Cases reported "Polyradiculoneuropathy"

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1/207. Chronic motor axonal neuropathy: pathological evidence of inflammatory polyradiculoneuropathy.

    Chronic immune and inflammatory motor neuropathies may resemble motor neuron disease, and the distinction may be particularly difficult if conduction block or GM1 antibodies are absent. The pathology of this axonal type of chronic motor neuropathy has not been characterized except in a few cases associated with paraproteinemia. We describe the clinical, electrophysiological, and pathological findings in a patient with a chronic motor axonal neuropathy, normal immunoelectrophoresis, and no GM1 antibodies. At autopsy the spinal cord was normal with the exception of chromatolytic motor neurons. All the ventral roots were greatly thinned. Of 10 mixed nerves and numerous spinal roots sampled, five showed areas of perineurial, perivascular lymphocytic infiltration. There was severe axonal loss in the motor roots that was not as evident in mixed nerves, and the sensory nerves and roots were virtually unaffected. Our findings suggest that a chronic motor axonal neuropathy without paraproteinemia or GM1 antibodies may, in some cases, result from an inflammatory process.
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2/207. AAEM case report 4: guillain-barre syndrome. American association of Electrodiagnostic medicine.

    A 57-year-old woman developed rapidly progressive, symmetric, extremity weakness, facial diplegia, ophthalmoplegia, respiratory insufficiency, and sensory ataxia over a 3-week period. Electrodiagnostic studies were performed on days 6, 13, and 50 following the onset of weakness. Motor nerve conduction abnormalities were the predominant findings. Prolonged motor distal latencies, prolonged or absent F waves, and partial motor conduction blocks were present and form the diagnostic features of an acquired, demyelinating polyneuropathy. Abnormalities in sensory nerve conductions and blink reflexes were also present. guillain-barre syndrome was diagnosed prompting the initiation of therapeutic plasma exchange. The patient's clinical status continued to worsen over the next 10 days before stabilizing. Considerable improvement in extremity strength, ocular motility, and respiratory function occurred in the subsequent weeks. Well-planned and well-executed electrodiagnostic studies generate key adjunctive data to the clinical diagnosis of guillain-barre syndrome.
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3/207. Chronic steadily progressive central and peripheral predominantly motor demyelination, involving the cranial nerves, responsive to immunoglobulins.

    The association of central and peripheral demyelination was reported previously. Most of the cases refer to central chronic relapsing demyelination with clinical criteria for multiple sclerosis associated with later signs of peripheral nerve involvement. Other authors, described central lesions in patients with chronic inflammatory demyelinating polyneuropathy and in guillain-barre syndrome, as a seldom occurrence. We report a patient in which a chronic steadily progressive central and peripheral predominantly motor nervous system demyelination, involving the cranial nerves, was identified. The patient improved after intravenous immunoglobulin suggesting an immune-mediated mechanism. To our knowledge this presentation was not described before.
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4/207. haemophilus influenzae has a GM1 ganglioside-like structure and elicits guillain-barre syndrome.

    The authors report a patient with an axonal guillain-barre syndrome (acute motor axonal neuropathy) associated with anti-GM1 antibody after haemophilus influenzae infection. The result of ELISA inhibition studies and cytochemical staining with cholera toxin suggest the presence of a GM1-like structure on the surface of H. influenzae isolated from the patient. A particular strain of H. influenzae may have a GM1-like structure and may elicit an axonal guillain-barre syndrome.
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5/207. Can immunoadsorption plasmapheresis be used as the first choice therapy for neuroimmunological disorders?

    The subjects were 31 patients in whom immunoadsorption plasmapheresis (IAPP) was performed as the first choice therapy for primary or recurrent neuroimmunological disorders. The clinical manifestations before and after IAPP and the use of corticosteroids were investigated in the present study. IAPP was clinically effective in all patients. The corticosteroids (CSs) administration was begun or CSs were increased after completion of IAPP in 11 patients. IAPP was performed as the first choice therapy, and favorable results were obtained in patients with guillain-barre syndrome and Miller-Fisher syndrome. IAPP alone was also effective in a patient with lupoid sclerosis. When IAPP was used alone in 2 patients with chronic inflammatory demyelinating polyradiculoneuropathy, it completely eliminated the clinical manifestations, but the symptoms recurred about 2 months later. Therefore, although IAPP could be performed as the first choice therapy for many neuroimmunological disorders, subsequent therapies should be carefully investigated.
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6/207. The guillain-barre syndrome following dengue fever.

    A 44 year old female presented with fever, muscle aches, rash and a low platelet count. IgM antibody to dengue virus was positive. Two weeks later she developed a flaccid areflexic quadriparesis. Nerve conduction studies showed a predominantly demyelitinating sensory motor polyneuropathy consistent with guillain-barre syndrome. Despite the relatively common occurrence of dengue fever, an associated polyradiculoneuropathy is distinctly uncommon.
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7/207. Multifocal polyradiculoneuropathy and carcinoma of the thymus.

    We studied a patient with polyradiculoneuropathy with anaplastic carcinoma of the thymus. Motor manifestations dominated. Postmortem examinations indicated that the primary changes were in the spinal nerve roots, peripheral nerves and, possibly, the spinal anterior horn cells. The posterior funiculi and posterior root ganglia were also affected, implying multifocal and multiphasic degeneration. This unusual polyradiculoneuropathy is a form of carcinomatous neuropathy.
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8/207. Encephalomyeloradiculoneuropathy following exposure to an industrial solvent.

    A 19-year-old male developed complaints including weakness of the lower extremities and right hand, numbness, dysphagia and urinary difficulties following a 2 month exposure to an industrial solvent constituted mainly of 1-bromopropane, but also containing butylene oxide, 1,3 dioxolane, nitromethane, and other components. Nerve conduction studies revealed evidence of a primary, symmetric demyelinating polyneuropathy. Evidence of CNS involvement came from gadolinium enhanced MRI scans of the brain, showing patchy areas of increased T2 signal in the periventricular white matter, similar scans of the spinal cord revealing root enhancement at several lumbar levels, and SSEP studies. The patient's symptoms had started to resolve following the discontinuation of the exposure, before he was lost to follow-up. Similar findings have been reported following 1-bromopropane exposure in rats. I hypothesize that this patient's symptoms may have been due to 1-bromopropane-induced neurotoxicity.
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9/207. mixed connective tissue disease associated with chronic inflammatory demyelinating polyneuropathy.

    We present a patient with mixed connective tissue disease (MCTD) and slowly progressing demyelinating polyradiculoneuropathy (CIDP). To our knowledge, the case described is the first reported MCTD case associated with definite CIDP.
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10/207. Acute polyradiculoneuropathy with cerebrospinal fluid eosinophilia.

    A 60-year-old woman who presented with quadriparesis, dysarthria and dysphagia after acute febrile illness was reported. Neurological examination and electrodiagnostic study were compatible with acute polyradiculoneuropathy. Lumbar puncture revealed cerebrospinal fluid eosinophilia. Her muscle power improved after supportive treatment.
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