Changes in the perioral muscle responses to cortical TMS induced by decrease of sensory input and electrical stimulation to lower facial region.

OBJECTIVE: To determine the changes in the motor cortex due to repetitive electrical stimulation and cutaneous anesthesia in lower facial region. METHODS: A total of 11 subjects participated in the study of repetitive electrical stimulation, and 10 other subjects in the study of lower facial anesthesia. Facial nerve root and face associated cortical MEPs by transcranial magnetic stimulation (eight-shaped coil) were recorded from perioral muscles pre- and post- electrical stimulation and lower facial anesthesia. Cheek near to the corner of the mouth was transcutaneously stimulated by bipolar surface electrode giving repetitive electrical shocks at 5 Hz. Five percent lidocain/prilocain local anesthetic cream was applied to left or right lip-cheek region. RESULTS: There was no significant change in perioral MEP responses after 10-30 min of 5 Hz electrical stimulation. We found a significant increase of amplitude in cortical MEP recordings during lower facial anesthesia especially in cases of cortical magnetic stimulations ipsilateral and contralateral to the anaesthetized side and in perioral recordings contralateral to the anaesthetized side. CONCLUSIONS: The present study demonstrates that topical anesthesia to the lower facial region leads to cortical modulation and fast plastic changes in both hemispheres that are directed to the normal side.     

Transcranial magnetic stimulation after conditioning stimulation in two adrenomyeloneuropathy patients: delayed but facilitated motor-evoked potentials

Two male patients were diagnosed with adrenomyeloneuropathy. Their chief problems were progressive spastic paraparesis, sensory impairment, hyperpigmentation and testis atrophy. Transcranial magnetic stimulation (TMS) does not easily elicit motor-evoked potentials (MEPs) in patients with a central nervous system dysfunction, even though a few methods, such as contraction of the target muscles and the Jendrassik maneuver (JM), are used in the attempt to facilitate them. In these two patients, we used a conditioning method (prior electrical stimulation over the cutaneous nerve of the left index finger) in order to facilitate MEPs, elicited by TMS, in the left tibialis anterior muscle. In patient 1, facilitation of MEPs was present at conditioning-test (C-T) intervals in the range 60-220 ms, with the maximal MEP recorded at C-T 160 ms; in patient 2, it occurred in the C-T interval range 110-140 ms, with the maximal MEP recorded at C-T 130 ms. By means of conditioning electrical stimulation, we can facilitate MEPs elicited by TMS in those subjects in whom MEPs are minimal or difficult to elicit even using the conventional JM or muscle contraction. The facilitation of MEPs by conditioning stimuli allowed us not only to assess central motor conduction time, but also to demonstrate the preserved continuity of the corticospinal tract in these two patients.     

Conditioning effect on the long latency potentials in the lower limb to transcranial magnetic stimulation

Objectives – We used an electrical conditioning stimulation followed by transcranial magnetic stimulation (TMS) to facilitate the occurrence of long latency potentials (LLPs) in order to study the relationship between primary motor evoked potentials (MEPs) and LLPs in the lower limbs. Materials and methods – The study group included 6 healthy subjects, 1 patient with right thalamic infarction, and 3 patients with spinal cord injuries. The subjects were subjected to electrical conditioning (C) stimulation delivered to the left big toe at 250 Hz in a train of pulses of 20 ms duration prior to TMS (T) from 0 to 150 ms at an increment of 10 ms. The surface electromyographic signals were recorded at the tibialis anterior and gastrocnemius medialis for 400 ms. Results – The C-T test facilitated both primary MEPs and LLPs with a pattern similar to the primary MEPs of its antagonist. There was no facilitation of the primary MEPs or LLPs in the affected limb of patients with thalamic or spinal cord lesions. Conclusion – At appropriate C-T interval, LLPs could be consistently provoked by TMS. The LLPs were absent in the patients with thalamic infarction and spinal cord injuries. It suggests that LLPs might be provoked through a supraspinal control.     

The role of cutaneous inputs during magnetic transcranial stimulation

Latency and amplitude characteristics of motor evoked potentials (MEPs) from abductor digiti minimi (ADM) and first dorsal interosseus (FDI) muscles were evaluated in 7 healthy volunteers via magnetic transcranial stimulation of the hemiscalp overlying contralateral motor areas. MEPs in complete relaxation and during contraction were recorded in two different experimental conditions: before and following anesthesia of median (sensory + motor) and radial (sensory) nerve fibers at wrist. This procedure induced a complete loss of skin sensation from dorsal and palmar aspects of the hand area “enveloping” the FDI muscle. On the other hand, the skin overlying the ADM muscle, as well as the strength of ulnar nerve-supplied muscles were spared. This selective sensory deprivation lead to the following short-term changes: the physiological latency “jump” toward shorter values in contracted MEPs vs. relaxation was partially lost in the FDI (3.0 ± 1.4 ms in basal condition, 1.8 ± 1.1 ms after anesthesia, P = 0.028), while it was still clearly evident in the ADM (3.7 ± 0.9 ms and 3.3 ± 1.0 ms, respectively). Moreover, minor amplitude changes of MEPs during active contraction in the two muscles were detected: MEPs recorded from the FDI muscle were less potentiated during voluntary contraction than those recorded from the ADM muscle. The role of the cutaneous input in governing latency/amplitude characteristics of MEPs is discussed. © 1996 John Wiley & Sons, Inc.     

Inhibition of ipsilateral motor cortex during phasic generation of low force.

OBJECTIVE: To study the effect of different types of unilateral pinch grips on excitability of the ipsilateral motor cortex. METHODS: In 9 healthy volunteers, transcranial magnetic stimuli (TMS) were applied over one motor cortex while the subjects performed either phasic or tonic ipsilateral pinch grips with different force levels (range 1-40% maximum voluntary contraction, MVC). Motor evoked potentials (MEP) were recorded from the relaxed contralateral first dorsal interosseous muscle (FDI) and were compared to MEPs obtained during muscle relaxation of both hands. In additional experiments, transcranial electrical stimuli (TES) were administered and F waves were recorded after electrical stimulation of the ulnar nerve. RESULTS: Phasic pinch grips with low force (1 and 2% MVC) induced a significant decrease of TMS-induced MEP amplitudes. The effect lasted for about 100 ms after reaching the force level and was similar for both right and left-handed pinch grips. TES-induced MEPs and F waves remained unchanged. In contrast, tonic contractions (20 and 40% MVC) enhanced MEPs in the homologous FDI. CONCLUSIONS: Phasic pinch grips with low force inhibit the motor cortex responsible for the contralateral homologous hand muscle. This effect, which is probably mediated transcallosally, might act at the level of the motor cortex.     

Effects of somatosensory input on central fatigue: a pilot study.

OBJECTIVE: Depression of motor evoked potentials (MEPs) following transcranial magnetic stimulation (TMS) may be a sign of central motor fatigue. As a pilot study, we have examined whether post-exercise MEP depression can be compensated by application of sensory stimuli prior to TMS. METHODS: We studied 15 healthy volunteers (aged 21-28 years) who were required to perform an exercise protocol of ankle dorsiflexion until force fell below 66% of maximum force. MEPs were recorded from the right tibialis anterior muscle. Prior to TMS, electrical stimuli were applied to the ipsilateral sural nerve with an individual interstimulus interval between 50 and 80 ms. RESULTS: MEP areas decreased after exercise. When a sensory stimulus was administered MEPs did not change. CONCLUSION: We conclude that the effects of central fatigue may be influenced by application of sensory stimuli.     

The silent period induced by transcranial magnetic stimulation in muscles supplied by cranial nerves: normal data and changes in patients.

The silent period induced by transcranial magnetic stimulation of the sensorimotor cortex (Magstim 200, figure of eight coil, loop diameter 7 cm) in active muscles supplied by cranial nerves (mentalis, sternocleidomastoid, and genioglossus) was studied in 14 control subjects and nine patients with localised lesions of the sensorimotor cortex. In the patients, measurements of the silent period were also made in the first dorsal interosseus and tibialis anterior muscles. In the controls, there was a silent period in contralateral as well as ipsilateral cranial muscle and the duration of the silent period increased with increasing stimulus intensities. The mean duration of the silent period was around 140 ms in contralateral mentalis muscle and around 90 ms in contralateral sternocleidomastoid muscle at 1.2 x threshold stimulation strengths. Whereas the duration of the silent period in ipsilateral mentalis muscle was shorter than on the contralateral side it was similar on both sides in sternocleidomastoid muscle. In patients with focal lesions of the face associated primary motor cortex and corresponding central facial paresis, the silent period in mentalis muscle was shortened whereas it was unchanged or prolonged in limb muscles (first dorsal interosseus, tibialis anterior) with stimulation over the affected hemisphere. By contrast, in a patient with a lesion within the parietal cortex, the silent period in mentalis muscle was prolonged with stimulation of the affected side.     

Significance of coil orientation for motor evoked potentials from nasalis muscle elicited by transcranial magnetic stimulation.

OBJECTIVE: In transcranial magnetic stimulation (TMS) of the motor cortex, the optimal orientation of the coil on the scalp is dependent on the muscle under investigation, but not yet known for facial muscles. METHODS: Using a figure-of-eight coil, we compared TMS induced motor evoked potentials (MEPs) from eight different coil orientations when recording from ipsi- and contralateral nasalis muscle. RESULTS: The MEPs from nasalis muscle revealed three components: The major ipsi- and contra-lateral middle latency responses of approximately 10 ms onset latency proved entirely dependent on voluntary pre-innervation. They were most easily obtained from a coil orientation with posterior inducing current direction, and in this respect resembled the intrinsic hand rather than the masseter muscles. Early short duration responses of around 6 ms onset latency were best elicited with an antero-lateral current direction and not pre-innervation dependent, and therefore most probably due to stimulation of the nerve roots. Late responses (>18 ms) could inconsistently be elicited with posterior coil orientations in pre-innervated condition. CONCLUSIONS: By using the appropriate coil orientation and both conditions relaxed and pre-innervated, cortically evoked MEP responses from nasalis muscle can reliably be separated from peripheral and reflex components and also from cross talk of masseter muscle activation.     

Functional recovery in hemiplegic cerebral palsy: ipsilateral electromyographic responses to focal transcranial magnetic stimulation.

The patterns of functional recovery after unilateral cerebral damage occurring in the prenatal to infantile periods were studied in nine patients with hemiplegic cerebral palsy. Motor evoked potentials (MEPs) recorded from the small hand muscles were investigated using focal transcranial magnetic stimulation (TMS). The MEPs findings could be separated into three subtypes based on the features of ipsilateral MEPs elicited by TMS over the unaffected motor cortex. Bilateral MEPs of similar latency were obtained in three patients. These patients each having a congenital lesion invariably exhibited mirror movements and severe hemiparesis. Meanwhile, ipsilateral MEPs with markedly prolonged latency were demonstrated in two other patients, who exhibited synergistic associated movements and severe hemiparesis caused by an acquired lesion. In the remaining four patients, who showed mild hemiparesis without such abnormal interlimb coordinations, there were no ipsilateral MEPs. Thus, we suggest that TMS is useful for confirming the electrophysiological findings relevant to functional recovery in hemiplegic cerebral palsy underlying such abnormal interlimb coordinations. Specifically, bilateral MEPs of similar latency were considered consistent with compensatory mirror movements originating from bilateral motor representation in the unaffected motor cortex.     

Effects of visual and auditory stimulation on somatosensory evoked magnetic fields.

DESIGN AND METHODS: We investigated the effects of continuous visual (cartoon and random dot motion) and auditory (music) stimulation on somatosensory evoked magnetic fields (SEFs) following electrical stimulation of the median nerve on 12 normal subjects using paired t test and two way ANOVA for the statistics. RESULTS: In the hemisphere contralateral to the stimulated nerve, the middle-latency components (35-60 ms in latency) were significantly enhanced by visual, but not by auditory stimulation. The dipoles of all components within 60-70 ms following stimulation were estimated to be very close each other, around the hand area of the primary sensory cortex (SI). In the ipsilateral hemisphere, the middle-latency components (70-100 ms in latency), the dipoles of which were estimated to be in the second sensory cortex (SII), were markedly decreased in amplitude by both the visual and auditory stimulation. CONCLUSIONS: These changes in waveform by visual and auditory stimulation are thought to be due to the effects of the activation of polymodal neurons, which receive not only somatosensory but also visual and/or auditory inputs, in areas 5 and/or 7 as well as in the medial superior temporal region (MST) and superior temporal sulcus (STS), although a change of attention might also be a factor causing such findings.     

Reinforcement of subliminal flexion reflexes by transcranial magnetic stimulation of motor cortex in subjects with spinal cord injury.

A 20 msec train (500 Hz; 0.1-0.2 msec duration) of percutaneous electrical stimulation (ES) applied to the plantar surface was used to condition muscle responses evoked in tibialis anterior (TA) by transcranial magnetic stimulation of the motor cortex in 8 subjects with traumatic spinal cord injury (SCI). The intensity of conditioning ES was adjusted to just subthreshold for evoking flexion reflexes in TA and was delivered at conditioning-test (C-T) intervals of 15-60 msec prior to cortical stimulation. Four subjects with clinically complete SCI revealed no muscle response to cortical stimulation or following combined subliminal percutaneous ES and cortical stimulation. Four subjects (3 clinically incomplete and 1 complete injury) demonstrated muscle responses with a latency of 70-80 msec time-locked to the percutaneous ES when the conditioning subliminal stimulation was delivered at C-T: 15-40 msec. These responses, resembling suprathreshold flexion reflexes, reflect the convergence of excitatory afferent and cortical inputs and provide evidence of preserved corticospinal innervation to the L4-5 segmental motoneuron or interneuron pools. In 3 of the subjects this preserved corticospinal influence was evident despite absence of motor evoked potentials (MEPs) following cortical stimulation. The effect of the combined electrical and cortical stimulation in yielding suprathreshold flexion reflexes, instead of the facilitated MEPs seen in control subjects, appears to be related to slowed central conduction, prolonged temporal dispersion of the motoneuron facilitation following cortical stimulation and segmental reflex changes associated with disrupted modulation of interneuronal pathways. The results show this conditioning paradigm to be useful in revealing preserved corticospinal innervation in some SCI subjects with absent MEPs.     

Cortical reorganization in patients with facial palsy

Possible changes in the organization of the cortex in patients with facial palsy, serving as a model of peripheral motor deefferentation, were investigated by using transcranial magnetic stimulation (TMS) and positron emission tomography (PET). With TMS, the size of the area producing muscle-evoked potentials (MEPs) of the abductor pollicis brevis muscle, the sum of MEP amplitudes within this area, and the volume over the mapping area were compared between both hemispheres in 8 patients. With PET, increases in regional cerebral blood flow, measured with the standard H₂ ¹⁵O₂ bolus injection technique, were compared between 6 patients and 6 healthy volunteers during sequential finger opposition. Patients moved the hand ipsilateral to the facial palsy, the control subjects the right hand. Of 9 patients in total, 5 participated in both experiments. With both methods, an enlargement of the hand field contralateral to the facial palsy was found, extending in a lateral direction, into the site of the presumed face area. The PET data showed that the enlargemement of the hand field in the somatosensory cortex (SMC) is part of a widespread cortical reorganization, including the ipsilateral SMC and bilateral secondary motor and sensory areas. We report for the first time, using two different noninvasive methods, that peripheral, mere motor deefferentation is a sufficient stimulus for reorganizational changes in the healthy adult human cortex.     

Intraoperative localisation of the primary motor cortex using single electrical stimuli.

A new method of intraoperative localisation of the primary motor cortex is described, based on the application of single anodal electric pulses to the brain surface. Patients were anaesthetised with propofol infusion, and neuromuscular blockade was temporarily alleviated to allow recording of surface EMG responses (CMAPs) to the stimuli. Primary motor areas could be localised in 18/19 patients studied. In the other patient, no responses were elicited, as the operative field was posterior to the motor cortex. When compared with MEPs elicited in awake patients by magnetic stimuli, responses to intraoperative anodal stimulation were of small amplitude (usually less than 10% of MEPs) and their latency was some 1 to 2 ms longer. One month after the operation, only 1/19 patients was left with a slight muscle weakness, although seven showed preoperative motor deficit. The procedure proved easy and fast, needing no preliminary surgery or time consuming preparation. It did not induce any detectable side effects.     

Altered mechanisms of motor-evoked potential generation after transient focal cerebral ischemia in the rat: implications for transcranial magnetic stimulation

We recently demonstrated that a long-lasting transmission defect in cortical synapses caused motor dysfunction after brief middle cerebral artery (MCA) occlusion in the rat despite rapid recovery of axons. In this experimental study, we have examined the impact of differential recovery of synapses and axons on generation of motor-evoked potentials (MEP) recorded from contralateral paralyzed and ipsilateral unaffected muscles, to gain insight into mechanisms of MEPs recorded from stroke patients by transcranial magnetic stimulation (TMS). MEPs generated by focal electrical stimulation of the forelimb area of motor cortex were simultaneously recorded from the brain stem, contra- and ipsilateral forelimb and contralateral hindlimb muscles in rats subjected to transient MCA occlusion. The effect of ischemia on cortical activity and axonal conduction was differentially studied by proximal or distal occlusion of the MCA. Regional cerebral blood flow changes in the forelimb area were monitored by laser-Doppler flowmetry during ischemia and reperfusion. In addition, synaptic transmission within the forelimb area of motor cortex was examined by intracellular and extracellular recording of potentials generated by stimulation of the premotor area. No MEP response was recorded during ischemia. Upon reperfusion: (i) motor axons readily regained their excitability and cortical stimulation caused successive pyramidal volleys (recorded as D waves from the brain stem) and a MEP from contralateral paralytic muscles although synaptic activation of motor pathways was not feasible; (ii) the amplitude of pyramidal volley was increased; (iii) MEPs with a longer latency were recorded from the ipsilateral forelimb. In conclusion, differential recovery of synapses and axons after ischemia may account for some previously unexplained findings (such as preserved MEPs in paralysed muscles) observed in cortical stimulation studies of stroke patients.     

Motor potentials of inferior orbicularis oculi muscle to transcranial magnetic stimulation. Comparison with responses to electrical peripheral stimulation of facial nerve.

Magnetic stimulation at the vertex evoked a motor potential (MP) in the inferior orbicularis oculi muscle of 10 healthy subjects with an onset latency of 8-13 msec. Its amplitude increased and its latency decreased when the muscle was contracted: the latency measured 9.5 +/- 1.3 msec with an intensity of stimulation 10-15% above threshold in the contracted muscle. This MP is secondary to excitation of the motor cortex. With the coil placed over the occipital scalp and the same stimulation intensity, an MP was recorded with an onset latency at 4.5 +/- 0.6 msec. This response reflects the activation of the facial nerve root. The peripheral electrical stimulation of the facial nerve at the mandible angle elicited an MP with an onset latency at 3.5 +/- 0.4 msec. Most records showed the presence of late components at about 30 msec for all types of stimulation.     

Influence of task-related ipsilateral hand movement on motor cortex excitability.

OBJECTIVE: The time course of the right motor cortex excitability in relation to a task-related voluntary right thumb twitch was studied using sub-threshold transcranial magnetic stimulation (TMS) to the right motor cortex. METHODS: Motor excitability was studied in 8 adult subjects who made a brief right thumb twitch to the predictable omission of every fifth tone in a series of tones 2.5 s apart. This paradigm avoided an overt sensory cue, while allowing experimental control of TMS timing relative to both movement and the cue to move. Motor excitability was characterized by several measures of motor evoked potentials (MEPs) recorded from the left thenar eminence in response to TMS over the right scalp with a 9 cm coil: probability of eliciting MEPs, incidence of MEPs and amplitude of MEPs. RESULTS: All subjects showed suppression of motor excitability immediately following a voluntary right thumb twitch (ipsilateral response), and up to 1 s after it. However, two distinctly different effects on motor excitability were observed before the response: two subjects showed excitation, beginning about 500 ms before response until 300 ms after it, followed by the post-movement suppression; 6 subjects displayed pre-movement suppression, beginning about 600 ms before the response and persisting for the duration. CONCLUSIONS: The net effect of an ipsilateral response on motor cortex can be either inhibitory or excitatory, changing with time relative to the response. These findings are compatible with two separate processes, inhibitory and excitatory, which interact to determine motor excitability ipsilateral to the responding hand.     

The second sensory area in humans: evoked potential and electrical stimulation studies

A patient with intractable seizures originating from a right frontal focus was evaluated for surgical treatment. This evaluation was carried out using a chronically implanted array of 96 stainless steel electrodes 1 cm apart and covering the perirolandic and frontal areas. Somatosensory evoked potentials and electrical stimulation of the subdural electrodes localized the primary sensory hand area. Evoked potentials of identical waveform but of lower amplitude and 2.4 ms longer latency were recorded in the inferior frontal gyrus immediately anterior to the face area of the motor strip. Electrical stimulation of that area elicited: (1) a "paralyzing" feeling in the left arm and face; (2) inhibition of rapid alternating movements of left fingers, left hand, and tongue; (3) inability to maintain a strong voluntary muscle contraction of the left hand or tongue; and (4) speech arrest. This appears to be the first report of a secondary sensory area in humans demonstrated by both electrical stimulation and evoked potential studies. Electrical stimulation showed that the secondary sensory area overlapped an area of complex motor control, suggesting that the secondary sensory area provides direct sensory feedback information for appropriate motor integration.     

Investigation of facial motor pathways by electrical and magnetic stimulation: sites and mechanisms of excitation.

A refined technique is described for non invasive examination of the facial motor pathways by stimulation of the extra- and intracranial segment of the facial nerve and the facial motor cortex. Surface recordings from the nasalis muscle rather than from the orbicularis oris muscle were used, since the compound muscle action potential (CMAP) from this muscle showed a more clearly defined onset. Electrical extracranial stimulation of the facial nerve at the stylomastoid fossa in 14 healthy subjects yielded a mean distal motor latency of 3.7 ms (SD 0.46), comparable with reported latencies to the orbicularis oris muscle. Using a magnetic stimulator, transcranial stimulation of the facial nerve was performed. The mechanism of transcranial magnetic facial nerve stimulation was studied using recordings on 12 patients who had facial nerve lesions at different locations, and with intraoperative direct measurements in four patients undergoing posterior fossa surgery. The actual site of stimulation could be localised to the proximal part of the facial canal, and a mean "transosseal conduction time" of 1.2 ms (SD 0.18) was calculated. The cerebrospinal fluid (CSF) played an important role in mediating the magnetically induced stimulating currents. Finally, with transcranial magnetic stimulation of the facial motor cortex, clearly discernible CMAPs could be produced when voluntary activation of several facial muscles was used to facilitate the responses. From this, a central motor conduction time of 5.1 ms was calculated (SD 0.60, 6 subjects).     

Origin of muscle action potentials evoked by transcranial magnetic stimulation in cats

We studied the effects of transcranial magnetic stimulation on ipsilateral and contralateral forelimb extensor muscles in anesthetized cats. A magnetic stimulator, operating at 100% intensity; was used through a circular coil which was placed tangentially over the midline scalp. Bilateral activation of extensor muscles was readily obtained in all animals. The onset latencies were 7.3 ± 1.1 and 7.07 + 0.8 msec for the contralateral and ipsilateral muscles, respectively. The amplitude of muscle response was unstable in magnitude, nevertheless, it did not show any significant difference between the two sides. The latency of response for ipsilateral and contralateral muscles was similar, which suggests simultaneous activation of motor pathways serving forelimb muscles. Lesioning or ablation of the motor cortex and decerebration at mid-colliculi level did not abolish the evoked responses elicited at high intensity magnetic stimulation. Stereotactic electrical stimulation of the vestibular nuclei complex was performed[ and satisfactory ipsilateral motor responses were obtained. Subsequently; a stereotactic radiofrequency lesion was made at the vestibular nuclei complex, with morphological confirmation. After this lesion, the motor evoked potentials (MEPs) were significantly diminished in amplitude. This finding strongly suggests that the generator of the MEPs resides in the brainstemi, mainly at the vestibular nuclei complex. [Neurol Res 1995; 17: 469-473]     

Motor cortex stimulation in patients with post-stroke pain: conscious somatosensory response and pain control

We analyzed the conscious sensory responses to cortical stimulation of 31 patients with post-stroke pain who underwent motor cortex stimulation (MCS) therapy. During surgery for electrode placement, a sensory response (tingle projected to a localized peripheral area) was elicited by high-frequency stimulation (50 Hz) in 23 (84%) from the somatosensory cortex, and in 16 (52%) from the motor cortex without muscle contraction. Unpleasant painful sensation was induced or their original pain was exacerbated in 12 patients (39%) when the somatosensory cortex was stimulated and in two (6%) when the motor cortex was stimulated. Somatosensory responses were induced in eight (25%) even by low-frequency stimulation (1-2 Hz) of the motor cortex at an intensity below the threshold for muscle contraction. In contrast, among 20 nonpain patients who underwent a similar procedure for cortical mapping in epilepsy or brain tumor surgery, a sensory response was produced by high-frequency stimulation in only eight (40%; p < 0.02) from the somatosensory cortex and four (20%; p < 0.03) from the motor cortex. Pain sensation was not induced by stimulation of the somatosensory cortex (p < 0.002) or motor cortex in any of these patients. In addition, none of these patients reported a sensory response to low-frequency stimulation. In both of the two post-stroke pain patients who reported abnormal pain sensation in response to stimulation of the motor cortex, MCS failed to control their post-stroke pain. These findings imply that the sensitivity of the perceptual system even to activity of the motor cortex is heightened in post-stroke pain patients, which can sometimes hinder pain control by MCS.