Peripheral neuropathies I: Clinical approach and investigations

Published on 10/04/2015 by admin

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Last modified 10/04/2015

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Peripheral neuropathies I

Clinical approach and investigations

Peripheral neuropathies are very variable, both in their clinical manifestations and in their aetiology (Table 1). These three sections give an overview of peripheral nerve disease, with the third concentrating on the common isolated peripheral nerve lesions.

Table 1 Relationship of presentation of neuropathy to aetiology

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Pathology

Peripheral nerves can be affected in three ways (Fig. 1). These mechanisms of injury are not mutually exclusive and in some conditions there are contributions from all three mechanisms:

1. Axonal degeneration.
2. Demyelination.
3. Vascular nerve damage.
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Fig. 1 Effects on peripheral nerve conduction of common neuropathies. (a) Normal; (b) axonal degeneration; (c) demyelination; (d) vascular lesion.

Axonal degeneration

The axon degenerates as a result of many different toxic, metabolic, nutritional and physical (such as cold or trauma) insults and in genetic conditions. The longest axons are most severely affected. These changes result in distal weakness, wasting or sensory loss depending on the involvement of motor and sensory fibres. If the neurone remains intact and the pathological process is reversed, there is scope for regeneration. If the neurone is lost, there is no scope for regeneration.

Demyelination

In this process, the myelin is lost but the axon is preserved. The demyelination prevents conduction and produces weakness but not wasting. Repair of demyelination, remyelination, can be quick. Many demyelinating neuropathies also have some associated axonal degeneration. Demyelination can occur in inflammatory diseases, when it tends to be patchy, and in inherited or metabolic neuropathies, when it tends to be uniform.

Vascular nerve damage

The blood supply to peripheral nerves can be disrupted, producing infarcts of peripheral nerves. This then produces isolated axonal degeneration in the axons distal to the site of infarct. This usually occurs with vasculitic illness.

Clinical features

Peripheral neuropathies can be sensory or motor, though usually there is a combination with one predominant. The clinical features depend on the underlying pathological process and the speed of onset. Axonal neuropathies result in wasting of muscles with loss of distal tendon reflexes. Demyelinating neuropathies are not associated with muscle wasting, but usually there is areflexia. In some types of neuropathy, the autonomic nervous system can also be affected.

There are four patterns of clinical presentation of peripheral nerve disease (Fig. 2):

1. Distal symmetrical neuropathy. This is the most common presentation of axonal neuropathies. There is distal sensory and motor dysfunction, affecting the legs more than the arms; sensory changes in the hands are noted when sensory changes in the legs get to the knees.
2. Multifocal neuropathies. There is an asymmetrical involvement, without involving specifically named nerves. This is usually the presentation of demyelinating or vasculitic neuropathies.
3. Mononeuropathies. The involvement of an individual named nerve. The most commonly affected nerves are described on page 106.
4. Mononeuritis multiplex.

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