Peripheral neuropathy and multiple myeloma in aging: a case report

A 67-year-old man affected by moderate weight loss, acral paresthesia and plantar burning sensation was admitted to our department. Electromyographic (EMG) and electroneurographic (ENG) studies confirmed a peripheral, asymmetrical, motor-sensorial polyneuropathy (PPN). Hematological data and bone marrow biopsy discovered a non-secerning multiple myeloma (MM). All other probable causes of peripheral neuropathy could be excluded, and the possible relationship between nerve damage and neoplasia was confirmed. Furthermore, all possibilities of association of MM with PPn, namely the osteosclerotic variant, the Crow-Fukase syndrome, and the amyloid one have been evaluated. The only finding of osteolytic bone areas by radiology, the absence of organomegaly, diabetes mellitus, skin alterations, and of amyloid deposition in muscles and nerves, exclude the possible connection of the case to any of the listed possibilities. On the other hand, some clinical aspects differ, in part, to others described in the literature. In conclusion, the association between PPN and MM as the result of multiform clinical variants could be considered.     

Peripheral neuropathy in the elderly

Peripheral neurologic deficits are commonly found during physical examination of older patients. Losses of vibratory sensation in the lower extremities and ankle reflexes are so common that they are often listed in geriatric textbooks as normal physical findings in very old people. In this population, the detection of peripheral neuropathy, which may lead to a serious disability, is an important contribution to the health care but there is very little information in the literature about its actual prevalence and etiology. The epidemiological, clinical, morphological, electrophysiological data on the peripheral nervous system abnormalities in elderly are reviewed. A strategy of investigations is proposed to improve the identification of the etiology of their peripheral neuropathy.     

Peripheral neuropathy associated with ethambutol

A woman developed peripheral neuropathy and optic neuritis while receiving ethambutol in the retreatment of drug-resistant pulmonary tuberculosis. There was prompt improvement in peripheral neuropathy and the ocular symptoms following the withdrawal of the drug. The clinical events in this case suggest that occasionally symptoms of peripheral neuropathy may precede the development of optic neuritis by several months, and thus serve as a warning for the subsequent development of the more serious visual toxicity.     

Peripheral neuropathy in liver cirrhosis

BACKGROUND AND AIMS: Neuropathy in association with chronic liver disease, including cirrhosis, is recognized; however, there are differences in the incidence and type of neuropathy reported. The causal relationship of liver disease to neuropathy has been questioned. This study was designed to evaluate the incidence and character of peripheral neuropathy in patients with liver cirrhosis. The effect of alcohol consumption, severity of liver disease and encephalopathy on the incidence and severity of neuropathy were also studied. METHODS: Patients having an identifiable cause of peripheral neuropathy, except alcohol, were excluded from the study. Patients with evidence of vitamin B12 deficiency or diabetes were also excluded from the study. In this study, 33 patients with liver cirrhosis were evaluated clinically and electrophysiologically to detect any evidence of peripheral neuropathy. Nerve conduction studies were performed in the upper and lower limbs using surface electrodes. These patients also underwent a detailed clinical examination. RESULTS: Clinical signs of peripheral neuropathy were found in seven (21%) patients. Nerve conduction studies were abnormal in 24 (73%) patients. The pattern of involvement was predominantly of an axonal sensory motor polyneuropathy. Neuropathy was found both in patients with alcohol-related and non-alcohol-related cirrhosis. The presence of encephalopathy did not have a significant bearing on the incidence and severity of neuropathy. The neuropathy was also not significantly related to the severity of liver disease. CONCLUSIONS: The present study reveals that a significant number of patients with liver cirrhosis show evidence of peripheral neuropathy, which is present regardless of the etiology of cirrhosis, and is subclinical in a majority of these patients. The cause of neuropathy was probably the liver disease itself, as the incidence and severity of neuropathy in the alcohol-related cirrhosis, although higher, was not significantly different from the neuropathy in patients with non-alcohol-related cirrhosis.     

Peripheral neuropathy in tropical pancreatic diabetes

Summary Electrophysiological evaluation of peripheral neuropathy was done in 16 patients with tropical pancreatic diabetes (TPD) and the data compared with those of a matched group of 16 NIDDM patients. Peripheral neuropathy was present in 6 TPD and 5 NIDDM patients. Abnormal motor conduction velocity in the lateral popliteal nerve was seen in 9 TPD patients and in 8 NIDDM patients and biothesiometry was abnormal in 7 patients in each group. One TPD patient had an abnormal F wave in the lower limb. An abnormal sensory potential was recorded in the sural nerve in 6 TPD and 8 NIDDM patients. The study showed that occurrence of peripheral neuropathy in TPD was similar to that in NIDDM. Subclinical neuropathy could be detected by electromyographic recording in both groups of patients.     

Peripheral neuropathy associated with temporal arteritis

Peripheral neuropathy is described in a patient with biopsy proven giant cell arteritis. Sural nerve biopsy showed myelin and axonal degeneration. Such an uncommon manifestation was resolved with corticosteroid therapy.     

Peripheral neuropathy in patients on leflunomide

SIR, Much progress has been made in understanding the pathogenesisof rheumatoid arthritis. This has resulted in the developmentof novel therapeutic strategies. Leflunomide is a disease-modifyinganti-rheumatic drug (DMARD) which is in vogue all over the world.The active metabolite of leflunomide, A77 1726, reversibly inhibitsdihydroorotate dehydrogenase (DHODH), the rate-limiting stepin the de novo synthesis of pyrimidines [1]. The side-effects     

Peripheral neuropathy in prediabetes and the metabolic syndrome

Peripheral neuropathy is a major cause of disability worldwide. Diabetes is the most common cause of neuropathy, accounting for 50% of cases. Over half of people with diabetes develop neuropathy, and diabetic peripheral neuropathy (DPN) is a major cause of reduced quality of life due to pain, sensory loss, gait instability, fall‐related injury, and foot ulceration and amputation. Most patients with non‐diabetic neuropathy have cryptogenic sensory peripheral neuropathy (CSPN). A growing body of literature links prediabetes, obesity and metabolic syndrome to the risk of both DPN and CSPN. This association might be particularly strong in type 2 diabetes patients. There are no effective medical treatments for CSPN or DPN, and aggressive glycemic control is an effective approach to neuropathy risk reduction only in type 1 diabetes. Several studies suggest lifestyle‐based treatments that integrate dietary counseling with exercise might be a promising therapeutic approach to early DPN in type 2 diabetes and CSPN associated with prediabetes, obesity and metabolic syndrome.