In the past, stereotactic surgical intervention for Parkinson's disease was considered indicated only in those patients with active motor manifestations that were refractory to pharmacological therapy, manifestations such as tremor, rigidity, dystonia, and dyskinesia. With the reintroduction and refinement of Leksell's posteroventral pallidotomy, both akinetic and hyperkinetic symptoms are now amenable to surgical treatment. We have analyzed the results of 126 patients who underwent either unilateral (n = 58) or bilateral (n = 68) posteroventral pallidotomies. The Unified Parkinson's Disease Rating Scale and Hoehn and Yahr Staging Scale were used for preoperative and postoperative objective assessments. Postoperative follow-up evaluation occurred initially at 1 week and subsequently at intervals between 1 and 12 months (mean = 4.5 months) after surgery. Although individual motor subscores on the Unified Parkinson's Disease Rating Scale were significantly reduced (n = 126, P < or = 0.01), the most dramatic findings were the reversal of akinetic symptoms and the elimination of dyskinesia and profound "off" periods. These clinical results, combined with intraoperative microelectrode records revealing pallidal neuronal hyperactivity, suggest a reconsideration of the pathophysiology of akinesia and point to possible mechanisms of akinesia improvement by posteroventral pallidotomy in some parkinsonian subgroups.

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The tethered cord syndrome is a clinical entity manifested by progressive motor and sensory changes in the legs, incontinence, back of leg pain, and scoliosis. In order to elucidate the pathophysiology involved in the tethered cord, the reduction/oxidation ratio (redox) was used in vivo of cytochrome alpha,alpha 3 to signal oxidative metabolic functioning in human examples of tethered cord and in animal models. Studies in experimental models indicate marked metabolic and electrophysiological susceptibility to hypoxic stress to lumbosacral cord under traction with greater weights (3, 4 or 5 gm). Similar effects were demonstrated in redox behavior of human tethered cord during surgical procedures. The authors conclude that symptoms and signs of tethered cord are concomitant with lumbosacral neuronal dysfunction which could be due to impairment of mitochondrial oxidative metabolism under constant or intermittent cord stretching. It is assumed that prolonged or accentuated neuronal dysfunction may lead to structural damage to the neuronal perikarya and later of the axons. Untethering procedures in human tethered cord improve oxidative metabolism, and probably facilitate the repair mechanism of injured neurons.

✓Tethered cord syndrome (TCS) is a stretch-induced functional disorder of the spinal cord due to the fact that its caudal portion is anchored by an inelastic structure. The functional lesion of TCS is generally situated in the lumbosacral cord, and many authors have shown that the syndrome is reversible via surgery to untether the cord. To clarify the expressions relevant to TCS, such as “cord tethering” and “tethered cord,” the authors have formulated three categories. These categories include cases that show the anatomical appearance of spinal cord stretching. Among them, Category 1 is isolated to represent the “true TCS.” The authors focus their discussion of the pathophysiology of TCS on Category 1 to explain the impaired oxidative metabolism and electrophysiological derangements within the tethered spinal cord, which is the primary intrinsic cause of the dysfunction. Furthermore, they extend the discussion to the extrinsic (outside the spinal cord) factors and other complex conditions that mimic TCS.