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PubMed1992

Origins and conducting pathways of motor evoked potentials elicited by transcranial magnetic stimulation in cats.

Spinal cord motor evoked potentials (MEPs-S) were elicited in cats by transcranial magnetic stimulation. The MEPs-S recorded from the epidural electrode at the first lumbar (L1) level consisted of four negative peaks (N1, 2.56; N2, 3.19; N3, 4.06; N4, 4.99 ms) followed by small, multiphasic waves. The mean conduction velocities of N1-N3 of the MEPs-S were calculated to be 90 to 115 m/s, which is consistent with extrapyramidal tract activation. A direct brain stem electrical stimulation and sequential transection of the spinal cord studies showed that N1-N3 of the MEPs-S originated primarily from the brain stem and conducted in the ventral funiculus of the spinal cord, which corresponded to the extrapyramidal tracts (e.g., the reticulospinal and vestibulospinal tracts). We also showed that N1 and N2 of the MEPs-S originated mainly from the lower medulla or upper cervical and that N3 originated from the lower pons or upper medulla (vestibular nucleus). On the other hand, N4 of the MEPs-S had a conduction velocity of 70 m/s, which disappeared by ablation of the sensorimotor cortex and pyramidotomy. A dorsal hemisection of the spinal cord, resulting in the disappearance of N4 of the MEPs-S, indicated that it conducted in the dorsolateral funiculus of the spinal cord. These results suggest that N4 of the MEPs-S originates from the sensorimotor cortex and conducts in the lateral corticospinal tract. MEPs-S by transcranial magnetic stimulation in cats constituted complex responses in both the pyramidal and extrapyramidal tracts.

Animals↗
PubMed2001

Transient spinal inhibition induced by electrical stimulation of the rat brain.

Intracortical electrical stimulation of the rat brain using single pulse induced motor evoked potentials (MEPs) with shorter onset latencies in the bilateral extremity muscles. The MEPs appeared in the stimulation of cortical areas outside the motor cortex (MI) and subcortical areas. Train-pulse stimulation of the MI at a stimulus intensity just above the threshold induced MEPs with longer onset latency in muscles corresponding to the somatotopy of the MI stimulated. This implies that the potential characterizing shorter onset latency is equal to responses induced via the extrapyramidal tract, and responses with longer onset latency originate in the pyramidal tract. Corresponding to MEPs, we recorded two types of spinal potentials (SPs) via extrapyramidal and pyramidal tracts. In paired-pulse stimulation of the extrapyramidal tract, second MEPs showed a long-lasting inhibition up to 3 s after the first MEPs, while the changes in second SPs were not remarkable. Extrapyramidal tract stimulation inhibited H-reflex in the same manner as MEPs. These results suggest that the electrical stimulation of rat brain has a long-lasting effect in inhibiting lower motoneuron excitabilities. Our method may be a useful experimental model to induce the transient inhibition of spinal motoneuron excitabilities caused by supraspinal structures.

Animals↗
PubMed1990

Experimental studies on spinal cord function using evoked action potentials.

Experiments were carried out on cats to determine the use of conductive evoked spinal cord action potentials in diagnosing motor function of the spinal cord. Direct stimulation from the dura produced three negative wave potentials, N1, N2 and N3. The intraspinal pathway of N2 and N3 was the dorsal column. The pathways of N1, determined by dorsal and ventral epidural recording, were the dorsilateral funicle and the extrapyramidal tracts. A collision experiment between potential N1 and pyramidal tract action potential did not reflect the function of the tract as the amplitude of the action potential was too small. Nevertheless, it is considered that conductive evoked spinal cord action potentials could become a valuable method of assessing spinal cord function as they reflect the function of the extrapyramidal tracts, as well as of the dorsilateral funicle and the dorsal column.

Action Potentials↗
PubMed1992

[A case of Machado-Joseph disease--cerebral blood flow and cerebral metabolic rate of oxygen].

A 51-year-old woman, with progressive gait disturbance and dysarthria, had been diagnosed as Menzel-type spinocerebellar degeneration. Later, she developed dystonic posture of upper limbs and bulging eyes. She was diagnosed as Machado-Joseph disease from neurological findings, which consisted of cerebellar signs, pyramidal tract signs and extrapyramidal tract signs and peripheral neuropathy. She died suddenly of unknown origin. Her illness lasted about 13 years. Neuropathological findings showed moderate neuronal loss with gliosis in the subthalamic nucleus, globus pallidus, substantia nigra, dentate nucleus, oculomotor and hypoglossal nucleus and anterior horn. Positron emission tomography (PET) using 15O steady state inhalation technique revealed reduction of cerebral blood flow and cerebral metabolic rate of oxygen in not only cerebellum but also cerebral cortex. These findings are different from typical PET findings of spinocerebellar degeneration.

Brain↗
PubMed1991

Origins and conducting pathways of motor evoked potentials elicited by transcranial (vertex-hard palate) stimulation in cats.

Spinal cord evoked potentials were elicited in cats by transcranial electrical stimulation with electrodes on the vertex and hard palate. Vertex motor evoked potentials (V-MEP) were also recorded. An extracellular microelectrode recording technique was then used to analyze the results by isopotential mapping. The relationship between the distribution of field potentials and the stimulation polarity was studied using the field potential distribution of the V-MEP in the lower thoracic spinal cord that had been represented on the isopotential maps. The first negative wave of the V-MEP showed maximal amplitude distribution in the anterior funiculus, which corresponds to the extrapyramidal tracts. This pattern was seen with both stimulation polarity arrangements: 1) stimulation with the cathode at the vertex and the anode at the hard palate, and 2) stimulation with the anode at the vertex and the cathode at the hard palate. When the cathode was at the vertex, the stimulation threshold was lower, and the response had higher amplitude than when the anode was at the vertex. Recording V-MEPs elicited by vertex cathode stimulation could provide an excellent method of monitoring the extrapyramidal tracts in cats.

Animals↗
PubMed2001

Protein thiol oxidation by haloperidol results in inhibition of mitochondrial complex I in brain regions: comparison with atypical antipsychotics.

Usage of 'typical' but not 'atypical' antipsychotic drugs is associated with severe side effects involving extrapyramidal tract (EPT). Single dose of haloperidol caused selective inhibition of complex I in frontal cortex, striatum and midbrain (41 and 26%, respectively) which was abolished by pretreatment of mice with thiol antioxidants, alpha-lipoic acid and glutathione isopropyl ester, and reversed, in vitro, by disulfide reductant, dithiothreitol. Prolonged administration of haloperidol to mice resulted in complex I loss in frontal cortex, hippocampus, striatum and midbrain, while chronic dosing with clozapine affected only hippocampus and frontal cortex. Risperidone caused complex I loss in frontal cortex, hippocampus and striatum but not in midbrain from which extrapyramidal tract emanates. Inhibition of the electron transport chain component, complex I by haloperidol is mediated through oxidation of essential thiol groups to disulfides, in vivo. Further, loss of complex I in extrapyramidal brain regions by anti-psychotics correlated with their known propensity to generate side-effects involving extra-pyramidal tract.

Animals↗
PubMed1991

[A case of Fahr's disease associated with juvenile rheumatoid arthritis].

We studied a case of Fahr's disease type idiopathic intracerebral calcification (Fahr's disease) associated with juvenile rheumatoid arthritis. The patient was a 15-year-old male with a chief complaint of gait disturbance. His family members had no similar signs and symptoms. His parents had no consanguinity. He was born with the normal perinatal course at 1967. He had repeated episodes of convulsive attacks during fever elevation from 2 years and 8 months to 9 years of age. Morning stiffness of bilateral hands, and pernio in the auricles, fingers, planta, and toes had occurred in every winter, since 6 years old. Swelling and pain of the bilateral knee and foot joints appeared, making ambulation difficult in 1983 (15 years old), and the patient was admitted to our hospital in July, the same year. On admission, congenital anomalies such as epicanthus and high-arched palate were noted, and swelling, deformation and contracture of limb joints, and Raynaud phenomenon were shown. His ocular fundus showed no arteriosclerotic change. He didn't have Albright's sign. Mild mental retardation and bilateral pyramidal tract signs were noted, but extrapyramidal tract and cerebellar signs, and sensory disturbance were absent. Laboratory findings exhibited markedly elevated ESR, positive CRP, RA, and antinuclear antibody. The levels of serum Ca, P, alkaline phosphatase and parathyroid hormone were normal. Peripheral blood study showed microcytic and hypochromic anemia. Anti-DNA antibody was negative. Ellsworth-Howard test was positive. Elevated antibody titer to toxoplasma, rubella virus, herpes simplex virus and cytomegalovirus were not proven. He had no chromosomal change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Suprathreshold brain stimulation activates non-corticospinal motor evoked potentials in cats.

In the feline model of the motor evoked potential (MEP) test, a multiphasic spinal cord signal can be elicited in response to bipolar or transcranial brain stimulation. Previous studies have shown that signals produced by threshold stimulation travel mostly in the corticospinal tract. However, from this study we show that suprathreshold stimulation produces very large amplitude MEPs which travel in the ventral funiculus and therefore are most likely associated with extrapyramidal tract activation. The data supporting this conclusion are: (1) apparent conduction velocities of the first two large amplitude peaks are at least 80 m/s with transcranial stimulation; (2) latency of the transcranial MEP at L2 in the cord is less than or equal to 3.50 ms; (3) large amplitude, positive monophasic potentials are recorded in the ventral but not dorsal-lateral funiculus for either bipolar or transcranial MEPs; (4) both bipolar and transcranial MEPs are significantly reduced or abolished by selective lesion of the ventral funiculus. The two tracts which we believe are responsible for mediating the suprathreshold MEP in the cat are the reticulospinal and vestibulospinal tracts. This is significant because suprathreshold MEPs can be used to monitor feline ventral cord function. Furthermore, combining the use of threshold and suprathreshold MEPs may provide a differential diagnostic test for pyramidal vs. extrapyramidal motor function.

Animals↗
PubMed2005

[Aicardi-Goutières syndrome: report of two new cases].

INTRODUCTION: Aicardi-Goutières syndrome is an early onset autosomal recessive progressive encephalopathy, clinically characterized by acquired microcephaly, severe psychomotor delay and involvement of pyramidal and extrapyramidal tracts. Intracranial calcifications, especially at the level of the basal ganglia, white matter abnormalities, lymphocytosis and raised interferon (IFN)-alpha in blood and cerebrospinal fluid (CSF) form part of this syndrome. CASES REPORTS: We describe two unrelated infants (a 3-month-old boy and an 11-month-old girl) who both presented with hypotonia, microcephaly, and psychomotor delay. Mild choreic and dystonic movements, as well as progressive spasticity, were also observed in the girl. Extensive investigations revealed intracranial calcifications, mild CSF lymphocytosis in the boy, and raised IFN-a in blood and CSF in both patients. COMMENTS: Aicardi-Goutières syndrome should be kept in mind when investigating microcephalic and retarded patients with cerebral calcifications initially suggestive of TORCH infection. Appropriate genetic counseling should be provided.

Brain Diseases↗
PubMedDate not supplied

Cranial MR in Wilson disease: abnormal white matter in extrapyramidal and pyramidal tracts.

PURPOSE: To describe abnormal white matter in the brain on MR in Wilson disease and to compare with anatomic location of white matter tracts. METHODS: Forty-six patients with Wilson disease were examined. Axial T1-weighted inversion-recovery, axial T2-weighted spin-echo, and coronal T2*-weighted gradient-echo MR images were performed. Imaging studies were compared with clinical data. RESULTS: Seventeen patients showed abnormalities in the region coinciding with the following white matter tracts: corticospinal tract (24%, n = 11), dentatorubrothalamic tract (24%, n = 11), and pontocerebellar tract (17%, n = 8). CONCLUSION: Abnormal extrapyramidal and pyramidal white matter tracts are part of the neuroimaging spectrum of Wilson disease. No significant correlation was found with neurologic groups and individual white matter tracts affected.

Basal Ganglia Diseases↗