Low performance in decision-making under ambiguity and abnormal social behavior distinguished PD patients with PG from those without this disorder. Dopamine replacement therapy may induce dysfunction of the ventromedial prefrontal cortex and amygdala-ventral striatum system, thus increasing the risk for developing PG.
Clinical idiopathic Parkinson's disease (PD) diagnosis requires following strict clinical criteria. Final definitive diagnosis can only be made after pathological confirmation and, despite following clinical criteria, several cases are misdiagnosed. We assessed sensitivity and specificity of acute challenge with levodopa (L-dopa) to predict sustained long-term L-dopa responsiveness as a major criterion for clinical diagnosis of PD. A consecutive series of 82 patients first seen at a movement disorders clinic with a parkinsonian syndrome without specific diagnosis was included. A second examiner, blind to the presumptive diagnosis, performed in each patient an acute challenge with 250/50 mg of L-dopa-carbidopa and rated the test as positive or negative according to whether values reached a minimal 30% of improvement on UPDRS scores. Positive tests were considered supportive of presumptive clinical diagnosis of Parkinson's disease. Blind to test results and according to clinical presumption, the first examiner started patient treatment with the necessary L-dopa dose or, alternatively, until reaching 1 g for 1 month in those who failed to display a positive test response. At 24 month follow-up, they were re-tested with 1 g for 1 month when required. At this point, clinical criteria of the U.K. Parkinson's Disease Society Brain Bank were applied and definitive clinical diagnosis of PD was made. Sensitivity, specificity, and positive predictive ratio for acute challenge were calculated. Overall sensitivity and specificity of acute L-dopa challenge to predict clinical diagnosis of PD was 70.9% and 81.4%, respectively; positive predictive ratio was 88.6%. When patients were divided into three groups according to their UPDRS motor section score at initial examination, sensitivity and specificity varied: Group I (or=21), 36.4% and 87%, respectively. Positive predictive ratio increased to 100% in Group I and to 87.5% in Group III. The positive result of initial acute L-dopa challenge predicts chronic L-dopa responsiveness as major criterion of PD in all patients with UPDRS motor scores lower than 10.
Current concepts regarding the organisation of the motor system indicate the existence of a frontoparietal circuit involved in prehension and manipulation, whose damage may result in a motor behavioural disorder strongly resembling the one originally described as limb-kinetic apraxia. To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three-dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb-kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb-kinetic apraxia in patients with corticobasal degeneration.
At the 1-year follow-up, microelectrode-guided PVP produced significant changes in patient motor status and disease progression versus a comparable group of patients who did not undergo surgery during the same period of time.
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