Faculty Bibliography

Our ongoing study of central pallidotomy for the control of Parkison's disease in selected patients has provided the opportunity to explore the topographical and somatotopic organization of the human globus pallidus. Utilizing microelectrode techniques we have obtained recordings which were correlated with data from MPTP-parkinsonian primates. In addition, we performed pre- and postoperative FDG/PET scans in these patients. Our studies reveal similarities between the MPTP-parkisonian primate model and human Parkinson's disease in terms of physiological recordings and responses. However, we have encountered significant differences between dominant and nondominant hemisphere representations, particularly for the hand, in the human. In addition, our PET studies confirmed, as in previous parkinsonian primate models, glucose hypermetabolism in the lenticular area of Parkinson's disease patients. This hypermetabolism is dramatically altered by creation of a lesion in the globus pallidus medialis. This is demonstrated by follow-up PET scans which reveal not only a decrease in metabolism of the operated lenticular region, but also in the frontal cortical projections. These combined observations of the cellular activity in globus pallidus and the observed changes in PET metabolism support the selection of the pallidum for lesioning and control of Parkinson's disease, and offer insight into the underlying physiology of this disorder. The above physiological and PET data will be clinically correlated with our ongoing series of 35+ patients

Poststroke pain syndrome is commonly regarded as an intractable disease. We describe four patients who responded to an intravenous lidocaine infusion for relief of central pain after a stroke. The infusion was administered over a 48-hour period after an initial bolus of 50 to 100 mg intravenously over 40 to 120 seconds. Pain intensity and pain relief were measured by visual analog and numeric scales. All patients reported some relief within the first 12 hours of infusion. All patients were subsequently given a trial of mexiletine, an oral congener of lidocaine. Two have continued taking the drug and report excellent relief at 12 months' follow-up; the other two had side effects that precluded further use of the drug. We conclude that lidocaine can reduce poststroke pain, and we propose a treatment algorithm based on our experience with 40 additional patients treated for other neuropathic pain states.

Central pain syndrome is defined as pain associated with a lesion of the central nervous system. It has a low incidence but is frequently intractable and does not have effective treatment. The cause of central pain is speculative; however, the single common sensory abnormality in patients with central pain is interruption of spinothalamocortical nociceptive pathways. It appears that severe central nervous system lesions, with total destruction of ascending sensory systems, do not lead to a central pain syndrome; and that setting of mild, moderate, or severe disruption of the anterolateral ascending system with partial or complete preservation of the dorsal column/medial lemniscus functions is most frequently associated with central pain syndrome. Furthermore, even during remission, dysesthesias and pain could be triggered by additional afferent input to the large fiber/dorsal column/medial lemniscus system and, once established, they may not be abolished by additional deafferentation

We studied a previously healthy 25-year-old woman with the anterior spinal artery syndrome, a rare thoracocervical myelopathy with multiple potential etiologies. Quantitative and clinical sensory examination showed dissociated loss of pin-prick and temperature discrimination below the level of the lesion, with normal light touch, vibratory, and position sense. Magnetic resonance imaging was consistent with cervical spinal cord infarction. Median SEPs showed normal Erb's potential with absent spinal N13- and normal scalp N20- latency. Tibial SEPs showed normal lumbosacral responses and normal scalp P30- latency. Both median and tibial nerve stimulation produced cortical responses of unusually large amplitude (median 38 microV, tibial 17 microV). We hypothesize that large SEP amplitudes in this patient resulted from loss of anterolateral inhibitory influences on the dorsal column-medial lemniscal system.

Three male and two female patients with anorgasmia and dissociated sensory loss due to an anterior spinal cord syndrome are described. Clinical, neurophysiological and quantitative sensory evaluation revealed preservation of the large fibre dorsal column functions from the lumbosacral segments with concomitant severe dysfunction or absence of the small fibre neospinothalamic mediated functions. These findings indicate a role for the spinothalamic system in orgasm.

A total of 13 patients with proved lesions of the cauda equina underwent neurological evaluation. All patients had video urodynamic testing, while 9 underwent a varying combination of pelvic floor electromyography, lumbosacral evoked potentials to tibial nerve stimulation and the sympathetic skin response from the perineum. All patients had detrusor areflexia with varying degrees of bladder neck incompetence. Reports of clinical and experimental studies are discussed in relation to the pathophysiology of bladder neck function following lesions of the pudendal and preganglionic pelvic nerve to explain why there have been conflicting reports in the literature regarding bladder neck function with lesions of the cauda equina. The adaptive changes observed in the experimental animal, consisting of random regeneration of the cholinergic neuroeffective junctions, adrenergic hyperinnervation and an increased sensitivity of the prejunctional inhibitory muscarinic receptors on the adrenergic nerve, may explain the degree of variability of bladder neck incompetence observed clinically.

In 5 cases suffering from intractable seizures and ictal onset in exquisite (primary somatosensory or language related) cortex, surgical therapy has been done consisting wholly or in part of multiple subpial transections. In two cases with involvement of the primary somatosensory cortex, good seizure control without detectable neurological deficit was achieved. In the other three cases with involvement of the language cortex, deficits were minimal and cleared with time. Patients became seizure-free