Polyneuropathy in elderly patients

Polyneuropathies comprise an extremely complex and heterogeneous group of peripheral nervous system syndromes, the progress of both diagnostic and therapeutic approaches against which have advanced in leaps during these last years. The aetiological investigation of polyneuropathies has been rendered now possible, for 87% of the cases, by means of neurophysiology, immunology, neuropathology and molecular genetics. This investigation is imperative, since 1/3 of those cases are observed within immunological disturbances and are effectively managed by administration of steroids, gamma-spherin, plasma-removal and immunosuppressives. The abundance of acquired (non genetic) neuropathies in people over 55 years of age reaches 3%. The lightening speed of invasion is a characteristic of ischemic and diabetic neuropathies. Acute onset (in a matter of days) is typically observed in inflammatory neuropathies and porphyria. Subacute onset (in a matter of weeks or months) is observed in toxic and paraneoplastic neuropathies, whereas, chronic onset (in a matter of years) is observed in genetic neuropathies. Multifocal motor neuropathy exhibits exaltations and remissions, whereas, Guillan-Barre syndrome only rarely remits (3-6%).

In this study we completed a retroactive epidemiological review of twelve patients (at a mean age of 70 years and a male-to-female ratio of 11:1) who demonstrated neurophysiologicaly confirmed polyneuropathy. Most of these patients complained of weakness and numbness of their lower and, to a lesser extent, upper extremities. The most common findings included loss of reflexes, distal symmetrical impairment of epidermal sensation, weakness in the distal parts of the limbs, as well as, significant diminution in vibratory sensation and nerve conduction velocities. Three of the patients (25%) demonstrated a sensory form of polyneuropathy, one (8%) a motor type and the rest (67%) a sensorimotor type of polyneuropathy. Four of the patients (33%) suffered from diabetes mellitus, three (33%) were alcoholic, whereas six (50%) demonstrated anaemia due to vitamin B12 deficiency, two (17%) were symptomatic of renal deficiency, five (41%) of heart problems, one (8%) of hyperthyroidism, one (8%) of Ca (lung) and one patient (8%) who expired during hospitalization due to intestinal perforation. In addition, one patient demonstrated both anaemia and positive Ra-test whereas another increased anti-nuclear antibodies.

Our results indicate that sensorimotor polyneuropathy is the most common type of polyneuropathies in elderly male patients, and it is usually associated with vitamin B12 (cobalamine) deficiency.

The spinal cord, optic nerves and peripheral nerves have been all found to be affected by vitamin B12 deficiency. At first, the patients manifest signs from their peripheral nerves, experiencing paresthesias involving their hands, and even their feet. Later comes the onset of distal and symmetrical impairment of epidermal sensation, more pronounced in the legs, and diminished tendon reflexes. The peripheral nerves may demonstrate a loss of myelin but there is no unequivocal evidence that the axonic fibres are significantly affected. Known pharmacological agents, such as neomycin, colchicine, vinplastine, biguanide, phenobarbitol, primidone and hormonal medication, deplete the stores of B12. Little is known about the exact role of cobalamine in the nervous system or the mechanism of nervous tissue damage in the case of cobalamine deficiency. One of the better understood functions of vitamin B12 is its role as a coenzyme in the methylmalonyl CoA-mutase reaction. A lack or failure of this mutase leads to the accumulation of propionyl CoA, which is the usual primer for the synthesis of even-chain fatty acids and it results in the anomalous insertion of odd-chain fatty acids into membrane lipids, such as myelin sheaths. This biochemical abnormality underlies the lesions of myelinated fibres that characterize the disease.

We believe the presented observations to be in aid in investigating the aetiology, the morphology and even the treatment of polyneuropathy in elderly patients.

Key words: Polyneuropathies, elderly patients, B12 (cobalamine) deficiency.