[Two patients with isolated vasculitis of the central nervous system]. / Twee patiënten met geïsoleerde vasculitis van het centrale zenuwstelsel.

Over the course of time, a 43-year-old woman and a 39-year-old man developed visual, sensory, motor, cerebellar and cognitive disturbances. Initially these occurred episodically, but later became continuous. Isolated vasculitis of the central nervous system was only diagnosed after brain biopsies were taken, upon which treatment with prednisone and cyclophosphamide was instituted. In both patients the symptoms persisted for 23 and 19 months, respectively, after treatment was initiated, but no new symptoms developed. The woman did, however, develop pancytopenia as a result of the cyclophosphamide treatment. Non-infectious vasculitis of the small veins and arterioles of the brain is lethal if left untreated. Leptomeningeal and cortical biopsy is essential in establishing the diagnosis in order to rule out other causative diseases. Combination therapy consisting of prednisone and cyclophosphamide for at least one year is recommended. The efficacy of this treatment is unknown due to the rarity of this disease.

Differentiation between reactive gliosis and diffuse astrocytoma by in situ hybridization.

The authors examined the use of chromosomal analysis by in situ hybridization to differentiate between nonneoplastic reactive gliosis and astrocytomas in cases in which routine histology was inconclusive. Numerical chromosomal aberrations were found in 80% of low-grade astrocytoma specimens and in none of the reactive gliosis specimens. Aneusomic tumor cells were detected in four of 13 stereotactic samples with an initially inconclusive tissue diagnosis, three of which were later diagnosed as astrocytoma. The in situ hybridization procedure may have additional value in the differential diagnosis of reactive gliosis versus low-grade astrocytoma.

[Computerized tomography markers of morphologically confirmed hemorrhagic brain infarct]. / Computertomographische Merkmale von morphologisch gesicherten hämorrhagischen Hirninfarkten.

Radiological differentiation between hemorrhagic infarction and intracerebral hemorrhage is important for patient management. To ascertain CT features of hemorrhagic infarction, we studied the findings in 19 cases with autopsy-proven hemorrhagic infarction. Most cases had multiple, mainly cortically located, small hyperdensities. However, some presented with a single hyperdensity, deeply located, that could be mistaken for primary intracerebral hematoma. Hemorrhagic infarctions usually present as multiple, small hyperdensities within a hypodense area compatible with an arterial territory. The shape can be round, slitlike, curvilinear, or spotted. Most often the hyperdensities are located cortically; however, some larger, deeply located hyperdensities may falsely suggest primary intracerebral hematoma. Some guidelines for a more reliable radiological separation between hemorrhagic infarctions and intracerebral hematomas are suggested.

Timing of autopsy-confirmed hemorrhagic infarction with reference to cardioembolic stroke.

We studied the temporal profile of hemorrhagic transformation in 34 cases with autopsy-confirmed hemorrhagic infarction who died within 15 days following a supratentorial brain infarct, provided they had undergone computed tomography. It appeared that within 4 days, at least 76% (95% confidence interval 39-100%) of 21 cardioembolic strokes had become hemorrhagic. We conclude that if anticoagulation is considered in cardioembolic stroke, such treatment should not be started sooner than at least 4 days after the onset of stroke, provided that computed tomography at that time shows no hemorrhagic infarction.

Hemorrhagic infarction on CT in cardioembolic stroke.

CT-scans of 103 patients anticoagulated following cardioembolic stroke were evaluated. Data were taken from a prospective registry on the risk of early anticoagulant treatment in patients with cardioembolic stroke. Ninety-three patients had CT within 24 hours after stroke onset. Sixty-six of 103 CT-scans showed infarction. On initial CT five hemorrhagic infarcts were found (5%). Of 35 follow-up CT-scans randomly performed during anticoagulant treatment, six (= 17%) showed hemorrhagic infarction without clinical worsening. It is argued that a cardioembolic cause of stroke cannot be infered by the presence of HI on CT. In patients with a cardioembolic stroke the value of CT lies in minimizing the risk of early anticoagulant treatment.

Cerebral hemorrhagic infarction at autopsy: cardiac embolic cause and the relationship to the cause of death.

In 48 patients dying within 15 days following a supra-tentorial cerebral infarct, the presence of hemorrhagic infarction at autopsy was related to a cardiac embolic cause of the infarct, and to the cause of death. Hemorrhagic infarcts were more common among patients dying from brain herniation than among those dying from a non-cerebral cause. Cardiac embolic strokes were more often hemorrhagic at autopsy than strokes without such cause; this could be explained by a significant higher rate of brain herniation and death after embolic stroke. On the other hand infarcts with extended hemorrhages more often tended to have a cardiac than a non-cardiac cause. These data, together with earlier clinical findings suggest that autopsy studies are biased in relating hemorrhagic infarction almost exclusively to a cardiac embolic cause of stroke, although cardiac emboli may produce more extended hemorrhages.