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.

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.

Recurrent Guillain-Barré syndrome following influenza vaccine.

Two patients recovered from an attack of Guillain-Barré syndrome and then had a second attack of this disease, with a shorter latent period, following monovalent influenza vaccination. These cases suggest that an attack of Guillain-Barré syndrome may result in greater risk of future episodes of the syndrome in conjunction with exposure to influenza or other vaccinations.

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.

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.

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.

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.

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.

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.

Effect of sleep on the electrographic manifestations of epilepsy.

Alterations in the level of arousal have profound predictable effects on the electrographic manifestations of epileptogenic abnormalities. The changes produced by sleep are dramatic in patients with generalized epilepsy as compared to patients with partial epilepsy. The epileptiform complexes associated with the generalized epilepsies show changes in spatial distribution, voltage, temporal sequencing, and waveform morphology. The changes are qualitatively similar in the different types of generalized seizure disorders but vary in the degree to which they are expressed in proportion to the "severity" of the seizure disorder. The presence of a generalized epileptogenic abnormality may result in alteration of K-complex waveform morphology. Multifocal spikes occurring in conjunction with bilateral synchronous discharges are frequently represented by a spatial field distribution consistent with a "horizontal dipole," during sleep especially in children.

Complex partial status epilepticus in paraneoplastic limbic encephalitis.

Paraneoplastic limbic encephalitis (PLE) results from tumor-related autoimmune mediated inflammation and degeneration of the mesial temporal structures. Cognitive and behavioral changes and seizures occur in PLE. Seizures are an uncommon presenting symptom of PLE occurring in 6 of 50 patients in one series. We present a report of complex partial status epilepticus (CPSE) as the presentation of PLE with anti-neuronal antibodies and improvement in mental status following treatment of seizures.

The human posterior tibial somatosensory evoked potential: synapse dependent and synapse independent spinal components.

Evidence has been obtained for the existence of two separate events occurring in the human spinal cord following posterior tibial nerve (PTN) stimulation. These events can be recorded on the surface in unanesthetized individuals. The first is an ascending wave which is conducted up to the cord at constant velocity and has a relatively short refractory period consistent with a compound nerve action potential. This represents the afferent volley traversing the lumbosacral plexus and the ascending dorsal columns. A second event, the N22/P22 complex, is surface negative on the back and surface positive anteriorly; its amplitude is maximal 5-15 cm above the level of the L4 spine and its peak latency remains constant at all levels. This activity has a relatively long refractory period. These characteristics of N22/P22 indicate that it is a localized synaptically dependent event conforming to a transverse dipole with dorsal negativity and a simultaneous anterior positivity. The N22/P22 is probably generated in the dorsal grey at the root entry zone. The N22/P22 is analogous to the stationary N13/P13 recorded over the neck following median nerve stimulation.

Short latency somatosensory evoked potentials following mechanical taps to the face. Scalp recordings with a non-cephalic reference.

Trigeminal somatosensory evoked potentials were recorded over the scalp using non-cephalic reference sites following mechanical taps to the face. A negative wave form, Nf17, was recorded bilaterally with its highest amplitude over the frontal scalp contralateral to the side of stimulation. A localized negative wave form, Np25, was recorded over the centro-parietal scalp contralateral to the side of stimulation. Np25 had an onset latency of 16.46 msec. The location and restricted spatial distribution of Np25 suggest that it represents the initial activation of the face area of the primary sensory cortex. The widespread bilateral nature of Nf17 and its latency of onset preceding that of Np25 suggest that Nf17 may be a 'far-field' potential reflecting activity in subcortical sensory pathways subserving the face.

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.

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.

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.

Somatosensory evoked potentials following median nerve stimulation. I. The cervical components.

Median somatosensory evoked potentials were studied in 20 normal adult volunteers. Recording electrodes were positioned over posterior, anterior and lateral neck, as well as on the scalp. Three distinct cervical potentials were identified. Immediately after the afferent volley passes Erb's point, a travelling wave is recorded in the lateral cervical electrodes ipsilateral to the side of stimulation. This represents the afferent volley approaching the spinal cord in the proximal brachial plexus and cervical roots and has been designated the 'proximal plexus volley' (PPV). Following PPV, a second travelling wave is recorded which increases in latency from low to high cervical levels. It represents the afferent volley in the dorsal column, and has been designated the 'dorsal column volley' (DCV). Following DCV, a stationary potential, designated CERV N13/P13, is recorded with characteristics of a transverse midline dipole having maximal negativity posteriorly and maximal positivity anteriorly. This potential may be generated by interneurons in the dorsal grey of the cervical cord. Each of these cervical travelling waves is accompanied by a negative far-field potential recorded at the scalp. The PPV is accompanied by a negative scalp deflection with a nominal latency of 10 ms (N10), and the peak of DCV at SC1 is accompanied by a scalp negativity with a nominal latency of 12 ms (N12). In view of these observations, it is necessary to reexamine assumptions regarding the polarity of scalp-recorded potentials generated by remote neural events.