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Biomedical subjects

A N Lieberman

Publications and source records attributed to A N Lieberman.

At least 19 recordsLinked to original sources
PubMed1995

Transient resolution of bilateral tremor after unilateral thalamotomy, associated with focal injury of the corpus callosum: case report.

We present a patient with Parkinson's disease whose bilateral tremor transiently resolved after a unilateral left ventrolateral thalamotomy. The transient resolution of the bilateral tremor was associated with a focal thalamic lesion and a second lesion in the corpus callosum. The mechanism of this phenomenon may be related to temporary disruption of descending bilateral corticostriate projections by the callosal lesion.

Corpus Callosum↗
PubMed1995

Novel heuristics of functional neural networks: implications for future strategies in functional neurosurgery.

A hypothesis is proposed that (a) the skeletomotor basal ganglia-thalamocortical loop functions as a model of the behavior of the body and the environment, and that (b) dopaminergic neurons of the substantia nigra pars compacta comprise the substrates of an error distribution system projecting to the striatum. This error signal initiates the learning process in the basal ganglia - learning starts with increasing intensity of the error signal and is complete when the signal is minimized. Parkinson's disease (PD) may be considered as a disruption of learning processes in the basal ganglia that results from progressive degeneration of the substrate that is the error distribution system for this functional motor loop. Numerous clinical and experimental observations obtained from functional procedures for PD that show identical clinical effects in alleviating parkinsonian symptoms, e.g. thermocoagulative lesions and chronic stimulation, can be explained through the use of this conceptual theory of basal ganglia function. Because any controlling neural network must possess a model of the behavior of its controlled object, the heuristics outlined in this theory are broadly applicable for explaining the function of the nervous system, as well as being useful for planning surgical procedures and future strategies in functional neurosurgery.

Basal Ganglia↗
PubMed1993

Temporal dissociation of the prehension pattern in Parkinson's disease.

This study assesses the reach to grasp movement of eight Parkinson and eight control subjects. The reach was of either 15, 27.5 or 40 cm. The grasp was either of a small (0.7 cm) or a large diameter (8 cm) dowel. When comparing Parkinson to control subjects, no differences were found in the regulation of movement parameters according to changes in object distance or size. However, for Parkinson's disease patients the onset of the manipulation component was delayed with respect to the onset of the transport component. It is proposed that this reflects a deficit in the simultaneous or sequential implementation of different segments of a complex movement.

Aged↗
PubMed1988

Biochemical analysis of caudate nucleus biopsy samples from parkinsonian patients.

Biochemical analyses of caudate nucleus biopsy samples from patients with Parkinson's disease undergoing autologous adrenal transplantation were performed. Activity of the dopamine biosynthetic enzyme tyrosine hydroxylase, and concentrations of dopamine and its primary metabolite homovanillic acid were significantly greater than anticipated on the basis of previously published postmortem values. These data suggest that postmortem changes in various biochemical parameters of dopamine function are more rapid than has been generally appreciated. Further analysis of striatal biopsy samples may reveal predictive relationships between striatal indices of dopamine function and therapeutic response to adrenal transplantation.

Adult↗
PubMed1988

Deprenyl in the treatment of symptom fluctuations in advanced Parkinson's disease.

Deprenyl, a selective inhibitor of monoamine oxidase, type B, which is free of the "tyramine effect," may ameliorate symptom fluctuations in advanced Parkinson's disease (PD). We randomized 96 patients with marked symptom fluctuations at three centers to receive either deprenyl 5 mg b.i.d. or placebo in parallel fashion in addition to a previously optimized levodopa/carbidopa (Sinemet) regimen. Disability was recorded hourly at home by patients 3 days weekly during the 2-week baseline and the 6-week treatment period. Disability during the "on" state was assessed each week by examination. Mean hourly self-assessment of gait improved in 28 of 50 patients (56%) receiving deprenyl (mean degree of improvement 0.25 points on a 0-2 scale) and in 14 of 46 (30.4%) taking placebo (mean 0.15). Mean hourly overall symptom control improved in 29 (58%) taking deprenyl (mean 0.34) and in 12 (26.1%) taking placebo (mean 0.15) (p less than 0.01 for each parameter). No significant improvement occurred in the objective quality of the "on" state with deprenyl. Mean daily Sinemet dosage decreases were 17% in the deprenyl group and 7% in the placebo group. Adverse effects included nausea, light-headedness, dyskinesias, and hallucinations, all of which abated after the Sinemet dose was reduced. We conclude that deprenyl is of moderate benefit in a majority of patients with symptom fluctuations complicating PD and is generally well tolerated.

Adult↗
PubMed1987

D-1 and D-2 agonists in Parkinson's disease.

We have evaluated 5 DA agonists-bromocriptine, lergotrile, lisuride, pergolide, and mesulergine in studies encompassing 278 patients with advanced PD. In most of our patients the DA agonist was added to levodopa. Most of our patients were no longer satisfactorily responding to levodopa. Previous attempts at managing these patients by changing the dose of levodopa (increasing or decreasing it), the treatment schedule, or the ratio of levodopa to carbidopa or by temporarily discontinuing levodopa [drug holiday] were unsuccessful. The majority of our patients had diurnal fluctuations in performance, either "wearing off" or "on-off" phenomena. The addition of a DA agonist resulted in a decrease in parkinsonian disability in most patients and a decrease in the severity of the diurnal fluctuations in performance. Improvement in many patients was maintained for at least 2 years. Adverse effects included mental changes, dyskinesias, orthostatic hypotension, and nausea. All of the adverse effects were reversible when the agonist was decreased or discontinued. As a group the agonists behaved similarly but individual patients often responded better to one agonist than another. The main role of agonists is in combination with levodopa in the treatment of patients with early PD who have not yet developed dyskinesias or diurnal fluctuations in performance.

Aged↗
PubMed1986

Efficacy of pergolide and mesulergine.

The activity of pergolide, a clavine ergolene, and mesulergine, an 8-alpha amino ergoline, were compared in 18 patients with advanced Parkinson's disease. All of the patients were no longer satisfactorily responding to levodopa, and 16 patients had diurnal oscillations in performance. Pergolide, mean dose 2.7 mg, when added to levodopa resulted in a significant (27%) decrease in Parkinson disability and a significant improvement in diurnal oscillations in performance (136% increase in hours 'on'). Twelve of the 18 patients (67%) improved. However, after 2 years pergolide was discontinued in all of the patients because of decreased efficacy, adverse effects, or both. At this time, mesulergine, mean dose 9.3 mg., when added to levodopa resulted in a significant (37%) decrease in Parkinson disability and a significant improvement in diurnal oscillations (61% increase in hours 'on'). Twelve of the 18 patients (67%) improved. Adverse effects (dyskinesias) were less with mesulergine than with pergolide. A declining response to one agonist does not preclude a successful response to another agonist of a different class.

Aged↗
PubMed1986

Management of levodopa failures: the use of dopamine agonists.

In the past decade, dopamine agonists have emerged as important treatment options for patients with Parkinson's disease. Originally, dopamine agonists were used only in patients with advanced disease in whom the response to levodopa had decreased (levodopa failures). The decreased response to levodopa, usually associated with diurnal oscillations in performance and the 'wearing-off' and 'on-off' phenomena, is secondary to disease progression with continued degeneration of the nigrostriatal neurons. In addition, chronic levodopa treatment itself may contribute to the decreased drug response and the diurnal oscillations in performance. Dopamine receptor agonists bypass the degenerating nigrostriatal neurons and directly stimulate the striatal dopamine receptors. Dopamine receptor agonists also permit a reduction in the dose of levodopa. Five ergoline dopamine agonists--bromocriptine, lergotrile, pergolide, lisuride, mesulergine, and the nonergoline agonist, ciladopa--have undergone clinical trials in Parkinson's disease. In 10 years, we treated a total of 278 patients with advanced Parkinson's disease, a declining response to levodopa, and diurnal oscillations in performance with five ergoline dopamine agonists (in addition to levodopa). The mean duration of treatment was one year (with a range of 1-60 months). Improvement was noted in 140 (50%) of our patients. Adverse effects necessitating discontinuation of the agonist occurred in 131 patients (46%). We compared our results with those of others who, unlike us, began treatment with a dopamine agonist earlier, using the agonist alone or adding it to levodopa before the response to levodopa had decreased. Many of the patients so treated had mild or moderate Parkinson's disease. A total of 1,599 patients were treated with ergoline dopamine agonists. Of these patients, 976 (61%) improved, while 407 (25%) experienced adverse effects. We believe that a greater number of these patients improved and fewer experienced adverse effects, in comparison to our patients, because the patients had less advanced disease.

Animals↗
PubMed1986

Parkinson's disease.

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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗