Healthy Hemisphere Research Articles

Poststroke Dysphagia Rehabilitation by Repetitive Transcranial Magnetic Stimulation: A Noncontrolled Pilot Study

Poststroke dysphagia is frequent and significantly increases patient mortality. In two thirds of cases there is a spontaneous improvement in a few weeks, but in the other third, oropharyngeal dysphagia persists. Repetitive transcranial magnetic stimulation (rTMS) is known to excite or inhibit cortical neurons, depending on stimulation frequency. The aim of this noncontrolled pilot study was to assess the feasibility and the effects of 1-Hz rTMS, known to have an inhibitory effect, on poststroke dysphagia. Seven patients (3 females, age = 65 +/- 10 years), with poststroke dysphagia due to hemispheric or subhemispheric stroke more than 6 months earlier (56 +/- 50 months) diagnosed by videofluoroscopy, participated in the study. rTMS at 1 Hz was applied for 20 min per day every day for 5 days to the healthy hemisphere to decrease transcallosal inhibition. The evaluation was performed using the dysphagia handicap index and videofluoroscopy. The dysphagia handicap index demonstrated that the patients had mild oropharyngeal dysphagia. Initially, the score was 43 +/- 9 of a possible 120 which decreased to 30 +/- 7 (p < 0.05) after rTMS. After rTMS, there was an improvement of swallowing coordination, with a decrease in swallow reaction time for liquids (p = 0.0506) and paste (p < 0.01), although oral transit time, pharyngeal transit time, and laryngeal closure duration were not modified. Aspiration score significantly decreased for liquids (p < 0.05) and residue score decreased for paste (p < 0.05). This pilot study demonstrated that rTMS is feasible in poststroke dysphagia and improves swallowing coordination. Our results now need to be confirmed by a randomized controlled study with a larger patient population.

Effect of cervical spinal cord stimulation on cerebral glucose metabolism

Objective: Syndromes resulting from decreased cerebral blood flow and metabolic activity have significant clinical and social repercussion. However, treatment options are limited. Cervical spinal cord stimulation has shown clinical benefit in the management of several ischemic syndromes. The aim of this report was to assess the effect of cervical spinal cord stimulation on cerebral glucose metabolism.Materials and methods: Between April 2000 and December 2005, 16 patients with brain tumors were assessed. Before and during spinal cord stimulation, they had cerebral glucose metabolism evaluated using 18fluoro-2-deoxyglucose positron emission tomography (18FDG-PET) in the healthy cerebral hemisphere contralateral to the lesion area.Results: Following cervical spinal cord stimulation, there was a significant (p<0.001) increase in glucose metabolism in healthy cerebral hemisphere. The measured increase was 37.7%, with an estimated potential maximal contribution of the first 18fluoro-2-deoxyglucose injection to the quantification of the second positron emission tomography study (carry-over effect) ≤ 16.6%.Conclusion: Cervical spinal cord stimulation can increase cerebral glucose metabolism. This result supports the potential usefulness of this neurosurgical technique as an adjuvant treatment in stroke and brain disorders that result from decreased blood flow and metabolism.

Cortical lateralization of bilateral symmetric chin movements and clinical relevance in tumor patients—A high field BOLD–FMRI study

Although unilateral lesion studies concerning the opercular part of primary motor cortex report clinically severe motor deficits (e.g. anarthria, masticatory paralysis), functional lateralization of this area has not yet been addressed in neuroimaging studies.Using BOLD–FMRI, this study provides the first quantitative evaluation of a possible cortical lateralization of symmetric chin movements (rhythmic contraction of masticatory muscles) in right-handed healthy subjects and presurgical patients suffering tumorous lesions in the opercular primary motor cortex. Data were analyzed according to “activation volume” and “activation intensity”.At group level, results showed a strong left-hemispheric dominance for chin movements in the group of healthy subjects. In contrast, patients indicated dominance of the healthy hemisphere. Here, a clinically relevant dissociation was found between “activation volume” and “activation intensity”: Although “activation volume” may be clearly lateralized to the healthy hemisphere, “activation intensity” may indicate residual functionally important tissue close to the pathological tissue. In these cases, consideration of BOLD–FMRI maps with the exclusive focus on “activation volume” may lead to erroneous presurgical conclusions.We conclude that comprehensive analyses of presurgical fMRI data may help to avoid sustained postoperative motor deficits and dysarthria in patients with lesions in the opercular part of primary motor cortex.

Jugular Bulb Oxygen-Desaturation Episodes During Functional Cerebral Hemispherotomies

To the Editor: Hemispherotomy, a modified functional hemispherectomy, is indicated in catastrophic unilateral epileptic syndromes where the substrate lies upon a diffuse hemispheric disease, with preservation of the contralateral hemisphere. Few published data describe anesthetic monitoring during this procedure (1–3). Monitoring jugular bulb venous oxygen saturation (Sjo2) in the healthy hemisphere gives useful information for maintaining adequate cerebral perfusion pressure and for setting the best ventilator characteristics to avoid hyperventilation and cerebral vasoconstriction (4,5). We report our experience with five patients with diffuse hemispheric disease, who underwent cerebral hemispherotomy. Because we continuously monitored Sjo2, we were able to detect and correct several episodes of severe desaturation. In each patient we inserted a fiberoptic oximetry catheter (Oximetrix, Abbott Critical Care Systems, North Chicago, IL) through the jugular vein ipsilateral to the healthy hemisphere, allowing us to continuously record Sjo2. In all patients, we detected several episodes of Sjo2 < 50% during neurosurgical procedures lasting from 7 h to 9 h 30 min. Representative episodes are shown in Table 1. These episodes were caused by modest hyperventilation, slight decreases in arterial blood pressure, or postural changes (e.g., reverse Trendelenburg position). Sjo2 normalized after we had several simultaneous adjustments: diminishing ventilation, increasing Fio2, and increasing arterial blood pressure. If we had not monitored Sjo2, we would have missed the impaired cerebral oxygenation, potentially resulting in intraoperative cerebral ischemia, increased postoperative morbidity, and impaired neurological outcome. All patients had good neurological outcomes.Table 1: Measured Hemodynamic and Respiratory VariablesNeus Fàbregas, MD, PhD Ivan Bel, MD Lydia Salvador, MD Ricard Valero, MD, PhD Enrique Carrero, MD Anesthesiology Department Hospital Clínic i Provincial de Barcelona University of Barcelona Barcelona, Spain [email protected] Jordi Rumià, MD Neurosurgical Department Hospital Clínic i Provincial de Barcelona University of Barcelona Barcelona, Spain

Sleep EEG Changes After Middle Cerebral Artery Infarcts in Mice: Different Effects of Striatal and Cortical Lesions

Hemispheric stroke in humans is associated with sleep-wake disturbances and sleep electroencephalogram (EEG) changes. The correlation between these changes and stroke extent remains unclear. In the absence of experimental data, we assessed sleep EEG changes after focal cerebral ischemia of different extensions in mice. Following electrode implantation and baseline sleep-wake EEG recordings, mice were submitted to sham surgery (control group), 30 minutes of intraluminal middle cerebral artery (MCA) occlusion (striatal stroke), or distal MCA electrocoagulation (cortical stroke). One and 12 days after stroke, sleep-wake EEG recordings were repeated. The EEG recorded from the healthy hemisphere was analyzed visually and automatically (fast Fourier analysis) according to established criteria. Striatal stroke induced an increase in non-rapid eye movement (NREM) sleep and a reduction of rapid eye movement sleep. These changes were detectable both during the light and the dark phase at day 1 and persisted until day 12 after stroke. Cortical stroke induced a less-marked increase in NREM sleep, which was present only at day 1 and during the dark phase. In cortical stroke, the increase in NREM sleep was associated in the wake EEG power spectra, with an increase in the theta and a reduction in the beta activity. Cortical and striatal stroke lead to different sleep-wake EEG changes in mice, which probably reflect variable effects on sleep-promoting and wakefulness-maintaining neuronal networks.

Causal visual interactions as revealed by an information theoretic measure and fMRI

In the present study, we evaluated the direction of the effective connectivity between fMRI activations in neural structures mediating preserved visual function in a patient with homonymous hemianopsia due to a posterior cerebral artery stroke. Although the lesion affected the primary visual cortex, the visual abilities of this patient included above-chance verbal reports of movement and color change as well as the discrimination of movement direction in his hemianopic field. These abilities were coupled with awareness (Riddoch syndrome). The strength and the direction of the interactions between visual regions were assessed by applying directed transinformation ( T), a nonparametric information theoretic causal measure sensitive to linear as well as to nonlinear interactions. In the healthy hemisphere, T identified a strong flow of information from visual area V1 to V5 during stimulation by visual movement and from V1 to V4/V8 during stimulation by color change. In addition, during color change stimulation, a bi-directional flow was observed between V4/V8 and V5, suggesting crosstalk between these regions. In the lesioned hemisphere, the color change stimulation evoked a stronger flow from V5 to V4/V8 and a flow from V4/V8 to V2. These observations provide support for the hypothesis that visual information is mediated via subcortical pathways that bypass V1 and project first to higher-tier visual areas V5 and V4/V8 then subsequently to lower-tier area V2.

Predictive value of Wada memory scores on postoperative learning and memory abilities in patients with intractable epilepsy

Surgery for refractory epilepsy often bestows significant relief but may cause memory impairment. The risk of postoperative memory loss can be determined by the intracarotid amobarbital procedure, or the Wada test. Chemical inactivation of the hemisphere on the side of the lesion is usually performed first, followed by inactivation of the contralateral hemisphere. Patients who demonstrate adequate memory capacity of the contralateral hemisphere following deactivation of the ipsilateral hemisphere are considered good candidates for anterior temporal lobectomy. Evidence for the contribution of deactivating the contralateral healthy hemisphere remains inconclusive. The authors analyzed results in 32 patients with intractable epilepsy who had undergone a bilateral Wada test followed by an anterior temporal lobectomy and in whom the findings of both pre- and postsurgical neuropsychological evaluations were available. The Wada memory scores were correlated with the difference in scores between pre- and postsurgical standardized memory test scores. Analyses revealed no significant relationship between the Wada memory scores in the contralateral hemisphere and postsurgical changes in memory abilities. There was, however, a significant negative correlation between the Wada memory score in the ipsilateral hemisphere and postsurgical memory changes, particularly in patients with right hemisphere epileptogenic lesions (p = 0.0007). The results of this study are discussed vis-à-vis two theories of hippocampal function, and the authors stress the importance of the functional status of the surgical hemisphere in the prediction of postsurgical memory changes.

Change of facilitation during voluntary bilateral hand activation after stroke

Background and purpose The relearning of daily activities after stroke also involves performance of bimanual tasks. This raises the possibility that concurrent activation of the healthy hemisphere interferes with reorganization processes in the affected hemisphere due to inhibitory pathways between homologous motor cortex representations. This study investigated the effect of voluntary, simultaneous activation of both hands upon the non-dominant (healthy subjects) or affected (stroke patients) hemisphere. Methods Eleven healthy subjects and 16 stroke patients were investigated using transcranial stimulation (TMS). TMS was applied over the non-dominant/affected hemisphere during performance of an isometric pinch grip at different force levels (10% or 50% of maximal voluntary contraction) with the contralateral hand. The ipsilateral hand had to perform the pinch grip at various force levels (10%, 50%, or 100% of maximal voluntary contraction) simultaneously. Peak-to-peak amplitudes of motor evoked potentials (MEPs) were compared to assess differences in motor cortex excitability. Results Unilateral activity of either hand alone exerted a facilitatory effect upon the non-dominant or affected hemisphere. In healthy subjects, the activation of the ipsilateral hand simultaneously with the contralateral hand did not produce any significant change of the MEP amplitudes compared to unilateral activation of the contralateral hand. In patients, however, the additional activation of the ipsilateral hand caused an additional increase of the peak-to-peak amplitudes. Conclusion In healthy subjects voluntary activation of the ipsilateral hand does not change the excitability of the motor cortex of the non-dominant hemisphere, when the contralateral hand is simultaneously activated. The facilitation of the contralateral hand seems to gate further facilitation by the ipsilateral hand. However, in stroke patients simultaneous activation of both hands causes an additional facilitation compared to activation of the affected hand alone.

Role of the healthy hemisphere in recovery after resection of the supplementary motor area

To determine the compensatory mechanisms involved in the recovery of motor function following surgical lesions of the supplementary motor area (SMA) and their relation to the clinical characteristics of recovery. Twelve patients were referred for surgery of low-grade gliomas located in the SMA, and compared to eight healthy controls using fMRI before and after surgery during self-paced movements of both hands, successively. Magnitude and volume of activation within regions of interest (primary sensorimotor cortex, premotor cortex, SMA, preSMA, and parietal lobes) were compared and tested for correlation with anatomic characteristics of the tumor and resection, and clinical data. Tumor growth induced preoperative underactivity in the adjacent SMA and overactivity in the opposite SMA. Postoperative recovery was associated with recruitment of a premotor network located in the healthy hemisphere including the SMA and the lateral premotor cortex. Postoperative premotor recruitment in the healthy hemisphere increased with the percentage of resection of preoperative SMA activation. Shortened onset and duration of recovery was associated with increased preoperative changes in activation levels. These findings suggest a dysfunction of the SMA ipsilateral to the tumor, partially compensated by a recruitment of the contralesional SMA which correlated with shortened postoperative recovery. SMA resection was compensated by the recruitment of a medial and lateral premotor circuitry in the healthy hemisphere.

Interhemispheric connection of auditory neural pathways assessed by auditory evoked magnetic fields in patients with fronto-temporal lobe infarction.

In auditory evoked magnetic fields (AEFs), the latency of temporal N100m response elicited by the ipsilateral ear stimulation (Ipsi-Stim) is generally longer than that of N100m response elicited by the contralateral ear stimulation (Cont-Stim). The reason for this difference remains unclear. We measured AEFs in patients with fronto-temporal or frontal lobe infarction to clarify this question. In the patients with fronto-temporal lobe infarction, the N100m peak latencies in the healthy hemisphere by Ipsi-Stim measurements were significantly longer than the corresponding normal values. Such a latency prolongation was not observed in the patients with frontal lobe infarction. The results suggest that auditory impulses originated from the ear may first arrive at the contralateral temporal cortex and then return to the ipsilateral temporal cortex mediating through the corpus callosum. The disturbance of interhemispheric conduction by ischemic temporal lesions likely delays the N100m latency at the contralateral temporal cortex. The mediation of interhemispheric route may, thus, make the ipsilateral N100m latency generally longer than the contralateral N100m latency.

Visual and Spectral Analysis of Sleep EEG in Acute Hemispheric Stroke

Background: Reports on the effects of focal hemispheric damage on sleep EEG are rare and contradictory. Patients and Methods: Twenty patients (mean age ± SD 53 ± 14 years) with a first acute hemispheric stroke and no sleep apnea were studied. Stroke severity [National Institute of Health Stroke Scale (NIHSS)], volume (diffusion-weighted brain MRI), and short-term outcome (Rankin score) were assessed. Within the first 8 days after stroke onset, 1–3 sleep EEG recordings per patient were performed. Sleep scoring and spectral analysis were based on the central derivation of the healthy hemisphere. Data were compared with those of 10 age-matched and gender-matched hospitalized controls with no brain damage and no sleep apnea. Results: Stroke patients had higher amounts of wakefulness after sleep onset (112 ± 53 min vs. 60 ± 38 min, p < 0.05) and a lower sleep efficiency (76 ± 10% vs. 86 ± 8%, p < 0.05) than controls. Time spent in slow-wave sleep (SWS) and rapid eye movement (REM) sleep and total sleep time were lower in stroke patients, but differences were not significant. A positive correlation was found between the amount of SWS and stroke volume (r = 0.79). The slow-wave activity (SWA) ratio NREM sleep/wakefulness was lower in patients than in controls (p < 0.05), and correlated with NIHSS (r = –0.47). Conclusion: Acute hemispheric stroke is accompanied by alterations of sleep EEG over the healthy hemisphere that correlate with stroke volume and outcome. The increased SWA during wakefulness and SWS over the healthy hemisphere contralaterally to large strokes may reflect neuronal hypometabolism induced transhemispherically (diaschisis).

Sleep electroencephalogram changes in acute hemispheric stroke

Background/objective: Since reports of the effects of cerebral hemispheric stroke on sleep architecture are rare and contradictory, we prospectively studied 24 patients with first acute supratentorial, extra-thalamic stroke. Methods: We assessed stroke severity, topography, and volume (on brain MRI). Sleep electroencephalogram recordings were performed a mean of 12 days after stroke onset, and scored for sleep stages over the healthy hemisphere. Sleep spindles and sawtooth waves were analyzed over both hemispheres. Data were compared with those of 17 age and gender-matched patients with normal brain imaging. Results: Compared to controls, stroke patients had lower total sleep time ( P<0.01), lower sleep efficiency ( P=0.02), and reduced amounts of NREM sleep stages 2–4 ( P=0.02). Sleep spindles and sawtooth waves were often bilaterally reduced in patients with stroke volumes >25 ml. Abnormalities of REM sleep were more common in sleep studies performed within 3 days after stroke onset. Compared to patients with poor outcome, those with good outcome had higher sleep efficiency ( P<0.01), more sleep time ( P=0.02), and more NREM sleep stage 2 ( P<0.01). Conclusion: Acute hemispheric stroke is accompanied by sleep EEG changes over the healthy hemisphere that correlate with stroke severity. These findings support the hypothesis that the cerebral hemispheres participate in the control of sleep.

Functional imaging correlates of recovery after stroke in humans.

The mechanisms that are responsible for the remarkable potential for functional recovery from stroke in humans remain unclear, and functional tomographic neuroimaging techniques increasingly are being used to investigate this issue. Such studies confirmed that recovery of function is related to the volume of penumbra tissue that escapes infarction. For language, reactivation of the primary functional areas in the dominant hemisphere is associated with the best prognosis. Evidence for functional plasticity in the immediate vicinity of infarcts, as demonstrated under experimental conditions with invasive methods, is still limited after stroke in humans, probably because of the limitations of spatial resolution of most currently available methods. Often, functional changes in the large-scale networks that support motor (for example, supplementary and premotor cortex) and language functions (for example, prefrontal cortex) have been found, more extensively after lesions acquired during childhood than at adult age. A frequent finding is an increase in the cerebral blood flow response in corresponding regions of the healthy hemisphere during unilateral motor activation or language activation. It is, however, not yet clear whether that is related to functional recovery, and there are several observations indicating that it is often inefficient. Further systematic follow-up studies and therapeutic intervention trials are needed to clarify these issues.

Early 99mTc-Ethylcysteinate Dimer Brain SPECT Patterns in the Acute Phase of Stroke as Predictors of Neurological Recovery

Objectives: Accurate prediction of outcome in acute stroke would help in identifying subgroups of patients for therapeutic trials and intravenous thrombolysis. The purpose of this study was to prospectively test the hypothesis that brain SPECT, with ^99mTc-L,L-ethylcysteinate dimer (ECD), a tracer sensitive to cell function, performed in the first hours after stroke onset, adds predictive power to concomitant neurological evaluation. Methods: Twenty-four patients with a first-ever middle cerebral artery stroke were prospectively studied with ECD-SPECT within 12 h after stroke onset. Neurological evaluation was performed using Orgogozo’s scale at admission and 3 months later in order to calculate the percent Martinez-Vila evolution indices (EI%). Semiquantitative visual analysis of SPECT images was performed in 6 cortical regions relevant for carotid artery territory. Both the extent and the intensity of cortical reduced ECD uptake were calculated, leading to an ‘ischemia’ score, corresponding to the sum of regions of interest (ROI) where ECD uptake was between 40 and 80% of the contralateral healthy hemisphere, and an ‘irreversibly damaged tissue’ (IDT) score, corresponding to an uptake below 40%, and a total score (ischemia + IDT). Each patient was assigned to one of three patterns: (1) pattern I with severe ECD cortical uptake reduction defined by at least one ROI with uptake under 40%, (2) pattern II with moderate ECD cortical uptake reduction (40–80%) only and (3) pattern III with normal ECD uptake. Results: There were 11 patients (46%) with pattern I ECD-SPECT. This group had almost invariably (10/11 patients) a poor outcome. The 12 patients (50%) classified in pattern II had a variable clinical outcome, ranging from improvement to deterioration. The single patient with a normal SPECT (pattern III) had a full clinical recovery. Both total score and IDT score were strongly significantly correlated with neurological recovery EI% (respectively p = 0.006 and 0.004). Their predictive value was significantly higher than, and independent of, day 0 neurological evaluation. No patient had an increased ECD uptake. Conclusion: Our results show that the degree of ECD cortical uptake reduction, measured on early brain SPECT, is a strong predictor of neurological recovery. ECD-SPECT data have a higher predictive value than day 0 neurological evaluation. The apparently better predictive value of ECD over hexamethylpropyleneamine oxime may reflect this tracer’s brain retention mechanisms which are weighted more towards cell function than towards perfusion. ECD-SPECT is easily obtainable and may help in selecting out from therapy those patients who are likely to have either very good or very poor spontaneous outcome, and thus improve the assessment of acute stroke and the choice of therapeutic strategy.

Plasticidad cortical y restauración de funciones neurológicas: una actualización sobre el tema

Neuroplasticity is a natural property of the nervous system to change its function and to reorganize due to a lesion or environmental changes. We review some of the main experimental and clinical experiences on cortical sensorimotor plasticity related to central nervous system (CNS) lesions. In the last 10 years increasing interest in neuronal plasticity has been prompted by several important discoveries. Long term potentiation and depression have been described as basic synaptic mechanism mediating functional recovery after CNS lesions, modulated by the up-down regulation of inhibitory-excitatory activity related to GABA, acetylcholine and glutamate between other neurotransmitters. In humans there are evidences from functional reorganization in the affected hemisphere in patients with hemispheric lesions, and the activation of homologues areas in the contralateral healthy hemisphere. Significative changes in the topography of cortical somatosensory and motor maps have been demonstrated using non invasive mapping techniques as multichannel EEG, evoked potential, transcranial magnetic stimulation, functional magnetic resonance imaging and positron emission tomography. Axonal and dendritic sprouting take place in animal models of brain lesions; but effective neural regeneration in the CNS does not seem to be a plausible mechanism for functional restoring. Plastic changes after CNS lesions make it possible the restoration of neurological functions in a high number of patients. It is important now to understand which changes are related to the clinical improvement of patients, and what might be done to promote or facilitate this changes and to inhibit maladaptive phenomena, for the design of rationale therapeutics strategies with modulatory influence on this process.

Modified activation of somatosensory cortical network in patients with right-hemisphere stroke.

To study the effects of parietal lesions on activation of the human somatosensory cortical network, we measured somatosensory evoked fields to electric median nerve stimuli, using a whole-scalp 122-channel neuromagnetometer, from six patients with cortical right-hemisphere stroke and from seven healthy control subjects. In the control subjects, unilateral stimuli elicited responses which were satisfactorily accounted for by modelled sources in the contralateral primary (SI) and bilateral secondary (SII) somatosensory cortices. In all patients, stimulation of the right median nerve also activated the SI and SII cortices of the healthy left hemisphere. However, the activation pattern was altered, suggesting diminished interhemispheric inhibition via callosal connections after right-sided stroke. Responses to left median nerve stimuli showed large interindividual variability due to the different extents of the lesions. The strength of the 20-ms response, originating in the SI cortex, roughly reflected the severity of the tactile impairment. Right SII responses were absent in patients with abnormal right SI responses, whereas the left SII was active in all patients, regardless of the responsiveness of the right SI and/or SII. Our results suggest that the human SI and SII cortices may be sequentially activated within one hemisphere, whereas SII ipsilateral to the stimulation may receive direct input from the periphery, at least when normal input from SI is interrupted.

Acquired `theory of mind' impairments following stroke

The ability to attribute thoughts and feelings to self and others (`theory of mind') has been hypothesised to have an innate neural basis and a dedicated cognitive mechanism. Evidence in favour of this proposal has come from autism; a brain-based developmental disorder which appears to be characterised by impaired theory of mind, despite sometimes good general reasoning skills/IQ. To date no case of specific acquired theory of mind impairment has been reported. The present study examined theory of mind in adults who had suffered right hemisphere stroke, a group known to show pragmatic and social difficulties. In one study using story materials and two using cartoons, patients' understanding of materials requiring attribution of mental states (e.g. ignorance, false belief) was significantly worse than their understanding of non-mental control materials. Data from healthy elderly subjects, and a small group of left hemisphere patients (who received the tasks in modified form), suggest that this impairment on mental state tasks is not a function of task difficulty. The findings support the notion of a dedicated cognitive system for theory of mind, and suggest a role for the healthy right hemisphere in the attribution of mental states.

Electrodermal level asymmetry in a unilateral brain-damaged patient

The purpose of this article is to report on a patient with right frontal damage who exhibited a strong left>right asymmetry of skin conductance levels (SCLs). Comparison with a control group indicates that this asymmetry resulted only from a higher SCL on the left hand. Such a result suggests that the frontal lesion has induced a contralateral disinhibition and is consistent with the idea of a contralateral inhibitory control of tonic electrodermal activity in the case of a healthy hemisphere. Peripheral factors, such as sweating or temperature seem unrelated to the SCL asymmetry and a possible influence of motor weakness is also rejected following comparison with a second patient who presented the same motor disorder without atypical SCL asymmetry. In contrast to SCLs, no asymmetry in skin conductance response amplitudes was observed in the former patient. This discrepancy is in line with previous observations showing that tonic and phasic EDA could depend on different neurophysiological controls.

Bilateral hemispheric activation in the early recovery of motor function after stroke.

Functional recovery after cerebral infarction is a complex phenomenon that depends on various factors. The aim of this study was to investigate changes in cerebral perfusion during motor activity in stroke patients with very early recovery of motor function. We included 9 consecutive patients hospitalized for acute-onset hemiparesis who showed complete functional recovery within 24 hours. CT of the brain showed an ischemic or hemorrhagic cerebral lesion in areas compatible with the symptomatology. Within 36 hours (range, 28 to 36) all patients were examined for the effects of a thumb-to-finger opposition task on cerebral blood flow in the middle cerebral arteries, evaluated by means of bilateral transcranial Doppler ultrasonography. Data were compared with those of 9 healthy subjects matched for age and sex. In patients, the evaluation was repeated 2 to 4 months later. A comparable increase in flow velocity (% mean+/-SD) was observed with respect to baseline in the contralateral middle cerebral artery during motor activity with patients' normal (8.8+/-2.0%) and recovered hand (9.7+/-4.1%) and with both hands of control subjects (10.6+/-1.4%). In the middle cerebral artery ipsilateral to the hand performing the motor task, the increase in flow velocity was significantly higher (P<0.0001) during movement of the recovered hand in patients (8.6+/-2.7%) than during movement of the normal hand in both patients (2.6+/-1.6%) and control subjects (1.4+/-0.7%). In patients, pattern of changes in flow velocity during motor performance remained the same in the second evaluation. These observations suggest that areas of the healthy hemisphere can be activated soon after a focal injury and contribute to the positive evolution of a functional deficit in some patients. This phenomenon of ipsilateral activation cannot be considered transient because it is evident months after stroke onset.

Ipsilateral motor activation in patients with cerebral gliomas.

The aim of this study is to provide neurophysiologic evidence of ipsilateral hemispheric activation in patients affected by intracerebral gliomas via the use of transcranial magnetic stimulation. The mechanisms involved in such ipsilateral activation have yet to be established, but they may involve preexisting routes that either are suppressed or undetected in the normal brain. Ipsilateral pathways may act in reserve, activated by the impairment of contralateral control. This hypothesis is suggested by the fact that the considerable size of the tumors in our patients is not matched by a proportionate loss of motor performance in the limbs contralateral to the affected hemisphere. However, it remains possible that ipsilateral motor-evoked potentials (iMEPs) may reflect reorganizational changes without significant functional effects. The effects of such activation were investigated using both focal and nonfocal coils stimulating cortical motor areas, with MEPs recorded from both left and right thenar muscles. Fifteen healthy control subjects and seven patients were examined. iMEPs were generally absent in normal subjects, but in contrast they were obtained in the patients by stimulating the healthy hemisphere using both round and figure-of-eight coils. Distinct from contralateral MEPs, iMEPs are obtained with higher thresholds (range, 60 to 80% of stimulator output) and display longer latencies (20.9 msec versus 19.4 msec). Taken in conjunction with recent research using functional imaging brain exploration and a variety of clinical, anatomic, and neurophysiologic studies, our results reflect a growing awareness of ipsilateral motor control and its potential compensatory role when contralateral routes are damaged.