Notes on the history of the postural reflexes.
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Ten rats were observed, before and after selective unilateral ablation of the SI and/or SII cortical area, for the ability to turn toward tactile stimuli to head, limbs, or trunk. Placing and hopping postural reflexes were also observed. SI damage caused greater contralateral deficits than SII damage in all these behavioral measures; combined ablation of SI plus SII caused the greatest contralateral deficits in all measures. Partial recovery of all behaviors was observed during six postoperative test sessions, spanning 2 months. In contrast to these rats, cats studied in earlier experiments in this laboratory had shown a double dissociation, with SI damage followed by contralateral deficits in posture and movement but not passive touch, and damage to SII plus subjacent cortex by contralateral deficits in passive touch but only very small deficits in posture and movement. In other species comparisons, normal rats oriented as vigorously as do cats to tactile cues and, like cats, showed tactile responsiveness in orientation-localization greater rostrally than caudally. In both species wrong-way orientations were occasionally observed during the early postoperative period following the largest unilateral lesions. Unoperated albino rats oriented much less readily than do unoperated cats toward appetitive auditory or visual cues signaling availability of food. An accompanying theoretical review paper further examines the nature of passive and active touch in terms of these and other comparative findings.
Inhalation of organic solvents has long been known to damage various nervous systems, including cerebellum, brainstem, and pyramidal tract. However, little is known about the damage of the dopaminergic system. We report two patients with occupational long-term solvent exposure who developed postural instability without other features of parkinsonism. The concentration of HVA in CSF was decreased and the retropulsion was dramatically improved after the administration of levodopa. These findings indicate that the nigrostriatal dopaminergic neurons were disturbed by chronic solvent exposure, resulting in the loss of postural reflexes.
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BACKGROUND AND PURPOSE: Intraluminal middle cerebral artery (MCA) occlusion in rats has been reported to cause hyperthermia assumed to be caused by hypothalamic damage. To clarify the effects of hypothalamic ischemia on body temperature and to obtain a model simulating lacunar infarction, we attempted to produce small infarcts in deep structures (including the hypothalamus). METHODS: A surgical suture was advanced to occlude the origin of the hypothalamic (HTA) and/or anterior choroidal arteries (AChA) without compromise of the anterior or middle cerebral artery origins. After treatment, rectal temperature and postural reflex were examined repeatedly for 3 days under nonanesthetic conditions. The AChA and HTA and their link with small deep infarction were then confirmed by TTC, hematoxylin and eosin, and TUNEL stains and by microsurgical dissection after colored silicone perfusion into the cerebral arteries. RESULTS: Advancement of the suture near to but not occluding the MCA origin (0.5 to 1.9 mm proximal) produced small, deep, nonneocortical strokes in 25 of 36 animals without producing MCA ischemic changes. These infarctions mainly affected the hypothalamus in 13 animals (HTA area: infarct volume 6+/-1 mm(3)) and involved both the internal capsule and hypothalamus in 12 animals (HTA+AChA area infarct volume 48+/-10 mm(3)). Rats with HTA infarction alone exhibited persistent hyperthermia for 72 hours; some also had transient mild postural abnormality. The AChA+HTA infarct group showed a transient elevation of body temperature for 24 hours and definitive postural abnormality. In the remaining 11 animals, the suture was inadvertently advanced across the MCA origin, producing a large infarct that affected both the neocortex (MCA territory) and nonneocortical structures (volume 381+/-30 mm(3), n=11). The MCA infarct group displayed a transient hyperthermia and severe postural abnormality. CONCLUSIONS: When properly positioned, the intraluminal suture method permits selective AChA and/or HTA obstruction without inducing MCA territory ischemia. This model confirms that selective hypothalamic infarction produces significant and sustained temperature regulation abnormalities. The model also may be useful in investigating the pathophysiology of small, deep, end-vessel infarction.
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AIMS/HYPOTHESIS: Assessment of autonomic dysfunction provides prognostic data in diabetic patients. Clinical tests are limited to heart rate variability and blood pressure measurements. We investigated whether a detailed analysis of postural reflexes of patients during short-term head-up tilting and standing erect (both for 3 min) would provide useful clinical data. METHODS: We studied 14 control subjects and 56 patients with Type 2 diabetes, stratified into four matched groups: uncomplicated, micro-albuminuria, macro-albuminuria and autonomic neuropathy, who were tilted 55 degrees three times and were standing erect. Non-invasive finger plethysmography blood pressure measurements, using the Portapres, and impedance cardiac output measurements, using the RheoCardioMonitor, were continuously recorded throughout the study. Wavelets of the response to tilting and standing were drawn. The wavelets for the three tilts were combined to improve definition. The degree of autonomic dysfunction was quantified by calculating the baroreflex sensitivity index from the heart-rate and blood-pressure variability data. RESULTS: Baroreflex sensitivity data confirmed that autonomic dysfunction increased as diabetic complications worsened (p<0.001). Both standing and tilting resulted in an initial decrease in blood pressure followed by recovery, an increase in heart rate which was more pronounced with standing and a decrease in stroke volume. Characteristic and incremental changes in these responses were noted as the complications of diabetes worsened (p<0.001). These were a greater decrease in blood pressure with loss of the recovery phase, a reduced heart-rate response and paradoxically an increase in stroke volume. CONCLUSION/INTERPRETATION: Non-invasive blood-pressure and stroke-volume measurements recorded during short-term tilting and standing promises to be useful in assessing diabetic autonomic dysfunction.
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The effect of moderate hypoxemia upon postural sympathetic vasoconstrictor reflexes in skeletal muscle was studied in five healthy young students, aged 20-30 years. The vasoconstrictor response to head-up tilt was studied in brachio radial muscle kept at heart level and in the anterior tibial muscle. The local sympathetic veno-arteriolar axon reflex was studied in the anterior tibial muscle placed at heart level and lowered 30-50 cm below heart level. Muscle blood flow was measured by the local 133Xe wash-out technique. The measurements were carried out with the subject breathing atmospheric air and with the subject breathing 10-11% oxygen. No sign of orthostatic intolerance was seen during hypoxaemia as arterial blood pressure remained constant in the tilted position. Hypoxaemia did not alter the head-up tilt induced vasoconstriction in brachio-radial and anterior tibial muscles. The vasoconstriction elicited by the local veno-arteriolar reflex was slightly reduced during hypoxaemia. The results suggest that central orthostatic vasoconstrictor reflexes to muscle are essentially normal during moderate hypoxaemia, but local veno-arteriolar reflexes are slightly attenuated. This does not, however, significantly alter blood pressure control during head-up tilt.
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Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by "toe-up" rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young-onset Parkinson's disease, and 4 patients with MPTP-induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4 degrees amplitude, (b) 10 serial (predictable) perturbations of 10 degrees amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10 degrees amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a "default" response emerged that anticipated the 10 degrees perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic-induced parkinsonism and young-onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP-induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.
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