Epileptic negative myoclonus: a combined study of EEG and [123I]iomazenil (123I-IMZ) single photon emission computed tomography indicating involvement of medial frontal area.

Negative myoclonus (NM) is a sudden brief atonia in muscle that causes jerky lapses of posture. This study employed an electrophysiological technique (silent-period-locked-averaging (SPLA) electroencephalography (EEG)) and a pharmacodynamic imaging technique (123I-IMZ-SPECT) to examine epileptic NM (ENM). Delayed-phase 123I-IMZ-SPECT images, which reflect the specific binding of the tracers to GABA-A receptors, exhibited significant decrease in the left medial frontal area. The deficit in GABA-A receptors indicated that abnormal synchronization was mediated by the lack of inhibitory postsynaptic mechanism. The SPLA-EEG recorded spike-like notches superimposed on the slope of negative slow activity in the contralateral fronto-central region. The slow activity started around 100 ms before and the peak of the spike-like component was 30 ms before the onset of ENM. Since the 123I-IMZ-SPECT shows the actual distribution of the tracers, the abnormal area associated with ENM in this particular patient was supposed to be on the left medial frontal lobe. Scalp EEG, though it cannot always accurately locate the abnormal area, was highly sensitive to be able to detect electrical activities transmitted through neuronal network or volume conductor. Combined use of the two methods provided high resolution both in spatial and temporal domain.

Generators of tibial nerve somatosensory evoked potential: recorded from the mesial surface of the human brain using subdural electrodes.

The generators of the initial cortical component of somatosensory evoked potentials in response to tibial nerve stimulation (Tib-somatosensory evoked potentials) are still uncertain. The purpose of this study is to localize the generators of it. A 15-year-old boy with intractable parietal lobe epilepsy was studied. Subdural electrodes were chronically implanted for presurgical evaluation of epilepsy surgery, covering the primary motor, primary sensory, and supplementary sensorimotor areas of the right leg. Tib-somatosensory evoked potentials were recorded from these areas. Highly localized prominent positive activities were recorded from electrodes on the primary motor area of the leg at 32.4 to 34.0 milliseconds. No corresponding large negative peak was recorded in any other electrodes. Weak negative activities distributed widely around the postcentral area at 33.2 to 33.6 milliseconds, accompanied by similar but positive activities in the precentral area at 32.8 to 33.2 milliseconds. There was an independent positive field on supplementary sensorimotor areas at 34.0 to 34.8 milliseconds. A small negative peak was also recorded but only from a single electrode within supplementary sensorimotor areas at 34.0 milliseconds. Our data suggest that the initial response of Tib-somatosensory evoked potentials has at least three independent generators: a radial dipole on the primary motor, a tangential dipole on the primary sensory area, and a dipole on the supplementary sensorimotor areas oriented perpendicularly to the mesial hemispheric surface.

Bilateral symmetric tonic posturing suggesting propagation to the supplementary motor area in a patient with precuneate cortical dysplasia.

We report a patient manifesting seizures with bilateral symmetric tonic posturing, which were markedly reduced after resection of the left precuneus. A 16-year-old man had sudden onset, complex partial seizures with bilateral symmetric tonic posturing since the age of eight years. Magnetic resonance fluid-attenuated inversion-recovery imaging revealed a hyperintense lesion in left precuneus. In almost all focal seizures recorded during an invasive EEG evaluation, ictal onset was detected from the inferomesial aspect of the lesion, but fast paroxysmal discharges from the ipsilateral supplementary motor area (SMA) were observed just before the clinical onset. After surgical excision of the EEG onset zone, including the lesion, seizure frequency was markedly (> 95%) reduced. By the 20th month after surgery, there were only brief nocturnal seizures involving slight elevation of both shoulders and slight abduction of both arms, with preservation of consciousness occurring once every few days. Invasive EEG findings and surgical outcome suggested that the epileptic activity originating from the epileptogenic zone may have propagated to the symptomatogenic zone including mainly the ipsilateral SMA. In summary, we report an interesting case of bilateral symmetric tonic posturing suggesting propagation to the SMA. MRI and invasive EEG confirmed the epileptogenic focus as a precuneate cortical dysplasia lesion.[Published with video sequences].

Long-term stimulation of the subthalamic nucleus in hemiparkinsonian rats: neuroprotection of dopaminergic neurons.

OBJECT: The goal of this study was to evaluate the neuroprotective effects conferred by long-term electrical stimulation of the subthalamic nucleus (STN) against degeneration of dopaminergic neurons by assessing motor functional and immunohistological findings in hemiparkinsonian rats. METHODS: In 13 of 25 rats, a concentric microelectrode was stereotactically implanted into the right STN under the guidance of extracellular microelectrode recording. After this had been done the animals were given an injection of 6-hydroxydopamine (6-OHDA) into the right striatum. Seven of the rats received continuous stimulation (frequency 130 Hz, intensity 80-100 microA) for 2 weeks (Group A); the other six did not receive any stimulation during this period (Group B). Twelve rats did not receive electrode implantation and underwent 6-OHDA injection only; these animals served as a control group (Group C). After 2 weeks, motor function in the rats was evaluated by conducting an amphetamine-induced rotation test. Finally, tyrosine hydroxylase-immunoreactive neurons in the pars compacta of the substantia nigra (SNc) were counted to evaluate the extent of degeneration of dopaminergic neurons. Ipsilateral rotation was significantly decreased in Group A, regardless of the effects of stimulation delivered during the test (p < 0.05). Rats in Group B demonstrated typical circling as did those in Group C, except that on stimulation Group B rats immediately stopped circling or changed direction. Tyrosine hydroxylase-immunoreactive neurons in the SNc were significantly preserved in the animals in Group A, whereas neurons in animals in Groups B and C were moderately depleted (p < 0.01). CONCLUSIONS: Acutely, STN stimulation improved rotation symmetry in rats with moderate SNc degeneration. When STN stimulation had been applied for the preceding 2 weeks, motor function was better and SNc neural degeneration was significantly milder. Subthalamic nucleus stimulation thus appears to protect dopaminergic neurons in this hemiparkinsonian model, in addition to improving motor function in these animals.