Changes In Cortical Silent Period Research Articles

Cortical Re-organization After Traumatic Brain Injury Elicited Using Functional Electrical Stimulation Therapy: A Case Report.

Functional electrical stimulation therapy (FEST) can improve motor function after neurological injuries. However, little is known about cortical changes after FEST and weather it can improve motor function after traumatic brain injury (TBI). Our study examined cortical changes and motor improvements in one male participant with chronic TBI suffering from mild motor impairment affecting the right upper-limb during 3-months of FEST and during 3-months follow-up. In total, 36 sessions of FEST were applied to enable upper-limb grasping and reaching movements. Short-term assessments carried out using transcranial magnetic stimulation (TMS) showed reduced cortical silent period (CSP), indicating cortical and/or subcortical inhibition after each intervention. At the same time, no changes in motor evoked potentials (MEPs) were observed. Long-term assessments showed increased MEP corticospinal excitability after 12-weeks of FEST, which seemed to remain during both follow-ups, while no changes in CSP were observed. Similarly, long-term assessments using TMS mapping showed larger hand MEP area in the primary motor cortex (M1) after 12-weeks of FEST as well as during both follow-ups. Corroborating TMS results, functional magnetic resonance imaging (fMRI) data showed M1 activations increased during hand grip and finger pinch tasks after 12-weeks of FEST, while gradual reduction of activity compared to after the intervention was seen during follow-ups. Widespread changes were seen not only in the M1, but also sensory, parietal rostroventral, supplementary motor, and premotor areas in both contralateral and ipsilateral hemispheres, especially during the finger pinch task. Drawing test performance showed improvements after the intervention and during follow-ups. Our findings suggest that task-specific and repetitive FEST can effectively increase cortical activations by integrating voluntary motor commands and sensorimotor network through functional electrical stimulation (FES). Overall, our results demonstrated cortical re-organization in an individual with chronic TBI after FEST.

NEUOPHYSIOLOGICAL CHANGES AFTER UPPER AND LOWER LIMB GRADED EXERCISE TESTING.

Aerobic exercise, including graded exercise testing (GXT), may cause neurophysiological changes of circuits in the primary motor cortex (M1) related to mechanisms of fatigue and/or plasticity. Investigating M1 inhibitory circuit changes over time in exercising compared to non-exercising muscles after GXT of the upper limbs (UL) and lower limbs (LL) may distinguish between different post-exercise mechanisms. PURPOSE: To evaluate M1 inhibitory circuit changes resulting from UL and LL GXT and determine their associations with fitness. METHODS: Six healthy subjects (30 ± 6 yrs) participated. Transcranial Magnetic Stimulation (TMS), Peripheral Nerve Stimulation (PNS), and Electromyography (EMG) were used for neurophysiological testing. Gas analysis was performed to evaluate VO2max (UL: 24.2 ± 4.8, LL: 35.1 ± 5.9 mL/kg/min) during GXTs. Surface electrodes were placed over the first dorsal interosseous (FDI) and tibialis anterior (TA) muscles. Measures of M1 and M1-related afferent inhibition included cortical silent period (CSP) and short-latency afferent inhibition (SAI), respectively. SAI inter-stimulus intervals (ISI) between PNS and TMS stimulations were 21-23ms (UL), and 32-35ms (LL). TMS coil orientation (CO) was altered between posterior-anterior (PA) and anterior-posterior (AP) for both measures of CSP and SAI. CSP and SAI were taken 0-45 min (POST1) and 45-90 min (POST2) post-exercise and compared to pre-exercise. Repeated measures ANOVAs were performed to evaluate effects of exercise type, CO, time, and ISI. RESULTS: CSP decreased at POST1 and increased at POST2 in FDI (97.9 ± 1.2% vs. 104.5 ± 2.5%, p < 0.05) with a trend toward significance in TA (99.3 ± 2.5% vs. 103.5 ± 4.9%, p = 0.19). Although SAI was found for the TA at 32ms (p<0.05) and FDI at 21-23ms (p < 0.05), the interaction of exercise type, CO, and ISI did not reach significance after Huynh-Feldt correction (FDI: p = 0.10, TA: p = 0.10). Univariate linear regression of VO2max and SAI revealed a potential relationship reliant on exercise type and CO (UL: R2 = 0.91, LL: R2 = 0.68). CONCLUSIONS: Changes in CSP suggest that exercise may cause early disinhibition followed by greater inhibition in M1 while changes in SAI may be influenced by fitness levels. Collectively, the results support UL and LL GXTs cause measurable M1 neurophysiological changes.

The Relationship Between Cortical Inhibition and Electroconvulsive Therapy in the Treatment of Major Depressive Disorder.

Dysfunctional cortical inhibition (CI) is postulated as a key neurophysiological mechanism in major depressive disorder. Electroconvulsive therapy (ECT) is the treatment of choice for resistant depression and ECT has been associated with enhanced CI. The objective of this study was to evaluate the relationship between CI and ECT response in resistant depression. Twenty-five patients with treatment resistant depression underwent an acute course of ECT. CI was indexed by the cortical silent period (CSP) and short-interval cortical inhibition (SICI), through TMS-EMG. CI and clinical response was measured prior to beginning an acute ECT course and within 48 hours of the last ECT treatment in the course. Clinical response to ECT was assessed by HDRS-17 before and after an acute course of ECT. We found that there was a significant difference in CSP at baseline between responder and non-responder groups (p = 0.044). Baseline CSP predicted therapeutic response to ECT with sensitivity of 80% and specificity of 60%. There were no changes in CSP or SICI after administration of the ECT course. Our findings suggest that duration of pre-treatment CSP may be a useful predictor of therapeutic response to ECT in patients with TRD.

Effects of repetitive transcranial magnetic stimulation on masseter motor-neuron pool excitability

ObjectiveRepetitive transcranial magnetic stimulation (rTMS) has been widely used to modulate the excitability of the cortical control of limbs muscles, but rarely in the cortical control of human masseter muscles. This study aims to investigate the effects of rTMS on masseter motor-neuron pool excitability in humans. Materials and methodsA total of 20 healthy participants were selected and received a total of three rTMS sessions involving stimulation of the right masseter-motor complex: one session of 10-Hz rTMS, one session of 1-Hz rTMS and one session of sham rTMS at an intensity of 80% of the active motor threshold (AMT). The masseter AMT, motor-evoked potentials (MEPs), cortical-silent period (CSP), and short-interval intracortical inhibition (SICI) were measured before and after each rTMS session. ResultsThe masseter SICI was significantly decreased following 10-Hz rTMS, with no significant changes in AMT, MEPs or CSP. No significant differences in masseter AMT, MEPs, CSP or SICI were observed in either the 1-Hz, or sham rTMS groups. ConclusionsThe present findings demonstrate that high-frequency rTMS increases masseter motor-neuron pool excitability.

113. Spinal Direct Current Stimulation modulates short intracortical inhibition

Transcutaneous spinal Direct Current Stimulation (tsDCS) is a new and safe technique for modulating spinal cord excitability. We evaluated healthy subjects before (T0) and at different intervals (T1 and T2) after anodal, cathodal and sham tsDCS (20 ′ ,2.0 mA) applied over the thoracic spinal cord (T10–T12). We assessed changes in cortical Silent Period (cSP), paired-pulse short intracortical inhibition (SICI, interstimulus interval, ISI = 3 ms) and intracortical facilitation (ICF, ISI = 10 ms). Motor Evoked Potentials (MEPs) were recorded from first digital interosseus (FDI) and tibialis anterior (TA) muscles. Cathodal tsDCS increased MEP amplitudes at ISI of 3 ms, while anodal one elicited opposite effects (FDI: p = 0.0023; TA: p = 0.0004); conversely, tsDCS left MEP amplitudes unchanged at ISI of 10 ms (FDI: p = 0.39; TA: p = 0.45). No significant change in cSP duration was found from upper ( p = 0.81) and lower limb ( p = 0.33). tsDCS modulates inhibitory GABA(A) ergic drive, as assessed by SICI, without interfering with cSP and ICF. tsDCS may be helpful to modulate spinal drive through non spinal mechanisms. tsDCS could represent an early rehabilitation strategy in patients with acute brain lesions and in the treatment of spinal diseases or pain syndromes.

1. A meta-analysis of the cortical silent period in epilepsies

The cortical silent period (CSP) following transcranial magnetic stimulation reflects GABAB-mediated inhibition in the primary motor cortex (M1), and could contribute to understand the pathophysiological substrates of epilepsies. Increased CSP duration has been reported in idiopathic generalized epilepsy (IGE) and in partial epilepsy (PE) involving the M1, although other studies yielded discordant findings. In this meta-analysis we systematically assessed the consistency of CSP changes in untreated epileptic patients. We searched for controlled studies evaluating the CSP in drug-naive or drug-free patients with IGE or PE. The mean difference between CSP duration obtained in patients and controls was calculated. Fourteen studies (267 patients and 234 controls) were included. A significant mean difference was found, with longer CSP in patients than in controls. The difference was still greater if IGE patients only were analyzed. CSP modifications did not depend from differences in motor threshold between patients and controls. Meta-analysis confirms CSP modifications in epilepsies, with enhancement of this cortical inhibitory measure in most IGE patients. This provides a rationale for investigations aiming to verify the hypotheses that increased CSP reflects compensatory neural phenomena counteracting transition from the interictal to ictal state, and that CSP variability reflects the pathophysiological heterogeneity of epileptic syndromes.

ID 323 – Shortening of the cutaneous silent period duration in tibialis anterior after fatiguing eccentric exercise

Objective Muscle afferent feedback (presumably mainly of spindle origin) contributes to the maintenance of alpha motoneuron firing during sustained muscle contraction. We aimed at investigating how a unilateral fatiguing eccentric exercise involving the tibialis anterior (TA) affects inhibitory control of muscle activity. Methods In 8 healthy subjects, we assessed the TA silent period (SP) to cortical magnetic stimuli (round coil) and to cutaneous nerve electrical stimulation (superficial peroneal nerve at the ankle) before and after 5 min of eccentric exercise. Results At baseline, SP duration was variable among subjects but cortical SP was always longer than cutaneous SP (111.6 ± 13.8 ms vs. 37.3 ± 10.2 ms). After exercise, there was a slight increase in background EMG activity. The cutaneous SP shortened significantly (24.3 ± 7.3 ms) at the expenses of onset latency delay (98.7 ± 14.0 ms in baseline to 112.2 ± 11.9 ms after exercise). There were no significant changes in cortical SP after exercise (106.2 ± 18.1 ms). Conclusions Eccentric exercise leads to a delay in onset latency of the cutaneous SP with no changes in cortical SP. An effect of fatigue on small nerve fibers, which are known to contribute to the onset of cutaneous SP, may partly explain our results.

Ipsilateral M1 transcranial direct current stimulation increases excitability of the contralateral M1 during an active motor task: Implications for stroke rehabilitation

Anodal transcranial direct current stimulation (a-tDCS) of the primary motor cortex (M1) elicits an increase in cortical excitability that outlasts the period of stimulation. However, little is known about effects of a-tDCS on the contralateral M1 during and after ipsilateral M1 stimulation. Therefore, we investigated the changes in corticospinal excitability and inhibition of the left M1 during and after 20 min of a-tDCS to the right M1. Eight healthy participants received real (2 mA) and SHAM a-tDCS to the right M1 randomized across 2 testing sessions. Single- and paired-pulse transcranial magnetic stimulation (TMS) was applied to the left M1 to measure changes motor-evoked potential (MEP) amplitude from the right extensor carpi radialis (ECR) at 130% of resting and active motor threshold, cortical silent period (CSP) and short-interval cortical inhibition (SICI). Active motor threshold was measured during a wrist extension contraction that was less than 5% of maximal electromyographic activation of the ECR. TMS measurements were recorded at baseline, every 5 min for 20 min during and 10 min after a-tDCS. The results showed a significant ( P < 0.05) increase in left M1 MEP amplitude and reduction in CSP duration during (10 and 15 min) and after (immediately and 10 min post) a-tDCS to the right M1, only during the active motor task. A significant reduction ( P < 0.05) in SICI during the active task was also found immediately and 10 min post a-tDCS. No significant changes in MEP amplitude, CSP and SICI were observed in the resting or active task during SHAM tDCS. The increase in left M1 MEP amplitude and reduction in CSP and SICI during and after 20 min of right M1 a-tDCS is most likely to be attributed to a reduction in interhemispheric inhibition that is modulated by a-tDCS during the performance of an active task. Our findings may have significant implications for stroke rehabilitation whereby the application of a-tDCS on the contralesional M1 during neurorehabilitation of the paretic limb may be beneficial for inducing neuroplasticity of the ipsilesional M1 to improve motor function.

A Meta-analysis of the Cortical Silent Period in Epilepsies.

The cortical silent period (CSP) following transcranial magnetic stimulation reflects GABAB-mediated inhibition in the primary motor cortex (M1) and could contribute to understand the pathophysiological substrates of epileptic conditions. Increased CSP duration has been reported in idiopathic generalized epilepsy (IGE) and in partial epilepsy (PE) involving the M1, although other studies yielded discordant findings. We used meta-analysis to systematically assess the consistency of CSP changes in untreated patients with epilepsies. Databases were searched for controlled studies evaluating the CSP in drug-naïve or drug-free patients with IGE or PE. For each study, the mean difference with 95% confidence intervals (CIs) between CSP duration obtained in patients and controls was calculated. The effect of motor threshold (MT) on the CSP duration has also been explored by meta-analysis and meta-regression. Fourteen studies (267 patients and 234 controls) were included. A significant mean difference (14.16ms, 95% CI, 1.20, 27.11ms) was found, with longer CSP in patients than in controls. The mean difference was still greater (18.05ms) if only the 202 IGE patients were analyzed. No MT difference emerged between patients and controls. Meta-regression showed no relationship between MT and CSP duration. Meta-analysis confirms CSP modifications in epilepsies, with enhancement of this cortical inhibitory measure at least in most IGE patients. This provides rationale for further investigations aiming to verify the hypotheses that increased CSP reflects compensatory neural phenomena counteracting transition from the interictal to ictal state and that CSP variability reflects the pathophysiological heterogeneity of epileptic syndromes.

Spinal Direct Current Stimulation Modulates Short Intracortical Inhibition.

Transcutaneous spinal direct current stimulation (tsDCS) is a new and safe technique for modulating spinal cord excitability. We assessed changes in intracortical excitability following tsDCS by evaluating changes in cortical silent period (cSP), paired-pulse short intracortical inhibition (SICI), and intracortical facilitation (ICF). Healthy subjects were studied before (T0) and at different intervals (T1 and T2) after anodal, cathodal, and sham tsDCS (20', 2.0 mA) applied over the thoracic spinal cord (T10-T12). We assessed changes in cSP, SICI (interstimulus interval, ISI = 3 ms) and ICF (ISI = 10 ms). Motor-evoked potentials (MEPs) were recorded from first digital interosseus (FDI) and tibialis anterior (TA) muscles. Cathodal tsDCS increased MEP amplitudes at interstimulus interval of 3 ms, while anodal one elicited opposite effects (FDI: p = 0.0023; TA: p = 0.0004); conversely, tsDCS left MEP amplitudes unchanged at ISI of 10 ms (FDI: p = 0.39; TA: p = 0.45). No significant change in cSP duration was found from upper limb (p = 0.81) and lower limb (p = 0.33). tsDCS modulates inhibitory GABA(A)ergic drive, as assessed by SICI, without interfering with cSP and ICF. The possibility to interfere with cortical processing makes tsDCS a useful approach to modulate spinal drive through nonspinal mechanisms. tsDCS could also represent an early rehabilitation strategy in patients with acute brain lesions, when other noninvasive brain stimulation (NIBS) tools are not indicated due to safety concerns, as well as in the treatment of spinal diseases or pain syndromes.

Transcranial magnetic stimulation follow-up study in early Parkinson's disease: A decline in compensation with disease progression?

A number of neurophysiological abnormalities have been described in patients with Parkinson's disease, but very few longitudinal studies of how these change with disease progression have been reported. We describe measures of motor cortex inhibition and plasticity at 6 and 12 mo in 12 patients that we previously reported at initial diagnosis. Given the well-known interindividual variation in these measures, we were particularly concerned with the within-subject changes over time. Patients were assessed clinically, and transcranial magnetic stimulation (TMS) was used to measure motor cortical excitability, inhibition (short interval intracortical inhibition, cortical silent period), and plasticity (response to excitatory paired associative stimulation protocol) in both hemispheres. All measurements were performed 6 mo and 12 mo after the baseline experiments. Asymmetry in clinical motor symptoms was reflected in asymmetry of plasticity and inhibition. In the group as a whole, little change was seen in any of the parameters over 12 mo. However, analysis of within-individual data showed clear correlations between changes in clinical asymmetry and asymmetry of response to paired associative stimulation protocol and cortical silent period. Longitudinal changes in cortical silent period and response to paired associative stimulation protocol in Parkinson's disease reflect dynamic effects on motor cortex that are related to progression of motor signs. They are useful objective markers of early disease progression that could be used to detect effects of disease-modifying therapies. The decline in heightened plasticity that was present at disease onset may reflect failure of compensatory mechanisms that maintained function in the preclinical state.

Neurophysiological Correlates of Central Fatigue in Healthy Subjects and Multiple Sclerosis Patients before and after Treatment with Amantadine.

In ten healthy subjects and in ten patients suffering from Multiple Sclerosis (MS), we investigated the cortical functional changes induced by a standard fatiguing repetitive tapping task. The Cortical Silent Period (CSP), an intracortical, mainly GABAB-mediated inhibitory phenomenon, was recorded by two different hand muscles, one acting as prime mover of the fatiguing index-thumb tapping task (First Dorsal Interosseous, FDI) and the other one not involved in the task but sharing largely overlapping central, spinal, and peripheral innervation (Abductor Digiti Minimi, ADM). At baseline, the CSP was shorter in patients than in controls. As fatigue developed, CSP changes involved both the “fatigued” FDI and the “unfatigued” ADM muscles, suggesting a cortical spread of central fatigue mechanisms. Chronic therapy with amantadine annulled differences in CSP duration between controls and patients, possibly through restoration of more physiological levels of intracortical inhibition in the motor cortex. These inhibitory changes correlated with the improvement of fatigue scales. The CSP may represent a suitable marker of neurophysiological mechanisms accounting for central fatigue generation either in controls or in MS patients, involving corticospinal neural pools supplying not only the fatigued muscle but also adjacent muscles sharing an overlapping cortical representation.

The acute effects of exercise on cortical excitation and psychosocial outcomes in men treated for prostate cancer: a randomized controlled trial.

Purpose: Regular exercise improves psychological well-being in men treated for prostate cancer (PCa). For this population and among cancer survivors in general, the effect of a single bout of exercise on self-report or objective measures of psychological well-being has not been examined. We examined the acute effect of a single bout of exercise on the cortical silent period (CSP) and on self-reported mood in men that have received treatment for PCa.Methods: Thirty-six PCa survivors were randomly assigned to 60 min of low to moderate intensity exercise or to a control condition. Outcomes were assessed immediately before and after either the exercise or the control condition.Results: No significant between-group differences were observed in CSP or mood were observed following the exercise session or control conditions. Participants with higher scores of trait anxiety had significantly shorter CSP at baseline, as well as those receiving androgen deprivation therapy. Age and baseline CSP had a low-moderate, but significant negative correlation. Changes in CSP following the exercise condition were strongly negatively correlated with changes in self-reported vigor.Conclusion: While we did not observe any acute effect of exercise on the CSP in this population, the associations between CSP and trait anxiety, age, and vigor are novel findings requiring further examination.Implications for Cancer Survivors: Exercise did not acutely affect our participants in measures of psychological well-being. Additional mechanisms to explain the chronic psychosocial benefits of exercise previously observed in men with PCa require further exploration.Clinicaltrials.gov Identifier: NCT01715064 (http://clinicaltrials.gov/show/NCT01715064).

Evaluating the feasibility of measures of motor threshold and cortical silent period as predictors of outcome after temporal lobe epilepsy surgery

Introduction Although it is well known that ES alters cortical excitability, little is known about the relationship between ES outcome and cortical excitability. Transcranial magnetic stimulation has been successfully used to evaluate cortical excitability in epilepsy patients. The present study aimed to assess the value of the motor threshold (MT) and cortical silent period (CSP) as predictors of the outcome of temporal lobe epilepsy surgery (TLES). Materials and methods Epileptic foci in the epilepsy patients were identified via video-electroencephalography (v-EEG) monitoring, brain magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT), and positron emission tomography (PET), and neurophysiological testing. MT, CSP-150, and CSP-max were measured in 10 epilepsy patients on both the ipsilateral and contralateral side of the epileptic focus 1 week before and 3 months after TLES. Pre- and post-operative MT and CSP measurements were compared, and the results were interpreted based on the clinical outcome of TLES. Results Mean follow-up period was 28.8 months. In all, 8 patients were seizure-free post TLES, whereas in 2 patients seizures persisted. No significant differences were observed in ipsilateral or contralateral hemisphere MT measurements before and after surgery. Both CSP-150 and CSP-max values in the non-focal hemispheres decreased in the 8 patients that were seizure-free post TLES, whereas no differences were observed in the 2 patients with seizures that persisted post TLES. Conclusions The present findings indicate that monitoring pre- and post-TLES CSP changes may be predictive of the early clinical outcome of TLES.

Vibration-induced effects in stroke patients with spastic hemiparesis – a pilot study

Spasticity manifesting as a dysbalance between extensor and flexor muscles may contribute to an impaired hand function. We studied clinical (n=10 patients) and electrophysiological (n=9 patients) changes produced by vibration of forearm extensor muscles (FEM) in chronic stroke patients with spastic hemiparesis. In Exp. 1, the Box and Block Test (BBT) was applied to test dexterity before and after 5 minutes of FEM vibration. In Exp. 2, transcranial magnetic stimulation was used to study the cortical silent period (CSP) before and during FEM vibration. Recordings were taken from the antagonistic flexor carpi radialis muscle. After vibration, performance of the BBT was improved by 20%. The effect persisted for at least 10-15 minutes. Vibration induced a prolongation of the CSP. This effect occurred in the affected and non-affected side to a similar degree. The magnitude of performance changes and CSP changes was not correlated. FEM vibration enhances inhibitory neuronal circuits targeting the antagonistic forearm flexor muscles and is associated with an improved dexterity in the spastic arm. It might become a supporting tool in the motor recovery of spastic hemiparesis.

Sensitivity of electrophysiological tests for upper and lower motor neuron dysfunction in ALS: A six‐month longitudinal study

By following a group of amyotrophic lateral sclerosis (ALS) patients longitudinally using lower motor neuron (LMN) and upper motor neuron (UMN) markers of dysfunction it may be possible to better understand the functional relationships between these motor systems in this disease. We used neurophysiological techniques to follow UMN and LMN dysfunction in a group of 28 patients with ALS, in comparison with the ALS functional rating scale (ALS-FRS) score and the forced vital capacity (FVC). We used motor unit number estimation (MUNE), compound muscle action potential (CMAP) amplitude, and the Neurophysiological Index (NI) to quantify the LMN disorder, and transcranial motor stimulation to study cortical motor threshold, motor-evoked response amplitude, central motor conduction time, and cortical silent period (CSP). The patients were studied shortly after diagnosis and then 6 months later, using both abductor digiti minimi muscles (ADM); ADM strength was initially >MRC 3 (Medical Research Council, UK). The NI and MUNE changed more than any other variable. CSP increased by about 30%, a change more marked than the slight increase observed in the cortical motor threshold (9%). The normal increase of CSP after acute muscle fatigue was preserved during disease progression. The CSP increase correlated with the MUNE rate of decay but not to the NI reduction, perhaps because NI includes F-wave frequency in itscalculation. There was no definite correlation between UMN and LMNdysfunction or progression, but there was a link between CSP and LMN changes in ALS. The CSP may be a useful variable in following UMN dysfunction in clinical practice and in clinical trials.

Cyclical excitability of the motor cortex in patients with catamenial epilepsy: A transcranial magnetic stimulation study

The pathophysiology of catamenial epilepsy is still unclear. Therefore, we investigated the cortical excitability of women with catamenial epilepsy during different phases of the menstrual cycle. Using transcranial magnetic stimulation, six patients suffering from catamenial epilepsy were investigated during ovulatory cycles. On days 8, -14, -7 and 2 of the cycle (day 1 being the first day of menstrual bleeding), resting motor threshold (RMT), cortical silent period (CSP), intracortical inhibition (ICI) and intracortical facilitation (ICF) were investigated. The non-parametric Friedman-test for multiple comparisons and Wilcoxon signed rank test were used for statistical analysis. Five patients suffered from focal epilepsy (three right hemispheric, one bitemporal, one unknown origin) and one patient had idiopathic generalized epilepsy. All patients experienced perimenstrual seizure clustering and two also showed an increased seizure frequency during the luteal phase. In the right hemispheres there was a significant change of CSP duration in the course of the menstrual cycle (chi(2)=8.3, P=0.041), due to a shorter CSP during the luteal phase (Z=-2.0, P=0.043) and menstruation (Z=-2.2, P=0.028) as compared to the follicular phase. There was no significant variation of CSP in the left hemispheres. RMT, ICI and ICF showed no significant changes in the course of the menstrual cycle. The CSP changes suggest a decreased inhibition involving GABA-ergic neurotransmission during the luteal phase and menstruation. These TMS alterations correlated with the clinical course of the epilepsies and were found in the hemispheres containing the majority of the epileptogenic zones.

Cortical excitability in cocaine-dependent patients: a replication and extension of TMS findings

Cortical excitability can be assessed by transcranial magnetic stimulation (TMS). Previously we observed that TMS motor threshold (MT) was elevated in abstinent cocaine-dependent subjects. In the current study we aimed at replicating our initial finding, exploring other TMS-based measures of excitability, and examining association with personality characteristics. Nineteen cocaine-dependent and 12 healthy control subjects were examined. Resting and activated motor thresholds (RMT and AMT) and duration of the cortical silent period (CSP) were examined. The Cocaine Experience Questionnaire (CEQ) was administered to assess cocaine-induced psychotic symptoms. The relationship between Minnesota Multiphasic Personality Inventory (MMPI) scales and cortical excitability measures was also examined. AMT was significantly elevated in cocaine-dependent subjects on both hemispheres. RMT was also significantly elevated on the right hemisphere. No CSP changes were noted. Patients with cocaine-induced paranoia had longer CSPs on the right hemisphere compared to subjects reporting no paranoid experiences. The patients displayed significantly elevated scores on several MMPI scales, though the scale scores did not correlate with cortical excitability measures. These data support our initial finding of decreased cortical excitability in abstinent cocaine-dependent subjects. We interpret this finding as a compensatory mechanism against the stimulating and epileptogenic effects of cocaine.

Cortical silent period in two patients with meningioma and preoperative seizures: a pre- and postsurgical follow-up study

Objectives: Prolongation of the cortical silent period (CSP) following transcranial magnetic stimulation has been reported in patients with partial epilepsy involving the primary motor cortex (M1). This study aimed to investigate the relationship between the expected intraindividual variations in risk factors for seizures and CSP duration. Methods: We studied a 59-year-old woman with a rolandic meningioma and simple motor partial seizures and a 71-year-old woman with a parietal/occipital meningioma and complex partial seizures. Both patients had seizure as their initial symptom with complete postsurgical remission. Repeated pre- and postoperative CSP recordings were made from both first dorsal interosseous muscles. We compared the results to those obtained in 13 normals. Results: In the patient with simple motor partial seizures, the CSP was significantly prolonged in preoperative recordings and 3 weeks after surgery. This CSP lengthening partly subsided 3 months after surgery. Finally, the CSP was normal 6, 8, and 18 months after surgery. In the patient with complex partial seizures, no CSP change was observed. Conclusions: In our patient with a rolandic meningioma, CSP prolongation was observed when the risk of seizure relapse was supposed to be higher (preoperative and early postoperative periods). This supports the view that CSP changes reflect compensatory mechanisms in M1 epilepsy.