Intravenous lisuride in the treatment of the neuroleptic malignant syndrome.

Four severe cases of the neuroleptic malignant syndrome (NMS) were successfully treated with intravenous infusion of the dopamine agonist lisuride in doses up to 0.25 mg per hour or 4.0 mg per day, respectively. Dramatic improvements of the clinical symptoms--in particular the extrapyramidal syndrome and state of consciousness-- could be observed in two cases. The pharmacological properties of intravenous lisuride seem to make it an alternative in the treatment of NMS, which merits further study.

Local hemostasis in subarachnoid hemorrhage.

Fibrinopeptide A (FPA), platelet-secreted protein, platelet factor 4 and beta-thromboglobulin were determined in the cerebrospinal fluid of patients who had suffered from subarachnoid hemorrhage and were treated with 6 g tranexamic acid or 4 million KIU aprotinin to prevent rebleeding. Platelet-secreted proteins and FPA were cleared from the cerebrospinal fluid within 3 days after bleeding. Their vasoactive and thrombotic capability is limited to the initiation period of vasospasm that usually comes to clinical observation 3-8 days after bleeding. Increased thrombotic activity of the cerebrospinal fluid, as reflected by high levels of FPA and platelet-secreted protein, seemed to promote the occurrence of neurological deficits.

Treatment of vasospasm due to subarachnoid hemorrhage with calcium entry blockers.

Cerebral vasospasm is the most important factor causing neurological deterioration later than 72 h after subarachnoid hemorrhage (SAH). The few clinical studies investigating the effect of calcium entry blockers on SAH demonstrate that patients treated with nimodipine have a better clinical outcome. The experimental data do not explain the mechanism of the observed clinical effect. Nimodipine does not reverse large vessel spasm, but it seems that it dilates microvessels and that it exerts a protective effect on nervous tissue by influencing metabolic processes not yet known.

The disposition of intraventricularly injected 14C-5,6-DHT-melanin in, and possible routes of elimination from the rat CNS. An autoradiographic study.

14C-5,6-DHT-Melanin was injected into the left lateral ventricle of adult rats and its fate followed by light and EM autoradiography and by TEM of structures identified as labeled in preceding light micrographs. Shortly after injection, melanin particles were seen ingested by supraependymal and epiplexus cells, by cells residing in the pia-arachnoid, i.e. free subarachnoidal cells and perivascular cells, and by subependymally located microglia-like cells with intraventricular processes. Up to day four, an increase in the number of labelled phagocytes in the CSF was noted which transformed into typical reactive macrophages. After this time, many intraventricular melanin-laden phagocytes formed rounded clusters; cells of such clusters were subsequently found to invade the brain parenchyma by penetrating the ependymal lining and to accumulate in the perivascular space of brain vessels. 14C-Melanin-storing macrophages were found in the marginal sinus of the deep jugular lymph nodes suggesting emigration of CNS-derived phagocytes via lymphatics or pre-lymphatics that contact the subarachnoidal space compartment. This does not exclude the possibility that some of the macrophages leave the brain via the systemic circulation by penetrating the vascular endothelium; these may be disposed of in peripheral organs other than the lymph nodes. The ability of supraependymal, epiplexus, free subarachnoidal and perivascular cells in the pia and of subependymal microglia cells to accumulate synthetic melanin by phagocytosis suggests that these cells are local variants of the same type of resting potential phagocytes of the mammalian brain. The present study shows that 14C-5,6-DHT-melanin is an ideal phagocytic stimulant and marker for phagocytosis.