Cases reported "Diabetic Neuropathies"

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1/7. Reversible tetraplegia due to polyneuropathy in a diabetic patient with hyperosmolar non-ketotic coma.

    critical illness polyneuromypathy has not previously been reported as a complication of diabetic coma. We describe a patient with hyperosmolar non-ketotic coma (HONK) complicating gram-negative sepsis in whom persistent coma and profound tetraplegia caused considerable concern. Although, initially, it was feared that the patient had suffered a central neurological complication such as stroke or cerebral oedema, a diagnosis of critical illness motor syndrome (CIMS) was subsequently confirmed neurophysiologically. Profound limb weakness associated with HONK is not necessarily due to a catastrophic cerebral event, rather it may be a result of CIMS, which has an excellent prognosis for full neurological recovery.
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2/7. Botulinum toxin treatment for upper airway collapse resulting from temporomandibular joint dislocation due to jaw-opening dystonia.

    To examine the effects of botulinum toxin injection application for the treatment of upper airway obstruction due to hyperactive lateral pterygoid muscle contraction, we applied botulinum toxin injection. A 20 year-old male patient had involuntary mouth opening after a diabetic coma. His mouth opened excessively (84 mm) particularly when he was in a nervous or stressed condition. This resulted in a bilateral temporomandibular dislocation and, consequently, upper airway collapse. The differential diagnosis of jaw-opening oromandibular dystonia was made. Botulinum toxin type A was bilaterally injected into the lateral pterygoid muscle. The excessive mouth opening was reduced, and the patient showed no temporomandibular joint (TMJ) dislocation or experienced any further airway collapse after the injections. We successfully applied botulinum toxin to a patient with upper airway obstruction and TMJ dislocation relative to jaw-opening dystonia.
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keywords = coma
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3/7. cerebrospinal fluid lactate in patients with diabetes mellitus and hypoglycaemic coma.

    cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 20 patients with diabetes mellitus but without disturbance of consciousness and five who recovered from hypoglycaemic coma. CSF lactate was slightly but significantly higher in diabetes mellitus (1.78, SEM 0.04 m mol/l) than that in 15 control subjects (1.40, SEM 0.05 m mol/l). In those who recovered from hypoglycaemic coma, CSF lactate was markedly elevated to 2.45-4.43 m mol/l. CSF glucose concentrations, however, were substantially the same between treated hypoglycaemic and diabetes mellitus groups. These findings indicate that CSF lactate levels increase with glycaemic levels in diabetes mellitus owing to enhanced glucose influx into glycolytic pathway of the brain, and also increases in treated hypoglycaemic coma probably due to mitochondrial dysfunction or damage.
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4/7. Coma preceded by severe dysphagia in type II diabetes mellitus.

    A 62-year-old man with 11 years' duration of type II diabetes was hospitalized because of non-ketotic diabetic coma. He had never noted any symptoms of swallowing difficulty until 3 days before admission when they developed gradually and he became comatous. He had never received special medication such as diuretics except anticonvulsants. Even after the recovery from diabetic coma he could hardly swallow solid foods or saliva for about 15 days, but these symptoms subsided gradually. Motility dysfunction of esophagus and pharynx in diabetes mellitus, in most cases they are mild, has been described, although diabetic coma preceded by dysphagia has not been documented except in one report. We studied, therefore, the autonomic nerve function of the present patient and discussed the relationship between dysphagia and diabetic coma together with the description of the clinical course of this patient. The relationship between this case and the previously reported cases were compared in terms of the sex, age, type of diabetes, clinical course, medication and the autonomic nerve function.
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keywords = coma
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5/7. Bilateral acute anterior ischemic neuropathy in diabetes: case report.

    A 51-year-old white man presented with an acute bilateral anterior ischemic optic neuropathy approximately 1 month following hospitalization for a hyperosmolar nonketotic diabetic coma. One eye treated by retrobulbar corticosteroids showed marked improvement. The literature reveals that diabetic anterior ischemic optic neuropathy is often diagnosed in the absence of diabetic retinopathy.
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6/7. Multiple cerebral haematomata and peripheral nerve palsies associated with a case of juvenile diabetic ketoacidosis.

    A 15-year-old girl presented de novo in diabetic ketoacidosis having been comatose for 24 h (day 1). A CT scan and lumbar puncture performed on admission were normal and her conscious level slowly improved over several days. On day 7 she had central neurological signs of bilateral knee clonus and an extensor plantar response. In addition, she had developed lower motor neurological signs of an ulnar nerve palsy of the left forearm, and ulnar, median, and radial nerve palsies of the right forearm. magnetic resonance imaging (MRI), performed on day 12, showed multiple small cerebral haematomata with appearances at least several days of age. The scattered lesions were localized particularly to the parieto-occipital region, with sparing of the basal ganglia and without cerebral oedema, a novel feature not previously described in juvenile ketoacidosis. Four months later there was minimal residual disability of her right arm. The clinical findings together with the MRI images suggested that the peripheral nerve and central lesions were temporally related, suggesting a common aetiology. However, it is likely that MRI showed cerebral lesions which may have been missed by the conventional CT scanning performed initially.
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keywords = coma
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7/7. Persistent chorea after recurrent hypoglycemia. A case report.

    In a 72-year-old woman with a 33-year history of diabetes mellitus bilateral chorea had occurred after a series of hypoglycemic comas at the age of 58. The choreiform movements remained untreated, persisted more than 10 years and inspite of intermittent exaggeration were tolerated by the patient. Except for the hyperkinetic movements, neurological examination of this patient was otherwise normal as was cranial computer tomography.
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