1/9. guillain-barre syndrome occurring in two women after ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus.We report two women who presented with a guillain-barre syndrome just after a ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus. One had characteristic clinical signs and the other had major motor involvement. At neurophysiologic investigations, one had typical demyelinating neuropathy whereas the second had mainly axonal degeneration. At ultrastructural examination of a peripheral nerve biopsy, features of macrophage-associated demyelination were present in both nerve specimens, thus confirming the diagnosis of acute inflammatory demyelinating polyneuropathy, i.e., guillain-barre syndrome. Prominent axonal involvement was also present in the motor nerves of the second patient. insulin therapy had to be permanently continued and these two cases are quite different from the transient diabetes sometimes observed in certain cases of guillain-barre syndrome. Both the latter and insulin-dependent diabetes mellitus probably have auto-immune mechanisms. It is likely that in our two patients both auto-immune diseases were triggered by a common event. Such cases of guillain-barre syndrome have to be distinguished from other acute diabetic neuropathies.- - - - - - - - - - ranking = 1keywords = inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
2/9. Childhood-onset chronic inflammatory demyelinating polyradiculoneuropathy with cranial nerve involvement.A 17-year-old male presented with chronic diplopia and generalized motor weakness. He was previously diagnosed with chronic inflammatory demyelinating polyradiculoneuropathy and acute disseminated encephalomyelitis in childhood. Cranial magnetic resonance imaging (MRI) revealed a rarely reported finding of thickening and enhancement of multiple cranial nerves. Nerve conduction studies and electromyography showed peripheral nerve demyelination with axonal involvement. There was improvement in the clinical examination, MRI, and electrophysiologic studies after combined corticosteroid and plasma exchange therapy. We review the clinical presentation, course, and response to therapy among children with chronic inflammatory demyelinating polyradiculoneuropathy, with specific emphasis on the frequency and pattern of cranial nerve involvement.- - - - - - - - - - ranking = 17.497900628062keywords = chronic inflammatory demyelinating, inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
3/9. Severe chronic sensory-motor polyneuropathy: coexistence of 3 unrelated etiologies in a type 1 diabetic patient. A case report and review of the literature.We present the case of a 58-year-old man, who has suffered from type 1 diabetes mellitus since he was young. He had monoclonal IgM kappa gammopathy of undetermined significance and high anti-MAG antibody titer. He developed a polyneuropathic picture with the clinical and laboratory features of chronic inflammatory demyelinating polyneuropathy within the span of approximately 2 years. He benefited from IV administration of high doses of immunoglobulins. Investigation of all parameters, but particularly of the clinical phenotype, can lead to a better definition of the polyneuropathic picture, especially for therapeutic and prognostic purposes.- - - - - - - - - - ranking = 2.9163167713437keywords = chronic inflammatory demyelinating, inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
4/9. Chronic inflammatory demyelinating polyneuropathy after campylobacter jejuni infection mimicking vasculitic mononeuritis multiplex in a diabetic.Chronic inflammatory demyelinating polyneuropathy (CIDP) is a clinically heterogeneous disorder. Recent reports suggest that CIDP could be more frequent in diabetics. We report here a case of CIDP presenting as mononeuritis multiplex with accompanying cranial nerve involvement in an insulin-dependent diabetic who presented a preceding campylobacter jejuni infection and misleading skin lesions. Treatment with intravenous immunoglobulins was successful. This case suggests that CIDP should be considered as a potential diagnosis in all diabetics with localized, acute or sub-acute onset, and multiple, or overlapping mononeuropathies.- - - - - - - - - - ranking = 4.9006583009843keywords = inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
5/9. Chronic inflammatory demyelinating polyradiculoneuropathy in two children with type 1 diabetes mellitus.An association between chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and type 1 diabetes has been described in adults, but not previously in children. Two adolescents with both CIDP and type 1 diabetes are reported here. In order to raise the awareness of CIDP among pediatricians, a description of the clinical and laboratory features, treatment, and prognosis of the condition is provided. A preliminary study was undertaken to determine whether responses to autoantigens in peri-islet schwann cells and schwann cells may account for the association between type 1 diabetes and CIDP. Lymphocyte proliferation in response to these autoantigens was abnormal in one of the two patients, but was also abnormal in one control subject.- - - - - - - - - - ranking = 6.8368434121312keywords = chronic inflammatory demyelinating, inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
6/9. Relapsing inflammatory demyelinating polyneuropathy in a diabetic patient.Inflammatory demyelinating polyradiculoneuropathies exhibit well-known ultrastructural lesions of the peripheral nerve, both in acute cases, i.e., guillain-barre syndrome, and in relapsing, sub-acute and chronic cases. We present a case of relapsing inflammatory demyelinating polyradiculoneuropathy in a diabetic patient with a biopsy exhibiting these lesions, as well as a widening of the outermost myelin lamellae in some fibers. Such associated lesions are classic in experimental inflammatory demyelinating polyradiculoneuropathies, but have not been reported in human pathology.- - - - - - - - - - ranking = 5.9006583009843keywords = inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
7/9. Successful treatment of neuropathies in patients with diabetes mellitus.OBJECTIVES: To report and characterize two forms of disabling progressive peripheral neuropathy in patients with diabetes mellitus, which respond to anti-inflammatory and/or anti-immune treatment. DESIGN: review of clinical, electrophysiologic, and pathologic findings and results of treatment. SETTING: University medical center. patients: Twenty-one patients with diabetes mellitus to whom we gave anti-inflammatory and/or anti-immune treatment for progressive peripheral neuropathy during the past 6 years. MAIN OUTCOME MEASURES: patients were interviewed and examined at intervals before and after beginning treatment with intravenous immunoglobulin (n = 15), prednisone (n = 13), cyclophosphamide (n = 5), plasma exchange (n = 3), and azathioprine (n = 1) (alone or in combination). RESULTS: Fifteen patients had evidence of axonal neuropathy by electrophysiologic studies (group A). All 15 patients had non-insulin-dependent diabetes mellitus, 10 patients had weight loss, and 13 patients had prominent involvement of thighs and/or thoracic bands consistent with diabetic amyotrophy or mononeuropathy multiplex. Small vessel disease was seen in all 10 patients who underwent biopsy, with perivascular or vascular inflammation seen in seven patients. Six patients had demyelinating neuropathy by electrophysiologic criteria (group B). All these patients had insulin-dependent diabetes mellitus, and no one had weight loss. The process was asymmetric in three patients and involved thoracic or abdominal regions in two patients. Onion bulbs were seen in all four patients who underwent biopsy, but no vascular inflammation or occlusion was seen. In all patients in both groups, worsening of their conditions stopped and improvement started after beginning treatment. CONCLUSION: Neuropathies responsive to anti-inflammatory and/or anti-immune therapy in patients with diabetes mellitus include (1) multifocal axonal neuropathy caused by inflammatory vasculopathy, predominantly in patients with non-insulin-dependent diabetes mellitus, indistinguishable from diabetic proximal neuropathy or mononeuropathy multiplex, and (2) demyelinating neuropathy indistinguishable from chronic inflammatory demyelinating polyneuropathy, predominantly in patients with insulin-dependent diabetes mellitus.- - - - - - - - - - ranking = 2.95605345095keywords = chronic inflammatory demyelinating, inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
8/9. Chronic inflammatory demyelinating polyneuropathy (CIDP) in diabetics.Seven diabetic patients developed a progressive, moderately severe, motor rather than sensory neuropathy predominantly affecting the legs. This met clinical and electrophysiological criteria for chronic inflammatory demyelinating polyneuropathy (CIDP). Nerve biopsies showed a variety of abnormalities, none of which clearly distinguished between diabetic polyneuropathy and CIDP. The patients were treated with combinations of corticosteroids, azathioprine, plasmapheresis and intravenous immune globulin; all improved substantially. We believe that CIDP may masquerade as unusually severe and progressive diabetic distal symmetric polyneuropathy. It is important to recognize CIDP in diabetics because, unlike diabetic polyneuropathy, CIDP is treatable.- - - - - - - - - - ranking = 6.8368434121312keywords = chronic inflammatory demyelinating, inflammatory demyelinating, demyelinating (Clic here for more details about this article) |
9/9. Uncommon early-onset neuropathy in diabetic patients.An acute neuropathy rarely occurs early in the course of diabetes mellitus. Five cases are described of adult patients who developed a peripheral neuropathy at the time or shortly after the onset or discovery of diabetes mellitus. Patient 1, an 80-year-old woman who developed a subacute tetraparesis with proximal and distal muscle weakness with normal cranial nerves, proved to have insulin-requiring diabetes mellitus. In the other patients, all men aged 23-34 years, symptomatic neuropathy occurred simultaneously (patient 2) or 1-6 months after the onset of insulin-dependent diabetes mellitus (IDDM) (patients 3-5). patients 2 and 3 developed a symptomatic multifocal neuropathy; patients 4 and 5, a painful distal symmetrical sensory polyneuropathy (DSSP) shortly after beginning treatment with insulin. Nerve biopsy showed active axonal lesions in patients 2 and 5 and mixed axonal and demyelinating lesions in the others, with severe axon loss in patients 4 and 5. Vasculitic lesions were found in patient 2, who improved without additional treatment. Neurological examination remained unchanged after 2 years in patients 3-5. Although a coincidence cannot be excluded for patients 1-3, whose neuropathy was not of the pattern commonly found in diabetes, it is suggested that acute disequilibrium in the diabetic status may facilitate the occurrence of a variety of neuropathies. Alternatively, the autoimmune process which led to IDDM may also trigger an autoimmune neuropathy with vasculitis (patient 2) or demyelinative nerve lesions. Only the distal symmetrical sensory polyneuropathy with severe axonal lesions observed in patients 4 and 5 seems directly related to diabetes mellitus. In spite of their occurrence shortly after beginning insulin therapy, the role of treatment with insulin in the onset is uncertain.- - - - - - - - - - ranking = 0.019868339803132keywords = demyelinating (Clic here for more details about this article) |