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At least 217 records · Page 12Linked to original sources
PubMed1989

[Soft palate myoclonus and opsoclonus in disorders of cerebrovascular circulation in the vertebrobasilar system].

In 4 patients with residual cerebral circulation disorders in the vertebrobasilar vascular bed, the myoclonus of soft palate, pharynx, larynx, tongue (in 2 cases comprising opsoclonus) developed among other signs of brainstem or cerebellar lesions. Myoclonic hyperkinesia emerged after 1.5 to 4 months of the disease, not in its acute period, and was not related to second stroke. With focal neurological signs analyzed, the syndrome of the soft palate myoclonus++ plus opsoclonus appeared in connection with the lesions of upper cerebellar crus where dento olivary++ pathway and the fibers connecting the cerebellar flocculus with oculomotor nuclei run. Soft palate myoclonus++ without opsoclonus emerges with lesions of cerebellar dental nucleus and central pathway of the brainstem tegmentum.

Adult↗
PubMedDate not supplied

Cerebrovascular circulation "steal" syndrome secondary to a voluminous retrotracheal goiter.

A case of recurrent transient ischaemic attacks in the brain resolved after removal of a voluminous retrotracheal goiter is presented. The presence of congenital atretic left vertebral artery, associated with impairment of left carotid artery blood flow by a very large inferior thyroid artery, probably caused the episodes to transient ischaemic attack.

Brain↗
PubMedDate not supplied

[Features of central hemodynamics in patients with ischemic disorders of cerebrovascular circulation].

Central hemodynamics was studied in 75 persons; 10 were healthy, 65 had abnormal tortuousness, stenosis, and thrombosis of the internal carotid arteries in the late post-stroke period. Twenty-one patients suffered from arterial hypertension. An increase in the cardiac output was revealed, which was associated with centripetal effects and was compensatory in character.

Adult↗
PubMed1996

[Regional cerebral blood circulation and cerebrovascular reserve capacity as indications for in vascular reconstructive surgery].

Effect of Extra-Intracranial Bypass and Carotid Thrombendarterectomy. The causal treatment of cerebral ischemia requires an exact analysis of the basic deficit of cerebral blood flow. Cerebral ischemia can be the result of hemodynamic insufficiency or frequently a consequence of thromboembolic event. The distinction of both forms of ischemia is possible only by dynamic measuring of regional cerebral blood flow and evaluation of the cerebral vascular reserve capacity. This allows to select of a small group of patients who suffer from carotid occlusion or a combined occlusion with stenosis of the contralateral side, where a characteristic disturbance of the cerebrovascular reserve capacity can be proved. By performing an extra-intracranial bypass, the cerebral collateral blood supply can be improved in order to reduce the risk of stroke. In this study 26 patients received an extra-intracranial bypass. 7 weeks after surgery a normalization of the limited cerebrovascular reserve capacity was observed. With regard to carotid stenosis, thrombendarterectomy was conducted in 63 patients. Although the cerebrovascular reserve capacity had not been impaired in this group preoperatively, a further increase was observed following thrombendarterectomy. It is indisputable that the indication for thrombendarterectomy is aiming towards elimination of the source of emboli. However, our results indicate that thrombendarterectomy has an additionally positive hemodynamic effect.

Adult↗
PubMed1984

Effects of barbiturates, phencyclidine, ketamine and analogs on cerebral circulation and cerebrovascular muscle.

Although barbiturates are often effective as therapeutic agents in several types of brain ischemia, there is no consensus as to their mechanisms of action. Exactly why other intravenous anesthetics such as ketamine are not effective therapies in brain ischemia is not known. Structural analogs of ketamine such as phencyclidine (PCP) not only exert potent hallucinogenic properties and are widely abused drugs, but often result in hypertensive encephalopathies and death. In view of the paucity of information on the cerebral circulatory actions of barbiturates, ketamine and PCP (and analogs), in-vivo (microcirculatory) and in-vitro studies were undertaken. Barbiturates, in anesthetic concentrations (e.g., 10(-5) to 10(-4) M), were found to exert direct vasodilator actions on cerebral arterial smooth muscle; these relaxant actions appear to be related to inhibition of calcium ion (Ca2+) influx in cerebral vessels. The latter may be important in the salutory actions of barbiturates in brain ischemia, head trauma and cerebrovasospasm. Unlike barbiturates, ketamine was found to exert spasmogenic actions on cerebral arteries, which may aid in explaining the inability of this anesthetic to be of therapeutic value in brain ischemia. PCP and its analogs, as well as other hallucinogenic molecules (e.g., LSD, mescaline) produced spasms in cerebral arterioles, venules and arteries in concentrations which mimic their hallucinogenic potencies. Distinct PCP-like receptors which subserve contraction appear to exist on large as well as microscopic cerebral blood vessels. Spasms induced by PCP, its analogs and ketamine can be readily reversed or prevented completely by calcium channel blockers. The latter agents could be quite useful, clinically, in prevention of cerebral infarction, hypertension and fatality associated with PCP (and analogs) intoxication.

Barbiturates↗