Severe Bradykinesia Research Articles

Combined stereotactic thalamotomy and posteroventral pallidotomy for Parkinson's disease

Stereotactic thalamotomy has traditionally provided good relief of tremor for patients with intractable tremor-dominant Parkinson's disease. However, bradykinesia, dyskinesia, and rigidity are often less reliably treated with this technique. Although posteroventral pallidotomy (PVP) can alleviate dyskinesias, appendicular bradykinesia, and rigidity, tremor may not be completely ameliorated. We have combined Vim/VOp junction thalamotomy and PVP in 29 patients with severe tremor, rigidity, and bradykinesia. Patients underwent unilateral Vim thalamotomy followed at the same sitting by PVP. The distinct physiological consequences of each procedure were documented by intraoperative electromyography (EMG) and video recording, revealing the effects on both tremor and agonist/antagonist co-contraction. Lack of reciprocal inhibition of antagonistic muscle groups often remained following thalamotomy but was eliminated by subsequent PVP. The complementary therapeutic effects of PVP and Vim thalamotomy may be due to the interruption of different neuronal circuits by the two procedures. The effect of Vim thalamotomy has been attributed to the interruption of the rubrothalamocortical loop. PVP interrupts the outflow of the globus pallidus interna (GPi), which may cause disinhibition of locomotor centers in the mesencephalon and spinal cord. There is no direct interruption of the rubrothalamocortical loop by PVP, explaining why this procedure sometimes exacerbates tremor in certain patients. The combination of the two procedures appears to provide excellent relief of the majority of symptoms in patients suffering from tremor-dominant Parkinson's disease.

Combined stereotactic thalamotomy and posteroventral pallidotomy for Parkinson's disease

Stereotactic thalamotomy has traditionally provided good relief of tremor for patients with intractable tremor-dominant Parkinson's disease. However, bradykinesia, dyskinesia, and rigidity are often less reliably treated with this technique. Although posteroventral pallidotomy (PVP) can alleviate dyskinesias, appendicular bradykinesia, and rigidity, tremor may not be completely ameliorated. We have combined Vim/VOp junction thalamotomy and PVP in 29 patients with severe tremor, rigidity, and bradykinesia. Patients underwent unilateral Vim thalamotomy followed at the same sitting by PVP. The distinct physiological consequences of each procedure were documented by intraoperative electromyography (EMG) and video recording, revealing the effects on both tremor and agonist/antagonist co-contraction. Lack of reciprocal inhibition of antagonistic muscle groups often remained following thalamotomy but was eliminated by subsequent PVP. The complementary therapeutic effects of PVP and Vim thalamotomy may be due to the interruption of different neuronal circuits by the two procedures. The effect of Vim thalamotomy has been attributed to the interruption of the rubrothalamocortical loop. PVP interrupts the outflow of the globus pallidus interna (GPi), which may cause disinhibition of locomotor centers in the mesencephalon and spinal cord. There is no direct interruption of the rubrothalamocortical loop by PVP, explaining why this procedure sometimes exacerbates tremor in certain patients. The combination of the two procedures appears to provide excellent relief of the majority of symptoms in patients suffering from tremor-dominant Parkinson's disease. J Image Guid Surg 1:133–140 (1995). © 1996 Wiley-Liss, Inc.

Cognitive and motor performance in multiple system atrophy and Parkinson's disease compared

Nineteen patients with multiple system atrophy (MSA) of striato-nigral degeneration type were tested to examine cognitive and motor performance. Parkinson's disease (PD) patients and healthy subjects served as controls. The MSA and PD patients showed similar cognitive dysfunction and motor impairment, performing poorly in the visuo-spatial organization, the construction tests and motor assessment tests. Movement times were much longer in MSA than PD patients. The association of nigral with putaminal damage may explain the more severe bradykinesia in MSA.

Grafts of Fetal Dopamine Neurons Survive and Improve Motor Function in Parkinson's Disease

Neural transplantation can restore striatal dopaminergic neurotransmission in animal models of Parkinson's disease. It has now been shown that mesencephalic dopamine neurons, obtained from human fetuses of 8 to 9 weeks gestational age, can survive in the human brain and produce marked and sustained symptomatic relief in a patient severely affected with idiopathic Parkinson's disease. The grafts, which were implanted unilaterally into the putamen by stereotactic surgery, restored dopamine synthesis and storage in the grafted area, as assessed by positron emission tomography with 6-L-[18F]fluorodopa. This neurochemical change was accompanied by a therapeutically significant reduction in the patient's severe rigidity and bradykinesia and a marked diminuation of the fluctuations in the patient's condition during optimum medication (the "on-off" phenomenon). The clinical improvement was most marked on the side contralateral to the transplant.

Neurobehavioral effects of intrathecal somatostatinergic treatment in subhuman primates.

We infused somatostatin and its long-acting analogue (SMS 201-995) into the intracranial subarachnoid space of eight monkeys. Chronic infusions of SMS 201-995 produced marked neurotoxic effects characterized by truncal ataxia, dysmetria, and severe bradykinesia, with normal level of consciousness. Subcutaneous injection of apomorphine, a dopaminergic agonist, promptly reversed these effects. Further studies are required before intrathecal somatostatin replacement therapy can be offered to patients with Alzheimer's disease.

Neuropsychological dysfunctions in Parkinson's disease: a study of 64 cases

Sixty-four cases of idiopathic Parkinson's disease were studied focusing the neuropsychological performance. To all subjects a brief mental status questionnaire was administered (30 items). Cases with a performance below normal and meeting the dementia criteria of the Diagnosis and Statistical Manual of Mental Disorders, third edition (DSM III), were considered demented. This evaluation showed that 12 of the 64 patients had dementia, a prevalence rate of 18.7%. Patients that had neuropsychological performance below normal showed more severe bradykinesia than normals. Short term memory, abstract thinking, visual gnosia, calculations, dynamic motor function of hands, constructional ability and recent memory were the most affected psychological functions. The significance of the mentioned findings is discussed and the literature reviewed.

Changes in sensorimotor function associated with the degree of bradykinesia of Parkinson's disease.

Changes in coordinated eye and hand movements associated with the progress of bradykinesia were studied in 31 parkinsonian patients and 8 age-matched healthy subjects. Among the parameters expressing the changes in motor behaviour, the interval between the onset of eye and hand movements was most sensitive. This parameter reflected the difference in the progress of the symptom in the two motor systems. An increase in the reaction time of the hand response appeared in patients of grade II bradykinesia; this was observed for eye movements only in patients with grade III (severe) bradykinesia. While the changes in ocular reaction time remained within the physiological range, a lengthening of the reaction time, a reduction in peak velocity, a decrease in the open-loop gain, a prolongation of movement duration, and a slow build-up in EMG activity, appeared from an early stage in hand movement. These signs of motor disturbance may appear eventually in every motor system at an advanced stage, but their development is not synchronous in different motor systems. An analysis of the responses recorded simultaneously from the two motor systems examined made it possible to evaluate the changes in the sensorimotor processes with different grades of bradykinesia. A comparison between reaction times for eye and hand movements may be useful for assessing the degree of bradykinesia in parkinsonian patients.

The corticomotoneurone connection is normal in Parkinson's disease.

Voluntary movements in Parkinson's disease are initiated and executed slowly. It is assumed that the motor cortex and its output pathway are intact and that bradykinesia is due to abnormal motor commands delivered to a normal corticospinal system. We have tested this assumption using electrical stimulation of the motor cortex through the scalp in three patients with severe Parkinson's disease, studied during fluctuations from relatively normal mobility when receiving drugs (ON) to severe bradykinesia when not receiving drugs (OFF). Thresholds and latencies for motor cortex stimulation to excite thumb flexor muscles and the resulting fast mechanical responses were the same in both ON and OFF conditions, even though the patients were unable to execute fast thumb flexion movements voluntarily when OFF. We conclude that the excitability and conduction velocity of the corticospinal motor pathways are normal in Parkinson's disease.

Disturbances in the voluntary recruitment order of anterior tibial motor units in bradykinesia of Parkinsonism.

The recruitment of motor units is studied with an electromyographic technique for secure identification of single motor unit potentials. It has been shown in previous studies that the recruitment order is different in tonic and in phasic activities; in tonic activity the recruitment order is stable and low frequency units are always recruited before high frequency units; in phasic activity, however, the recruitment order is unstable and units with a higher frequency range may be recruited before units with lower frequency range. In this investigation the shifts between tonic and phasic recruitment order in voluntary contraction were compared in normal subjects and in patients with severe bradykinesia of Parkinsonism. Upon initiation of a voluntary contraction in a normal subject, phasic recruitment order may be used for a few 100 msec but tonic recruitment order then takes over. In bradykinetic patients, however, this shift from phasic to tonic recruitment order is delayed. After termination of tonic voluntary contraction in a normal subject, phasic recruitment order can again be used after a few seconds. In bradykinetic patients, however, the shift back from tonic to phasic recruitment order is also delayed. In favourable experimental situations the shift from phasic to tonic recruitment order can be normalized by passive stretch of the muscle and the shift from tonic to phasic recruitment pattern by unloading the muscle. It is discussed whether the pathological recruitment in bradykinesia might be due to disturbed gamma loop function.

Severe bradykinesia as a manifestation of toxicity to antiepileptic medications

Severe bradykinesia as a manifestation of toxicity to antiepileptic medications