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31/105. Extrapontine myelinolysis in a patient with systemic lupus erythematosus: a case report.

    Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in systemic lupus erythematosus (SLE) is rare and related pathologic changes in brain images have not been reported. We report the case of a 49-year-old woman with SLE who developed extrapontine myelinolysis (EPM) following gradual correction of marked hyponatremia caused by SIADH. EPM was caused by the hyponatremia, which resulted in cerebral hypoxia and brain swelling. SIADH was most likely induced by the occult vasculitis of SLE. After partial correction of hyponatremia, she regained consciousness, but gradually developed parkinsonism including rigidity, bradykinesia, and tremors 1 week later. magnetic resonance imaging revealed bilateral symmetrical brain lesions at the putamen, globus pallidus, and part of the thalamus. These symptoms improved gradually after administration of levodopa. Mild jerky tremors of both hands persisted 4 months later. The EPM lesions differ from those observed in central pontine myelinolysis (CPM), which is immediately induced by acute correction of hyponatremia. Therefore, hyponatremia in lupus-related SIADH should be carefully corrected to prevent CPM or EPM. ( info)

32/105. Efficacy of clozapine in a non-schizophrenic patient with psychogenic polydipsia and central pontine myelinolysis.

    clozapine is an atypical antipsychotic drug that has been demonstrated to be a highly effective treatment for polydipsia in schizophrenic patients. The authors report the first case of a non-schizophrenic patient affected by polydipsia and central pontine myelinolysis who was successfully treated with clozapine. ( info)

33/105. A 47-year-old alcoholic man with progressive abnormal gait.

    Central pontine myelinolysis should be considered in the differential diagnosis of a patient with a history of alcoholism and malnutrition presenting with ataxia, regardless of serum sodium values. T2-weighted images are the most sensitive imaging technique, but changes may not be evident for weeks after the insult, and in addition, the insult may not be known. Supportive care is important to prevent complications, but no treatment has been found to be effective in treating the illness. Patient outcomes vary considerably and are difficult to predict. ( info)

34/105. Evolving spectrum of movement disorders in extrapontine and central pontine myelinolysis.

    Extrapontine (EPM) and central pontine myelinolysis (CPM) are rare and frequently related to rapid correction of hyponatremia. We describe a 60-year-old woman who developed an unusual evolving spectrum of movement disorders secondary to EPM and CPM following intravenous sodium replacement therapy for severe hyponatremia. She presented initially with confusion, generalized coarse postural limb tremor, myoclonic jerks and quadriparesis. Subsequently her mental state improved and her tremor and weakness resolved. Over the following months, she developed progressive painful dystonia of her facial musculature and lower limbs. This gradually became generalized and associated with choreoathethosis in her limbs. In addition, she had increasing bradykinesia and rigidity, which responded poorly to levodopa treatment. Our case illustrates that while the myelin destruction occurs during the initial insult of the osmotic demyelinating process, its delayed clinical effects resulting from ineffective reorganization of neuronal structures may be progressive, evolve with time, and difficult to treat. ( info)

35/105. EBV associated hemophagocytic syndrome accompanied by central pontine myelinolysis.

    The development of central pontine myelinolysis (CPM) has rarely been reported in association with hemophagocytic syndromes (HPS). Here we report a unique case of Epstein-Barr Virus (EBV)-related HPS which was accompanied with CPM. A 72-year-old man who had no significant medical history was admitted to our hospital due to high fever and progressing dysphasia and dysarthria. physical examination revealed anisocoria of the right pupil, fixed reaction to light, and paralysis of the left vagus nerves. magnetic resonance imaging revealed low signal intensity on T1-weighted images and high signal intensity T2-weighted images in the patient's central midpontine lesion. Initial work-up showed anemia and thrombocytopenia with elevated levels of serum ferritin, lactate dehydrogenase, and soluble IL-2 receptor. bone marrow aspiration revealed hemophagocytosis. The EBV genome was detected in the peripheral blood using the polymerase chain reaction method. He was diagnosed as having EBV-related HPS and CPM. Despite intensive treatment with methylpredonisolone, immunoglobulin, and etoposide, he died due to progressive disease and fungal septicemia. The etiology and relation between CPM and HPS are discussed. ( info)

36/105. Central pontine myelinolysis secondary to cytomegalovirus hepatitis in a 10-month-old child.

    We present a 10-month-old child with central pontine myelinolysis (CPM) secondary to chronic active hepatitis due to cytomegalovirus (CMV) infection. A total of 35 paediatric cases of pontine and/or extrapontine myelinolysis are reported and, to our knowledge, CPM secondary to CMV hepatitis in an infant has not been previously reported. The MRI findings are highlighted. ( info)

37/105. Does uremia protect against the demyelination associated with correction of hyponatremia during hemodialysis? A case report and literature review.

    Rapid correction of chronic hyponatremia is known to cause demyelination syndromes, which are attributed to the rapid shift of water out of the brain. In uremic patients with hyponatremia, depending on the dialysate sodium concentration and delivered Kt/V, serum sodium levels may be rapidly corrected inadvertently during the hemodialysis (HD) session. It is not known whether uremic patients are as susceptible to the development of demyelination as patients with normal renal function. Since urea diffuses slowly across the blood-brain barrier, it can act as an effective osmole between plasma and the brain if levels are changed abruptly. During HD, blood urea levels drop suddenly and significantly and cerebral edema may develop (dialysis disequilibrium syndrome). This effect may counteract the fluid shift out of the brain during correction of hyponatremia. Therefore, theoretically, uremic patients may be less prone to develop demyelination. We present a patient with renal failure whose hyponatremia was corrected rapidly during HD to illustrate the potential problem. The patient tolerated rapid correction of hyponatremia without sustaining any neurologic damage. We performed a literature search looking for similar case reports and reviewed the scientific evidence behind the above hypothesis. ( info)

38/105. Central pontine myelinolysis associated with hypokalaemia in anorexia nervosa.

    A 31-year-old man was admitted to hospital with of anorexia, binge eating, and self induced vomiting. On admission, he showed a pronounced low weight and disturbance of the body image and was diagnosed as having anorexia nervosa. In addition, electrolyte abnormalities, mainly hypokalaemia, and increased serum renin and aldosterone concentrations were recorded, suggesting pseudo-bartter syndrome as a complication. Under frequent monitoring of the serum potassium and sodium concentrations, serum electrolytes were gradually corrected, but brain magnetic resonance imaging revealed reversible central pontine myelinolysis (CPM). Although attention has been mainly paid to the association of CPM with rapid correction of hyponatraemia and abnormal osmolality, this case report strongly suggested the involvement of hypokalaemia in the pathogenesis of CPM. ( info)

39/105. Central pontine myelinolysis manifested by temporary blindness: a possible complication of lithium toxicity.

    Central pontine myelinolysis (CPM) is removal of myelin material from neural elements in a way that is not clearly known as yet. In this case of CPM, blindness was encountered and was thought to be "hysterical." The blindness went away after four months. After reviewing the literature we suggest the CPM was a complication of lithium toxicity which affected the lateral geniculate nucleus which produced blindness. ( info)

40/105. Treating hyponatremia in an empty sella syndrome patient complicated with possible myelinolysis.

    hyponatremia as the presenting manifestation of empty sella syndrome is rare. There is little clinical experience in the management of this problem and its possible therapeutic complications. We herein report on a 44-year-old woman with a past history of massive postpartum hemorrhage who was admitted because of hyponatremia and disturbed consciousness. Initial biochemical data suggested the effects of antidiuretic hormone, but fluid restriction alone offered limited benefit. Later, hormonal levels indicated hypopituitarism. magnetic resonance imaging and cisternography led to a diagnosis of empty sella. Although glucocorticoid substitution was initiated and the clinical condition initially improved, possible myelinolysis subsequently became a complication. With early recognition and immediate replacement of hypotonic fluid, the patient completely recovered. We report this case to illustrate the fact that glucocorticoid substitution and concurrent fluid restriction can probably lead to myelinolysis in empty sella syndrome patients. We suggest that the serum sodium level should be frequently monitored and that much more attention should be paid to the neurologic signs when substituting glucocorticoids in these patients, even though the increment in the serum sodium level is acceptable. Once possible myelinolysis develops, early recognition is critical, and the immediate replacement of hypotonic fluid is suggested. ( info)
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