Gavin Yamey presents a practical approach to a widely feared task Neurology has always had an image problem. It conjures up an arcane world where educated men in bow ties elicit startling diagnoses with a hat pin or a single glance. Lesser mortals can barely pronounce Gerstmann-Sträussler-Scheinker syndrome or Pelizaeus-Merzbacher disease (both true entities, I'm afraid). The result is that when we come to perform a neurological examination ourselves, we feel incompetent and afraid. This article makes only one claim - to give you some guidance through the thorny thicket so that you will hopefully emerge triumphant. Under exam conditions, being polite and courteous to patients will always score highly, so make sure that they are comfortable and always cover them once the exam is over.

Exam technique - the keys are familiarity and repetition

Neurological cases are common in finals, because the signs are striking and static. You will not be asked to examine the entire nervous system. Instead, be prepared to assess cranial nerves, limbs, gait, speech, or higher mental functions. Looking hard before acting may reveal a huge amount (obvious facial palsy? Fasciculations? Walking stick?).
 

Cranial nerves

A cranial nerve examination can be done in under a minute, by practising the routine hundreds of times on family and friends. Any deviation from this routine is usually startling. Always compare left with right.

When you see a sign, it is sometimes hard to remember where the pathology lies. A unilateral palsy of the glossopharyngeal or vagus nerves (IX and X) causes the palate to move away from the affected side when the patient says "Aah." In contrast, a unilateral lesion of the hypoglossal nerve causes the tongue to deviate towards the affected side when it is protruded. So: "Palate away, tongue towards" (fig 1).

Limbs

Examining the limbs is not synonymous with examining the peripheral nervous system, since you will be assessing aspects of both upper and lower motor neurone function. Again, be comparative, so assess tone in one arm, then in the other, before moving on to power.

Gait

Ask the patient to stand with his/her eyes open, then closed, to walk, turn around, walk on his/her heels and then his/her toes. In a spastic gait the patient drags his/her affected leg, with the foot plantar flexed and inverted, and the toes scuffing the ground (fig 2). The Parkinsonian gait is shuffling, with difficulty initiating movements and turning. An ataxic gait is unsteady and broad based, and it can be exaggerated by asking the patient to walk heel-toe as if on a tightrope. The two main causes of gait ataxia are cerebellar disease and sensory loss. In the latter, the patient relies on being able to see and place his feet as s/he walks, since s/he is missing positional feedback. If s/he closes his/her eyes, his/her unsteadiness worsens - this is a positive Romberg's sign. In a foot drop, owing to a lateral popliteal nerve palsy or L5 root lesion, the patient has to lift the affected foot high off the ground, and it returns with a distinctive "slap."

Hypoglossal nerve palsy

Speech

Your routine questions should distinguish between dysphonia (poor voice production), dysarthria (a mechanical disorder of articulation) and dysphasia (a language or communication disorder). Remember that we are all temporarily dysarthric, but not dysphasic, after a visit to the dentist or the pub. Examiners are impressed if you can distinguish between a receptive dysphasia, where comprehension is impaired, and an expressive type where it remains intact, although they usually coexist.

Begin a conversation with your patient, perhaps by asking his/her name and address, and listen for clues. If his/her speech sounds dysarthric, this sign can be exaggerated by asking him/her to say something complicated ("West Register Street"). Next, ask him/her to obey a simple command - which will be difficult if s/he has a receptive dysphasia. A common expressive dysphasia entails difficulty in naming objects (nominal dysphasia), so point to your pen or tie and ask what it is. You can confirm an isolated expressive problem by giving a range of possibilities: "Is it a torch? Is it a hammer? Is it a pen?" and the patient will nod appropriately.

Higher mental functions

In your medical finals, a simple 10 point mental test will suffice. Learn one by heart, and avoid the Queen's name and the world wars, since they are too culturally specific. You may be asked the causes of acute confusion versus chronic cognitive decline (dementia). In psychiatry exams, be prepared to perform a thorough cognitive assessment - you could use the well known 30 point mini mental state examination.

Localisation - keep it simple

The lesion will be in one (or more) of these places: brain, brain stem, spinal cord, nerve roots, peripheral nerves, neuromuscular junction, muscles.

The most important distinction is between upper and lower motor neurone lesions (table). "Upper" refers to the brain, brain stem, and cord, and the rest is "lower". Keep in mind a patient with a stroke as a paradigm of upper motor neurone signs, with weak and stiff limbs down one side, brisk reflexes, and an extensor plantar. This weakness is said to have a pyramidal tract distribution. In the affected arm the flexors are stronger than the extensors, so the stroke patient holds his arm tightly flexed. In the affected leg the converse is true, with stronger extensors causing the leg to be held out straight. Remember that multiple sclerosis is a disease of the brain and cord, so it only produces upper motor neurone signs.
 

As a paradigm of lower motor neurone loss, think of a patient with polio - leading to a wasted, fasciculating, flaccid, weak limb. You can further localise peripheral nerve problems by considering if the signs fit a glove and stocking distribution (a peripheral neuropathy - for example, in diabetes mellitus), a single nerve lesion (a mononeuritis - for example, ulnar nerve palsy) or multiple discrete nerve lesions (mononeuritis multiplex - for example, in a vasculitis).

Mixed upper and lower motor neurone lesions are often the result of problems of the cervical cord (with lower motor neurone signs at the level of the lesion, and upper motor neurone signs below it), or motor neurone disease.

If you suspect a spinal cord lesion, you should try and elicit sensory or motor signs that roughly indicate the level.

You should have a basic idea of the functions of different regions of the brain and the clinical consequences of lesions in each, such as personality change and disinhibition in a frontal lobe syndrome . Cerebellar signs are common in exams, and easy to remember (box).
 

Learn only a few causes - concentrate on common diseases

If asked for the cause of a cranial nerve lesion, don't mention Wegener's granulomatosis first of all. In fact, all cranial nerve lesions can be caused by trauma, tumours, diabetes mellitus, or multiple sclerosis. Most lists of causes can be stripped down in this way.

In your exam, and in clinical practice, you can predict the commonest conditions. Make sure you have examined patients with stroke, multiple sclerosis, Parkinson's disease, dementia, peripheral and cranial nerve lesions.

Finally

For those interested, Gerstmann-Sträussler-Scheinker syndrome is a prion disease, usually familial, and slower in progression than Creutzfeldt-Jakob disease. Pelizaeus-Merzbacher disease (X-linked sudanophilic leukodystrophy) is a hereditary spastic paraparesis. Now strike these from your memory banks, in view of the above.