Does the extent of axonal loss and demyelination from chronic lesions in multiple sclerosis correlate with the clinical subgroup?
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OBJECTIVE: To determine non-invasively the relation between the degree of axonal loss and the extent of demyelination in chronic lesions visible on MRI in patients with different subgroups of clinically definite multiple sclerosis using (1)H magnetic resonance spectroscopy ((1)H MRS) and magnetisation transfer imaging (MT). Conventional MRI is unable to differentiate between the various pathological processes occurring in the multiple sclerosis lesion. There are, however, newer MR techniques which show promise in this respect. METHODS: (1)H MRS and MT were performed in 18 patients with clinically definite multiple sclerosis who had a wide range of disability and disease duration. RESULTS: A significant correlation was found between a reduction in the concentration of N-acetyl aspartate (NAA; an in vivo marker of axonal loss or dysfunction) and a reduction in MT ratio (a probable marker of demyelination) in patients who had entered the secondary progressive stage of the disease. Patients with minimal disability after a disease duration of greater than 10 years-so called benign multiple sclerosis-showed a relative preservation of NAA and MT. CONCLUSIONS: Because a reduction in MT seems to be a relative marker for demyelination and a reduction of NAA from chronic lesions is indicative of axonal loss, this study supports the hypothesis that demyelination and axonal loss occur in the same chronic multiple sclerosis lesions. In addition, the degree of axonal loss and demyelination correlates with clinical heterogeneity. (+info)
Slowly progressive dystonia following central pontine and extrapontine myelinolysis.
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A 28-year-old woman was hospitalized with dysarthria and oro-mandibular and upper limb dystonia. Approximately 8 years prior to the current admission, the woman became severely hyponatremic due to traumatic subarachnoid hemorrhage-related SIADH. Brain MRIs showed a signal increase in the central pons, thalamus and striatum on T2 weighted images compatible with central pontine and extrapontine myelinolysis. From a few months after that event, dystonia progressed slowly over the subsequent 8 years. We speculate that the particular damage chiefly to the myelin structures by myelinolytic process may have caused an extremely slow plastic reorganization of the neural structures, giving rise to progressive dystonia. (+info)
Treatment of severe hyponatremia: conventional and novel aspects.
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Hyponatremia is a frequent electrolyte disorder. A hyponatremia is called acute severe (<115 mM) when the duration has been <36 to 48 h. Such patients often have advanced symptoms as a result of brain edema. Acute severe hyponatremia is a medical emergency. It should be corrected rapidly to approximately 130 mM to prevent permanent brain damage. In contrast, in chronic severe hyponatremia (>4 to 6 d), there is no brain edema and symptoms are usually mild. In such patients, a number of authors have recommended a correction rate <0.5 mM/h to approximately 130 mM to minimize the risk of cerebral myelinolysis. Sometimes it is not possible to diagnose whether a severe hyponatremia is acute or chronic. In such cases, an initial imaging procedure is helpful in deciding whether rapid or slow correction should be prescribed. The modalities of treatment of severe hyponatremia have so far consisted of infusions of hypertonic saline plus fluid restriction. In the near future, vasopressin antagonists will become available. Preliminary experience has already demonstrated their efficiency of inducing a sustained water diuresis and a correction of hyponatremia. (+info)
MR imaging of seven presumed cases of central pontine and extrapontine myelinolysis.
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MRI was performed in seven patients with presumed central pontine and extrapontine myelinolysis. The underlying diseases were diabetes, lung cancer, Wilson disease, trauma, alcoholism, renal insufficiency and hemodialysis. CPM was found in four cases (in two of them extrapontine lesions were considered as resulting from Wilson disease), CPM and EPM in three patients. The localization of extrapontine changes included cerebellum, cerebral peduncles, caudate and lentiform nuclei, internal capsules, white matter and cortex of the cerebrum. (+info)
Decreased diffusion in central pontine myelinolysis.
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Two patients with central pontine myelinolysis (CPM) were studied with diffusion-weighted MR imaging 1 week after onset of tetraplegia. In both patients, affected white matter showed hyperintensity on diffusion-weighted images associated with a decrease in apparent diffusion coefficient (ADC) values. In one patient studied serially, ADC values normalized by 3 weeks after tetraplegia. Early in the clinical course, diagnosis of CPM can sometimes be difficult. Hyperintensity on diffusion-weighted images may therefore have diagnostic utility. Decreased lesional ADC values support the notion that CPM is a consequence of relative intracellular hypotonicity. (+info)
Serial magnetic resonance imaging of central pontine myelinolysis.
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Central Pontine Myelinolysis (CPM) is a rare neurologic complication after liver transplantation. The true incidence of CPM after orthotopic liver transplantation remains an estimate. However, with the introduction of magnetic resonance imaging, early recognition became feasible. In this report, we present a case of rapid resolution of CPM followed by serial magnetic resonance imaging scans. (+info)
A 47-year-old alcoholic man with progressive abnormal gait.
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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)
Central pontine myelinolysis associated with hypokalaemia in anorexia nervosa.
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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)