Evoked potentials I

Evoked potentials I

$34 GUIDED POSTER SESSIONS IPs-o2.o31 Evoked potentials I Dynamic changes of somatosensory evoked potentials following finger ischemia demonstrate...

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GUIDED POSTER SESSIONS

IPs-o2.o31

Evoked potentials I

Dynamic changes of somatosensory evoked potentials following finger ischemia demonstrated by direct recording from human cerebral cortex. E.Urasaki, S.Wada, T.Genmoto, N.Akamatsu. University of Occupational and Environmental Health, Kitakyushu, Japan.

Objective: We examined the dynamic changes of sensory processing in the human adult brain by analyzing cortical somatosensory evoked potentials (SEPs) following finger ischemia. They were compared with the effect of tactile stimulation on SEPs. Methods: SEPs were directly recorded in the vicinity of central sulcus in 4 patients with intractable epilepsy who required implantation of chronic subdural electrodes. During electrical stmiulation to a selected finger, ischemic anesthesia was induced by the ligation of other finger's base using a rubber band. The effect of tactile interference was examined during electrical stimulation to the selected finger, by applying tactile stimulation to another finger (surround inhibition) or the electrically stimulated finger (partial saturation). Results: (1) During ischemic anesthesia of finger(s), SEP changes became gradually apparent and tended to persist in the post ischemic stage. (2) SEP changes during tactile interference were in part similar to those during ischemia. The tactile interference effects were seen in the subdural electrodes where area 3b responses (N20/P30) or area 1 responses (P25/N35) were recorded. Conclusions: Dynamic changes of SEP wavelbrms during finger ischemia were demonstrated by a direct recording study from the human adult cortex. Certain similarities of SEP changes in the ischemia and tactile interference suggest the involvement o f a common sensory pathway or network. Additionally, the persisting SEP changes following finger ischemia may indicate a new conditioning of sensory cortex.

Retinal dysfunction in Chagas disease based on electrophysiological studies. S.C.Matsumoto, M.Roncoroni, H.Gori, R.Jurgelevicius, A.Grillo, P.Manfredi, L. Gimenez, J. Mitelman. Hospital Dr Teodoro Alvarez, Buenos Aires, Argentina. Chagas disease is a chronic endemic infectious disease caused by Trypanosoma cruzi, well known for its cardiac and gastrointestinal complications. We have performed electroretinographic (ERG) studies in 35 patients (28E 7M; age ranged from 28 to 61) with confirmed Chagas disease and without other ophtalmological risk factors. Monocular electroretinosxaphic stimulation was performed with white, red and blue flashes and recorded according to standarized criteria. The obtained a-wave, b-wave latencies and b-wave amplitudes were measured and compared with those of age matched 35 normal controls (27F, 8M, age ranged from 30 to 60). Results in otherwise ophtalmologically asymptomatic patients showed dissociated ERG responses in comparison to controls, mostofthe time in an asymmetric pattern. Responses to white and blue flash stimulations were similar to those of controls but in 8 cases failed to be evoked with red flash stimulation (bilaterally in three). Mean latency values of b-wave obtained with red flash stimulation were slightly increased but the reduction of b-wave mean amplitude compared to those of controls was most remarkable. The results suggest a dissociated subclinical retinal involvement in Chagas disease.

Propagation of visual inflow demonstrated by VEPmapping. D.Ratiu, M.Matei, D.M.Psatta. Center of Neuroseiences Bucharest, Romania.

Background: Previous studies in our laboratory showed by electroclinical correlations on a great number of cases (N > 5000), that various components of visual evoked potential (VEP) have different generators: N20 from the retina, N40 from the lateral geniculate body, N70 and P100 from the striatal cortex, NI50 from the reticular ascendent activatory system, and N220P300 from the deep structures o f the temporal lobe (hippocampus?). Objectives: The present study investigated the propagation of visual impulses in the central nervous system (CNS) through VEP components mapping. Methods: VEPs were recorded on 19 leads (10 - 20 international system) with source derivation, by binocular flash stimulation. VEP amplitude maps were obtained by interpolation in 20 normal controls. Results: Comparing VEP maps at critical intervals in control normals with the latency of the previously mentioned components, it was found that N20 projects at the frontal poles, N40 on the rolandic line slightly lateral (lateral geniculate body projection area?), and N70 and PI00 at the occipital pole. Sometimes pathways activated between these areas were apparent. N 150 occurred on the midline in Cz (midline thalamus propagation area) and N220-P300 in the posterior temporal region and in Pz. Conclusions: These areas of propagation confirm our data obtained by electro-clinical correlation. Source derivation was by far superior to monopolar recording for the assessment of visual inflow propagation in the CNS. VEP components propagation data are useful in the investigation of visual disorders of central origin.

Cerebral generators of the early scalp somatosensory evoked potentials after tibial nerve stimulation. M.Valeriani. '." A.Insola, ' D.Restuccia," D.Le Pera, ' P. Mazzone, ~V.Santillig c C.Barba," ETonali '~."Universitgt Cattolica del Sacro Cuore. Roma, Italy. Casa di Cura San Raffaele Pisana, Roma, Italy. ~CTO, Roma, Italy. The cerebral sources underlying the early responses alter tibial nerve stimulation have not been largely investigated. We approached this problem from three different points of view. 1) The modifications oftibial nerve SEPs due to the phenomenon of gating were examined in 11 healthy subjects. We showed that while the early scalp positive response (P40) is usually focused on the Cz vertex, its topography shifts toward the parietal region ipsilateral to stimulation, if the subject is asked to voluntarily move the stimulated foot (active gating). 2) We performed the dipolar source modelling of tibial nerve SEPs recorded in 10 healthy subjects and found that two different generators in the contralateral hemisphere are activated in the 40 ms latency range. One dipole is radially oriented and may represent the source o f the P40 subcomponent at the vertex; the other dipole is perpendicular to the mesial hemispheric surface and probably generates both the fronto-temporal N37 potential and the parietal subeomponent of the P40 SEP. Active gating reduces the activity strength of the radial dipole more than that of the tangential source. 3) Tibial nerve SEPs were recorded in 16 drug-resistant Parkinsonian patients, who underwent thalamic or globus pallidus stimulation for extrapyramidal symptoms relief. Recording from the thalamic or globus pallidus electrodes showed a N40 potential at the same latency of the vertex P40 response. Voluntary movement of the stimulated foot reduced the amplitude of both the subcortical N40 and the vertex P40 SEP components, leaving the frontotemporal N37 and the parietal P40 potentials unaffected. Our results strongly suggest that centro-parietal positivity recorded after tibial nerve stimulation has two different subcomponents: a vertex subcomponent generated by a radial dipolar source, whose negative counterpart can be recorded by thalamic or globus palidus electrodes, and a parietal subcomponent, which represents the positive counterpart of the same tangential dipole generating also the fronto-temporal N37 potential.

Evoked potentials

Conduction velocity of the thermal-pain pathway in the human spinal cord. ~_

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" A. Truini ~, A. Romaniello ~, R. Isabella ~, G. Cruccu ~.2.

IDepar~. . . . 'urological Sciences, University of Rome "La Sapienza "', 2 Neuromed lnstitul~, Pozzilli (Is), Italy. Laser radiant heat pulses, exciting mechano-thermal nociceptors in the superficial skin layers, selectively activate A-delta or C free nerve endings and evoke brain potentials (LEPs, laser evoked potentials). CO 2 laser pulses (wavelength 10,6 lam, intensity 1,5-15 W, diameter 2,5-5 mm, duration 1550 ms) were delivered to the dorsal skin at different spinal levels from C5 to TI0; brain LEPs were recorded in 15 healthy subjects. AS-fiber stimulation easily evoked reproducible brain potentials, consisting of a negative wave with a latency o f about 200 ms (N200) followed by a positive wave with a latency of about 320 ms (P320). C-fiber stimulation evoked brain potentials in 10 subjects only; these potentials consist of a single positive wave with a mean latency of 450 ms (P450). Brain potentials induced by both A-delta and C-fiber inputs reached their highest amplitude at the vertex. The mean conduction velocity o f the A-delta pathway along the spinal cord was approximately 20 m/s, whereas that of the C-fiber pathway was about 3 m/s. For beth pathways the conduction velocity along the spinal cord was higher than the reported velocity of the corresponding primary sensory neurons.

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year history of blindness following giant cell arteritis, not a Braille reader. Both patients had elementat~ hallucinations; one also showed the complex type (case 2). No one had neurological deficits. Middle Latency Somatosensory Evoked Potentials (MI.,-SEPs), EEG with tapping (EEG-T), Transcranial Magnetic Stimulation (TMS) of the motor and occipital areas. EEG-T showed spikes on vertex and eentro- temporal derivations elicited by tactile stimulation o f the right limbs in patient I and o f the left foot in patient 2. At ML-SEPs, both patients showed high amplitude fronto-parietal components ( > I 0 uV: giant M L-SEPs), following stimulation of the median and posterior tibial nerves. TMS of the motor,cortex was normal in both patients. In both cases, magnetic stimulation o f occipital cortex evoked homolateral flashes of light to the stimulated side. In the Braille reader the occipital stimulation occasionally impaired reading. The neural representation ofnonvisual sensory stimuli is different in blind and in sighted people. Recent studies with TMS and SEPs showed the cortical representation of the reading finger of blind braille readers to be expanded if compared to that of sighted subject fingers. In patients with visual hallucinations by cortical blindness, PET imaging showed activation of the parieto-occipital cortex. Giant MLSEPs are a common feature in children with and without rolandic epilepsy. They usually disappear after age 14. Giant ML-SEPs are not described in adults. In our cases, giant ML-SEPs may represent a neurophysiological correlate o f somatosensory cortical hyperexcitability due to visual deafferentation. In our experience, the effect of the magnetic occipital stimulation may give a new insight on neuronal plasticity.

The postoperative changes in somatosensory evoked potentials and magnetic resonance imaging findings in cervical myelopathy.

Sensory perception correlates with the amplitude of long latency somatosensory evoked potentials (LLSEPs) changes to paired mechanical and eletrical stimuli.

T. Hayashida,T. Ogura, H. Hase,T. Osawa,Y. Hirasawa. Kyoto Prefectural UniversiO, of Medicine. Kyoto, Japan.

M. Veciana, J. Vails-Sol6. Servei de Neurologia. Hospital Clinic. Barcelona. Although imaging and electrophysiological techniques have made rapid progress, there is no conclusion whether the morphological intramedullary changes of the spinal cord permit the prediction of postsurgical outcome. The purpose of this study is to clarify the relationship between the spinal cord dysfunction using short-latency somatosensory evoked potentials (SSEPs) and the morphological changes of the spinal cord using highresolution magnetic resonance imaging (MRI) in cervical myelopathy patients treated surgically. We studied 20 patients with cervical myelopathy. There were 11 men and 9 women. The average age was 64.5 years, ranging from 45-80 years. All patients underwent cervical laminoplasty from posterior approach by the same surgeon. The SSEPs recordings were performed before surgery and 4, 12, 24 and 48 weeks tbllowing surgery. MRI examinations were performed betbre and after surgery. The compression ratio and the postoperative recovery rate of the cervical cord were measured from MRI. For clinical evaluation, we used the rating score (clinical score) and the recovery rate developed by the Japanese Orthopaedic Association. All patients (1 lcases) with a postoperative normal spinal N 13 amplitude recovered at least 15.5 clinical score points (average, 15.9), and the recovery rate of the cervical cord was significantly increased (p<0.01). With regard to the prognosis factor for the postoperative outcome, in all patients with normal spinal N 13 amplitude at 24 weeks postoperatively, the sufficient amplitudes o f spinal N13 were kept at 48 weeks after surgery. The postoperative restoration of the spinal N 13 response was closely related to the recovery rate of the cervical cord and the prognosis of the cervical cord function. In this study we can't find positive preoperative indicators for surgical outcome from SSEPs or MRI.

Spain. The LLSEPs are partly generated after cognitive processing of afferent inputs. Sensory volleys can be modulated by afferent inputs from other sensory modality by the action of gating mechanisms. In this study, we wanted to know how the gating effect modifies the LLSEPs and the subject's sensory perception. This study was carried out in 7 healthy volunteers. We recorded the LLSEPs to electrical stimuli to the 3 "~finger at an intensity of 120% above perception threshold. In test trials, we applied the same stimuli preceded by a mechanical stimulus to the dorsum of the hand at an interstimulus interval (ISI) of 0 to 800 ms. Other ISis were tested in some individuals. Mechanical stimuli were applied alone. We recorded the subject's evaluation of the sensory perception with a visual analog scale (VAS). The amplitude of the LLSEP decreased significantly to then disappear at ISis of 0 or 50 ms, and the value of VAS indicated absence of the subject's sensory perception. The amplitude of the LLSEP and the value of the VAS showed a progressive recovery that was not complete even at the ISI of 800 ms. In conclusion, the amplitude of the LLSEPs showed a significant positive correlation with the sensory perception, with a significant decrease at short ISis after the modulatory stimuli. Gating mechanisms are very effective in modulating both sensory perception and LLSEPs. Our study shows the possibility of quantifying gating effects on cognitive potentials.

Abnormal premovement gating of the somatosensory evoked potentials (SEPs) in Parkinson disease. Cortical hyperexeitability in blind subjects with visual hallucinations. R.PlasmatL F.Salvi, F.Pastorelli, M.C.Malaguti, C.A.Tassinari. Department of Neurological Sciences, Bellaria Hospital, University of Bologna, Italy. To determine cortical hyperexcitability in two acquired blind subjects with visual hallucinations. Patient 1: a 40 year old man; recurrent uveitis led to blindness at age of 27. He is an occasional Braille reader. Patient 2: a 76 year old woman, with a 3

N. Murase t, R. Kaji 2, N. Kohara ~, J. Kimura ~, H. Shibasaki I and JC. RothwellTM Department of Neurology, Kyoto University, Kyoto City, Japan;

2Depm'tment of Neurology and Clinical Otology Hospital of the University ofTokushima, TokushimaCity, Japan; JMRC Human Movement and Balance Unit, Institute of Neurology. Queen Square, London, UK.

Aim: Patients with Parkinson disease often show improvement by sensory guidance, which suggests abnormal sensory-motor integration. We reported abnormal pre-movement gating of the SEPs in writers" cramp which shows

Evoked potentials

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another abnormal sensory-motor integration (sensory trick) (Murase et al., Brain 123, 1813-29, 2000) and suggests abnormal central sensory processing before movement. We investigated this again in Parkinson disease. Method: Eight patients (mean age 63.8) and 7 age-matched normal controls were studied. The first sound stimulation (S 1) was followed by the second electric stimulation of mixed median nerve ($2) at the right wrist just one second later. Subjects were instructed to perform brisk finger extension immediately after they felt $2 stimulation at their wrist (pre-movement gating of SEP) and were compared at rest (control SEPs). Results: In the pre-movement gating, normal subjects showed significant attenuation of the amplitude of frontal N30a (p=O.006 in paired-t analysis) and the patients showed less significant gating (p=0.047). They also showed the gating of N20 (p=0.048). These results were distinct from those in writers' cramp, in which only frontal P22 component was gated. Conclusions: In Parkinson disease, the sensory gating in movement preparation may occur at the thalamocortical projection to the primary somatosensory area and use different sensory central processing for movement from that of writers' cramp.

The effect of different stimulus rates on somatosensory evoked potentials (SEPs) in patients with focal brain lesions. T, Genmoto. E. Urasaki, S. Wada. University of Occupational and

Environmental Health, Kitakyushu, Japan. Purpose: The aim of this study was to investigate whether the SEPs changes with focal brain lesions are enhanced by the different stimulus rates of peripheral sensory inputs. Method: The effect of different stimulus rates on SEPs were studied in 12 normal controls and 12 patients with focal cerebral lesions, including 3 frontal, 3 central, and 6 parietal lesions. The median nerve was electrically stimulated at the wrist with the stimulus rate of 1.3, 3.3, 6.3, 12.3 and 18.3 Hz. Cortical SEPs were recorded from frontal and parietal scalp electrodes contra-lateral to the side of stimulation. The amplitude of frontal (P22- N27) and parietal (N20- P25) components was measured from peak to trough. Results: in normal subjects, the amplitudes of frontal P22- N27 and parietal P25 components were decreased by the higher stimulus rates. The amplitude of N20 was decreased only when the high stimulus rate of 18.3 Hz was applied.

The frontal P22- N27 components were absent in 2 patients with frontal lesions and I with parietal lesions. When the median nerve was stimulated at higher rates, the amplitude decrease of N20 became apparent in 2 patients with central lesions. Paradoxically the amplitude increase of frontal P22N27 and parietal P25 components were observed in 2 patients with parietal lesions at the higher stimulus rates. Conclusion: These findings suggest that the change in stimulus rates is a useful method to detect the alternation of the sensory process in patients with focal cerebral lesions.

Somatosensory evoked potential and quantitative sensory testing abnormalities in patients with spinal sensory loss. B.E. Smith, EP Bosch. Mayo Clinic Scottsdale, Scottsdale, AZ, USA. Patients with isolated symptomatic sensory loss are most often found to have disease of the distal sensory axon. Uncommonly, the dorsal root ganglion (DRG) cell body can be affected by inflammatory, pamneoplastic, toxic, or other conditions (sensory polyganglionopathy). Rarely the distal sensory axon and DRG cell body are spared while the central sensory axon is the site of disease; this third group constitutes an unusual condition with isolated spinal sensory loss. Medical records of patients seen in the authors' neurology (n=7,509) and clinical neurophysiology practice (n=14,225) between 1994 and 2000 were reviewed for individuals meeting four criteria: 1) abnormal sensation on clinical neurological examination, 2) normal strength and absence of upper motor neuron findings on neurological examination, 3) normal sensory nerve conduction studies, and 4) central abnormalities on somatosensory evoked potential testing and/or abnormal quantitative sensory testing (CASE IV). Five patients, M:F 2:3, median age 58 years (range 44-75) were identified. Two had painless posterior midline C3.4 disk protrusion, one was diagnosed with chronic lymphocytic leukemia (CLL), a fourth had biopsy-proven Sj6gren syndrome, and the fifth no identifiable underlying disorder. The combination of non~al peripheral sensory nerve conduction studies and either central abnormalities on somatosensory evoked potential testing or quantitative sensory abnormalities, can aid in the identification of patients with isolated spinal sensory loss.