Central pontine myelinolysis

Landers, James W.; Chason, Jacob L.; Samuel, Viji

doi:10.1212/wnl.15.10.968

Cited by 24 publications

(8 citation statements)

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“…Various predisposing factors have been implicated in the pathogenesis of cerebral venous thrombosis. These are pregnancy, puerperium, synthetic steroid contraceptives (2,6,7,9,10,14,24), blood dyscrasias including increased coagulability of blood (6,24), anaemias (14,24) and dehydration (14,17). Infection is a well recognized predisposing factor and cases with infection as a predisposing factor have been excluded from this report.…”

Section: Discussionmentioning

confidence: 99%

Dural sinus and cerebral venous thrombosis

Nagpal¹

1983

Neurosurg. Rev.

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Eighty patients with 'primary' dural sinus and cerebral venous thrombosis were seen over a period of 16 years. There was an equal distribution amongst the sexes and the largest number of patients presented in the third decade. The commonest predisposing factors were puerperium, pregnancy, synthetic steroid contraceptives and anaemia. Seventy patients presented in an acute fashion with headache, focal or generalized seizures and focal neurological deficits. Ten patients presented in a subacute to chronic manner, with features to suggest an intracerebral space-occupying lesion. The investigation of choice was angiography. Thirty-five patients were treated conservatively with anticonvulsants, low molecular weight dextran and anti-oedema measures. Anti-coagulants were not used for fear of haemorrhage in the associated red infarcts. Antibiotics were not needed as infection played no part in the pathogenesis. Thirty-four patients needed an operation which took the form of a decompressive craniotomy and dural closure with the aid of a pericranial graft. The conservatively treated group appeared to fare better only because it included patients with a milder ictus. Forty patients improved, three remained unchanged and 37 expired. Autopsy in the 35 of the 37 patients showed cortical vein and sinus thrombosis and oedema with a haemorrhagic infarct. Long term follow-up showed good recovery of neurological function, but epilepsy was a troublesome sequel and needs regular anti-epileptic drug treatment.

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Section: Discussionmentioning

confidence: 99%

Dural sinus and cerebral venous thrombosis

Nagpal¹

1983

Neurosurg. Rev.

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“…Bei dem Versuch, die Genese der ZPM zu kl~iren, ist man trotz unterschiedlichster Denkansgtze aus klinischer, pathophysiologischer, biochemischer und anatomischer Sicht bis heute nicht zu einem befriedigenden Ergebnis gekommen [1,10,24,35,45,57,62,69,74,82,86]. H6chstwahrscheinlich liegt nicht eine einzige isolierte Sch~idigung vor, sondern ein Syndrom mit kreislaufbedingter St6rung der Mikrozirkulation, C)dembildung und Austritt von myelintoxischen Substanzen.…”

Section: Fallunclassified

“…Die Lokalisation der Herde im Bereich des ,,zentralen Brfickensumpfes", einer Stelle, an der bevorzugt auch Sekund~ire Hirnstammblutungen nach supratentorialer Volumenzunahme zu finden sind [91], l~gt den Rfickschlug zu, dab es in Verbindung mit einem m6glicherweise passageren Hirn6dem zur Schrankenst6rung kommt und myelintoxische Produkte austreten, die zu einem Prozel3 ft~hren, der sich entweder selbst unterhaltend oder bei weiterbestehender Noxe zentrifugal ausdehnt [12,50,57]. M6glicherweise reicht dazu eine einmalige StOrung nicht aus, sondern es sind h~iufigere Episoden erforderlich.…”

Section: Fallunclassified

Zentrale pontine Myelinolyse Morphologie und forensische Bedeutung

Bratzke

Neumann

1989

Z Rechtsmed

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Central pontine myelinolysis (CPM) evidently occurs more frequently than had been assumed up to now owing to the cases that have been substantiated solely on the basis of pathological anatomy. Its genesis is still unclarified. Computed tomography and magnetic resonance methods allow detection of the foci while the affected person is still alive. They are clearly capable of regression and are not automatically accompanied by a poor prognosis. Since an iatrogenic factor (forced compensation of hyponatremia) is increasingly under discussion as the cause of CPM, the condition also has substantial significance from a forensic point of view. On the basis of a prospective study on CPM confirmed in 100 brains of alcoholics, as well as 4 further cases from the forensic autopsy material, it is shown that hyponatremia is not likely to be the sole triggering factor. The course of the condition in the cases investigated shows that the capacity for action may be preserved up to death (which has occurred for other reasons) in not very pronounced CPM. In questionable violent and other unclear deaths, CPM must also be considered a possible cause of death. The various hypotheses on its etiology in the extensive literature are compared with the findings in our own cases and discussed.

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“…In such instances, altered levels of consciousness have been reported. The features of the pontine-extrapontine form of the disease have recently been discussed in detail 1471.A second advance has been the increasingly strong association of CPM with derangements of serum sodium, usually hyponatremia [1,9,11,13,22,27,37,40, 471. Wright, Laureno, and Victor f47f correlated the time of occurrence of the sodium derangements with the histological age of the pontine lesions.…”

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confidence: 99%

Central pontine myelinolysis following rapid correction of hyponatremia

Laureno

1983

Annals of Neurology

228

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Central pontine and extrapontine myelinolysis was experimentally produced in dogs by the rapid correction of severe, sustained, vasopressin-induced hyponatremia. Hyponatremia alone or slowly corrected hyponatremia did not produce the disease. Affected dogs showed rigid quadriparesis. The central pons, lateral aspects of the thalamus and adjacent internal capsules, deep layers of cerebral cortex and subjacent white matter, cerebellum, and other regions were symmetrically involved. Myelin and oligodendroglia were affected out of proportion to axons and neurons. Thus, the clinical features, the distribution of the lesions, and their histological features closely resemble the human disease. These experiments document an electrolyte manipulation that can cause permanent neuropathological lesions. Taken with the available clinical data on human patients, the experimental results indicate that human myelinolysis may be due to a rapid increase in serum sodium from previously low levels, and that rapid normalization of severe, sustained hyponatremia should therefore be avoided.

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Central pontine myelinolysis

Cited by 24 publications

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Dural sinus and cerebral venous thrombosis

Dural sinus and cerebral venous thrombosis

Zentrale pontine Myelinolyse Morphologie und forensische Bedeutung

Central pontine myelinolysis following rapid correction of hyponatremia

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