Biomedical subjects
Publications and source records attributed to F Shima.
A 47-year-old female diagnosed as having juvenile parkinsonism at age 38 years developed progressive motor fluctuation while receiving levodopa medication. She underwent right posteroventral pallidotomy which achieved only a transient effect on the wearing-off. An additional procedure on the left pallidum resulted in long-lasting relief of the parkinsonian symptoms.
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Fetal graft research and renewed interest in Leksell's postero-ventral pallidotomy (PVP) stimulated reconsideration of surgical therapy for Parkinson's disease (PD), particularly with regard to improving akinetic symptoms previously thought resistant to surgical lesions. Review of our series and other published results of PVP and fetal graft show that PVP has beneficial effects on both akinetic and hyperkinetic symptoms that better the results reported for fetal graft implantation and other conventional stereotactics. Presented are the results of 60 consecutive patients, 55 of whom underwent PVP, and 5 who underwent fetal graft implantation. Using the Unified Parkinson's Disease Rating Scale (UPDRS), we found that PVP gave significant (P < 0.05) reductions in akinetic symptomatology including freezing, arising from a chair, posture, gait, postural instability, and bradykinesia. Fetal graft patients had significant reductions in two akinetic symptoms: bradykinesia and postural instability. PVP's dramatic therapeutic effects on akinesia may be explained by interruption of amplified collateral inhibitory output from the pallidum to brain stem locomotor centers such as the pedunculopontine nucleus, whereas interruption of collaterals to ventral lateral thalamus by PVP may account for the elimination of hyperkinesia. The excellent results of PVP represent a significant advance in the surgical treatment of PD.
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Sixty-eight stereotactic radiofrequency (rf) thalamic lesions in 57 patients with movement disorders were evaluated by magnetic resonance (MR) imaging. Postoperative periods ranged from 5 days to 4 years and 9 months. All 68 rf lesions were clearly detected on T2-weighted images (T2WI). Changes in signal intensity on T2WI were classified into five patterns, as follows: Pattern I: lesions with three concentric zones consisting of an inner hypointense, middle hyperintense and outer hypointense zone (31 lesions); Pattern II: lesions consisting of an inner hypointense and outer hyperintense zone (4 lesions); Pattern III: lesions consisting of an inner hyperintense and outer hypointense zone (27 lesion); Pattern IV: lesions of a hyperintense area alone (2 lesions); Pattern V: lesions of a hypointense area alone (4 lesions). The outer hypointense rim in Patterns I and III is thought to represent hemosiderin deposition. The abnormal signal intensity on T2WI caused by rf ranged from 2 to 12 mm in diameter, and lesions in the late phase were smaller than lesions in the early phase.
Striatal 18F-Dopa uptake and glucose metabolism were studied by positron emission tomography with 6-L-[18F]fluorodopa and [18F]fluorodeoxyglucose, respectively, in 8 patients with idiopathic dystonia. Patients with abnormal findings on the brain CT and MRI were excluded from this study. The clinical diagnosis consisted of torsion dystonia in 3 patients, focal dystonia limited in the arm in 3 and cervical dystonia (spasmodic torticollis) in 2. The 18F-Dopa uptake, corrected by nonspecific retention in the cerebellum, at 120 min post-administration was evaluated, and increased 18F-Dopa uptake in the putamen and in the caudate head was observed in the patients with idiopathic dystonia compared to the normal controls. The striatal glucose metabolism in the patients with idiopathic dystonia showed no difference with the normal controls. These findings suggest that pathogenetic mechanism of idiopathic dystonia involves increased presynaptic activity of the dopaminergic system in the striatum.
To elucidate the neuronal mechanism of the motor disturbances of the Rolling mouse Nagoya (rolling, genotype rol/rol), an experimental neurologic mutant mouse, we studied the physiological characteristics of neurons of the globus pallidus (GP) in rolling, comparing them with those of the behaviorally normal heterozygotes (+/rol) and normal controls (+/+). Forty-nine units in rolling, 41 in heterozygotes and 48 in controls were recorded under urethane anesthesia. The group mean of the interspike interval (ISI) of the spontaneous unit discharges was significantly shorter in rolling (42.2 +/- 2.6 msec, mean +/- SEM) than that of controls and of heterozygotes (55.4 +/- 2.4 msec, P < 0.001 and 50.4 +/- 2.6 msec, P < 0.05, respectively), indicating a significantly higher rate of spontaneous unit activity in the GP of rolling. In the controls and heterozygotes, about 60% of the GP neurons responded to striatal (ST) electrical stimulation with a predominantly inhibitory response, whereas a significantly smaller number of the GP neurons (22%, P < 0.001) exhibited inhibitory responses in rolling. The positive field potentials recorded in the GP evoked by ST stimulation were significantly smaller in amplitude in rolling (1.04 +/- 0.10 mV, mean +/- SEM) than that of the controls and heterozygotes (1.78 +/- 0.15 mV, P < 0.001 and 1.97 +/- 0.17 mV, P < 0.001, respectively). These results are in agreement with our previously reported findings of increased glucose metabolism and reduced concentration of GABA in the GP and substantia nigra pars reticula (SNr) in rolling.(ABSTRACT TRUNCATED AT 250 WORDS)
To elucidate the role of the basal ganglia on neck movement control and thus clarify the side of targets for stereotactic surgery of spasmodic torticollis, effects of electrical stimulation to the globus pallidus-entopeduncular nucleus complex (GP-EP) upon the activities of the sternocleidomastoid (SCM) muscle motoneurons were studied in cats. Repetitive stimulation of the ipsilateral GP-EP increased discharge rate in the majority of the SCM motoneurons, whereas contralateral GP-EP stimulation caused a decrease in discharge rate. These effects were gradually enhanced in the course of repetitive stimulation and lasted even after its cessation. Bilateral ablation of the motor and premotor cortices did not influence the effects of GP-EP stimulation. Latency studies suggested that the pallidal control of the SCM motoneuron is mediated by polysynaptic pathways on both sides; however, these same studies produced evidence of an ipsilateral oligosynaptic connection, as well. Repetitive antidromic stimulation of the accessory nerve caused a gradual increase in discharge rate of the SCM motoneurons, similar to the augmentation induced by ipsilateral GP-EP stimulation. Features of the responses indicate that the pallidal control on the neck muscles involves reverberating circuits in the brain stem and spinal cord. These experimental findings suggest that stereotactic thalamotomy of the ventrolateral nucleus for spasmodic torticollis should be performed on the side ipsilateral to the contracting SCM muscle.
To improve the localization of stereotactic targets, somatosensory evoked potentials (SEPs) were recorded from the thalamus and subthalamic area using a specially designed semimicroelectrode in 61 patients and a conventional "macroelectrode" in 17 patients. By means of the semimicroelectrode, median nerve stimulation evoked two distinct SEPs, consisting of a diphasic wave with a huge positivity restricted to the nucleus ventrocaudalis (Vc) and a triphasic wave of lower amplitude with a major negativity in the ventral part of the nucleus ventrointermedius (Vim) and nucleus ventrooralis posterior (Vop) as well as the subthalamic lemniscal pathway. The Vim-Vc junction could thus be clearly delineated by an abrupt transition of SEPs from one type to the other with a precision of 1 mm. The parvicellular part of the Vc (Vcpc), situated in its basal region, was distinguishable from the Vc proper by a significant reduction of the positivity elicited by stimulation of the median nerve and by a rapid growth of a diphasic SEPs to stimulation of the posterior tibial nerve. In the other thalamic nuclei, stimulation of the median nerve elicited triphasic SEPs of a very small amplitude, suggesting a volume conduction current from the lemniscal pathway. With the macroelectrode, the positivity in the Vc was sensitive to electrode manipulation and the thalamic nuclei could not be distinctly outlined. SEP monitoring using the semimicroelectrode significantly improved the precision of target localization, which allowed minimizing of the volume of the therapeutic lesion without losing surgical effectiveness, while avoiding complications associated with increased penetration of the coagulating electrode. It is suggested that recording serial thalamic SEPs with the semimicroelectrode is a practical method to refine stereotactic targets in the thalamus.
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To investigate the mechanism of analgesia noted with electrical stimulation of the thalamic sensory relay nucleus and medial thalamus, modulations of neuronal activities in the periaqueductal gray matter (PAG) were studied in response to electrical stimulations of the ventroposterolateral nucleus (VPL) and parafascicular nucleus (Pf) and to peripheral noxious stimulations in rats. Extracellular single-unit activities were recorded from 102 neurons in the PAG and the adjacent area in animals under halothane anesthesia. A large population (83%) of the PAG neurons reacted to Pf stimulations with a predominantly excitatory response, whereas smaller numbers (43%) responded to VPL stimulations. There was a significant correlation between the response characteristics of Pf and noxious stimulations, whereas no correlation was found between VPL and noxious stimulations. The PAG neurons that were verified antidromically to project to the nucleus raphe magnus showed a similar pattern of response. The excitatory response to the Pf stimulation was partially attenuated by systemic administration of naloxone, whereas that to the VPL stimulation was not affected. These results suggest that part of the analgesic mechanism of medial thalamus stimulation involves activation of the descending pain suppression system by exciting the PAG neurons through the opioid system, while the analgesia produced by sensory relay nucleus stimulation does not involve the PAG neurons or the opioid system.
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A successful GABA replacement therapy for choreo-ballistic status in a 9-year-old girl, who had been previously treated medically or surgically without beneficial results, was reported. Involuntary movements completely ceased after intravenous administration of GABA (the maximal doses: 533 mg/kg/day) of 3 weeks' duration. Chorea and ballism are assumed to be caused by hypofunction of the GABA-neurons in the basal ganglia. Administration of GABA has been considered to be ineffective for these involuntary movements, since GABA has been believed not to cross the blood-brain barrier. The present case suggests that a large amount of intravenous administration of GABA gives a chance to treat involuntary movements caused by deficiency of GABA-neurons, although the essential mechanism of intracerebral penetration of GABA remains uncertain.
To investigate the mechanism of analgesic effect of electrical stimulation of the thalamic parafascicular nucleus (Pf), we studied modulations of neuronal activities in the periaqueductal gray (PAG) and the adjacent reticular formation (RF) in response to Pf electrical and peripheral noxious stimulations in the rat. Extracellular single unit activities were recorded from 129 neurons in the PAG and adjacent RF under light halothane anesthesia. Pf stimulation caused neuronal responses in approximately 80% of the PAG and adjacent RF neurons, and noxious stimulation in 75%, with predominant excitatory responses to either stimulation. When the responses to the two stimuli were tested in the same neurons (n = 69), 91% responding to noxious stimuli also responded to Pf stimuli, again with predominant excitatory responses to either stimulation. The PAG and adjacent RF neurons that were verified antidromically to project to the nucleus raphe magnus (NRM), showed a similar pattern of response (n = 20). These results suggest that a sizeable population of neurons in the PAG and adjacent RF receives excitatory effects from the Pf and noxious afferents, and that part of these neurons projects to the NRM, which inhibits the dorsal horn cells of the spinal cord (the descending pain suppression system). Thus, part of the mechanism of the analgesic effects of Pf stimulation is due to activation of the descending pain suppression system by exciting the PAG and adjacent RF neurons. A possible role of noxious afferents on the negative feedback to pain mediation through this descending system also has to be considered.