Quantitative 2-deoxyglucose mapping of the cerebellum.
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Biomedical subjects
Publications and source records attributed to R J Schwartzman.
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An i.v. bolus of (14C) deoxyglucose was injected into 4 groups of rats which simultaneously were embolized through the internal carotid artery. 15 and 30 min post embolization there was a massive decrease in (14C) deoxyglucose uptake in both deep and cortical structures. At 4 h a small zone of increased (14C) deoxyglucose uptake persisted around each embolized microsphere.
Ten Macaca mulatta monkeys were operantly conditioned to perform three motor paradigms designed to evaluate single and combination finger movements. Eight of these monkeys were retested after left medullary pyramidotomy; 2 monkeys underwent left medullary pyramidotomy prior to conditioning. All animals were tested for three years after operation. Monkeys with a completely sectioned medullary pyramid could, with time, perform difficult motor paradigms that required: (1) both individual and combination finger movements; (2) proximal upper extremity motor control; (3) thumb and index finger pincer grasp; and (4) the ability to preprogram and then execute a precision hand movement. The greater the extent of pyramidal tract destruction, the longer the time necessary for recovery of both discrete finger movement and pincer grasp, the greater the effort needed to attain recovery of hand function, and the weaker the affected musculature. The 2 animals in which pyramidotomy of at least 70% of the tract preceded efforts at operant conditioning learned and performed difficult motor paradigms. In all animals, neurological examination revealed that the most enduring and functionally most important deficit that interferes with hand function following pyramidotomy is loss of contactual hand orienting responses and failure of reflex sensorimotor adjustments.
To eliminate the morbidity associated with thymectomy, we used high-dose corticosteroids perioperatively in 32 patients who had Class II and III myasthenia gravis. All patients were extubated within 2 hours after the operation, and none required respiratory support postoperatively. The average stay in the intensive care unit was 20 hours and the average hospital stay, 6 days. Addition of high-dose corticosteroids to the perioperative managment of patients with myasthenia gravis undergoing thymectomy improved the immediate operative results and eliminated the morbidity associated with this procedure.
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We discuss five patients who had cerebral air embolisms. Clinically, these patients had early seizures, focal neurological findings, or failure to awaken from anesthesia. The patients that survived had minimal neurological deficits. We also discuss the pathophysiology of cerebral air embolism and its differentiation from "the bends." The necessity for recognizing this entity early is important in order to administer appropriate therapy.
Three sisters with benign intracranial hypertension are reported. This is the first documentation of benign intracranial hypertension in three family members. Obesity is a striking feature in these patients as well as five of the six previously reported patients with familial benign intracranial hypertension. Pregnancy and chronic dysfunctional uterine bleeding, well known predisposing factors in this syndrome when it occurs sporadically, were present in two of the sisters. A familial metabolic defect may be responsible for the intracranial hypertension in these patients.
Total external ophthalmoplegia was observed in five patients consequent to the oral or intravenous administration of phenytoin. Coincident with the ophthalmoplegia, the state of consciousness varied from drowsiness to coma and the blood levels of phenytoin ranged from 36 to 55 mug per milliliter. Initially, the eyes were fixed in midposition, and oculocephalic and oculovestibular stimulation failed to evoke either horizontal or vertical eye movements. The return of vestibulo-ocular responsiveness lagged behind the return of consciousness and other reflex activity. The mechanism underlying this ophthalmoplegia may be related to the ability of phenytoin to potentiate inhibitory synapses in the vestibulo-oculomotor pathway which utilize gamma aminobutyric acid, and to increase the discharge rate of Purkinge cells which exert an inhibitory influence on the same structures.
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