Cases reported "Guillain-Barre Syndrome"

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1/91. Familial guillain-barre syndrome.

    There are few reports of guillain-barre syndrome (GBS) occurring in families. We have encountered a mother, who developed acute inflammatory demyelinating polyradiculoneuropathy at age 35 years, whose son developed the bulbar form of GBS 7 years later. Both shared HLA DR2.
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keywords = neuropathy
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2/91. Lumbosacral acute demyelinating polyneuropathy following hepatitis b vaccination.

    We report a patient who presented with an acute inflammatory demyelinating polyneuropathy, that followed the second injection of a hepatitis b vaccination, and characterized by motor and sensory deficit restricted to lower limbs and perineum, and persistent bladder dysfunction. The relationship between the preceding event and neurological disease is discussed.
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keywords = neuropathy
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3/91. Acute axonal polyneuropathy in chronic alcoholism and malnutrition.

    In contrast to the classic, slowly progressive polyneuropathy in alcoholic patients, acute forms, clinically mimicking guillain-barre syndrome, are rare. We present a patient who developed motor weakness and sensory loss in all four limbs within four days. Laboratory data were consistent with long-term alcohol abuse and documented thiamine deficiency. Repeated cerebrospinal fluid examinations were normal. Electrophysiological studies showed an acute sensorimotor polyneuropathy with predominantly axonal involvement. We conclude that acute alcoholic neuropathy has to be distinguished from guillain-barre syndrome and other forms of acute polyneuropathy by using clinical, laboratory, and electrophysiological data. Both ethanol toxicity and vitamin deficiency could play a role in the pathogenesis.
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keywords = neuropathy
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4/91. Acute sensory neuropathy in an adolescent girl following BCG vaccination.

    A 13-year-old girl developed a sensory neuropathy following bacille Calmette-Guerin (BCG) vaccination, consistent with acute inflammatory demyelinating polyradiculoneuropathy or acute sensory axonal neuropathy.
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ranking = 121.16169372484
keywords = axonal neuropathy, neuropathy
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5/91. Ganglioside-induced antiganglioside antibodies from a neuropathy patient cross-react with lipopolysaccharides of campylobacter jejuni associated with guillain-barre syndrome.

    Antiganglioside serum antibodies from a patient treated with gangliosides were examined for cross-reactivity with lipopolysaccharides (LPSs) of campylobacter jejuni strains associated with guillain-barre syndrome (GBS). The patient had no preceding infection with C. jejuni and developed chronic progressive motor polyneuropathy following parenteral ganglioside treatment. serum IgG antibodies recognised GM1 and GD1b gangliosides as well as asialo-GM1, and cross-reactivity was observed with LPSs from C. jejuni O:2, O:4, O:19 and O:41. The results give a clear indication that gangliosides and LPSs from C. jejuni serotypes associated with GBS share common epitopes.
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ranking = 5
keywords = neuropathy
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6/91. Neurogenic stunned myocardium in guillain-barre syndrome.

    Neurogenic stunned myocardium (NSM), a syndrome of reversible left ventricular dysfunction best described after subarachnoid hemorrhage, has not been associated with peripheral neuropathy. We describe a woman with guillain-barre syndrome in whom a syndrome compatible with NSM developed in the setting of a physiologically documented increase in sympathetic cardiovascular tone. This case supports the presumed unifying role of excessive sympathetic nervous system activation in the pathogenesis of NSM.
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keywords = neuropathy
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7/91. filtration of cerebrospinal fluid for acute demyelinating neuropathy in systemic lupus erythematosus.

    We report a patient with systemic lupus erythematosus complicated by an acute demyelinating neuropathy. Conventional therapy with intravenous immunoglobulins and immunoadsorption complemented by pulse methylprednisolone and cyclophosphamide failed. Institution of filtration of the cerebrospinal fluid was followed by a rapid improvement of the paresis.
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keywords = neuropathy
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8/91. 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.
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ranking = 2
keywords = neuropathy
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9/91. Acute axonal form of guillain-barre syndrome in a multiple sclerosis patient: chance association or linked disorders?

    multiple sclerosis (MS) is characterized by inflammation, demyelination and gliosis, involving the central nervous system (CNS) and commonly sparing the peripheral nervous system (PNS). Coexistence of CNS and PNS chronic demyelination has been rarely demonstrated in chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) and in MS, but the occurrence of acute polyradiculoneuropathy in a patient with MS is even more unusual. We describe the case of a woman with relapsing-remitting MS who presented with an acute severe tetraparesis. cerebrospinal fluid (CSF) examination together with neurophysiological data and sural nerve biopsy study demonstrated an axonal form of guillain-barre syndrome (GBS). It remains unresolved if the association of an axonal form of GBS and MS is fortuitous or, on the contrary, is indicative of the coexistence in some individuals of common pathogenetic mechanisms.
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keywords = neuropathy
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10/91. Event-related potentials in patients with total locked-in state due to fulminant guillain-barre syndrome.

    A series of electrophysiological investigations were performed over a 6-month period in two patients affected by fulminant Guillain-Barre polyradiculoneuropathy, who developed an ascending paralysis leading, within 72 h, to flaccid quadriplegia, internal and external ophthalmoplegia, absence of all brainstem reflexes and no respiratory effort: the clinical state resembled brain death. brain CTs were normal and spinal fluid examination revealed albuminocytological dissociation. All motor nerves tested were unexcitable, whereas sensory responses were markedly abnormal but present. Sequential EEG recordings revealed normal, partially reactive alpha rhythm in both patients. In one patient, normal auditory event-related potentials (ERPs: peak N1, P2, N2, P3, evoked in an 'oddball' paradigm) and CNV-like potentials could be recorded not earlier than the 20th day into the illness. In earlier recordings, N1 and P2 peaks as well as mismatch negativity (MMN) were present over the frontal and central scalp electrodes. This patient has now partially recovered motor functions and no cognitive defects are present, but he has little recollection of the events occurring in the first 2 weeks spent in the ICU, when he was completely paralyzed. The other patient generated normal N1 and P2 ERP peaks, but no N2, P3 and MMN were detected in a series of recordings. He died without having ever regained appropriate behavioral responses. The ERP abnormalities observed raise the matter of the origin of cognitive dysfunction in patients with severe and prolonged de-efferentation/de-afferentation. ERPs allow monitoring the level of alertness and attention and appear more specific than EEG in identifying a state of awareness in patients in which communication is severely impaired as a consequence of neurological disorders.
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