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Biomedical subjects

M Seyal

Publications and source records attributed to M Seyal.

At least 19 recordsLinked to original sources
PubMed2001

Transcranial magnetic stimulation of left prefrontal cortex impairs working memory.

OBJECTIVES: Several lines of evidence suggest that the prefrontal cortex is involved in working memory. Our goal was to determine whether transient functional disruption of the dorsolateral prefrontal cortex (DLPFC) would impair performance in a sequential-letter working memory task. METHODS: Subjects were shown sequences of letters and asked to state whether the letter just displayed was the same as the one presented 3-back. Single-pulse transcranial magnetic stimulation (TMS) was applied over the DLPFC between letter presentations. RESULTS: TMS applied over the left DLPFC resulted in increased errors relative to no TMS controls. TMS over the right DLPFC did not alter working memory performance. CONCLUSION: Our results indicate that the left prefrontal cortex has a crucial role in at least one type of working memory.

Adult↗
PubMed1999

Anticipation and execution of a simple reading task enhance corticospinal excitability.

OBJECTIVE: Electromyographic responses (EMG) evoked in the right hand by transcranial magnetic stimulation (TMS) of the left motor cortex are enhanced during continuous reading. This enhancement is the result of increased excitability of the motor cortex. We proposed that anticipation and reading of single words would also enhance corticospinal excitability. We studied the temporal course of corticospinal excitability changes following left and right hemisphere TMS. METHODS: Ten normal volunteers were studied. A warning stimulus (S1) was followed by an imperative stimulus (S2) whereupon a word was presented. Subjects responded by reading the word aloud or reading it silently. In other conditions, no word was displayed and the subjects responded to S2 by saying the word 'Cat', pursing their lips, or doing nothing. EMG was recorded over the contralateral hand following a TMS pulse over the motor cortex during and after the S1-S2 period. RESULTS: Enhancement of EMG amplitudes was significantly greater following left hemisphere TMS. The enhancement in the S1-S2 period and that following S2 had a time course similar to several event-related brain potentials. CONCLUSIONS: There may be a common mechanism underlying both corticospinal excitability and the contingent negative variation, readiness potential and N400.

Adult↗
PubMed1998

Increased excitability of the human corticospinal system with hyperventilation.

OBJECTIVES: Hyperventilation is effective in inducing generalized spike-wave discharges in patients with absence seizures and improves visual function and normalizes visual function in patients with multiple sclerosis. Hyperventilation increases the excitability of cutaneous and motor axons. In experimental animals, hyperventilation increases excitability of hippocampal neurons. There is however no direct evidence of a hyperventilation-induced increase in neuronal excitability within the central nervous system in humans. In this study we determined the effects of hyperventilation on the human corticospinal system. METHODS: We studied the effects of hyperventilation on (1) motor evoked potentials (MEPs) induced by transcranial magnetic pulse stimulation of the motor cortex and (2) F-wave responses. Six subjects were studied. RESULTS: Hyperventilation resulting in an end-tidal pCO2 of 15 mm Hg or less enhanced the amplitude of the MEP and resulted in a shortened onset latency. F-wave amplitudes were enhanced without any change in onset latency. CONCLUSIONS: These findings indicate that hyperventilation increases the excitability of the human corticospinal system. A hyperventilation-induced increase in excitability within the central nervous system may account for clinical phenomena such as facilitation of spike-wave discharges.

Adult↗
PubMed1998

Generators of short latency human somatosensory-evoked potentials recorded over the spine and scalp.

Somatosensory evoked potentials (SEPs) are most commonly obtained after stimulation of the median nerve and the posterior tibial nerve. SEPs reflect conduction of the afferent volley along the peripheral nerve, dorsal columns, and medial lemniscal pathways to the primary somatosensory cortex. Short-latency SEPs are recorded over the spine and scalp. After posterior tibial nerve stimulation, the following waveforms are recorded: N22, W3, the dorsal column volley, N29, P31, N34, and P37. After median nerve stimulation, the brachial plexus volley, dorsal column volley (N11), N13, P14, N18, N20, and P22 potentials are recorded. We discuss the current state of knowledge about the generators of these SEPs. Such information is crucial for proper interpretation of SEP abnormalities.

Afferent Pathways↗
PubMed1997

Suppression of spatial localization of a cutaneous stimulus following transcranial magnetic pulse stimulation of the sensorimotor cortex.

Transcranial magnetic pulse stimulation (TMS) over the region of the sensorimotor cortex impairs both perception and tactile localization of cutaneous stimuli delivered to the fingers of the contralateral hand. The region of the scalp over which TMS results in impaired cutaneous localization coincides with the region over which TMS suppresses simple perception. TMS has a more profound effect on tactile localization than on simple detection of cutaneous stimuli. TMS disrupts tactile localization for 400 ms after tactile perception has returned to normal.

Electric Stimulation↗
PubMed1995

Increased sensitivity to ipsilateral cutaneous stimuli following transcranial magnetic stimulation of the parietal lobe.

Transcranial magnetic stimulation of the sensorimotor cortex results in decreased sensitivity of threshold electrical stimuli to fingers of the contralateral hand. It has been suggested that one factor contributing to neglect contralateral to a unilateral parietal lesion is a release of the normal hemisphere from reciprocal interhemispheric inhibition by the damaged hemisphere. Consistent with this account, the current study demonstrated that transcranial magnetic stimulation over the parietal cortex results in increased sensitivity to cutaneous stimulation ipsilateral to the stimulation. The likely mechanism is a transcranial magnetic stimulation-induced transient dysfunction of the ipsilateral parietal cortex that then results in disinhibition of the contralateral parietal cortex.

Adolescent↗
PubMed1993

Brainstem bilirubin toxicity in the newborn primate may be promoted and reversed by modulating PCO2.

The auditory brainstem response (ABR) was monitored during infusion of bilirubin in six ventilated newborn rhesus monkeys (138-145 d gestation) while acute changes in pH were produced by varying inspired CO2. Prolonged respiratory acidosis without bilirubin infusion produced minimal changes in the ABR (one animal). CO2 exposure, usually initiated when the bilirubin level reached approximately 20 mg/dL, decreased arterial pH to values ranging from 6.85 to 7.10. ABR changes, including prolongation of the wave II-IV peak to peak intervals and decreased wave amplitudes, first developed 2-4 h after initial exposure to CO2. Total and unbound bilirubin levels at this time ranged from 376 to 564 mumol/L (22-33 mg/dL) and 38 to 65 nmol/L (2.5-3.8 micrograms/dL), respectively. Correction of respiratory acidosis produced partial to complete reversal of ABR changes within 3 to 20 min. Reexposure to CO2 immediately reproduced the ABR abnormality. Production and reversal of the abnormal ABR was obtained through two to three cycles in three animals. Thus, when the brainstem bilirubin level was near the threshold for toxicity, the effect of changes in PCO2 on the ABR were immediate, suggesting that auditory pathway toxicity is initially mediated by a reversible pH-dependent bilirubin-membrane complex. In contrast to humans, in monkeys auditory toxicity appeared to be a late manifestation of bilirubin toxicity, inasmuch as all monkeys were obtunded and apneic 30-70 min before ABR abnormalities appeared. Notwithstanding these limitations, the results support the hypothesis that bilirubin toxicity can be both promoted and reversed by modulating brain pH.

Acidosis, Respiratory↗
PubMed1992

Automated interictal EEG spike detection using artificial neural networks.

Feed-forward, error-back-propagation artificial neural networks were applied to recognition of epileptiform patterns in the EEG. The inherent network properties of generalization and variability tolerance were effective in identifying wave forms that differed from the training patterns but still maintained 'epileptiform' spatio-temporal characteristics. The certainty of recognition was measured as a continuous function with a range of 0-1. Two levels of certainty (0.825 and 0.900) were used to indicate recognition of spikes and sharp waves (SSW). An average 94.2% (+/- 7.3) of the SSW were recognized; 20.9% (+/- 22.9) of all recognized SSW were false-positive recognitions. The time required for pattern recognition was well within the time required for digitizing the analogue data. This study provides evidence that neural network technology is, in principle, an effective pattern recognition strategy for identification of epileptiform transients in the EEG. The analysis is sufficiently rapid to be of potential value as a strategy for data reduction of long recordings stored on bulk media.

Electroencephalography↗
PubMed1992

Suppression of cutaneous perception by magnetic pulse stimulation of the human brain.

We have demonstrated that magnetic pulse stimulation of the sensorimotor cortex suppresses perception of threshold electrical stimuli to the fingers of the contralateral hand. Maximum suppression of perception occurs when the fingers are stimulated 30-90 msec after the magnetic pulse. Thereafter, errors in perception of the cutaneous stimulus decrease to control levels by 300-400 msec after the magnetic pulse. The period of maximum suppression of perception coincides with the period during which cortically generated somatosensory evoked potentials (SEPs) are enhanced following magnetic pulse stimulation of the brain. The duration of suppression of perception, however, outlasts the duration of SEP enhancement. When the magnetic pulse is delivered after finger stimulation there is also suppression of perception. The suppression of perception is maximal when the magnetic pulse occurs 20-30 msec after finger stimulation. This interval coincides with the arrival of the afferent volley at the primary sensory cortex.

Electric Stimulation↗
PubMed1991

Cortical reflex myoclonus. A study of the relationship between giant somatosensory evoked potentials and motor excitability.

The excitability cycles of the N1-P1-N2 waveforms of the scalp-recorded somatosensory evoked potential (SEP) and of the long-latency, cortical loop reflex electromyographic (EMG) activity were studied in two patients with cortical reflex myoclonus. Long-latency cortical loop reflex EMG activity in the thenar muscles and giant SEPs occurred following median nerve stimulation. The excitability cycle of the EMG paralleled that of the SEP. There was an initial period of attenuation of SEP and EMG amplitude at interstimulus intervals (ISIs) of less than 40 ms followed by a period of amplitude enhancement at an ISI of up to 200 ms followed by a second period of attenuation. The excitability cycle is abnormal and the SEP and EMG amplitude changes parallel each other. It is therefore likely that a common mechanism determines the abnormal excitability cycle. The substrate for this mechanism is unknown and may be diffuse or restricted. Oral 5-hydroxytryptophan (5-HTP) in therapeutic doses altered the SEP excitability cycle. 5-HTP did not attenuate the giant SEPs but did attenuate the long-latency reflex EMG. Therefore, 5-HTP's site of action may be different from the substrate underlying the mechanism that results in the giant SEPs. Additionally, spinal latency reflex EMG activity occurred following treatment with 5-HTP but was absent when the patient discontinued 5-HTP.

5-Hydroxytryptophan↗
PubMed1990

Stiff-man syndrome: a GABAergic autoimmune disorder with autoantigenic heterogeneity.

Autoantibodies that reacted with cell bodies and axon terminals of gamma-aminobutyric acid (GABA)ergic neurons were present in the serum and cerebrospinal fluid in a patient with stiff-man syndrome with type I diabetes. Immunoblot experiments using this patient's serum and cerebrospinal fluid did not corroborate an earlier observation that these autoantibodies are directed against the GABAergic cytosolic enzyme, L-glutamic acid decarboxylase. While L-glutamic acid decarboxylase autoantibodies may be associated with this syndrome, they do not appear to be easily demonstrated.

Adult↗
PubMed1989

Spinal segmental somatosensory evoked potentials in lumbosacral radiculopathies.

We studied 21 patients with lumbosacral radiculopathy with segmental somatosensory evoked potentials (SEPs) recorded over both spine and scalp following saphenous, superficial peroneal, and sural nerve stimulation. Spinal SEPs were abnormal in 10 patients. In 3 patients, SEPs detected abnormalities not seen on EMG examination. With 1 exception, all anatomic levels of SEP abnormalities matched that of radiographic, EMG, or clinical abnormalities. SEPs were abnormal in 41% of nerve roots shown to be involved by other techniques. SEPs added to the clinical evaluation in 4 patients, but were less accurate than a combination of EMG and radiography in indicating the extent of nerve root involvement. We conclude that spinal SEPs following segmental sensory stimulation are useful in the evaluation of lumbosacral radiculopathies and complement information provided by the EMG. In contrast, scalp-recorded segmental SEPs rarely provide additional useful clinical information.

Adult↗
PubMed1988

Spinal somatosensory evoked potentials following segmental sensory stimulation. A direct measure of dorsal root function.

Dorsal root function cannot presently be measured directly. The H-reflex is an indirect measure of dorsal root function but only for the S1 root. Spinal somatosensory evoked potentials (SEPs) following dermatomal stimulation of the legs have the potential of providing direct data reflecting dorsal root function but have not been reliably recorded in normal subjects. We have developed a reliable technique for recording SEPs at the lumbar root entry zone following segmental sensory stimulation of the legs. The saphenous, superficial peroneal, and sural nerves were stimulated representing the L3/L4, L5 and S1 roots respectively. Reproducible responses (N-wave) were recorded over the lumbar spine in all 60 normal limbs examined. The N-wave peak latency was significantly correlated with lower limb length. The conduction velocities from the stimulation sites to the lumbar spine were similar to published values for peripheral conduction velocities in these nerves. The mean inter-limb latency differences for the N-wave peak were: L3/L4 0.61 msec; L5 0.35 msec; and S1 0.57 msec. The mean N-wave amplitudes were: L3/L4 0.11 microV; L5 0.28 microV; and S1 0.23 microV. This technique is a direct measure of dorsal root integrity. Unlike scalp recorded SEPs, the lumbar N-wave is not state-dependent and is unaffected by lesions within the brain and rostral cord.

Adult↗
PubMed1987

Generators of human spinal somatosensory evoked potentials.

Somatosensory evoked potentials recorded over the spine with a noncephalic reference following posterior tibial nerve stimulation have several components. (1) A stationary, synapse-dependent, negative potential (N22) occurs synchronously with a positive potential, P22, recorded ventral to the spinal cord and is localized to the lumbar region overlying the lumbar root entry zone. The N22/P22 complex is attributed to activation of interneurons in the dorsal gray of the lumbar cord. (2) A traveling negative potential with a gradually increasing latency may be recorded from the sacral to the cervical region. Its short refractory period indicates that it is not dependent on transmission across a synapse. This activity is attributed to transmission of the afferent volley through the lumbosacral plexus, roots, and the dorsal columns of the spinal cord. (3) N29, a stationary, synapse-dependent negative potential, localizes to the rostral cervical spine and is attributed to activation of the gracile nucleus relay cells. Following stimulation of the median nerve or fingers, the waveforms recorded over the cervical spine with a noncephalic reference include (1) the proximal plexus volley, a traveling negative potential reflecting transmission through the proximal brachial plexus and roots; (2) the dorsal column volley (DCV), the latency of which gradually increases from the caudal to rostral cervical region (the DCV is attributed to transmission of the afferent volley through the dorsal columns of the cervical cord); and (3) N13, a stationary negative waveform, with a long refractory period consistent with its dependence on transmission across a synapse. Experimental animal and human studies indicate that the N13 waveform is dependent on activity of at least two generator sites, namely the dorsal gray of the cervical cord and the cuneate nucleus.

Evoked Potentials, Somatosensory↗
PubMed1987

Effect of movement on human spinal and subcortical somatosensory evoked potentials.

Sensory transmission in dorsal column nuclei is inhibited during voluntary movement in experimental animals. We have studied the human response by recording spine and scalp somatosensory evoked potentials. Finger movement attenuated the amplitude and duration of the cervical N13 and the scalp N18 and N20 waves. Foot movement did not alter the lumbar N22 after foot stimulation, but the scalp P38 was attenuated. N22 results solely from activation of interneurons in the dorsal gray of the cord at the root entry zone, but N13 may receive contributions from the nucleus cuneatus. Therefore, the movement-induced attenuation of N13 is attributed to decreased contribution from the nucleus cuneatus.

Action Potentials↗
PubMed1987

Cervical synapse-dependent somatosensory evoked potential following posterior tibial nerve stimulation.

We have demonstrated the presence of a localized, synapse-dependent negativity (N29) recorded over the upper cervical spine after bilateral stimulation of the posterior tibial nerves at the ankle. The amplitude of N29 is maximal at the level of the second cervical spine and decreases at more rostral and caudal levels. The peak latency of N29 remains constant at all levels. N29 has a long refractory period when compared with the refractory period of the afferent volley recorded at either the sacral or thoracic level. N29 is most likely generated by activation of the nucleus gracilis by the afferent volley. The cervical N13 after median nerve stimulation probably has multiple generator sites, including the nucleus cuneatus.

Electric Stimulation↗