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Neuropathy Patients (neuropathy + patient)
Selected AbstractsImpairment of cerebral autoregulation in diabetic patients with cardiovascular autonomic neuropathy and orthostatic hypotensionDIABETIC MEDICINE, Issue 2 2003B. N. Mankovsky Abstract Aims Impaired cerebrovascular reactivity and autoregulation has been previously reported in patients with diabetes mellitus. However, the contribution of cardiovascular diabetic autonomic neuropathy and orthostatic hypotension to the pathogenesis of such disturbances is not known. The purpose of this study was to evaluate cerebral blood flow velocity in response to standing in patients with diabetes and cardiovascular autonomic neuropathy with or without orthostatic hypotension. Methods We studied 27 patients with diabetes,eight had cardiovascular autonomic neuropathy and orthostatic hypotension (age 46.4 ± 13.5 years, diabetes duration 25.0 ± 11.0 years), seven had autonomic neuropathy without hypotension (age 47.3 ± 12.7 years, diabetes duration 26.4 ± 12.1 years), and 12 had no evidence of autonomic neuropathy (age 44.1 ± 13.8 years, diabetes duration 17.1 ± 10.2 years),and 12 control subjects (age 42.6 ± 9.7 years). Flow velocity was recorded in the right middle cerebral artery using transcranial Doppler sonography in the supine position and after active standing. Results Cerebral flow velocity in the supine position was not different between the groups studied. Active standing resulted in a significant drop of mean and diastolic flow velocities in autonomic neuropathy patients with orthostatic hypotension, while there were no such changes in the other groups. The relative changes in mean flow velocity 1 min after standing up were ,22.7 ± 16.25% in patients with neuropathy and orthostatic hypotension, +0.02 ± 9.8% in those with neuropathy without hypotension, ,2.8 ± 14.05% in patients without neuropathy, and ,9.2 ± 15.1% in controls. Conclusions Patients with diabetes and cardiovascular autonomic neuropathy with orthostatic hypotension show instability in cerebral blood flow upon active standing, which suggests impaired cerebral autoregulation. [source] Structure Of Campylobacter Jejuni Lipopolysaccharides Determines Antiganglioside Specificity And Clinical Features Of Guillain-Barre, And Miller Fisher PatientsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2002CW Ang Ganglioside mimicry in the lipopolysaccharide (LPS) fraction of Campylobacter jejuni isolated from Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) patients was compared with isolates from patients with an uncomplicated enteritis. The antibody response to C. jejuni LPS and gangliosides in neuropathy patients and controls was compared as well. LPS from GBS and MFS-associated isolates more frequently contained ganglioside-like epitopes compared to control isolates. Almost all neuropathy patients showed a strong antibody response against LPS and multiple gangliosides in contrast to enteritis patients. Isolates from GBS patients more frequently had a GM1-like epitope than isolates from MFS patients. GQ1b-like epitopes were present in all MFS-associated isolates and was associated with anti-GQ1b antibody reactivity and the presence of oculomotor symptoms. These results demonstrate that the expression of ganglioside mimics is a risk factor for the development of post-Campylobacter neuropathy. This study provides additional evidence for the hypothesis that the LPS fraction determines the antiganglioside specificity and clinical features in post-Campylobacter neuropathy patients. [source] CLINICAL, MRI, AND SKIN BIOPSY FINDINGS IN SENSORY GANGLIONOPATHIESJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000A. Sghirlanzoni Unlike peripheral motor disorders, sensory disturbances are rarely diagnosed by the probable site of pathology. This approach is useful in the differential diagnosis between chronic sensory axonal neuropathies and ganglionopathies, in which routine clinical and neurophysiological evaluation alone often do not provide definite clues. Methods: Thirty patients with peripheral sensory disturbances were investigated. MRI was performed at cervical level in all cases. Four patients also underwent thoracic and lumbar MRI. Seventeen patients underwent skin biopsy at the proximal thigh and the distal leg. In 4 of them, further skin biopsies were taken at C5 dermatome and at the hand. Density of intra-epidermal nerve fibers (IENF) was quantified. Results: In 22 patients, sensory ganglionopathy was suspected. Disease was idiopathic in 7 cases; paraneoplastic in 3 cases; and associated with Sjögren, AIDS, autoimmune chronic hepatitis, and cisplatin neurotoxicity in 4 cases. One patient had a hereditary sensory autonomic neuropathy. Four patients had vitamin E deficiency and 3 patients a spinocerebellar syndrome. In 8 patients, sensory axonal neuropathy related to diabetes, alcoholism, and AIDS on antiretroviral treatment, and monoclonal gammopathy of undetermined significance was diagnosed. MRI findings: All ganglionopathy patients showed posterior columns hyperintensity on T2-weighted MRI. Conversely, MRI was negative in all axonal sensory neuropathy patients. Skin biopsy findings: In neuropathies, IENF density was significantly lower at the distal leg than at the proximal thigh, while ganglionopathies did not show any change with respect to the rostral:caudal orientation. A similar pattern of epidermal denervation was observed in the arm. Discussion: The degeneration of both central and peripheral sensory pathway in a fashion that is not length-dependent localizes the disease to T-shaped sensory neurons Early ataxia and cutaneous sensory symptoms involving the proximal regions of the body reflect this pattern of denervation and should prompt the diagnosis of ganglionopathy. This can be confirmed by T2-weighted hyperintensity in the posterior columns and a distinct pattern of IENF loss. [source] | ||||||||||