Cases reported "Muscle Weakness"

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1/93. Lessons to be learned: a case study approach: prolonged methaemoglobinaemia due to inadvertent dapsone poisoning; treatment with methylene blue and exchange transfusion.

    The authors present a case of methaemoglobinaemia of acute onset, with an unusually protracted course. The long persistence of this disorder led to a search for the cause which was eventually traced to medication with dapsone. The latter was found to be inappropriately being taken by the patient instead of an antispasmodic that had been prescribed for a spinal condition; this was because the tablets had been incorrectly labelled and dispensed in a pharmacy. The patient took increasing doses of the presumed 'antispasmodic' tablets as they seemed to lack clinical effect, thus further exacerbating the toxic consequences. Moreover, the patient brought his wrongly labelled tablets into hospital and was allowed to use them there, contrary to normal hospital policy. As treatment for the methaemoglobinaemia both bolus and continuous infusions of methylene blue were used, which probably contributed to the severe haemolysis which followed. Furthermore, the development of a rare side effect of dapsone toxicity, namely that of a sensorimotor neuropathy, is reported.
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2/93. An unusual manifestation of diabetes mellitus.

    MEDICAL history: Type 2 diabetes mellitus for five years; unexplained 35-lb weight loss three years ago; Bell's palsy on right side many years ago. MEDICATIONS: glipizide, 10 mg/day. family history: Father died of leukemia at age 65; mother has kidney stones; no diabetes or neuromuscular disease. SOCIAL history: insurance salesman; heterosexual, promiscuous, uses condoms; smokes (25 pack years); does not drink. physical examination: Well-nourished, well developed, not in acute distress; had difficulty rising from a sitting position because of right lower extremity weakness. blood pressure, 154/74; pulse, 88; temperature, 36.6 degrees C; respiratory rate, 16. head, eyes, ears, nose, and throat: normal. neck: normal. heart: S4. Lungs: clear. abdomen: mildly obese. extremities: no cyanosis, clubbing, or edema; atrophy and weakness of right thigh and both calves; wide-based gait; able to walk on toes but not heels. Neurologic responses: cranial nerves intact; deep tendon reflexes, 1 symmetrically; plantar reflexes, flexor bilaterally. Skin: macular rash in sun-exposed areas. LABORATORY FINDINGS: Hemoglobin, 13.2 gm/dL; mean corpuscular volume, 80 micron 3; white blood cell count, 7,200/mm3 (normal differential); platelet count, 137,000/mm3. serum: electrolytes, normal; blood urea nitrogen, 18 mg/dL; creatinine, 0.8 mg/dL; glucose, 308 mg/dL; total protein, albumin, liver enzymes, and creatine kinase, normal. urine: 1 glucose. Venereal disease test: nonreactive; hiv test: negative. DIFFERENTIAL diagnosis: dermatomyositis; heavy-metal poisoning; diabetic amyotrophy. HOSPITAL COURSE: The patient was given 50 mg/day of oral amitriptyline to alleviate the painful paresthesias and was switched to 20 U/day of subcutaneously injected neutral protamine Hagedorn (NPH) insulin to normalize the blood glucose level. Histologic studies of skin and muscle showed sun damage and neuropathic changes, respectively. There was no evidence of vasculitis. Screening for heavy-metal toxins produced negative results.
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ranking = 8.3250543216016E-5
keywords = deep
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3/93. hypereosinophilic syndrome: progression of peripheral neuropathy despite controlled eosinophil levels.

    Idiopathic hypereosinophilic syndrome (HES) is a disorder of the hematopoietic system, characterized by persistent elevation in the total eosinophil count (> 1500/microliter) for over 6 months, associated with organ damage and no detectable underlying cause. Treatment is centered on the reduction of total circulating eosinophils, which generally leads to remission of symptoms. We report a 68-year-old female patient with HES and peripheral neuropathy, presenting with cutaneous lesions, mental changes, cardiac and pulmonary symptoms, followed by right foot drop and eventually paraparesis, which caused an inability to ambulate. Weakness progressed to include the upper extremities despite adequate control of eosinophilia by steroids. Worsening of the peripheral neuropathy can occur despite lowering of the eosinophil levels.
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ranking = 6
keywords = neuropathy
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4/93. Proximal diabetic neuropathy presenting with respiratory weakness.

    A patient is described with proximal diabetic neuropathy presenting with respiratory weakness. A 50 year old man developed progressive shortness of breath over 2 months. He also had weakness of hip flexion. phrenic nerve responses were absent, and spontaneous activity was seen in the intercostal and lumbar paraspinal muscles with long duration neurogenic MUPs and reduced recruitment in the diaphragm. Without treatment, the patient began to improve with resolution of his proximal leg weakness and breathing difficulties. Proximal diabetic neuropathy is another cause of neuromuscular respiratory weakness.
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keywords = neuropathy
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5/93. amantadine-induced peripheral neuropathy.

    We report a 48-year-old woman with a 17-year history of PD who developed a peripheral sensory-motor neuropathy secondary to chronic administration (8 years) of amantadine. Discontinuation of amantadine resulted in resolution of trophic skin ulcers, paresthesias, and distal weakness. amantadine may be hazardous to patients with severe and chronic livedo reticularis.
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ranking = 5
keywords = neuropathy
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6/93. Hereditary neuropathy and vocal cord paralysis in a man with childhood diphtheria.

    We present the case of a 37-year-old Afghani man with a history of childhood diphtheria, who was diagnosed with bilateral vocal cord paralysis at age 15 years. At about this time he developed progressive muscular wasting and distally predominant weakness, and subsequently developed respiratory insufficiency, necessitating nocturnal ventilatory support. His examination suggested a distal symmetric sensorimotor neuropathy, and his brother was similarly affected, although to a lesser degree. electromyography (EMG) and nerve conduction studies revealed this process to be purely axonal. A diagnosis of possible hereditary motor and sensory neuropathy (HMSN) type IIc, hereditary axonal polyneuropathy with vocal cord paralysis, is proposed, although the question of early diphtheritic involvement of the vocal cords and peripheral nerves is also considered.
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ranking = 7
keywords = neuropathy
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7/93. cauda equina syndrome due to lumbosacral arachnoid cysts in children.

    We describe the clinical, neuroradiological and surgical aspects of two children in whom symptoms attributable to cauda equina compression were caused by spinal arachnoid cysts. The first patient presented with recurrent urinary tract infections due to neurogenic bladder dysfunction, absent deep tendon reflexes and sensory deficit in the lower limbs. The second child presented with unstable gait as a result of weakness and diminished sensation in the lower extremities. Spinal magnetic resonance imaging revealed a lumbosacral arachnoid cyst in both patients. During surgery the cysts were identified and excised. Two years after surgery, the sensory deficits of the first patient have disappeared and patellar and ankle reflexes can be elicited, but there is no improvement in bladder function. Neurological examination of the second patient was normal. We conclude that the diagnosis of cauda equina syndrome should prompt a vigorous search for its aetiology. Lumbosacral arachnoid cysts are a rare cause of cauda equina syndrome in children.
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ranking = 8.3250543216016E-5
keywords = deep
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8/93. Idiopathic sciatic mononeuropathy.

    sciatic nerve lesions are usually painful and secondary to compression, trauma, infarction or part of a systemic illness. The etiology is usually defined by radiographic or blood studies, or by exploratory surgery. In rare cases, as the one being presented, there is clear clinical and electrophysiological evidence for a lesion of the sciatic nerve, but no morphological correlate or defined etiology. These idiopathic sciatic mononeuropathies seem to occur in the nerves of the legs in young adults.
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ranking = 4
keywords = neuropathy
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9/93. Chronic demyelinating hypertrophic brachial plexus neuropathy.

    A patient with unilateral, painless, chronic progressive upper limb sensorimotor deficit showed electrophysiological evidence of a focal demyelinating neuropathy with almost complete conduction block across the brachial plexus. magnetic resonance imaging disclosed marked brachial plexus hypertrophy. Intravenous immunoglobulin led to fast and complete recovery, maintained by intermittent perfusions. Hypertrophic brachial plexus neuropathy can be a presentation of focal chronic inflammatory demyelinating polyradiculoneuropathy. Objective and quantitative assessment of hand function is useful to evaluate treatment results and to optimize treatment regimens.
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ranking = 7
keywords = neuropathy
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10/93. A man with worsening weakness.

    The contemporary presence of organomegaly, skin manifestations, polyneuropathy, endocrinopathy and monoclonal component characterises the poems syndrome, often associated with osteosclerotic myeloma and Castelman's disease and more frequent in the Japanese. Clinical manifestations seem to be related to the production of many interleukins, mainly IL-1, IL-6 and TNF. Several endocrinopathies have been described, the most frequent being diabetes. Only one previous case of hypoparathyroidism associated with the syndrome has been described in medical reviews. Polyneuropathy is often sensitivo-motory and skin disease accounts for Raynaud phenomenon, skin pigmentation, hypertricosis and others. We describe the case of a 74-year-old man who underwent clinical examination for weakness mainly in the legs. Clinical and instrumental data showed rhabdomyolysis due to hypoparathyroidism. The contemporary presence of a monoclonal band of light chains on proteic electrophoresis, organomegaly and distal leg neuropathy allowed us to make a diagnosis of poems syndrome.
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ranking = 3
keywords = neuropathy
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