Examination of Patients with Polyneuropathies
Neuropathy can be suspected in a patient based on the presence of certain symptoms and the pattern of distribution of the neurological deficit. Assessment of the time of disease onset, risk factors, and involvement of other organs and systems can play a key role in establishing the diagnosis. The specificity and sensitivity of individual symptoms in different forms of neuropathy remains relatively low, from 44%-75% depending on etiology, whereas their comprehensive assessment, including vibration sensitivity, has a substantially higher sensitivity of 95%.
Thus, patients with length-dependent neuropathy and involvement of large sensory fibers present with complaints of numbness and unsteady gait. However, with slow progression of the pathological condition, as in cases of hereditary neuropathies, the patient may not be aware of the sensory deficit. Most patients with acquired forms of such neuropathies will present with a clinical picture of distal symmetric neuropathy, accompanied by neuropathic pain in about 1/3 of cases. When motor fibers of peripheral nerves are involved, patients develop muscle atrophy and weakness, and tendon reflexes decrease and disappear.
Patients with involvement of small sensory fibers will mainly present with complaints of neuropathic pain in the arms and legs, while the motor and large sensory fibers of the peripheral nerves are not affected, which manifests as the absence of sensory impairment, muscle weakness, normal tendon reflexes, and no changes on routine EMG.
Neuropathies that are independent of nerve fiber length include multifocal neuropathies, neuronopathies, polyradiculopathies, and polyradiculoneuropathies. Progressive muscle weakness with the development of atrophy, which may be associated with cramps and fasciculations, as well as the absence of sensory impairment, is characteristic of motor neuronopathy. The pattern of distribution of muscle weakness and the course of the disease depend on the cause of the pathological condition. Hereditary forms are typically characterized by symmetric weakness predominating in proximal muscle groups. Motor neuronopathies of infectious or degenerative origin usually begin focally, and the addition of upper motor neuron signs to the clinical picture should raise suspicion of ALS.
At first glance, sensory neuropathies may appear to have a length-dependent pattern, since such a prominent symptom as sensory ataxia is common to all sensory neuropathies. However, if sensory disturbances first appeared in the hands and then in the legs, such an onset, atypical for length-dependent neuropathies, suggests a different origin of the disease. An atypical pattern — patchy numbness in the hands, trunk, or head — should also raise suspicion of a sensory neuropathy. Multifocal neuropathies are characterized by asymmetric, stepwise development of neurological deficit and are more often suspected based on the results of neurophysiological testing rather than the clinical picture. The differential diagnosis includes polyradiculopathies, the onset of motor neuron disease, and others.
Assessment of the autonomic status of a patient with unexplained neuropathy should include examination of pupillary reactions, salivary and lacrimal gland function, sweating, poor tolerance of increased ambient temperature, gastrointestinal disturbances (nausea, vomiting, early satiety, abdominal pain, alternating constipation and diarrhea), and increased urinary frequency.
The presence of acute neuropathic pain with the simultaneous development of a profound motor deficit (plegia) limited to the innervation zone of a single nerve should raise suspicion of the phenomenon of focal constriction of the peripheral nerve of the "hourglass" type, especially if it affects such vulnerable areas as the anterior and posterior interosseous nerves and the radial nerve. The development of unilateral pain, more often in the shoulder girdle region, followed by delayed motor and sensory deficit in this area, is a characteristic clinical feature of Parsonage-Turner neuralgic amyotrophy. In this symptom complex, differential diagnosis with compressive neuropathies and radiculoischemia is especially important.
Thus, despite improvements in instrumental diagnostic methods, a thorough neurological examination of patients with suspected polyneuropathy has high sensitivity.
Text author: Dmitry Druzhinin, MD, Doctor of Medical Sciences
