Recently, motor evoked potential(MEP) using cortical surface of transcranial stimulation have been used to monitor the integrity of motor pathways and map motor cortex in human and animal. The primary concept using motor evoked potentials(MEPs) for test of motor pathways was based on the assumtion that pyramidal neurons in the motor cortex are activated by electrical stimulation applied on the cerebral cortex and synchronized compound action potentials are conducted mainly along the corticospinal tracts in the spinal cord. However, the origins and the descending pathways of these MEPs in small animals may be different from those of potentials evoked by intracortical microstimulation because of current spread. Our previous study revealed that the origns of the MEPs in rats differed from those previously believed and may be reticular nuclei. To further clarify those results and localize the intraspinal pathways conduction MEPs, consecutive vertical and/or horizontal sections of the spinal cord were performed at T9 cord level in twelve rats. MEPs were recorded at T2/3 and L2/3 before and after each section and sequential alterations of MEPs were observed. In six rats, the stimulation was alternated between the right and left cortex and the lateralities of conduction pathways were compared. All six cases showed no differences of MEPs and pattern of wave abolition after each section between right and left brain stimulation. The alteration of MEPs after each consecutive section was categorized by analyzing latency shift, amplitude change, and disappearance of waves. We divided a cross section of T9 spinal cord into forty-six squares. If one of the categorized changes occurrd after cutting an area, the appropriate score was given for the area since more change of waves meant more significant contribution of the cut area to conduction of MEPs. The score of twelev rats were summed in each forty-six spots and map showing the distribution of MEPs was constructed. The map revealed that MEPs were conducted along the wide area of ventral and lateral funiculus of the spinal cord but mainly along the medial portion of the ventral funiculus of the spinal cord but mainly along the medial portion of the ventral funiculus and ventral portion of the larteral funiculus through which reticulospinal and vestibulospinal tracts pass. No conduction of MEPs along the corticospinal tracts was confirmed. This finding supports the result of our previous study. However, this extrapyramidal MEP conducted along ventral spinal cord in addition to somatosensory evoked potential(SSEP) which is conducted along posterior funiculus can be useful to monitor the integrity of the whole spinal cord. Moreover, the extrapyramidal MEP can be more useful than pyramidal MEP in rats because the reticular formation plays a more important role in motor function and pyramidal tract is located in posterior funiculus.
Action Potentials ; Animals ; Brain ; Cerebral Cortex ; Efferent Pathways ; Electric Stimulation ; Evoked Potentials, Motor* ; Extrapyramidal Tracts ; Humans ; Motor Cortex ; Neurons ; Pyramidal Tracts ; Rats* ; Reticular Formation ; Spinal Cord

Extrapyramidal tract motor disorder in calcification of basal ganglia probably occurs when the deposition of acid mucopolysaccharides in the basal ganglia is severe enough to lead to neuronal loss. Basal ganglia calcification has been noted to occur with higher incidence and intensity in encephalitis lethargica, carbon monocide intoxication, anoxia, tuberous sclerosis, toxoplasmosis, hypothyroidism and hypoparathyroidism. The neurologic disorder is frequently reversible with treatment in patients with basal ganglia calcification who have hypoparathy-roidism. We report a patient with idiopathic hypoparathyroidism associated with bilateral calcification of the basal ganglia and athetoid movement. This is the first case report in Korea.
Anoxia ; Athetosis* ; Basal Ganglia* ; Carbon ; Cefonicid ; Encephalitis ; Extrapyramidal Tracts ; Glycosaminoglycans ; Humans ; Hypoparathyroidism* ; Hypothyroidism ; Incidence ; Korea ; Nervous System Diseases ; Neurons ; Toxoplasmosis ; Tuberous Sclerosis

Motor evoked potential(MEP) produced by cortical surface or transcranial stimulation has evolved as a new clinical and experimental tool to monitor the integrity of motor pathways and to map motor cortex. Clinical assessment of motor system using MEP has further advanced with recent development of the magnetic stimulator. The primary concept using MEPs for test of motor pathways was based on the assumption that pyramidal neurons in the motor cortex are activated by electrical stimulation applied on the cerebral cortex and synchronized compound action potentials are conducted mainly along the corticospinal tracts in the spinal cord. However,recent studies indicated that the origins of the Meps in non primates may differ from those previously believed. In order to use MEPs as a clinical or experimental tool, it is essential to clarify the origin of MEPs. Therefore, goals of this study were : (1) to investigate the origin of MEPs, and (2) to design the most reliable but simple method to evoke and monitor MEPs. In a total of fifteen rats, MEPs were produced by cortex to cortex stimulation and were monitored using a pair of epidural electrodes. Using varying stimulus intensities, the amplitudes and latencies of MEPs were statistically analyzed. The latencies and amplitudes of the MEPs in these animals showed surprisingly large standard deviations, which were partially resulted in these animals showed surprisingly large standard deviations, which were partially resulted from convergence of neighboring waves during high stimulation intensities. Wave forms of MEPs were also varied greatly depending on the position of recording electordes. At low stimulus intensities, most consisten MEPs were obtained when the stimulating electrodes were placed on the hard palate and the temporal muscle, not on the motor cortex. This observation indicates that the primary source of MEPs is not the motor cortex in the rat. When the potentials generated by direct stimulation of motor cortex and those generated by reticular nuclei were monitored epidurally in the same preparation using the same electrodes, these potentials generated by different sources actually identical in their latencies and wave forms. However, the threshold stimulus intensities evoking these potentials were quite different in the two metholds. The threshold was much lower to evoke potentails by reticular nuclei stimulation. It suggests that MEPs are geneated by the reticular nuclei or brain structure located in the brain stem. The observation that the motor cortex play no major roles in generating MEPs was confirmed by sequential sections of neural axis from the motor cortex to brain stem in three rats. All these findings suggested that neither direct motor cortex stimulation not transcranial stimulation did evoke MEPs originating from the motor cortex in rat. These stimulating methods activate reticular nuclei by stimulus current spread to the brain stem. Since the reticular formation plays an important role in motor function in rats, MEP originated from reticular nucleus can be an important testing of the motor function in rats. Moreover, transcranial stimulation of the brain is technically easy. This technique producing MEPs originated from reticular nucleus can be useful to monitor the integrity of motor pathways.
Action Potentials ; Animals ; Axis, Cervical Vertebra ; Brain ; Brain Stem ; Cerebral Cortex ; Efferent Pathways ; Electric Stimulation ; Electrodes ; Evoked Potentials, Motor* ; Extrapyramidal Tracts ; Motor Cortex ; Neurons ; Palate, Hard ; Primates ; Pyramidal Tracts ; Rats* ; Reticular Formation ; Spinal Cord ; Temporal Muscle

OBJECTIVE: To investigate neuroradiological and neurophysiological characteristics of patients with dyskinetic cerebral palsy (CP), by using magnetic resonance imaging (MRI), voxel-based morphometry (VBM), diffusion tensor tractography (DTT), and motor evoked potential (MEP). METHODS: Twenty-three patients with dyskinetic CP (13 males, 10 females; mean age 34 years, range 16-50 years) were participated in this study. Functional evaluation was assessed by the Gross Motor Functional Classification System (GMFCS) and Barry-Albright Dystonia Scale (BADS). Brain imaging was performed on 3.0 Tesla MRI, and volume change of the grey matter was assessed using VBM. The corticospinal tract (CST) and superior longitudinal fasciculus (SLF) were analyzed by DTT. MEPs were recorded in the first dorsal interossei, the biceps brachii and the deltoid muscles. RESULTS: Mean BADS was 16.4+/-5.0 in ambulatory group (GMFCS levels I, II, and III; n=11) and 21.3+/-3.9 in non-ambulatory group (GMFCS levels IV and V; n=12). Twelve patients showed normal MRI findings, and eleven patients showed abnormal MRI findings (grade I, n=5; grade II, n=2; grade III, n=4). About half of patients with dyskinetic CP showed putamen and thalamus lesions on MRI. Mean BADS was 20.3+/-5.7 in normal MRI group and 17.5+/-4.0 in abnormal MRI group. VBM showed reduced volume of the hippocampus and parahippocampal gyrus. In DTT, no abnormality was observed in CST, but not in SLF. In MEPs, most patients showed normal central motor conduction time. CONCLUSION: These results support that extrapyramidal tract, related with basal ganglia circuitry, may be responsible for the pathophysiology of dyskinetic CP rather than CST abnormality.
Basal Ganglia ; Cerebral Palsy* ; Classification ; Deltoid Muscle ; Diffusion ; Diffusion Tensor Imaging ; Dystonia ; Evoked Potentials, Motor ; Extrapyramidal Tracts ; Female ; Hippocampus ; Humans ; Magnetic Resonance Imaging ; Male ; Neuroimaging ; Parahippocampal Gyrus ; Putamen ; Pyramidal Tracts ; Thalamus

OBJECTIVE: To investigate neuroradiological and neurophysiological characteristics of patients with dyskinetic cerebral palsy (CP), by using magnetic resonance imaging (MRI), voxel-based morphometry (VBM), diffusion tensor tractography (DTT), and motor evoked potential (MEP). METHODS: Twenty-three patients with dyskinetic CP (13 males, 10 females; mean age 34 years, range 16-50 years) were participated in this study. Functional evaluation was assessed by the Gross Motor Functional Classification System (GMFCS) and Barry-Albright Dystonia Scale (BADS). Brain imaging was performed on 3.0 Tesla MRI, and volume change of the grey matter was assessed using VBM. The corticospinal tract (CST) and superior longitudinal fasciculus (SLF) were analyzed by DTT. MEPs were recorded in the first dorsal interossei, the biceps brachii and the deltoid muscles. RESULTS: Mean BADS was 16.4+/-5.0 in ambulatory group (GMFCS levels I, II, and III; n=11) and 21.3+/-3.9 in non-ambulatory group (GMFCS levels IV and V; n=12). Twelve patients showed normal MRI findings, and eleven patients showed abnormal MRI findings (grade I, n=5; grade II, n=2; grade III, n=4). About half of patients with dyskinetic CP showed putamen and thalamus lesions on MRI. Mean BADS was 20.3+/-5.7 in normal MRI group and 17.5+/-4.0 in abnormal MRI group. VBM showed reduced volume of the hippocampus and parahippocampal gyrus. In DTT, no abnormality was observed in CST, but not in SLF. In MEPs, most patients showed normal central motor conduction time. CONCLUSION: These results support that extrapyramidal tract, related with basal ganglia circuitry, may be responsible for the pathophysiology of dyskinetic CP rather than CST abnormality.
Basal Ganglia ; Cerebral Palsy* ; Classification ; Deltoid Muscle ; Diffusion ; Diffusion Tensor Imaging ; Dystonia ; Evoked Potentials, Motor ; Extrapyramidal Tracts ; Female ; Hippocampus ; Humans ; Magnetic Resonance Imaging ; Male ; Neuroimaging ; Parahippocampal Gyrus ; Putamen ; Pyramidal Tracts ; Thalamus

OBJECTIVE: To explore plastic changes in the red nucleus (RN) of stroke patients with severe corticospinal tract (CST) injury as a compensatory mechanism for recovery of hand function. METHODS: The moderate group (MG) comprised 5 patients with synergistic hand grasp movement combined with limited extension, and the severe group (SG) included 5 patients with synergistic hand grasp movement alone. The control group (CG) included 5 healthy subjects. Motor assessment was measured by Motricity Index (MI). Diffusion tensor imaging was analyzed using fractional anisotropy (FA) and radial diffusivity (RD) in the individual regions of interest (ROIs)—bilateral internal capsule and anterior pons for CST injury and bilateral RN for rubrospinal tract (RST) injury. RESULTS: The SG showed a significantly lower MI score than the MG mainly due to differences in hand subscores. Significantly reduced FA was observed in both MG and SG compared with CG, while SG showed increased MD and RD in the affected ROIs of CST, and increased FA on the unaffected side compared with CG. However, in the RN ROI, a significantly increased FA and decreased RD on the unaffected side similar to the affected side were found only in the SG. The relative index of FA was lower and RD in SG was higher than in CG in RST. CONCLUSION: The diffusion metrics of RST showed changes in patients with severe CST injury, suggesting that RST may play a role in the recovery of hand function in patients with severe CST injury.
Anisotropy ; Diffusion Tensor Imaging ; Diffusion* ; Extrapyramidal Tracts ; Hand ; Hand Strength ; Healthy Volunteers ; Humans ; Internal Capsule ; Neuronal Plasticity ; Paraplegia ; Plastics ; Pons ; Pyramidal Tracts* ; Recovery of Function ; Red Nucleus* ; Stroke* ; Upper Extremity