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1/15. Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia.

    We report the case of a 54-year-old alcoholic female patient who was hospitalized for neurologic alterations along with a severe hyponatremia (plasma Na : 97 mEq/l). She suffered from potomania and was given, a few days before admission, a thiazide diuretic for hypertension. A careful correction of plasma Na levels was initiated over a 48-hour period (rate of correction < 10 mEq/l/24h) in order to avoid brain demyelination. After a 2-day period of clinical improvement, her neurologic condition started to deteriorate. By the 5th day of admission, she became tetraplegic, presented pseudobulbar palsy, ataxia, strabism, extrapyramidal stiffness and clouding of consciousness. Scintigraphic and MRI investigations demonstrated pontine and extrapontine lesions associated with Gayet-wernicke encephalopathy. After correction of ionic disorders (hyponatremia, hypokaliemia) and vitamin B (thiamine) deficiency, the patient almost completely recovered without notable disabilities. This case illustrates that profound hyponatremia, in a paradigm of slow onset, can be compatible with life. It also demonstrates that demyelinating lesions, usually considered as a consequence of a too fast correction of hyponatremia, may occur despite the strict observance of recent guidelines. There is increasing evidence to suggest that pontine swelling and dysfunction may sometimes occur in alcoholic patients even in absence of disturbance in plasma Na levels. It is therefore of importance, while managing a hyponatremic alcoholic patient, to identify additional risk factors (hypokaliemia, hypophosphoremia, seizure-induced hypoxemia, malnutrition with vitamin b deficiency) for brain demyelination and to correct them appropriately.
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2/15. Central pontine myelinolysis in a patient with anorexia nervosa.

    Myelinolysis may occur as a severe complication of eating disorders, especially anorexia nervosa (AN). One of the most important reasons can be a rapid correction of hyponatremia caused by tubulopathy, water intoxication (WI), or abuse of diuretics in individuals with AN. METHOD AND RESULTS We report on a 24-year-old female patient with an 8-year history of AN. A rapid correction of severe hyponatremia and hypokalemia induced by WI led to central pontine myelinolysis, which was confirmed by magnetic resonance imaging (MRI) examination. Besides affective lability, incoherence, and an acute confusional state, surprisingly, no severe neurological symptoms emerged. CONCLUSION: Thus, physicians should be aware of the risk of pontine myelinolysis with new psychiatric symptoms emerging in the absence of obvious neurological deficits.
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3/15. 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.
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4/15. 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.
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5/15. 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.
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6/15. Central pontine and extrapontine myelinolysis owing to disequilibrium syndrome.

    Neurologic disorders can be seen in patients with end-stage renal failure owing to complications of hemodialysis or peritoneal dialysis. The disequilibrium syndrome can be seen, usually soon after or toward the end of dialysis. We report a patient with central pontine and extrapontine myelinolysis owing to disequilibrium syndrome. The patient had depressed consciousness, agitation, tremor, stupor and hyperactive deep tendon reflexes toward the end of the second peritoneal dialysis. A brain computed tomographic (CT) scan showed hypodense lesions in pontine and extrapontine locations without radiocontrast medium enhancement After 2 days, the patient had only minimal memory deficits. A control brain CT scan 1 week later showed a decrease of the lesions in central pontine and extrapontine locations. Central pontine and extrapontine myelinolysis should be suspected and investigated in the acute neurologic disorders of dialysis patients.
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7/15. Central pontine myelinolysis central pontine myelinolysis manifesting with massive myoclonus.

    Central pontine myelinolysis is a rare neurologic disorder defined by symmetric demyelination in the central base of the pons. It usually manifests with neurologic signs such as impaired consciousness, ataxia, spastic quadriparesis, pseudobulbar signs, and the locked-in syndrome which is related to a disconnection syndrome at the pontine level. We report a 17-month-old patient with kwashiorkor and hyponatremia who developed acute massive myoclonus. magnetic resonance imaging revealed a central pontine lesion. Central pontine myelinolysis is rare in infants, with only a few cases reported in the literature so far. This report presents the first infantile case of central pontine myelinolysis manifesting with massive myoclonus.
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8/15. Central pontine and extrapontine myelinolysis associated with type 2 diabetic patient with hypokalemia.

    Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with the demyelination of extrapontine areas of the central nervous system. Although the etiology and pathogenesis are unclear, CPM is usually associated with hyponatremia or its rapid correction, and chronic alcoholism is also a common underlying condition. We observed a 43-year-old man with diabetes mellitus who developed central pontine and extrapontine myelinolysis with no apparent evidence of hyponatremia, serum hyperosmolality or associated rapid correction, or history of alcohol abuse. On admission, the patient was lethargic with dysarthria, dysphagia, and mild tetraparesis and his face and lower extremities were severely edematous. Laboratory examination showed normoglycemia and normonatremia, although hypokalemia, elevated HbA1c, and nephrotic syndrome were also present. magnetic resonance imaging (MRI) revealed abnormal signal intensity in the pons, the deep layers of the cerebral cortex, and the adjacent white matter consistent with central pontine and extrapontine myelinolysis. Generalized edema was reduced by the use of diuretics and extracorporeal ultrafiltration without significant changes of serum sodium or osmolality. His consciousness level and paresis gradually improved within a few weeks. Our patient is a rare case of CPM associated with diabetes without apparent evidence of sodium or glucose imbalances.
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9/15. Asymptomatic pontine myelinolysis.

    A 43-year-old lady presented with bilateral foot drop due to alcohol-related peripheral neuropathy. There was no history of electrolyte disturbance or altered consciousness. Cranial nerve, bulbar and pyramidal symptoms and signs were absent. Nerve conduction studies confirmed the neuropathy. Inadvertently requested neuroimaging of brain demonstrated signal change typical of central pontine myelinolysis. Asymptomatic pontine myelinolysis occurs rarely in alcoholics in the absence of bulbar dysfunction. It is important for physicians to be aware of the clinical entity of asymptomatic pontine myelinolysis to avoid misinterpretation of abnormalities detected on cerebral imaging in alcoholic individuals.
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10/15. Central pontine myelinolysis.

    The case is described of a 46 year old female alcoholic, presenting with confusion, jaundice and reduced level of consciousness. The patient was hyponatraemic on admission and despite gradual correction of serum sodium the patient deteriorated neurologically. magnetic resonance imaging scan of the brain revealed characteristic findings of Central Pontine Myelinolysis (CPM). We provide an overview of the first published cases of CPM. The clinical and pathological features of CPM are described. No specific therapy has been shown to improve outcome; current literature advocates supportive management. Identification of patients at risk and gradual correction of hyponatraemia is recommended.
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