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Query: UMLS:C0848771 (neurological disability)
 928 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with peripheral neuropathy and a solitary plasmacytoma are presented, and the literature is reviewed. It is suggested that middle-aged men with an obscure progressive sensorimotor neuropathy, a raised CSF protein, and otherwise negative investigations should have a full skeletal survey since irradiation of a plasmacytoma may lead to a considerable improvement in the associated neurological disability.
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PMID:Peripheral neuropathy and solitary plasmacytoma. 20 45

The effect of retrograde axonal transport of doses of acrylamide ranging from 50 to 500 mg/kg was studied in sensory nerve of rats. Accumulation of trichloroacetic acid-phosphotungstic acid-insoluble label was measured in a collection segment distal to a double ligature placed on the sciatic nerve at intervals 9-15 h and 9-24 h following injection into the dorsal root ganglion of the fifth lumbar root of [35S]methionine and [3H]fucose. After a dose of 100 mg/kg of acrylamide no neurological signs of neuropathy had yet appeared, but retrograde buildup of protein label was significantly reduced for the long interval (2.20 +/- 0.49 arbitrary units (AU) (mean +/- SD) versus 2.81 +/- 0.57 AU in controls, 2p = 0.034). No abnormality of the short interval appeared before a dose of 500 mg/kg was reached. The retrograde transport abnormality was dose-related (r = -0.85, n = 28, and 2p = 1.2 x 10(-8)), as was the degree of neuropathy evaluated by "blind" neurological scoring (r = 0.88, n = 14, and 2p = 2.8 x 10(-5)). After a dose of 500 mg/kg, when the rats were severely disabled with almost total incoordination of the hindlegs, the retrograde accumulation of the long interval was profoundly depressed (1.08 +/- 0.28 AU versus 2.81 +/- 0.57 AU in controls, 2p = 1.2 x 10(-7)). Similar changes were seen in accumulation of glycoprotein label. After the rats had recovered for 4-10 weeks neurological signs of neuropathy had disappeared and the transport abnormality had improved. To test the specificity of acrylamide on the retrograde transport defect N-hydroxymethylacrylamide and methylene-bisacrylamide, which do not induce neuropathy, were studied. None of these related compounds influenced the transport. These observations imply that in acrylamide intoxication a defect in the amount of material carried by retrograde axonal transport rather than in "turnaround" time or in transport velocity is present, that the transport abnormality precedes the development of neuropathy, and that it is related to the degree of the neurological disability. We suggest that the retention of protein in the distal axons in the functional counterpart of the well-known accumulation of vesicular organelles in the preterminals.
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PMID:Early and dose-dependent decrease of retrograde axonal transport in acrylamide-intoxicated rats. 618 37

Peripheral neuropathies constitute an important cause of neurological disability in the tropics. The clinical manifestations of tropical peripheral neuropathies are identical to those observed by neurologists elsewhere and their aetiologies are also similar. However, the frequency of occurrence, or prevalence, of the different types of neuropathy is clearly different from that observed in developed nations, ranging from epidemic outbreaks of optic and peripheral sensory neuropathy caused by malnutrition--such as in the outbreak recently observed in Cuba--to the endemic problems of leprosy and HTLV-1 infection. A large variety of plant and animal poisons and industrial neurotoxins frequently affect the peripheral nervous system in warm climates. In addition to their public health importance, tropical neuropathies constitute unexplored natural models of disease worthy of clinical and laboratory studies.
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PMID:Tropical neuropathies. 859 21

The isokinetic muscle strength in 56 IDDM patients with > 20 years of diabetes duration and in their individually sex-, age-, weight-, and height-matched control subjects was assessed. Peak torque of foot dorsal and plantar flexion and knee and wrist extension and flexion was measured. The neuropathic condition was assessed by a neurological disability score, a neuropathy symptom score, nerve conduction studies, and quantitative sensory examination. All results were summed to obtain a neuropathy rank-sum score for each patient. According to their renal albumin excretion, the patients were classified to have normo-, micro-, or macroalbuminuria. In addition, according to their retinal status, patients were classified as having no, simple, or proliferative retinopathy. The IDDM patients had a 21% reduction of muscle strength of both ankle dorsal (P < 1 x 10(-4)) and plantar flexors (P < 0.01), compared with control subjects. A 16% reduction of knee extensors (P < 0.005) and a 17% reduction of knee flexors (P < 0.01) was found. In contrast, muscle strength in wrist flexors and extensors was not significantly reduced (10 and 11%, respectively [NS]). In patients with the most severe weakness, muscle strength of the calf muscles was only 50% of the expected performance. Correlations were found between the neuropathy rank-sum score and the muscle strength of ankle dorsal (r = -0.66, P < 1 x 10(-7)) and plantar flexors (r = -0.51, P < 0.0005), knee extensors (r = -0.51, P < 0.0005) and flexors (r = -0.44, P < 0.005), and wrist flexors (r = -0.41, P < 0.005). No correlation was found for wrist extensors (r = 0). Neither were there any relationships between muscle strength at the ankle and knee and the degree of albuminuria or retinopathy. In conclusion, motor performance is substantially impaired in long-term IDDM patients, and the weakness is related to the presence of neuropathy but not to albuminuria or retinopathy per se.
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PMID:Isokinetic muscle strength in long-term IDDM patients in relation to diabetic complications. 860 65

In contradistinction to older populations, immune-mediated disorders (principally demyelinating processes) account for nearly half of peripheral neuropathies in childhood. The largest single diagnostic entity is GBS, which makes up approximately 25% of sensorimotor neuropathies in patients under 18 years of age. The clinical features are similar to those encountered in adults, although the prognosis in youngsters appears to be better than in older populations. Despite the absence of prospective data, plasmapheresis seems to be an effective modality for hastening recovery during GBS in children. The use of human immunoglobulin has gained acceptance for the treatment of GBS in adults, but insufficient data exist to draw firm conclusions about it role in the management of paediatric GBS. CIDP is the second most common cause of chronic sensorimotor neuropathy in children. The clinical manifestations of this disorder are extremely variable, and it can mimic the phenotype of several genetically determined neuropathies. The prognosis in this disorder is also relatively good, although a small number of children have significant neurological disability or treatment side-effects. Other immune-mediated neuropathies are relatively infrequent in our experience. When they occur, they are often associated with collagen-vascular diseases or bone marrow transplantation. Peripheral neuropathy in association with HIV infection in children appears to be rare.
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PMID:Immune neuropathies in childhood. 873 10

In order to evaluate the clinical and prognostic role of common neurophysiological parameters, we examined 114 patients selected from a population of 2500 diabetics, observed in the period 1973-1986. The follow-up lasted 9 to 16 years (mean = 10). For prognostic purposes the patients were divided into 3 groups according to the motor conduction velocity (MCV) of the peroneal nerve: A) 47 cases with normal MCV (more than 44 m/s); B) 38 cases with mild neuropathy (MCV between 44 and 39 m/s); C) 29 cases with severe neuropathy (MCV less than 39 m/s). The natural history was evaluated on the basis of the following parameters: neurological symptom score (NSS), neurological disability score (NDS), patient's self-evaluation (PE) and neurologist's evaluation (ME). At the initial examination, there was a significant correlation between MCV and NDS/ME. At the final examination, MCV was reduced to groups A and B, unchanged in group C. NSS, NDS, PE and ME were worsened, but a significant correlation was found only between MCV and NDS: neuropathic groups (B and C) showed a more severe evolution than the normal group (A). In conclusion, a) MCV is progressively reduced as diabetes evolves, but--once it has reached a plateau--it stabilizes; b) MCV only has a prognostic value when it is considered together with clinical neurological signs.
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PMID:Conduction studies as prognostic parameters in the natural history of diabetic neuropathy: a long-term follow-up of 114 patients. 878 31

Peripheral nervous system disorders in COPD (chronic obstructive pulmonary disease) have been found more frequently than usual neurologic practice. We planned this prospective clinical and electrophysiological study to determine the incidence and characteristics of neuropathy in patients with COPD. We studied 49 patients with COPD in whom other causes of polyneuropathy had been excluded. COPD patients were divided into two groups: 21 hypoxemic and 28 normoxemic. Age and sex matched, nonsmoker, 21 healthy subjects were included as the control group. We investigated the results of clinical (neurological symptom score-NSS, neurological disability score-NDS and vibration perception thresholds- VPT) and neurophysiological evaluations in COPD patients and the control group. A value over the mean +/- 2.5 SD of control group were accepted pathologic. NSS results were pathologic in 34% of COPD patients, NDS in 42% and VPT in 94%. Carpal tunnel syndrome was found in 24% of the patients, neuropathy in 55%, and polyneuropathy in 44.8%. In conclusion, the incidence of neuropathy was more than expected, the rate of axonal neuropathy was significantly higher in the hypoxemic group than normoxemic group and the severity of neuropathy was correlated with the degree of hypoxemia.
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PMID:Subclinical peripheral neuropathy associated with chronic obstructive pulmonary disease. 1140 11

The aim of this study was to determine the prevalence and risk factors for neuropathy in type 2 diabetic patients attending a major Turkish diabetes center. Eight hundred and sixty-six consecutive type 2 diabetic patients were included in the study. A single observer performed biothesiometry studies on these patients. The presence of diabetic neuropathy was investigated using neurological symptom scale (NSS) and neurological disability score (NDS) performed. Neuropathy was determined with standardized neurological examinations and defined as the presence of abnormal NSS and NDS together with abnormal sensory or motor signs and symptoms as well as decreased great toe vibration perception. Overall, 60% (n = 520) of the patients were diagnosed as having neuropathy. The prevalence of neuropathy increased with age (p < 0.001) and duration of diabetes (p < 0.001). Multiple logistic regression analysis revealed the duration of diabetes (p < 0.001) and HbA1c levels (p < 0.001) as the risk factors for neuropathy. The overall prevalence of neuropathy in Turkish type 2 diabetic population was 60%. Age, duration of diabetes, and poor glycemic control were considered to be the risk factors for neuropathy.
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PMID:Prevalence of peripheral neuropathy in type 2 diabetic patients attending a diabetes center in Turkey. 1564 75

The aim of the study was to determine the progression of muscle weakness in long-term diabetes and its relation to the neuropathic condition. Thirty patients were recruited from a cohort of 92 diabetic patients who participated in a study on muscular function 6-8 years earlier. Nine subjects were nonneuropathic, 9 had asymptomatic neuropathy, and 12 had symptomatic neuropathy. Thirty matched control subjects who participated in the initial studies were also included. At follow-up, isokinetic dynamometry at the ankle, electrophysiological studies, vibratory perception thresholds, and clinical examination (neuropathy symptom score and neurological disability score [NDS]) were repeated. The annual decline of strength at the ankle was 0.7 +/- 1.7% in control subjects, 0.9 +/- 1.9% in nonneuropathic patients, 0.7 +/- 3.1% in asymptomatic neuropathic patients, and 3.2 +/- 2.3% in symptomatic neuropathic patients. In the symptomatic patients, the decline of muscle strength at the ankle was significant when compared with matched control subjects (P = 0.002) and with the other diabetic groups (P = 0.023). Also, the annual decline of muscle strength at the ankle was related to the combined score of all measures of neuropathy (r = -0.42, P = 0.03) and to the NDS (r = -0.52, P = 0.01). In patients with symptomatic diabetic neuropathy, weakness of ankle plantar and dorsal flexors is progressive and related to the severity of neuropathy.
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PMID:Muscle weakness: a progressive late complication in diabetic distal symmetric polyneuropathy. 1650 47

Obstructive sleep apnoea (OSA) has previously been described in a large family suffering from Charcot-Marie-Tooth disease type 1 (CMT1). In the present study, we used a case control design to establish whether this suggested link between OSA and CMT1 may also be found when studying genetically non-related patients. 12 patients with CMT1 and 24 control patients matched for age, sex and body mass index (BMI) were included in the study. Neurological disability was graded with a previously established 6 point score. All patients underwent overnight polysomnography. The mean apnoea-hypopnoea index (AHI) of patients with CMT1 was 10.5 (16.3) which was significantly higher than that of the control group (1.5 (1.3)). Five out of 12 patients with CMT1 had an AHI > or =10/h compared with 1 of 24 control patients (p<0.01). In patients with CMT1, a significant correlation between AHI and neurological disability was found (Spearman r = 0.62; p = 0.031) while BMI and age were not related to AHI. CMT1, in particular CMT1A, predisposes with disease progression to the development of OSA. Pathophysiologically, one may assume that CMT1 related pharyngeal neuropathy increases the collapsibility of the upper airway which in turn leads to recurring obstructive respiratory events.
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PMID:Increased prevalence of obstructive sleep apnoea in patients with Charcot-Marie-Tooth disease: a case control study. 1855 57


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