Fumio Shima

Clinical studies of the movement-related cortical potential (MP) and the relationship between the dentatorubrothalamic pathway and readiness potential (RP).

SummaryIn order to investigate the influence of basal ganglia and cerebellar involvement on the preparatory state of the cerebral cortex for voluntary movement, the cortical potential preceding finger movement was studied in 20 patients with Parkinsons disease and 20 patients with cerebellar ataxia. Readiness potential (RP) was abnormal in 90% of the Parkinson group and in 55% of the cerebellar ataxia group. The most frequent abnormality was a depressed amplitude and earlier onset of RP in both groups. The most remarkable finding in the present study was the complete absence of RP with dyssynergia cerebellaris myoclonica (presumed Ramsay Hunt syndrome) whereas normal RP was obtained with cerebellar cortical degeneration. In addition, RP was absent or severely depressed in patients with a unilateral vascular lesion of the midbrain (Benedikts syndrome) and in patients with Parkinsons disease who underwent unilateral intermedioventral (Vim) thalamotomy. These facts suggest a possible important role of the dentatorubro-thalamic or dentatothalamic pathway in the physiogenesis of RP.ZusammenfassungKortikale Potentiale vor der willkürlichen Fingerbewegung wurden bei 20 Patienten mit Parkinsonscher Krankheit und bei 20 mit cerebellärer Ataxie studiert, um den Effekt der Stammganglien- und Kleinhirnläsion auf den Bereitschaftszustand der Großhirnrinde für Willkürbewegungen zu untersuchen. Das Bereitschaftspotential war abnorm bei 90% der Parkinsonpatienten und bei 55% der Patienten mit Ataxie. Die häufigste Abnormität war eine Depression und ein früherer Anstieg des Bereitschaftspotentials bei beiden Patientengruppen. Der bemerkenswerteste Befund war ein vollständiges Fehlen des Bereitschaftspotentials bei Patienten mit wahrscheinlicher Dyssynergia cerebellaris myoclonica (Ramsay Hunt Syndrom), während ein normales Bereitschaftspotential bei Patienten mit cerebellärer kortikaler Degeneration gefunden wurde. Das Bereitschaftspotential fehlte oder war auffallend niedrig bei Patienten mit einseitiger vaskulärer Mittelhirnläsion (Benedikt Syndrom) und bei Patienten mit Parkinsonscher Krankheit nach einseitiger Thalamotomie (Nukleus ventralis intermedius). Diese Befunde weisen auf eine wichtige Rolle der dentato-rubro-thalamischen oder dentato-thalamischen Bahn in der Pathogenese des Bereitschaftspotentials hin.

Brain shift: an error factor during implantation of deep brain stimulation electrodes

OBJECT The goal of this study was to focus on the tendency of brain shift during stereotactic neurosurgery and the shifts impact on the unilateral and bilateral implantation of electrodes for deep brain stimulation (DBS). METHODS Eight unilateral and 10 bilateral DBS electrodes at 10 nuclei ventrales intermedii and 18 subthalamic nuclei were implanted in patients at Kaizuka Hospital with the aid of magnetic resonance (MR) imaging-guided and microelectrode-guided methods. Brain shift was assessed as changes in the 3D coordinates of the anterior and posterior commissures (AC and PC) with MR images before and immediately after the implantation surgery. The positions of the implanted electrodes, based on the midcommissural point and AC-PC line, were measured both on x-ray films (virtual position) during surgery and the postoperative MR images (actual position) obtained on the 7th day postoperatively. RESULTS Contralateral and posterior shift of the AC and PC were the characteristics of unilateral and bilateral procedures, respectively. The authors suggest the following. 1) The first unilateral procedure elicits a unilateral air invasion, resulting in a contralateral brain shift. 2) During the second procedure in the bilateral surgery, the contralateral shift is reset to the midline and, at the same time, the anteroposterior support by the contralateral hemisphere against gravity is lost due to a bilateral air invasion, resulting in a significant posterior (caudal) shift. CONCLUSIONS To note the tendency of the brain to shift is very important for accurate implantation of a DBS electrode or high frequency thermocoagulation, as well as for the prediction of therapeutic and adverse effects of stereotactic surgery.

The interaction of the somatosensory evoked potentials to simultaneous finger stimuli in the human central nervous system. A study using direct recordings

In order to investigate the interaction of sensory electrophysiologic fields arising from the adjacent second (II) and third (III) fingers and the distant second and fifth (V) fingers, direct recordings of somatosensory evoked potentials (SEPs) were performed from the sensory and motor cortices, the sensory thalamic nucleus (nucleus ventralis caudalis, VC) and the cuneate nucleus in humans during neurosurgical operations. Electrical stimulation was given to the II, III or V fingers individually, and also to pairs of either the II and III fingers or the II and V fingers simultaneously. The interaction ratio (IR) was devised as the ratio of amplitude attenuation caused by the simultaneous stimulation to two fingers compared with the amplitude of the arithmetically summed SEPs to the individual stimulation of two fingers. The IRs were calculated on N20 and P25 from the sensory cortex, P22 from the motor cortex, P17thal from the VC, and N16cune and P35cune from the cuneate nucleus. With both stimulations to the II and III fingers and the II and V fingers, P25 showed the greatest IR, followed by P22, then by P17thal, with N16cune exhibited the smallest IR. N20 and P35cune showed similar IRs and significantly greater IRs with II and III finger stimulation compared with II and V finger stimulation. These results thus indicate that the interaction of somatosensory impulses occurs in several structures along the sensory pathway in CNS, including the cuneate nucleus, the sensory thalamic nucleus, as well as sensory and motor cortices, with the greatest IRs in the cerebral cortices and the weakest ones in the brain-stem.(ABSTRACT TRUNCATED AT 250 WORDS)

Subcortical thalamic and cortical somatosensory evoked potentials to median nerve stimulation

Subcortical and cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 16 normal controls, 3 patients with Parkinsons disease, and 2 patients with thalamic lesions. Multiple electrodes were placed over the scalp and cervical spines and connected with a hand electrode or Fz in grid II. Thalamic SEPs were recorded directly from the Vim nucleus in 3 patients with Parkinsons disease during the stereotaxic operation. SEPs recorded from the scalp-hand derivations were composed of 4 negative (N9, N11, N16, N18) and 3 positive potentials (P8, P10, P12), whereas, at the scalp-Fz electrode, only one negative peak was identified (N20). N18 is of higher amplitude on the parieto-occipital areas and corresponds to N20. On the other hand, N16 can be identified more clearly on the fronto-central areas at scalp-hand derivations because of intermixture with N18 on the posterior head areas and disappears at scalp-scalp derivation. This suggests that N16 represents a subcortical component that is picked up as a far-field potential at the scalp electrodes. Components preceding N16 at scalp-hand derivations are also interpreted as far-field potentials because of their short latency and wide distribution over the scalp. The peak latency of N16 is not significantly different from the major negativity recorded directly from the thalamus, whereas N18 (N20) occurs significantly later. From this we conclude that N16 is most probably generated in the thalamus with the potentials of shorter latency originating caudal to the thalamus and N18 rostral to the thalamus.

Origin of scalp far-field N18 of SSEPs in response to median nerve stimulation

To identify the origin of scalp-recorded far-field negativity of short-latency somatosensory evoked potentials to median nerve stimulation (designated N18), direct records were made from the thalamus and ventricular system during 4 stereotaxic and 3 posterior fossa operations. In the thalamus a negative potential with almost the same latency as the scalp N18 was restricted to the Vim nucleus, but there was a large positive potential in the VC nucleus and medial lemniscus. Vim negativity increased in amplitude when high frequency stimulation was given to the median nerve, indicative of a facilitation effect. In contrast, the amplitude of scalp N18 decreased at high frequency stimulus. Direct recordings made through the medulla oblongata to the mid-brain showed a negative potential with gradually increasing latency. Above the upper pons, there was stationary negativity with no latency shift. The similarity between this negative potential and N18 is shown by their having the same latency and same response to the amplitude reduction and latency prolongation produced by high frequency stimulus. Our data suggest that scalp N18 comes from brain-stem activity between the upper pons and the mid-brain rather than from the thalamus.

Surgical control of akinesia in Parkinson's disease

Posteroventral pallidotomy (PVP) was carried out in 86 patients with Parkinsons disease, who presented marked bradykinesia, freezing of gait and postural defect associated with rigidity and tremor in 82 patients (bradykinesia type), and similar gait and postural problems with minimum signs of rigidity and tremor in 4 (pure akinesia type). The stereotactic coordinates of Leksells device were calculated from MRI and conventional ventriculography. The final target was defined by microelectrode techniques in the basal ganglia. The microrecording study revealed a very high background activity in the internal pallidum in patients of the bradykinetic type, however, a much lower pallidal activity in patients of the pure akinesia type. Fifty-eight patients underwent unilateral PVP, and 28 underwent bilateral surgery. Following PVP, rigidity tremor and poor reciprocal movements were significantly improved especially in the contralateral extremities. The most dramatic findings were the reversal of akinetic symptoms and wearing-off phenomena. The patients were followed up for 3-30 months (mean = 8) after surgery. Of the 82 bradykinesia type patients, good result were obtained in 48 (58%), fair results in 26 (32%), and minor improvement or no change in 8 (10%). In all the 4 patients of the pure akinesia type, recurrence of the akinetic symptoms occurred after a temporal improvement lasting a few days to 3 month after surgery. There was worst dysarthria in 3 patients, hemiparesis in 1 and partial motor aphasia in 1. The visual field problem was not complicated in any patients. These findings suggest that akinetic symptoms in PD are implicated in overactive pallidal outputs with putative GABAergic modulator by excessively inhibiting pedunculopontine nucleus activity (midbrain locomotor and posture regions) as well as thalamic activity. Partial interruption of the pallidal efferents eliminates the akinetic symptoms by disinhibitory effects on the target structures. The pathology of PD of the pure akinesia type is supposedly in the brainstem and should be excluded from indication of pallidotomy.

Diagnosis and surgical treatment of spasmodic torticollis of 11th nerve origin

Of 22 patients with spasmodic torticollis, 7 were treated by microsurgical decompression of the 11th nerve. In these patients, there was an intermittent horizontal torticollis characterized by aggravation of the symptoms when in a resting posture, presenting with a striking contrast to the torticollis of extrapyramidal origin that was alleviated while in the resting posture and aggravated by postural stress. A tight neurovascular contact was observed at the C1 level, occurring between the principal 11th nerve and the vertebral or posterior inferior cerebellar artery. Nerve decompression was achieved in 2 by transposing the compressing artery and in 5 by sectioning at C1 or C2 the branching root of the 11th nerve that had caused the tight cross contact by locking the nerve trunk to the dura mater. The symptoms had improved after an interval of 1 to 4 weeks. After an average follow-up of 3 years, full or satisfactory relief had been obtained in 5 and some improvement had occurred in 2 patients. Possible neural mechanisms related to torticollis of 11th nerve origin are discussed.

Tremor induced by toluene misuse successfully treated by a Vim thalamotomy

A 22 year old man developed a vigorous tremor of 5 Hz in his right hand, after a 7 year history of toluene misuse. T2 Weighted MRI depicted marked decreases in the signal intensity of the basal ganglia, red nucleus, and thalamus on both sides. The stereotactic coagulation of the left nucleus ventrointermedius (Vim) of the thalamus abolished the tremors in his right hand. This patient clearly exhibited the pathological involvement of rubral lesions in generation of a toluene induced tremor on MRI. Toluene induced tremor is an irreversible symptom which persists even after stopping toluene misuse, therefore in medically intractable cases, it should be positively treated by a Vim thalamotomy.

Effects of thalamic parafascicular stimulation on the periaqueductal gray and adjacent reticular formation neurons. A possible contribution to pain control mechanisms

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.

Local cerebral glucose utilization altered in rats with unilateral electrolytic striatal lesions and modification by apomorphine

Alterations in local cerebral glucose utilization (LCGU) in rats with unilateral striatal lesions and the modification by apomorphine were investigated. Electrolytic lesions were made in the rostral part of the right striatum, and 1, 7, and 30 days later, LCGU was observed in terms of relative and absolute LCGU values, using the [14C]deoxyglucose method. A definite change in the pattern of LCGU was seen only at 7 days. These were increases in LCGU in the globus pallidus, entopeduncular nucleus and substantia nigra pars reticulata, and decreases in the ventroanterior-ventrolateral (VAL) and ventromedial (VM) thalamic nuclei and lateral habenula, all on the lesioned side. The circling behavior following the lesion, however, was maximal after 2 days and disappeared after 7 days. Intravenous administration of apomorphine (1.5 mg/kg) produced different modifications in the LCGU pattern between the intact and lesioned sides, at 7 days after producing the lesions. On the intact side, there were increases in LCGU in the striatum, globus pallidus, entopeduncular nucleus, substantia nigra pars reticulata and subthalamic nucleus, and a decrease in the lateral habenula. No such changes were observed on the lesioned side. These results indicate firstly that electrolytic striatal lesions induce LCGU increases or decreases in the structures which receive the striatal input, secondly that the mechanism of this change differs from that of the circling behavior seen in case of striatal lesions, and finally that the majority of the LCGU changes in the basal ganglia and thalamus following intravenous administration of apomorphine are brought about by an altered input of neuronal activity from the striatum to these structures.