diabetic fingerprick marks, dupuytrens contracture, telangiectasias, signs of chronic liver disease)
If time allows: examine lower limbs (heel shin testing, tone, power, reflexes, look for pes cavus)
Present to the examiner:
This patient has a bilateral cerebellar syndrome as evidenced by:
Ataxic wide based gait
Inability to walk heel to toe
Rhombergs test was negative but there was increased stability with the feet together
Dysdiadochokinesis, past pointing, intention tremor, rebound phenomenon
Heel shin ataxia
Nystagmus
Ataxic dysarthria
Comment on tone (reduced), power, reflexes (pendular) and sensation. NB: increased tone and reflexes and pyramidal weakness suggests corticospinal tract involvement
In terms of aetiology:
There was (no) internuclear opthalmoplegia (INO)/ RAPD/ UMN weakness/sensory disturbance to suggest demyelinating disease
There was (no) cachexia/clubbing/tar staining to suggest paraneoplastic cause
There was (no) weakness or visual field defect to suggest a stroke/space occupying lesion as the cause
There was (no) CN V, VII, VIII to suggest cerebellar pontine angle lesion
There was (no) parkinsonism to suggest multi systems atrophy
There was (no) gum hypertrophy to suggest phenytoin use
There was (no) dupuytrens contracture/stigmata of chronic liver disease to suggest alcohol as the cause
There was (no) opthalmoplegia to suggest Miller Fischer as the cause
There was (no) pes cavus to suggest Friedreich’s Ataxia as the cause
Alternatively……
This patient has a right/left sided unilateral cerebellar lesion as evidenced by:
Ataxic wide based gait with veering towards to right on heel toe walking
Rhombergs test was negative but there was increased instability with the feet together
Dysdiadochokinesis, past pointing, intention tremor, rebound phenomenon
Right heel shin ataxia
Gaze-evoked nystagmus on rightward gaze
Ataxic dysarthria
Comment on tone (reduced), power, reflexes (pendular) and sensation. NB: increased tone and reflexes and pyramidal weakness suggests corticospinal tract involvement
In terms of aetiology:
There was (no) internuclear opthalmoplegia (INO)/ RAPD/ UMN weakness/sensory disturbance to suggest demyelinating disease
There was (no) weakness or visual field defect to suggest posterior circulation stroke/space occupying lesion as the cause
There was (no) CN V, VII, VIII to suggest cerebellar pontine angle lesion
There was (no) Horner’s syndrome to suggest lateral medullary syndrome
To complete my examination I would like to perform fundoscopy (Optic atrophy in demyelinating disease, papilloedema in space-occupying lesion), a full lower and upper limb motor and sensory examination, full cranial nerve examination
Most likely causes of bilateral cerebellar syndrome are:
Demyelination (Multiple Sclerosis)
Paraneoplastic conditions
Bilateral posterior circulation strokes/space-occupying lesions
Other causes of bilateral cerebellar syndrome include:
Multiple System Atrophy
Drugs: phenytoin, carbamazepine, lithium
Toxins: Alcohol
Metabolic: hypothyroid, wilson’s disease, coeliac, B12 deficiency
Infective: HIV, enteroviruses, syphilis, CJD, toxoplasmosis, lyme disease
Inflammatory: Miller Fischer variant of GBS
Hereditary: Friedreich’s Ataxia, ataxic telangiectasia, spinocerebellar ataxias, von hippel landau
Bilateral cerebellar pontine angle lesion eg. neurofibromatosis
Most likely causes of unilateral cerebellar syndrome are:
Demyelination (Multiple Sclerosis)
Posterior circulation infarction/haemorrhagic stroke
Space occupying lesion in the posterior fossa eg. tumour, abscess
Other causes of unilateral cerebellar syndrome:
Cerebellar pontine angle lesion eg. neurofibromatosis
Lateral medullary syndrome
Ataxic hemiparesis following lacunar stroke
Multiple System Atrophy
Causes of spastic paraparesis and cerebellar signs:
- Demyelination (Multiple sclerosis)
- Friedreich’s ataxia
- Spinocerebellar ataxia
- Arnold Chiari Malformation
- Syringomyelia
Investigations according to most likely cause:
MRI brain and spinal cord
Bloods: TFT, copper studies, paraneoplastic screen, coeliac, screen for infection and inflammation, FBC, LFT, B12, drug levels (phenytoin, carbamazepine, lithium)
Lumbar puncture to examine CSF (eg. for oligoclonal bands)
EMG and nerve conduction studies
Genetic testing
Manage according to cause
Multiple Sclerosis
This is a progressive demyelinating disease of the central nervous system (brain and spinal cord)
CNS inflammation is disseminated in time and place
Involvement of spinal cord, cerebellum, brainstem, optic nerve
*does not affect peripheral nerves*
Visual evoked potentials are reduced (slow conduction in optic nerve)
CSF: increased protein, increased lymphocytes, unmatched oligoclonal bands
MRI: active inflammation, hyperintense on T2 (periventricular white matter lesions, corpus callosum, brainstem, cerebellar, spinal cord, optic nerve)
Management: MDT approach, high dose iv steroid acutely, symptom management eg. antispasmodics, disease modifying therapies
Written by Dr Sarah Kennedy
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