java barcode reader library free Paresthesias are more variable Acute dysautonomia may be life-threatening in Objective-C

Creator QR Code in Objective-C Paresthesias are more variable Acute dysautonomia may be life-threatening

Paresthesias are more variable Acute dysautonomia may be life-threatening
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A General Considerations
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This acute or subacute polyradiculoneuropathy sometimes follows infective illness, inoculations, or surgical procedures There is an association with preceding Campylobacter jejuni enteritis The disorder probably has an immunologic basis, but the precise mechanism is unclear
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B Clinical Findings
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1 Symptoms and signs The main complaint is of weakness that varies widely in severity in different patients and often has a proximal emphasis and symmetric distribution It usually begins in the legs, spreading to a variable extent but frequently involving the arms and often one or both sides of the face The muscles of respiration or deglutition may also be affected Sensory symptoms are usually less conspicuous than motor ones, but distal paresthesias and dysesthesias are common, and neuropathic or radicular pain is present in many patients Autonomic disturbances are also common, may be severe, and are sometimes life-threatening; they include tachycardia, cardiac irregularities, hypotension or hypertension, facial flushing, abnormalities of sweating, pulmonary dysfunction, and impaired sphincter control The axonal subtypes of the syndrome (acute motor axonal neuropathy [AMAN] and acute motor and sensory axonal neuropathy [AMSAN]) are caused by antibodies to gangliosides on the axon membrane and especially by antibodies to GM1, GM1b, and GD1a (and GalNac-GD1a to AMAN) 2 Laboratory findings The cerebrospinal fluid characteristically contains a high protein concentration with a normal cell content, but these changes may take 2 or 3 weeks to develop Electrophysiologic studies may reveal marked abnormalities, which do not necessarily parallel the clinical disorder in their temporal course Pathologic examination shows primary demyelination or, less commonly, axonal degeneration
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8 Chronic Inflammatory Polyneuropathy
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Chronic inflammatory demyelinating polyneuropathy, an acquired immunologically mediated disorder, is clinically similar to Guillain-Barr syndrome except that it has a relapsing or steadily progressive course over months or years and that autonomic dysfunction is generally less common It may present as an exclusively motor disorder or with a mixed sensorimotor disturbance In the relapsing form, partial recovery may occur after some relapses, but in other instances there is no recovery between exacerbations Although remission may occur spontaneously with time, the disorder frequently follows a progressive downhill course leading to severe functional disability Electrodiagnostic studies show marked slowing of motor and sensory conduction, and focal conduction block Signs of partial denervation may also be present owing to secondary axonal degeneration Nerve biopsy may show chronic perivascular inflammatory infiltrates in the endoneurium and epineurium, without accompanying evidence of vasculitis However, a normal nerve biopsy result or the presence of nonspecific abnormalities does not exclude the diagnosis Corticosteroids may arrest or reverse the downhill course Treatment is usually begun with prednisone, 60 mg daily, continued for 2 3 months or until a definite response has occurred If no response has occurred despite 3 months of treatment, a higher dose may be tried In responsive cases, the dose is gradually tapered, but most patients become corticosteroid-dependent, often requiring prednisone, 20 mg daily on alternate days, on a long-term basis IVIG can be used in place of or in addition to corticosteroids and is best used as the initial treatment in pure motor syndromes When both IVIG and corticosteroids are ineffective, plasma exchange may be worthwhile Immunosuppressant or immunomodulatory drugs (such as azathioprine) may be added when the response to other measures is unsatisfactory or to enable maintenance doses of corticosteroids to be lowered Symptomatic treatment is also important
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Albers JW et al Porphyric neuropathy Muscle Nerve 2004 Oct;30(4):410 22 [PMID: 15372536]
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C Differential Diagnosis
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When the diagnosis is made, the history and appropriate laboratory studies should exclude the possibility of porphyric, diphtheritic, or toxic (heavy metal, hexacarbon, organophosphate) neuropathies The temporal course excludes other peripheral neuropathies Poliomyelitis, botulism, and tick paralysis must also be considered as they cause weakness of acute onset The presence of pyramidal signs, a markedly asymmetric motor deficit, a sharp sensory level, or early sphincter involvement should suggest a focal cord lesion
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