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SS-12-3 PET studies on basal ganglia function
Satellite syrnpostum 12. Basal ganglia disorders
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of the recently postulated scheme of segregated basal gangliathalamocortical circuits and the intrinsic "direct" and "indirect" striatopallidal pathways. It now appears that the signs and symptoms of Parkinson's disease, although resulting from the lost of dopamine-containing midbrain neurons, must, ultimately, be the result of altered basal ganglia output and the resulting changes in brainstem and thalamocortical activity. The basal ganglia are viewed as components of larger circuits that influence the activity of selective frontal areas. The basal ganglia must play an important role in the normal functions of these cortical areas and, in disorders such as Parkinson's disease, they produce disturbances of motor and cognitive function that depend on altered cortical activity. There is now mounting evidence that increases in tonic and phasic activity in the basal ganglia-thalamocortical "motor" circuit, induced by degeneration of the dopaminergic nigrostriatal pathway, can explain the major motor abnormalities of Parkinson's disease, including akinesia, the most disabling symptom. Evidence for the importance of the "indirect" striatopallidal pathway and, in particular the subthalamic muscles, in this disorder has continued to accumulate. Recent neuroimaging studies provide new insights as well as support for this scheme. New therapeutic strategies in Parkinson's disease, including drug treatments, transplantation approaches, and technically improved stereotactic procedures, should therefore aim primarily to reduce the increased basal ganglia outflow. Pallidotomy appears to be an effective treatment for relieving the motor signs and symptoms of PD as well as the drug-induced dyskinesias and motor fluctuations.
SS-12-3
] PET studies on basal ganglia function
David J. Brooks. MRC Cyclotron Unit, Hammersmith Hospital,
London, UK Over the years, a number of possible roles have been postulated for the basal ganglia in the control of movement. These include: determination of the force and velocity of movements, suppression of unwanted movements, facilitation of sequential and bimanual movements, facilitation of novel or rewarded movements, development of automaticity, and facilitation of motor learning and planning. H2150 PET activation studies allow us to examine, in vivo, the brain systems involved in these various aspects of motor function and to determine whether the basal ganglia have a specific role. Our PET studies find that there is no differential activation of the lentiform nuclei when arm movements are performed more frequently or forcefully although the level of motor cortex blood flow increases. Arm movements in both freely selected and instructed directions activate the lentiform nucleus equally. This suggests the basal ganglia are not primarily involved in determining the basic parameters of motion or in making motor decisions.
The level of lentiform nucleus activity also remains constant while learning a sequence of movements until automatic or acquiring a motor skill. Performing increasingly complex learned sequences of finger movements produces increasing levels of SMA, but not lentiform nucleus, activity. The lentiform nucleus is, however, activated when arm movements are imagined. These PET findings suggest that the basal ganglia do not play a high level role in the control of movement but help prepare and facilitate all actions. In Parkinson's disease, where basal ganglia-frontal projections are underactive, bradykinesia results. Conversely, in dystonia and chorea the basal ganglia are abnormally overactive suggesting that they may normally act to suppress unwanted movements.
LSS-12-41 Surgical treatment on Parkinson's
disease
Hirotaro Narabayashi. Neurological Clinic, Tokyo, Japan In the history of human stereotaxic surgery since around 1950, the main subject has been treatment of involuntary movement due to basal ganglia pathology. It started from pallidotomy on choreic movement. Soon Parkinson's disease (PD) became the main topic, and target of surgery was gradually changed to thalamotomy, but all these procedures were in the pre-levodopa era. Recently again posteroventral pallidotomy (PVP) is being interested, although the target within globus pallidus internum (GPi) seems to be slightly different from the earlier time. Lesions within GPi and also ventrolateral nucleus (VL) of the thalamus which receives pallidal projection are known to eliminate rigidity. However, this effect of reducing rigidity is experienced more marked by 3.5-4.0 mm diameter small lesion within the VL than pallidal lesion of the same size. To achieve similarly marked reduction of rigidity by pallidal lesion, we need to produce larger lesion such as 4-5 x 810 mm lesion including ansa lenticularis. Usually cogwheeling and resting tremor do not disappear immediately after making pallidal lesion and remains but in slighter degree. In contrast, tremor and cogwheeling are almost completely diminished by ventral intermediate nucleus (Vim) lesion. Secondary akinesia or hypokinesia due to muscle rigidity is improved by either procedure, but more markedly by thalamotomy. Primary akinesia remains even after almost complete elimination of rigidity but is improved by levodopa. It may not depend on these structures but presumably on the caudate-reticular zone of the substantia nigra projection, escaping from surgical lesioning. Another important possibility is that the PVP lesion may involve the limbic-motor projection from ventral striatum to ventral pallidum and then projecting to dorsomedial nucleus of the thalamus and pedunculo-pontine nucleus. It should be recognized that several patients by PVP presented some psychological changes and k E G slowing, although transiently for one to several weeks.
$82
of the recently postulated scheme of segregated basal gangliathalamocortical circuits and the intrinsic "direct" and "indirect" striatopallidal pathways. It now appears that the signs and symptoms of Parkinson's disease, although resulting from the lost of dopamine-containing midbrain neurons, must, ultimately, be the result of altered basal ganglia output and the resulting changes in brainstem and thalamocortical activity. The basal ganglia are viewed as components of larger circuits that influence the activity of selective frontal areas. The basal ganglia must play an important role in the normal functions of these cortical areas and, in disorders such as Parkinson's disease, they produce disturbances of motor and cognitive function that depend on altered cortical activity. There is now mounting evidence that increases in tonic and phasic activity in the basal ganglia-thalamocortical "motor" circuit, induced by degeneration of the dopaminergic nigrostriatal pathway, can explain the major motor abnormalities of Parkinson's disease, including akinesia, the most disabling symptom. Evidence for the importance of the "indirect" striatopallidal pathway and, in particular the subthalamic muscles, in this disorder has continued to accumulate. Recent neuroimaging studies provide new insights as well as support for this scheme. New therapeutic strategies in Parkinson's disease, including drug treatments, transplantation approaches, and technically improved stereotactic procedures, should therefore aim primarily to reduce the increased basal ganglia outflow. Pallidotomy appears to be an effective treatment for relieving the motor signs and symptoms of PD as well as the drug-induced dyskinesias and motor fluctuations.
SS-12-3
] PET studies on basal ganglia function
David J. Brooks. MRC Cyclotron Unit, Hammersmith Hospital,
London, UK Over the years, a number of possible roles have been postulated for the basal ganglia in the control of movement. These include: determination of the force and velocity of movements, suppression of unwanted movements, facilitation of sequential and bimanual movements, facilitation of novel or rewarded movements, development of automaticity, and facilitation of motor learning and planning. H2150 PET activation studies allow us to examine, in vivo, the brain systems involved in these various aspects of motor function and to determine whether the basal ganglia have a specific role. Our PET studies find that there is no differential activation of the lentiform nuclei when arm movements are performed more frequently or forcefully although the level of motor cortex blood flow increases. Arm movements in both freely selected and instructed directions activate the lentiform nucleus equally. This suggests the basal ganglia are not primarily involved in determining the basic parameters of motion or in making motor decisions.
The level of lentiform nucleus activity also remains constant while learning a sequence of movements until automatic or acquiring a motor skill. Performing increasingly complex learned sequences of finger movements produces increasing levels of SMA, but not lentiform nucleus, activity. The lentiform nucleus is, however, activated when arm movements are imagined. These PET findings suggest that the basal ganglia do not play a high level role in the control of movement but help prepare and facilitate all actions. In Parkinson's disease, where basal ganglia-frontal projections are underactive, bradykinesia results. Conversely, in dystonia and chorea the basal ganglia are abnormally overactive suggesting that they may normally act to suppress unwanted movements.
LSS-12-41 Surgical treatment on Parkinson's
disease
Hirotaro Narabayashi. Neurological Clinic, Tokyo, Japan In the history of human stereotaxic surgery since around 1950, the main subject has been treatment of involuntary movement due to basal ganglia pathology. It started from pallidotomy on choreic movement. Soon Parkinson's disease (PD) became the main topic, and target of surgery was gradually changed to thalamotomy, but all these procedures were in the pre-levodopa era. Recently again posteroventral pallidotomy (PVP) is being interested, although the target within globus pallidus internum (GPi) seems to be slightly different from the earlier time. Lesions within GPi and also ventrolateral nucleus (VL) of the thalamus which receives pallidal projection are known to eliminate rigidity. However, this effect of reducing rigidity is experienced more marked by 3.5-4.0 mm diameter small lesion within the VL than pallidal lesion of the same size. To achieve similarly marked reduction of rigidity by pallidal lesion, we need to produce larger lesion such as 4-5 x 810 mm lesion including ansa lenticularis. Usually cogwheeling and resting tremor do not disappear immediately after making pallidal lesion and remains but in slighter degree. In contrast, tremor and cogwheeling are almost completely diminished by ventral intermediate nucleus (Vim) lesion. Secondary akinesia or hypokinesia due to muscle rigidity is improved by either procedure, but more markedly by thalamotomy. Primary akinesia remains even after almost complete elimination of rigidity but is improved by levodopa. It may not depend on these structures but presumably on the caudate-reticular zone of the substantia nigra projection, escaping from surgical lesioning. Another important possibility is that the PVP lesion may involve the limbic-motor projection from ventral striatum to ventral pallidum and then projecting to dorsomedial nucleus of the thalamus and pedunculo-pontine nucleus. It should be recognized that several patients by PVP presented some psychological changes and k E G slowing, although transiently for one to several weeks.