PubMed · 4617660
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1974-10-11. Sinemet.. https://pubmed.ncbi.nlm.nih.gov/4617660/
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It has been known for some time that patients with Parkinson's disease (PD) have difficulty executing simultaneous motor acts, yet the pathophysiology underlying this impairment remains uncertain. We examined the possibility that these dual-task deficits stem from defective sensorimotor mechanisms producing interference between the motor programs underlying the two tasks. Patients with PD and normal control subjects were tested on their ability to maintain steady-state force with one hand while performing a force-reaction time task with the other hand. Although performance was worse on the dual-task than on the single-task condition for both subject groups, only the patients with PD demonstrated significant interference between the two tasks. The interference across tasks improved in 87% of the patients with PD when tested after treatment with carbidopa/levodopa (Sinemet). These findings support the contention that, in patients with PD, disturbances in the execution of simultaneous motor performance may be due to sensorimotor disinhibition.
A new high-sensitive spectrophotometric method for the determination of microquantities of carbidopa is described. The method is based on the reduction of neotetrazolium chloride by carbidopa in an alkaline ethanolic medium. The formazan formed exhibits an absorption maximum at lambda = 507 nm, with an apparent molar absorptivity of epsilon = 6.63 x 10(4) M-1 cm-1 and a corresponding Sandell's sensitivity of 3.68 ng cm-2. Beer's law is obeyed over the range of 0.10-6.0 micrograms mL-1 while the optimum concentration range is 0.125-5.0 micrograms mL-1. The regression line equation was calculated as: A = 0.271C + 0.0023 with a correlation coefficient of 1.0000 (n = 28). The accuracy and the precision of the method were considered as very satisfactory. The results obtained from the determination of carbidopa using both the described procedure and the corresponding USP. XXII and BP 1988 clinical methods were statistically compared by means of Student's t-test as well as by the variance ratio F-test, and no significant difference was observed.
Dopa-sensitive dystonia has been recognised for twenty years. It may occur in the first years of life. It first affects the lower limbs, then generalized becomes, as in torsion dystonia. Eight clinical cases are presented in five boys and three girls. The absence of the disorder in the parents, but its presence in siblings in three cases suggests that it might be recessively inherited. The symptoms are severe enough to cause major functional disability. In some cases, the intensity of the motor disorder varies during the days being, less pronounced in the morning or after a nap and more marked in the evening. Nonetheless, this feature is not constant and thus cannot be considered as an essential diagnostic criterion. Treatment with levodopa gives remarkable and durable results, but it must be continued indefinitely. Abnormal movements accompany an overdose but regress when the dosage is decreased. Unlike Parkinson's disease, it is not necessary to increase or fragment doses to avoid fluctuations in the efficacy of treatment during the day. On the contrary, after several years of the illness a decrease in daily dosage sometimes to a single dose is possible. Discontinuing treatment leads to reappearance of dystonia after two or three days. There are no established biological criteria to aid diagnosis. However, a decrease in urine levels of homovanillic acid was observed in two cases. Dopa-sensitive dystonia should be regarded as distinct from juvenile Parkinson's disease, firstly because of its symptomatology and secondly, and more importantly, because of its particular course, since fluctuations in therapeutic efficacy are never observed. It is the only known example of dopaminergic insufficiency that is chronically almost completely controlled by a modest exogenous supply of levodopa.