1) Have a quick look at the patient for coarse pill rolling tremor at rest (cf essential tremor: fine, higher frequency, on exertion) facial hypomimia (decreased facial expressions) hunched posture. Don’t comment on them at this stage; just keep them in mind.

2) Get them up and ask them to walk back and forth looking for failure of ignition, enlarging steps, shuffling gait, hunched posture, unilateral loss of armswing, postural instability (unsteadiness turning corners and when shoved). When these features have been demonstrated, ask the patient to sit down again.

3) Look for and comment on resting tremor. Distract by asking them to count back from 20 or moving the other arm around (synkinesis).

4) Ask about pain. If none, take their hand in yours and test each upper limb joint in turn for cogwheel rigidity (a combination of rigidity and tremor). If you want, make a big show of taking the patient’s wrist in one hand and repeatedly flexing and extending the fingers. Cogwheeling can be exaggerated by distraction again.

5) Demonstrate bradykinesia by asking them to hold their arms up and make large rapid opposing movements between their fingers and thumb (look for diminution on affected side with time). Asking them to touch their thumb to each finger in turn is a more rigorous test if symptoms mild.

For honours, one could look for the Parkinson Plus^(c) syndromes:

6) Look at their face and examine eye movements: nystagmus suggests multiple system atrophy (as does postural hypotension and erectile dysfunction), impaired downgaze or central fixed gaze with intact doll’s eyes (supranuclear plasy) suggests progressive supranuclear palsy (along with axial rigidity). If they have a dystonic arm held in a strange posture, it could be corticobasal degeneration (look also for sensory inattention, alien limb phenomena, and myoclonus).

“Examine this patient’s speech”

Note: Dysarthria = difficulty articulating (remember that this can be anything from white matter disease to brain-stem dysfunction to cranial neuropathy, including Guillain-Barré and structural pathology, to neuromuscular junction weakness to facial myopathy). Dysphonia = altered/quiet voice due to vocal cord disease. Dysphasia = dominant higher centre disorder of language.

1) Ask the patient to talk freely e.g. “describe the room” noting the character, content, and fluency. Pseudobulbar palsy is an UMN weakness — spastic dysarthria. Slurring may be due to facial weakness or cerebellar lesions. Bulbar weakness — nasal speech. Extrapyramidal disease — slow, monotonous speech.

2) Test for receptive dysphasia by giving three-stage command.

3) Test for nominal aphasia by asking the patient to name objects.

4) Test cerebellar speech by asking them to say “baby hippopotamus” or “West Register Street” or even “British constitution” if you feel like it. Listen for disordered speech rhythm, scanning, and slurring.

Honours candidates might ask the patient to say “Muh, muh, muh then luh, luh, luh then cuh cuh cuh then guh guh guh” and comment on the area that is affected (muh=lips i.e. facial weakness, luh=tongue i.e. cranial nerve or cerebellar or UMN spasticity, cuh=soft palate, guh=lower pharynx)

“Examine this patient’s cerebellum”

1) Look at their eyes for nystagmus.

2) Ask them to stick their tongue out and move it from side to side: slowed (this could also be due to spasticity however e.g. in pseudobulbar palsy).

3) Again, to test cerebellar speech by asking them to say “baby hippopotamus”, “West Register Street” or “British constitution”. Listen for disordered speech rhythm, scanning, and slurring.

4) In the arm, look for dysdiadochokinesis (the inability to diadochokinese i.e. rapidly alternate hand movements — dysdiadochokinesis is the abnormality, not the test), rebound of outstretched arms pushed downwards (a form of dysmetria), past-pointing on the finger-nose test (also a form of dysmetria).

5) In the legs test heel-shin coordination.

6) Ask the patient to sit up and cross their arms, looking for
truncal ataxia.

7) Ask the patient to walk up and down looking for inability to succeed with heel-toe walking (this could be the only sign in a midline cerebellar vermis lesion), and broad-based, ataxic gait.

Now for honours:

8) If obvious unilateral cerebellar problem, examine cranial nerves V, VII, and VIII for evidence of cerebellopontine angle problem. Check fundi for papilloedema.

9) If evidence of midline lesion (truncal ataxia, poor heel-toe, abnormal speech) comment on the possibility of a midline tumour.

10) Bilateral signs suggest Multiple Sclerosis, Friedreich’s ataxia, alcoholic cerebellar degeneration.

“This patient is having problems walking, please examine their legs”

Immediately start thinking about causes: weakness (upper motor neurone or lower motor neurone or both — motor neurone disease [but never say this in the exam setting — use the euphemism of anterior horn cell disease or degenerative motor neuropathy]), sensory or cerebellar ataxia, Parkinson’s etc.

1) Look around the bed for clues: wheelchair, stick, frame etc. Show sensitivity by citing these items as your reason for not asking the patient to walk.

2) Ask the patient to get up and walk back and forth if they can. Looking for:

•   Parkinson’s (failure of ignition, enlarging steps, shuffling gait, hunched posture, unilateral loss of arm swing, postural instability)

•   Cerebellar ataxia         (inability to succeed with heel-toe walking, and broad-based, ataxic gait)

•   Sensory ataxia             (normal gait with eyes open possibly with foot stamping)

•   UMN weakness and spacticity           (leg extended, toes pointed downwards abduction and circumduction at the hip. So called scissor gait)

•   LMN weakness (high stepping gait is classical of loss of pretibial and peroneal muscle weakness [i.e. foot drop, probably due to L4-L5 or common peroneal nerve lesion]).

•   Proximal myopathy shows as a “waddling gait”

•   Frontal lobe lesions produce an apraxic gait (“feet stuck to floor”)

•   Widespread small vessel cerebrovascular disease can produce the “march en petit pas” gait.

3) Ask the patient to do heel-toe walking (tandem gait). Difficulty with this may illustrate early cerebellar ataxia.

4) Perform Romberg test looking for sensory ataxia. Make sure to start with feet together and let the patient get their bearings before closing their eyes. Do not risk them falling over in the exam — if they can’t do it with eyes open, they certainly can’t do it with eyes closed! If they are unsteady with their eyes open as well as closed, this may indicate cerebellar ataxia.

5) Lie the patient down and get correct exposure (underwear only). Run through standard tone, power, reflexes, coordination, and sensation.

If you suspect cerebellar ataxia or Parkinson’s, run through the relevant examinations. If you suspect UMN lesions, bring out those signs in the general lower limb exam: increased tone, clonus, weakness, hyperreflexia.

If you suspect LMN weakness, try to determine whether or not it is associated with a nerve root or a peripheral nerve and note LMN signs on general examination: wasting, fasciculations, areflexia (remember to test with reinforcement but then have the courage to report reflexes as absent rather than that you “couldn’t get them”), weakness of specific muscles, sensory loss if weakness associated with peripheral nerve lesion.

Proximal weakness (such as a proximal myopathy) may be illustrated by difficulty with standing from sitting.

“Please examine this patient’s cortical function”

1) Run through MMSE. If you don’t know it, learn it! Know what you are actually testing in terms of brain function with each question: orientation in time and place, short term and long term memory, understanding commands both verbal and written, concentration, etc

2) Frontal signs: pout reflex, grasp reflex, palmomental reflex

3) Parietal signs: neglect (clock drawing etc), astereognosis (can’t tell what objects in hand are with eyes shut — carry a 50p coin and a single key), apraxia (inability to perform purposeful movements e.g. comb hair or wave goodbye — this is more specifically ideamotor apraxia) or constructional dyspraxia (inability to copy diagrams — classic of hepatic encephalopathy), prosopagnosia (inability to recognise faces — classic of late Alzheimer’s), agraphia (inability to write), alexia (inability to read), acalcula (inability to do arithmatic).

Neil Eisenstein is a 6th year medical student at Jesus College, Oxford and Dr Martin Turner is a Neurology SpR at the Radcliffe Infirmary.