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Vibration Sense (vibration + sense)
Selected AbstractsThe value of the Rydel-Seiffer tuning fork as a predictor of diabetic polyneuropathy compared with a neurothesiometerDIABETIC MEDICINE, Issue 6 2004T. Kästenbauer Abstract Aims The aim of the study was to investigate the predictive value of the Rydel-Seiffer tuning fork for detecting diabetic neuropathy and to compare it with an electronic neurothesiometer. Methods In 2022 consecutive diabetic subjects, peripheral polyneuropathy was diagnosed by vibration perception threshold (VPT) at the tip of both great toes using a 128-Hz tuning fork and a neurothesiometer, by simple bedside tests and by the presence of neuropathic symptoms. These evaluations were further combined to diagnose peripheral nerve dysfunction (abnormal bedside tests) and symptomatic neuropathy. VPT was also measured in 175 non-diabetic control subjects to define normal values. Results VPT was normal in 1917 subjects and abnormal in 105 (5.2%) patients when measured by the tuning fork. Patients with an abnormal vibration test were significantly (P < 0.0001) older than subjects with a normal vibration sense, while diabetes duration and HbA1c of the former were also significantly elevated. The same was true for the percentages of an abnormal 10-g monofilament test (66.7% vs. 7.2%, P < 0.0001) and a missing Achilles' tendon reflex (68.6% vs. 24.8%, P < 0.0001). Finally, the VPT measured by the neurothesiometer was 2.5 times higher in patients with an abnormal tuning fork test (32.0 ± 9.8 vs. 12.5 ± 6.4 V, P < 0.0001). The plot of the difference of both methods against their mean yielded a good agreement of the two VPT measurements, and the tuning fork had a high sensitivity and positive predictive value for the diagnosis of abnormal bedside tests and for symptomatic neuropathy. Conclusion The tuning fork reliably detected peripheral neuropathy in comparison with the neurothesiometer. A tuning fork is a useful screening test for diabetic neuropathy. [source] A population-based intervention study on elevated serum levels of methylmalonic acid and total homocysteine in elderly people: results after 36 months of follow-upJOURNAL OF INTERNAL MEDICINE, Issue 5 2004K. Björkegren Abstract. Objectives., To study the effects of vitamin B12 and folic acid treatment on haematological measures, reported symptoms and clinical findings over a 3-year period. Design., A longitudinal two-cohort study. Setting., A mid-Swedish community. Subjects., A 20% random sample of persons 70 years or older in a defined geographical area were invited to a survey (n = 266). Sixty-nine persons who had serum cobalamin <300 pmol L,1 and serum methylmalonic acid (MMA) ,0.37 ,mol L,1 or serum total homocysteine (tHcy) ,15 ,mol L,1 and who had no vitamin B12 or folic acid substitution were selected for treatment. Main outcome measures., Serum cobalamin, folate, MMA and tHcy. Presence of gastrointestinal, neurological, psychiatric and some other symptoms, obtained by questionnaire, and Mini Mental State Examination (MMSE) score, vibration sense measurement and findings at a physical examination. Results., After combined vitamin B12,folic acid treatment, all persons normalized their serum tHcy and MMA levels and the effect remained after 3 years. The study design allowed separation of pure vitamin B12 deficiencies from folate and combined deficiencies. There was a tendency towards improvement of vibration sense, especially in the long nerve paths, and improvement of neurological symptoms and oral mucosa findings. No improvement was seen for other symptoms, reflex activity or MMSE score. Conclusions., Vitamin treatment of elderly people in the early phase of the condition may reverse damage that otherwise would become irreversible. If initiated, the treatment should be combined with vitamin B12 and folic acid. [source] AUTOMIC FAILURE AND NORMAL PRESSURE HYDROCEPHALUS IN A PATIENT WITH CHRONIC DEMYELINATING INFLAMMATORY NEUROPATHYJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002M. Laurà A 75-year-old man with HCV hepatitis developed at the age of 70 presented with rest and action tremor localized at both hands and progressive cognitive impairment with memory loss. Four years later he begun to complain of progressive fatigue, occasional falls, numbness at the extremities and orthostatic hypotension. One month after admission, he rapidly worsened with inability to walk, mainly because of autonomic failure. Neurological examination revealed gait disturbances, including a wide base of support and short stride, slurred speech, reduction of upward gaze, rest and action tremor at both hands, intrinsic hand muscle and anterior tibialis muscle wasting and weakness on both sides, absent deep tendon reflexes, loss of vibration sense at lower limbs, and bilateral pes cavus. Routine laboratory studies, autoantibodies, thyroid function, neoplastic markers and immunoelectrophoresis were normal. Cryoglobulins were absent, whereas CSF protein content was increased (142 mg/dl). Autonomic nervous system investigation detected severe orthostatic hypotension. Nerve conduction studies showed absent sensory potentials and a marked reduction of compound motor action potential amplitudes and of motor conduction velocities. A sural nerve biopsy revealed remarkable onion bulb-like changes, endoneurial and perivascular infiltrations of inflammatory cells. Psychometric tests showed mild cognitive impairment. Brain MRI was consistent with normotensive hydrocephalus. The findings indicated the presence of chronic inflammatory demyelinating polyneuropathy, autonomic nervous system involvement and normal pressure hydrocephalus. A condition of multiple system atrophy (MSA) might be taken into account, even if somatic peripheral nerve involvement may rarely occur in MSA. Moreover the normal pressure hydrocephalus could be due to the high protein content in CSF (Fukatsu R et al., 1997). [source] Mutations in PEX10 are a cause of autosomal recessive ataxiaANNALS OF NEUROLOGY, Issue 2 2010Luc Régal MD Peroxisomal biogenesis disorders typically cause severe multisystem disease and early death. We describe a child and an adult of normal intelligence with progressive ataxia, axonal motor neuropathy, and decreased vibration sense. Both patients had marked cerebellar atrophy. Peroxisomal studies revealed a peroxisomal biogenesis disorder. Two mutations in PEX10 were found in the child, c.992G>A (novel) and c.764_765insA, and in the adult, c.2T>C (novel) and c.790C>T. Transfection with wild-type PEX10 corrected the fibroblast phenotype. Bile acid supplements and dietary restriction of phytanic acid were started. Peroxisomal biogenesis disorders should be considered in the differential diagnosis of autosomal recessive ataxia. ANN NEUROL 2010;68:259,263 [source] Neuromuscular involvement in various types of Ehlers,Danlos syndrome,ANNALS OF NEUROLOGY, Issue 6 2009Nicol C. Voermans MD Objective Ehlers,Danlos syndrome (EDS) is a clinically and genetically heterogeneous group of heritable connective tissue disorders characterized by joint hypermobility, skin hyperextensibility, and tissue fragility. Muscle involvement is plausible based on recently discovered interactions between muscle cells and extracellular matrix molecules; however, muscle symptoms are only sporadically reported. We designed a cross-sectional study to find out whether neuromuscular features are part of EDS. Methods Standardized questionnaires, physical examination, nerve conduction studies, electromyography, muscle ultrasound, and muscle biopsy were performed in 40 EDS patients with the vascular, classic, tenascin-X (TNX),deficient type EDS, and hypermobility type of EDS caused by TNXB haploinsufficiency. Results Muscle weakness, myalgia, and easy fatigability were reported by the majority of patients. Mild-to-moderate muscle weakness (85%) and reduction of vibration sense (60%) were common. Nerve conduction studies demonstrated axonal polyneuropathy in five patients (13%). Needle electromyography myopathic features in nine patients (26%) and a mixed neurogenic-myopathic pattern in most (60%). Muscle ultrasound showed increased echo-intensity (48%) and atrophy (50%). Mild myopathic features were seen on muscle biopsy of five patients (28%). Overall, patients with the hypermobility type EDS caused by TNXB haploinsufficiency were least affected. Interpretation Mild-to-moderate neuromuscular involvement is common in various types of EDS, with a remarkable relation between residual TNX level and degree of neuromuscular involvement, compatible with a dose,effect relation. The findings of this study should increase awareness of neuromuscular symptoms in EDS patients and improve clinical care. They also point to a role of the extracellular matrix in muscle and peripheral nerve function. This is an updated version of this article that originally published online on June 29, 2009. Ann Neurol 2009;65:687,697 [source] Ataxia with vitamin E deficiency in southeast Norway, case reportACTA NEUROLOGICA SCANDINAVICA, Issue 2009J. Koht Background,, Ataxia with vitamin E deficiency (AVED) is a rare cause of hereditary ataxia in north European countries with unknown prevalence. Few cases are reported from these countries. Methods ,Through a systematic population based study of hereditary ataxia in southeast Norway subjects were classified and investigated. Aims , To report a subject with ataxia due to vitamin E deficiency in Norway. Results , One patient with AVED was identified. The subject was a 45 years old woman with progressive ataxia from preschool age. When she was 12 years old Friedreich's ataxia was diagnosed after neurological examination. At the age of 45 re-evaluation and re-examination was performed and genetic analysis of the Frataxin gene was negative. At that time she had truncal and extremities ataxia, titubation of the head, pes cavus, inverted plantar response, loss of proprioceptive and vibration sense and a severe sensory neuropathy. Vitamin E in serum was undetectable and genetic analysis detected a compound heterozygous mutation, p.A120T and p.R134X, in the ,-tocopherol transport protein gene on chromosome 8q13. Discussion , Vitamin E should always be assessed in progressive ataxia of genetic or unexplained causes and especially with a Friedreich's ataxia-like phenotype since treatment is available. Conclusion,, AVED is rare in Norway, but exists, and we here report the first genetically confirmed subject with ataxia due to vitamin E deficiency in Norway. [source] Long-term neurologic and peripheral vascular toxicity after chemotherapy treatment of testicular cancer,CANCER, Issue 10 2010Jennifer L Glendenning MD Abstract BACKGROUND: Testicular cancer is curable in the majority of men, and persisting treatment toxicity is a concern. The authors report a cross-sectional study of the long-term effects of chemotherapy (C) on neurologic function and development of Raynaud phenomenon. METHODS: Seven hundred thirty-nine patients who were treated between 1982 and 1992 gave consent to enter the study. Patients were classified according to the receipt of C (n = 384) or no C (n = 355). Patients completed a general health questionnaire and a quality-of-life form (the European Organization for Research and Treatment of Cancer Quality-of-Life C30 questionnaire with testicular module). Symptom scores of 3 or 4 were considered clinically significant. Patients were assessed in the clinic, and clinical history was used to diagnose Raynaud phenomenon (RP) and tinnitus. Examinations included peripheral nerve function testing for light touch and vibration sense. Five hundred seventy-seven patients underwent audiometry. RESULTS: On physician assessment, peripheral neuropathy and RP were more common after C (21.7% vs 9.1% [P<.001] and 20.3% vs 1.7% [P<.001], respectively). Similar results were obtained for symptom scores (12.5% vs 5.5% [P = .002] and 9.7% vs 3.7% [P<.001], respectively). On multivariate analysis, for peripheral neuropathy, the significant predictors were cisplatin dose, carboplatin dose, and age. For RP, the significant predictor was bleomycin. Significant differences in hearing thresholds were noted at 8000 hertz only and, on multivariate analysis, were related to age, cisplatin dose, and vincristine dose. Auditory symptom scores did not differ between groups. CONCLUSIONS: With long-term follow-up, peripheral neuropathy and RP remained detectable in approximately 20% of patients and caused significant symptoms in 10% of patients. Detectable effects on high frequency remained but caused little symptomatic problem. These effects persisted and were related to the cumulative chemotherapy dose. Cancer 2010. © 2010 American Cancer Society. [source] | ||||||||||