The aim of this study is to assess brain activity measured during continuous performance of design tracing tasks. Three issues were addressed: identification of brain areas involved in performing maze and square tracing tasks, investigation of differences and similarities in these areas related to dominant and nondominant hand performance, and most importantly, examination of the effects of practice in these areas. A total of 32 normal, right-handed subjects were instructed to move a pen with the dominant right hand (16 subjects) or nondominant left hand (16 subjects) continuously through cut-out maze and square patterns with their eyes closed during a 40-s positron emission tomography (PET) scan to measure regional blood flow. There were six conditions: 1) holding the pen on a writing tablet without moving it (rest condition); 2) tracing a maze without practice; 3) tracing the same maze after 10 min of practice; 4) tracing a novel maze; and tracing an easily learned square design at 5) high or 6) low speed. To identify brain areas generally related to continuous tracing, data analyses were performed on the combined data acquired during the five tracing scans minus rest conditions. Areas activated included: primary and secondary motor areas, somatosensory, parietal, and inferior frontal cortex, thalamus, and several cerebellar regions. Then comparisons were made between right- and left-hand performance. There were no significant differences in performance. As for brain activations, only primary motor cortex and anterior cerebellum showed activations that switched with hand of performance. All other areas, with the exception of the midbrain, showed activations that were common for both right- and left-hand performance. These areas were further analyzed for significant conditional effects. We found patterns of activation related to velocity in the contralateral primary motor cortex, related to unskilled performance in right premotor and parietal areas and left cerebellum, related to skilled performance in supplementary motor area (SMA), and related to the level of capacity at which subjects were performing in left premotor cortex, ipsilateral anterior cerebellum, right posterior cerebellum and right dentate nucleus. These findings demonstrate two important principles: 1) practice produces a shift in activity from one set of areas to a different area and 2) practice-related activations appeared in the same hemisphere regardless of the hand used, suggesting that some of the areas related to maze learning must code information at an abstract level that is distinct from the motor performance of the task itself.

We evaluated sensorimotor processing in patients with writer's cramp using PET and H2(15)O blood flow scans. The study included six right-handed patients with unilateral writer's cramp and eight right-handed normals. Subjects had blood flow scans at rest and during vibration of either the "affected" or "unaffected" hand. Vibration produced a consistent peak response in primary sensorimotor area (PSA) and supplementary motor area (SMA), both contralateral to the vibrated hand. Both responses were significantly reduced approximately 25% in patients with writer's cramp (PSA, p = 0.002; SMA, p = 0.02) whether vibrating the affected or unaffected hand. This indicates that patients with unilateral writer's cramp have bilateral brain dysfunction. These data provide objective evidence of abnormal central sensorimotor processing in writer's cramp.

Regional cerebral blood flow responses to vibrotactile stimulation were studied in 11 patients with predominantly unilateral idiopathic focal dystonia and 18 normal subjects using PET and H2(15)O. Stimulation produced a consistently localized and robust peak response in primary sensorimotor cortex contralateral to hand vibration in normal subjects (averaged hemisphere response 10.97 ml/(100 g.min) +/- 2.53). The sensorimotor response in dystonic patients was also consistently localized to the same area, but significantly reduced in magnitude whether vibrating the affected (8.35 ml/(100 g.min) +/- 2.29) or unaffected hand (8.40 ml/(100 g.min) +/- 2.15). Furthermore, vibration induced a dystonic cramp in the stimulated arm/hand in 6 patients, but not in any normal subjects. To determine whether the cocontraction of agonist and antagonist muscles could, in itself, attenuate the regional blood flow response, 10 normal subjects were studied with vibration during voluntary cocontraction of appropriate hand and forearm muscles, as well as with vibration alone. Vibration with voluntary cocontraction (mean = 12.57 ml/(100 g.min) +/- 2.13) produced a significantly greater response than vibration alone (mean = 10.30 ml/(100 g.min) +/- 2.20, P less than 0.00008). This abnormal sensorimotor response may have important implications for understanding the pathophysiology of idiopathic dystonia.

Previous studies of cerebral oxygen metabolism and extraction in patients with subarachnoid hemorrhage (SAH) have yielded conflicting results. We used positron emission tomography (PET) to measure the regional cerebral metabolic rate for oxygen (rCMRO2), oxygen extraction fraction (rOEF), and cerebral blood flow (rCBF) 16 times in 11 patients with aneurysmal SAH. All studies were performed preoperatively; no patient had hydrocephalus or intracerebral hematoma on brain CT. Eight patients with no arteriographic vasospasm who were studied on days 1-4 post-SAH had a significant 25% reduction in global CMRO2 compared to age-matched controls, and no significant change in global OEF, suggesting a primary reduction in CMRO2 caused by SAH. Four patients studied seven times during arteriographic vasospasm had significantly increased rOEF with unchanged CMRO2 in arterial territories affected by arteriographic vasospasm compared to territories without vasospasm, indicative of cerebral ischemia without infarction. No brain regions studied with PET were infarcted on follow-up CT. We conclude that the initial aneurysm rupture produces a primary reduction in CMRO2, and that subsequent vasospasm causes ischemia.