Morphology of defectively perfused brains in patients with persistent extracranial circulation.
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Biomedical subjects
Publications and source records attributed to J Korein.
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A placebo-controlled crossover study of behavioral effects of triiodothyronine (T3) was conducted in 30 young clinically euthyroid autistic children. Multiple independent raters and multiple rating scales were used. Except for a few symptoms that were reduced on T3, the drug did not differ from placebo. Time itself accounted for most of the improvement in the whole sample. As a group, the lower IQ children responded to T3. The individual children who were responders could not be defined by any parameter.
An innocuous intravenous portable radioisotopic test using technetium 99m pertechnetate was employed to demonstrate the deficit of cerebral blood flow associated with brain death. The results are compared to those of bilateral carotid and vertebral angiography in 20 patients. Absence of a bolus tracing from the head in the presence of a control tracing of a bolus from the femoral artery in two successive studies one hour apart reliably correlated with the clinical and electroencephalographic findings signifying cerebral death in comatose, apneic patients. Angiography indicated absence of intracranial circulation in 10 patients. Stasis filling or retrograde emptying of arterial vessels (or both) occurred in 7 patients. There was no evidence of venous filling in any of these 17 patients; all of them had either an absent head bolus or an "intermediate tracing." Results indicate that either form of tracing represents a critical decrease of cerebral blood flow. Two other patients had evidence of severely impaired abnormal posterior fossa circulation without angiographic evidence of cerebral circulation; both of these patients had an absent head bolus. An additional patient had an unusually small head bolus, and angiography revealed extravasation of radiopaque material but no evidence of intracranial circulation. We conclude that the bolus technique is a helpful adjunct in diagnosing brain death.
Diffuse necrosis and autolysis were found in the brains from 6 comatose, respirator-supported patients in whom the bolus technique demonstrated no cerebral blood flow during a period exceeding 20 hours prior to cardiac death. When blood flow was insufficient to produce a bolus, there was no evidence of active tissue response to necrosis. In 6 similar patients, when cerebral blood flow was detected by the bolus technique, less extensive necrosis was observed postmortem and there was active tissue response.
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Brain insults, regardless of etiology, may disrupt the CNS servosystems concerned with patterned voluntary movements and result in disorders of such movement. To aid functional recovery, we applied in these patients oscilloscopic display of digitally integrated EMG, monitored from malfunctioning primary movers, during attempted execution of movement (sensory feedback therapy). Such display provided the patient with an immediate and continuous visual feedback loop reflecting the events underlying the movement and occuring in the monitored muscle (force, displacement and rate). This information is essential for motor control of patterned voluntary movement. Coupled with auditory reward for optimal performance, such feedback also assumed reinforcing qualities and motivated the patient to execute voluntary movements with progressive improvement. Sixty patients with longstanding CNS insult, resulting in motor impairment, were treated and followed for periods of four months to four years. One half of these patients learned and retained voluntary movements that significantly improved their functional capabilities. Temporary substitution of feedback information about fundamental events in dysfunctional muscles can apparently be of lasting value in treatment of some patients with brain insult.
Total cerebral angiography has been performed on five patients who were demonstrated to have a cerebral circulatory deficit by the bedside isotope flow determination. In all five instances cerebral angiography confirmed the results of the isotope examination.
In summary, then, without consideration of specific circuits or transmitter agents, one can conceive of a hypothetical model that involves both learning and the functional nature of the defect in torticollis and focal dystonia to describe the results obtained. The model must be further elaborated upon and tested, preferably in a quantitative manner. Naturally, the specific finding of a defective transmitter agent (e.g., GABA) such as described in parkinsonian syndrome (dopamine) or the interruption of a specific pathway that causes and improves a dyskinesia is desirable. In this chapter we have described the use of integrated EMG feedback for the treatment of focal dystonia or spasmodic torticollis. Although we have achieved significant results, it remains clear that further research in the treatment of these disorders is required. However, since this treatment does not require medication or surgery and the possibility for significant improvement is greater than 40%, it should be attempted in patients with focal dystonia or torticollis prior to other forms of therapy. SFT should be considered as a standard mode in the medical armamentarium used for the treatment of these disorders, either primarily or in conjunction with other forms of medical, surgical, and physical therapy.
Advances in the understanding of the relationship of proprioceptive (kinesthetic) feedback to motor physiology have prompted the study of therapeutic effects of audiovisual displays of EMG activity. Patients with various manifestations of disturbed neuromotor control were studied prospectively for three years. This group included 114 patients with hemiparesis, torticollis, dystonia, and spinal cord or peripheral nerve injury. Initially, all but one of these patients had some residual volitional motor activity, which was insufficient for adequate function, and all patients had had conventional therapy with little or no functional recovery. Prior to EMG feedback therapy, the duration of illness was from three months to 35 years. The shaping of a patient's motor responses usually occurred gradually, often over an 8 to 12 week period. This modification was accomplished by feeding processed audio-visual signals back to the patient. These signals were proportional to the degree of activity of the muscles responsible for the defective function. The concept of microvolt-second, as a unit of muscle activity, is introduced and defined. Patterned movements, which were previously defective were observed to improve to varying degrees. Following the initial course of treatment, reinforcement was required by some patients. The mechanisms of improvement after EMG feeback therapy are not well understood; however, some hypotheses are presented. The results of this study indicate that EMG feedback therapy may induce significant functional recovery in patients with disturbed neuromotor control.
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Dopamine Beta Hydroxylase (DBH) activity was determined in 24 deeply comatose patients enrolled in the Collaborative Study of Cerebral Survival. All patients had been without cerebral responsiveness or spontaneous respirations for at least 15 minutes. Patients were examined, EEGs performed and blood for DBH drawn within 24 hours of the cerebral insult. DBH activity was lower in the deeply comatose patients than in a group of 51 age matched normal individuals. It is postulated that destruction or inactivation of the central nervous system (CNS) and particularly of the cerebrum may result in lowered serum DBH activity through decreased activation of sympathetic nerve terminals.
A portable radioisotopic technique was developed to demonstrate cerebral circulatory deficit, as part of a collaborative study to define and diagnose cerebral death simply and rapidly, in comatose, apneic patients with electrocerebral silence. The method involves an intravenous injection of 2mCi of 99mTcO4, and recording time/activity curves over the cranial cavity and a femoral artery simultaneously, using twin probe radioisotope detector equipment. Eight comatose, apneic patients had 142 studies in conjunction with clinical electroencephalographic and other laboratory evaluations. The results indicate that the absence of a bolus tracing from the head, as contrasted to the usual bolus seen is indicative of significant circulatory deficit to the cerebrum. This test may be used as an adjunct in confirming the diagnosis of cerebral death. A normal bolus tracing should be simultaneously observed over a femoral artery and this is used as a control. The method is safe and simple and offers significant information about the irreversibility of cerebral blood flow. Although further studies are indicated, the method appears to be most promising as a fundamental bedside laboratory test in the diagnosis of cerebral death in conjunction with other clinical and laboratory criteria.
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