Chest percussion artifact.
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Levels of PLCgamma, a phospholipase C (PLC) isozyme, were significantly increased in the cytosol in the injured left cortex (LC) at 5, 30 and 120 min after brain injury. In the same site, although levels of membrane PLCgamma did not alter at 5 and 30 min, they were found to be decreased at 2 h after brain injury. In general, the levels of both cytosolic and membrane PLCgamma were unaltered in the contralateral right cortex (RC), ipsilateral left hippocampus (LH) and contralateral right hippocampus (RH) between 5 and 120 min after brain injury. These results suggest that, in addition to well-proposed excitatory neurotransmitter-receptor systems, increased levels of PLCgamma may also contribute to alterations in PIP2 signal transduction pathway, particularly in the greatest injury site (LC) after lateral FP brain injury.
Five normal men and 70 spinal cord injury male patients underwent 100 studies with the multiple pressure recording technique, incorporating the continuous infusion principle for sphincter pressure monitoring. Gross cystosphincteric dyssynergia was noted in the majority of patients with complete upper motor neuron bladders less than 2 years in duration. Some form of synergic voiding patterns was noted, mostly in patients with incomplete upper motor neuron bladders. The external sphincter tends to be synergic in late cases of upper moto neuron bladders. Internal sphincter dyssynergia is uncommon in cases of injuries less than 2 years in duration, with the exception of patients who have autonomic dysreflexia. Bladder neck obstruction seems to be more common in late lesions secondary to global hypertrophy of the bladder. Rehabilitation maneuvers and bethanechol chloride administration may exaggerate detrusor sphincter dyssynergia and injudicious use of such procedures could be detrimental to the urinary tract.
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