Sternocleidomastoid muscle responses to transcranial magnetic stimulation in patients with cervical dystonia

Ten cervical dystonia (CD) patients, with involuntary head rotation to one side and contralateral sternocleidomastoid muscle (SCM) hypertrophy, were investigated with transcranial magnetic stimulation, and the results were compared to those of 10 healthy subjects. Monopolar needle electrodes with isolated shafts were used for bilateral electromyographic recordings in the SCMs of the motor evoked potentials (MEPs) elicited by the magnetic stimulator. The latencies of ipsilateral SCM MEPs were shorter in the CD patients than in the control subjects (P<0.001). The latencies of SCM activity suppression by TMS were longer in the CD patients than in the control group when stimuli were given on the contralateral side (P<0.05). Both the clinically dystonic and the contralateral SCM of the CD patients exhibited significantly abnormal latencies of the ipsilateral SCM MEPs (P<0.01) and of the SCM suppression (P<0.05). Three CD patients also had consistent activity in the SCM counteracting the direction of head rotation during the suppression experiments. The latencies of the suppression of this abnormal activation were shorter (P<0.05), than the latencies of the suppression in the SCM during normal voluntary activation by these CD patients (i.e. rotation of the head in the contrary direction). The results suggest bilaterally enhanced motoneuronal excitability and disturbed inhibitory regulation in patients with CD.     

Physiological studies of the corticomotor projection to the hand after subcortical stroke.

OBJECTIVE: The mechanisms which lead to recovery of motor function after a stroke are poorly understood. Functional reorganization of cortical motor centres is thought to be one of the factors which may contribute to recovery. We have investigated the extent of reorganization which occurs at the level of the primary motor cortex after a lesion of the corticospinal pathway. METHODS: Transcranial magnetic stimulation was used to map the topography of the primary corticomotor projection to the abductor pollicis brevis muscle and study changes in cortical motor thresholds and corticospinal conduction in a group of 20 subjects with subcortical infarcts of varying duration (1 week to 15 years) and varying degrees of motor deficit. RESULTS: There was a broad correlation between motor evoked potential (MEP) amplitude and motor thresholds on the one hand and the severity of motor deficit and site and extent of the lesion on the other. Shifts in the cortical motor maps were found in both early and late cases, irrespective of the site of the lesion, but were more frequent in the longer standing cases. Shifts were usually along the mediolateral axis but anteroposterior shifts were found in some late cases. CONCLUSION: Our findings indicate that there is functional reorganization of the corticomotor projection in subjects who regain a degree of motor control following a subcortical lesion sparing the motor cortex.     

Primary writing tremor: motor cortex reorganisation and disinhibition.

BACKGROUND: Primary writing tremor (PWT) is a task-specific tremor of uncertain origin. There has been debate as to whether PWT represents a variant of essential tremor or a tremulous form of focal dystonia related to writer's cramp. In writer's cramp there is evidence of changes in intracortical inhibition (ICI), as well as cortical motor reorganisation. OBJECTIVE: To study corticomotor organisation and short-latency ICI in a patient with typical task-specific PWT. METHODS: Transcranial magnetic stimulation mapping of the corticomotor representation of the hand and studies of ICI using paired-pulse stimulation were performed in a 47-year-old right-handed woman with a pure task-specific writing tremor. RESULTS: The motor maps for the hand were displaced posteriorly on both sides and reverted to a normal position after treatment with botulinum toxin. Short-latency ICI was reduced for the dominant hand. CONCLUSION: The findings indicate reorganisation and disinhibition of the corticomotor projection to the hand and point to the participation of cortical centres in the origin of PWT.     

Long-term changes in motor cortical organisation after recovery from subcortical stroke

The present study has investigated the long-term changes in the organisation of the corticomotor projection to the hand in a group of subjects who had sustained a subcortical hemispheric stroke up to 15 years previously and had subsequently recovered normal or near-normal motor function. Transcranial magnetic cortical stimulation (TMCS) was employed to map the topography of the primary corticomotor projection to the hand and to obtain measures of cortical motor threshold, long-latency intracortical inhibition and corticospinal conduction. Changes in motor threshold and in motor-evoked potential (MEP) amplitude and latency in keeping with persisting impairment of conduction in the corticospinal pathway were still present in the majority of subjects, whereas the duration of the post-MEP silent period, reflecting the strength of long-latency intracortical inhibition, was usually normal. Topographic shifts in the corticomotor representation relative to the unaffected side were found in the majority of subjects. In some the shifts were in the mediolateral axis suggesting reorganisation within the primary motor cortex, while in the others anteroposterior shifts were present in keeping with recruitment of premotor or postcentral cortex. The present findings indicate that changes in the physiological properties of the corticomotor projection to the hand are frequently present in subjects who have recovered motor function after a subcortical stroke and may persist indefinitely. We postulate that these changes are the result of reorganisation at cortical level and that cortical reorganisation is one of the processes which contribute to motor recovery after a subcortical lesion and which may compensate for persisting impairment of conduction in the corticospinal pathway.     

Sensory tricks in cervical dystonia: perceptual dysbalance of parietal cortex modulates frontal motor programming

Cervical dystonia is a disabling basal ganglia disorder characterized by an involuntary head deviation to one side. A typical but also mysterious feature is the impressive improvement of muscle spasms and involuntary head posture by application of a sensory facial stimulus (sensory trick). Here, we report the effect of a sensory trick on cortical activation patterns in 7 patients with cervical dystonia by using H2(15)O positron emission tomography. The application of the sensory trick stimulus, resulting in a near-neutral head position, led to an increased activation mainly of the superior and inferior parietal lobule (ipsilateral to the original head turn) and bilateral occipital cortex and to a decreased activity of the supplementary motor area and the primary sensorimotor cortex (contralateral to the head turn). We propose that a perceptual dysbalance induced by a sensory trick maneuver leads to a relative displacement of the egocentric midvertical reference to the opposite side and a decrease in motor cortex activity. This modulation of motor programming gives novel insights into the mechanisms involved in sensorimotor integration in movement disorders.     

Assessment of postexcitatory inhibition in patients with focal dystonia

The aim of our present study was to detect whether a generalized disturbance of intracortical inhibitory mechanisms as assessed by transcranial magnetic stimulation (TMS) can be observed in a movement disorder with localized clinical expression, that is, in focal cervical dystonia. We measured motor threshold intensity, central motor conduction time and the duration of postexcitatory inhibition evoked by single and paired stimuli TMS from a small hand muscle in 20 patients with idiopathic cervical dystonia, and 21 healthy volunteers. A significant difference could not be found in any of the neurophysiological parameters between patients and controls. These findings are unlike the observations made in Parkinson's disease and Huntington's disease, where significant changes of postexcitatory inhibition after TMS can be observed. This suggests a lack of widespread change in activity of underlying cortical inhibitory mechanisms, as seen in other diseases of the extrapyramidal system with more generalized clinical involvement.     

Differences in sensory and motor cortical organization following brain injury early in life

There have been a number of physiological studies of motor recovery in hemiplegic cerebral palsy which have identified the presence of novel ipsilateral projections from the undamaged hemisphere to the affected hand. However, little is known regarding the afferent projection to sensory cortex and its relationship to the reorganized cortical motor output. We used transcranial magnetic stimulation (TMS) to investigate the corticomotor projection to the affected and unaffected hands in a group of subjects with hemiplegic cerebral palsy, and also performed functional magnetic resonance imaging (fMRI) studies of the patterns of activation in cortical motor and sensory areas following active and passive movement of the hands. Both TMS and fMRI demonstrated a normal contralateral motor and sensory projection between the unaffected hand and the cerebral hemisphere. However, in the case of the affected hand, the TMS results indicated either a purely ipsilateral projection or a bilateral projection in which the ipsilateral pathway had the lower motor threshold, whereas passive movement resulted in fMRI activation in the contralateral hemisphere. These results demonstrate that there is a significant fast-conducting corticomotor projection to the affected hand from the ipsilateral hemisphere in this group of subjects, but that the predominant afferent projection from the hand is still directed to the affected contralateral hemisphere, resulting in an interhemispheric dissociation between afferent kinesthetic inputs and efferent corticomotor output. The findings indicate that there can be differences in the organization of sensory and motor pathways in cerebral palsy, and suggest that some of the residual motor dysfunction experienced by these subjects could be due to an impairment of sensorimotor integration at cortical level as a result of reorganization in the motor system.     

Reorganization of cortical motor area in prior polio patients.

OBJECTIVE: Focal transcranial magnetic stimulation (TMS) was used to study the motor maps of upper limb muscles in 7 adult patients with a history of paralytic poliomyelitis. The aim of the study was to verify the potential for long-term cortical reorganization of a selective peripheral motor neuron lesion suffered early in life. METHODS: Patient selection was based on the prevalent involvement of proximal muscles in only one of the upper limbs. Motor evoked potentials (MEPs) were recorded from deltoid and abductor pollicis brevis (APB) muscles. Each muscle map was characterized by area (no. of excitable positions), volume (the sum of MEP amplitudes at all scalp positions), maximal amplitude (the highest MEP recorded). RESULTS: In the patients, the mean area, volume and maximal amplitude were significantly greater in affected vs. contralateral deltoid (P<0.05) and vs. controls (P<0.01). No significant differences were found in APB map parameters. The APB/deltoid ratio for area was lower in the affected compared with the unaffected side and controls (P = 0.06). Cortical reorganization was not significantly correlated with motor performance. CONCLUSION: These findings are consistent with a rearrangement in human motor pathways targeting muscles affected by a lower motor neuron lesion.     

Doxorubicin chemomyectomy as a treatment for cervical dystonia: Histological assessment after direct injection into the sternocleidomastoid muscle

The sternocleidomastoid muscle (SCM) is one of the major muscles involved in producing abnormal head position in cervical dystonia patients. This study tested whether doxorubicin chemomyectomy, direct injection of doxorubicin into the SCM to permanently remove muscle fibers, has the potential to be a nonsurgical, permanent treatment for cervical dystonia. The right SCM of rabbits was injected with either 1 or 2 mg doxorubicin. Animals were sacrificed 1–2 months postinjection. The SCM was prepared for histological examination of muscle fiber loss and fiber type composition. In all cases, direct injection of doxorubicin resulted in significant decreases in total muscle cross-sectional areas ranging from 75% up to 98%. Individual myofiber cross-sectional areas were smaller than normal after 2 mg doxorubicin treatment, but similar to normal fiber size after 1 mg doxorubicin. There were increased numbers of myofibers that expressed slow and neonatal myosin heavy chain isoforms in these remaining muscle fibers compared to the untreated SCM on the contralateral side. Developmental myosin heavy chain (MHC) was also present in 53% of the remaining myofibers of the treated muscles. The fiber type composition of muscles contralateral to the doxorubicin injections was compared to the fiber type composition of SCM from normal, untreated controls; no difference was seen in the proportions of fast, slow, and neonatal MHC fiber types in these SCM muscles. In summary, the direct injection of doxorubicin into the SCM resulted in significant muscle loss. This supports the use of doxorubicin chemomyectomy as a potential permanent, nonsurgical treatment for cervical dystonia. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21: 1457–1464, 1998     

Fluoxetine facilitates use-dependent excitability of human primary motor cortex.

OBJECTIVES: In poststroke patients, fluoxetine, a selective serotonin-reuptake inhibitor, as an adjunct to physical therapy provided a better functional recovery from motor deficits. The aim of this study was to investigate the effect of a single dose of 20 mg fluoxetine on motor learning and associated cortical changes in healthy right-handed subjects in order to get deeper insight into its facilitating influence on human motor cortex. METHODS: Subjects performed a motor task consisting of a simultaneous co-contraction of the abductor pollicis brevis (APB) and the deltoid muscle with and without fluoxetine in a placebo-controlled double-blinded crossover study design. Immediately before and after motor learning motor output maps of the APB muscle were assessed in order to get insight into plastic changes of the muscle representation. RESULTS: We found a significantly improved motor performance under both conditions without having substantial differences between placebo and fluoxetine. After the completion of the motor task there was a medial shift of the APB muscle motor output map. Only after the administration of fluoxetine the sum of MEP amplitudes (SOA) increased and the motor output map enlarged. CONCLUSIONS: These findings provide evidence for a use-dependent facilitating effect of fluoxetine on cortical excitability but not on motor performance. SIGNIFICANCE: Our findings are not in line with previous experiments in poststroke patients. However, long-term treatment with fluoxetine may additionally improve motor function by upregulating serotonergic receptors. Further studies investigating the influence of long-term treatment on cortical excitability and psychophysics may therefore provide deeper insight into a possible therapeutical efficiency of fluoxetine in poststroke patients.     

Electroencephalographic measurement of motor cortex control of muscle activity in humans.

OBJECTIVE: To detect and measure correlation between cortical and muscle activities, coherence analysis was used. METHODS: The electroencephalogram (EEG) and electromyogram (EMG) were recorded in 9 normal volunteers during tonic contraction of upper and lower limb muscles on the right side. Coherence between EEG and EMG was computed to analyze their linear association. RESULTS: EEG over the contralateral sensorimotor area was coherent with EMG, with peak coherence at 11-36 Hz (mean, 22 Hz). For the abductor pollicis brevis (APB) muscle, peak coherence, as determined by functional brain mapping with focal transcranial magnetic stimulation (TMS), was over or slightly posterior to the hand area on the primary motor cortex determined by focal transcranial magnetic stimulation (TMS). Peak coherence over the scalp was somatotopically organized. The temporal relation between EEG and EMG was analyzed with a new model for interpreting the phase shift ('constant phase shift plus constant time lag' model). For the APB muscle, the phase relation between cortical and muscular oscillations differed in the frequency ranges of 3-13 Hz and 14-50 Hz, respectively, suggesting that different coupling mechanisms operate in different bands. Only the phase shift between cortical and motoneuronal firing at 14-50 Hz was reliably estimated by a linear model. At 14-50 Hz, motoneuronal firing was led by surface-negative cortical activity with a constant time lag that depended on the cortical-muscular distance. For the APB muscle, the time lag was slightly shorter than the cortical-muscular conduction time determined by TMS. Vibratory stimulation (100 Hz) of a muscle tendon during tonic contraction had no significant effect on cortical-muscular coherence, indicating that cortical oscillation reflected motor rather than sensory activity. CONCLUSIONS: The present findings suggest temporal coding of the oscillatory motor control system (3-13 Hz vs. 14-50 Hz), and confirm the functional importance of cortical beta and gamma rhythms in the motor efferent command. Cortical-muscular synchronization is most likely mediated by the direct corticospinal pathway within the frequency range of 14-50 Hz.     

Hand preference and transcranial magnetic stimulation asymmetry of cortical motor representation

Human handedness may be associated with asymmetry in the corticospinal motor system. Previous studies measuring the threshold for eliciting motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) have provided evidence consistent with this hypothesis. However, TMS asymmetry observed in previous studies may have reflected cortical or spinal differences. We therefore undertook this investigation to test the hypothesis that handedness is associated with asymmetry in cortical motor representations. We used TMS to map contralateral cortical motor representations of the right and left abductor pollicis brevis (APB) and flexor carpi radialis (FCR) muscles in nine normal subjects (three left-handed). Using focal stimulation with a figure-of-8 shaped magnetic coil, we found no differences in MEP threshold or MEP size between the preferred and the nonpreferred hand. However, we observed that the number of scalp stimulation sites eliciting MEPs was statistically greater for APB and FCR muscles of the preferred limb. We found significant asymmetry between right-handed and left-handed subjects, such that in right-handers, the representation of the right APB was larger than that of the left APB, but in left-handers the representation of right APB was smaller than that of the left APB. These results suggest that handedness is associated with asymmetry in cortical motor representation.     

Representation of cricothyroid muscles at the primary motor cortex (M1) in healthy subjects, mapped by navigated transcranial magnetic stimulation (nTMS)

Objectives

To establish a methodology for mapping of primary motor cortex (M1) for cricothyroid (CTHY) muscles in a group of healthy subjects using three-dimensional (3D) magnetic resonance imaging (MRI) navigated transcranial magnetic stimulation (nTMS).

Methods

Two independent measurements were performed. Twelve right-handed healthy subjects were included in the study. In the first measurement, mapping of the abductor pollicis brevis (APB) muscle was followed by mapping of the M1 for CTHY. This was performed in 11 subjects. Second, to avoid bias concerning using a hand knob as a landmark, mapping of M1 for CTHY muscle was followed by mapping of M1 for APB. This was performed in three healthy subjects.The nTMS was used, with selective recordings of motor evoked potentials (MEPs) from APB muscle and corticobulbar motor evoked potentials (CoMEPs) from the CTHY muscle. For recording the responses from the CTHY muscle two hook wire electrodes (the size of 76 μm of diametre passing through 27 gauge needle) were inserted in the muscle. For the recording of MEPs from APB muscle, surface electrodes were used.

Results

First measurement: Stimulation over the left M1 for APB muscles elicits MEPs in the contralateral APB muscle with a mean latency of 22.8 ± 1.69 ms. Stimulation over the left M1 for the CTHY muscle elicits CoMEPs in the contralateral CTHY muscle with a mean latency of 11.89 ± 1.26 ms. The distance between the cortical representation for APB and CTHY was 25.19 ± 6.52 mm, with CTHY muscle representation lateral to the APB muscle.Second measurement: The results of second measurement of the distance between M1 for CTHY and M1 for APB and their cortical localisation were comparable to the results of the first measurement.

Conclusion

This is the first study with the aim to determine the exact cortical localisation of CTHY muscle with nTMS. Mapping of M1 for CTHY and APB muscles by nTMS was successfully performed in all healthy subjects. The exact location of the stimulating points over M1 muscles eliciting responses in CTHY and APB muscles was determined and superimposed over 3D MRI images. The data show that M1 for CTHY muscle is about 25 mm more lateral with regard to M1 for the APB muscle.

Significance

Mapping of M1 for CTHY muscle might represent an important neurophysiologic marker for facilitating preoperative mapping of motor speech-related cortical areas due to the proximity of motor cortical representation for laryngeal muscles and opercular part of the Broca area.     

Facilitation and reciprocal inhibition by imagining thumb abduction.

It is well known that motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) of the motor cortex are facilitated by voluntary muscle contraction. We evaluated the effects of imagination of movements on MEP latencies of agonist and antagonist muscles in the hand using TMS. Twenty-two healthy volunteers were studied. TMS delivered at rest and while imagining tonic abduction of the right thumb. MEPs were recorded in response to magnetic stimulation over the scalp and cervical spine (C7-T1), and central motor conduction times (CMCT) were calculated. MEPs were recorded from right abductor pollicis brevis muscle (APB) and adductor pollicis muscle (AP) simultaneously. Imagination of abduction resulted in a shortened latency of MEPs in the APB muscle, and a prolonged latency in the AP muscle. But the imagination caused no significant change in the latency of MEPs elicited by stimulation over the cervical spine. The changes of the CMCT may account for these latency changes with imagination of movement. These findings indicate that imagination of thumb abduction facilitates motoneurons of agonist muscle and has an inhibitory effect on those of antagonist muscle (reciprocal inhibition).     

Modulation of motor cortex excitability after upper limb immobilization.

OBJECTIVE: To examine the mechanisms of disuse-induced plasticity following long-term limb immobilization. METHODS: We studied 9 subjects, who underwent left upper limb immobilization for unilateral wrist fractures. All subjects were examined immediately after splint removal. Cortical motor maps, resting motor threshold (RMT), motor evoked potential (MEP) latency and MEP recruitment curves were studied from abductor pollicis brevis (APB) and flexor carpi radialis (FCR) muscles with single pulse transcranial magnetic stimulation (TMS). Paired pulse TMS was used to study intracortical inhibition and facilitation. Compound muscle action potentials (CMAPs) and F waves were obtained after median nerve stimulation. In 4/9 subjects the recording was repeated after 35-41 days. RESULTS: CMAP amplitude and RMT were reduced in APB muscle on the immobilized sides in comparison to the non-immobilized sides and controls after splint removal. CMAP amplitude and RMT were unchanged in FCR muscle. MEP latency and F waves were unchanged. MEP recruitment was significantly greater on the immobilized side at rest, but the asymmetry disappeared during voluntary muscle contraction. Paired pulse TMS showed an imbalance between inhibitory and excitatory networks, with a prevalence of excitation on the immobilized sides. A slight, non-significant change in the strength of corticospinal projections to the non-immobilized sides was found. TMS parameters were not correlated with hand dexterity. These abnormalities were largely normalized at the time of retesting in the four patients who were followed-up. CONCLUSIONS: Hyperexcitability occurs within the representation of single muscles, associated with changes in RMT and with an imbalance between intracortical inhibition and facilitation. These findings may be related to changes in the sensory input from the immobilized upper limb and/or in the discharge properties of the motor units. SIGNIFICANCE: Different mechanisms may contribute to the reversible neuroplastic changes, which occur in response to long-term immobilization of the upper-limbs.     

Central motor conduction in cervical dystonia with cervical spondylotic myelopathy

OBJECTIVES: It has been known that cervical dystonia develops secondarily to spinal cord injuries as secondary dystonia. However, little is known about the pathophysiological mechanism. PATIENTS AND METHODS: We examined motor and sensory conduction in six patients with symptomatic cervical dystonia by transcranial magnetic stimulation (TMS). All of the patients exhibited unilateral head rotation. They had symptoms corresponding to cervical myelopathy and felt discomfort in the neck, shoulders or arms before involuntary movement occurred. RESULTS: Although the overall central motor conduction time (CMCT) was not different from that of normal controls, contralateral CMCT was significantly delayed compared to ipsilateral CMCT (p<0.05). The results of somatosensory evoked potential study demonstrated that contralateral central conduction time (CCT) was not significantly different from ipsilateral CCT. CONCLUSION: These findings indicate that there is a selective interference with the contralateral corticospinal tract in patients with symptomatic cervical dystonia.     

Motor outcome after subcortical stroke correlates with the degree of cortical reorganization.

OBJECTIVE: The contribution of cortical reorganization to motor recovery after a subcortical stroke is uncertain. The purpose of the study was to investigate the relationship between changes in motor cortex organization, and the degree of motor function after a subcortical stroke. METHODS: Transcranial magnetic stimulation mapping of the corticomotor projection to the hand was performed in 27 patients who had suffered a subcortical ischemic stroke resulting in an upper limb motor deficit up to 23 years previously. Corticospinal conduction was assessed by measurements of motor evoked potential latency, amplitude and threshold. Motor function in the upper limb was assessed using the Motor Assessment Scale for Stroke and measurements of grip strength. RESULTS: Motor maps for the hand were displaced on the affected side relative to the unaffected side in 17 patients. In 10 of these patients in whom corticospinal conduction had normalized, there was a strong positive correlation between the magnitude of the map shift and grip strength in the affected hand (r=0.79; P=0.006). In the other seven patients with a map shift, in whom corticospinal conduction was still impaired, there was a tendency for a larger map area to be associated with better motor function, and in the group as a whole there was a correlation between map area and grip strength (r=0.52; P=0.005). CONCLUSIONS: The present findings provide evidence that the cortical plasticity and reorganization that occurs after a subcortical stroke is functionally significant and contributes to motor outcome.     

Electromyographic evaluation of cervical dystonia for planning of botulinum toxin therapy

The success of botulinum toxin (BT) injections for treatment of cervical dystonia depends on precise identification of dystonic muscles and on quantification of their dystonic involvement. Conventionally, this is attempted by clinical examination analysing the dystonic head position. In this presentation, a more systematic approach is sought by using an electromyography (EMG)-based evaluation procedure. In 10 consecutive patients with cervical dystonia not previously exposed to BT clinical examination, analysing the dystonic head position was performed to classify patients into four groups with similar dystonic head positions. Additionally, a 2-channel concentric needle EMG was used to measure the amplitudes of dystonic and maximal voluntary activities in sternocleidomastoid (SCM), splenius capitis (SC) and trapezius/semispinalis capitis (T/SS) muscles bilaterally. The ratio between both amplitudes, the dystonia ratio, was used to quantify dystonic muscle involvement. In all patients dystonia ratios could be calculated. In patients with similar head positions, EMG evaluation revealed different qualitative and quantitative dystonic involvement patterns. In six patients, there were discrepancies in identification of dystonic muscles between clinical examination and EMG evaluation. EMG evaluation excluded dystonic involvement in five patients. All excluded muscles were SCM. In one of these patients, additional T/SS involvement was detected by EMG evaluation. In one patient, SC involvement was revealed by EMG evaluation. All dystonic muscle involvement detected by EMG evaluation represented genuine dystonic muscle coactivation rather than compensatory muscle activity. The EMG evaluation presented allows quantitative and qualitative identification of dystonic muscle involvement which cannot be achieved by clinical examination. Both pieces of information may be helpful for optimization of BT therapy.     

Reduced cerebral cortex inhibition in dystonia: Direct evidence in humans

ObjectiveA loss of inhibition in central motor circuits resulting in abnormal motor control is the hypothesised cause of dystonia. So far, changes in inhibitory function of cerebral cortex in dystonia, have been revealed only indirectly by recording muscle responses evoked by transcranial magnetic stimulation (TMS) of the brain. The aim of present study was to evaluate more directly cerebral cortex changes in dystonia. We had the almost unique opportunity to record directly motor cortex output after brain stimulation, in a dystonic patient who had epidural electrodes implanted in the upper cervical cord.MethodsWe evaluated descending activity evoked by single and paired pulse TMS together with the inhibitory effects produced by afferent stimuli on TMS evoked activity, and compared the results with those obtained in thirteen subjects with no central nervous system abnormality who also had cervical spinal electrodes.ResultsThe intrinsic inhibitory activity produced by paired TMS of the motor cortex, and the inhibitory effects produced by afferent inputs, were suppressed in the patient with dystonia.ConclusionsThese findings provide a direct evidence of the abnormality in motor cortex inhibitory systems in dystonia.SignificanceThe abnormality in cortical inhibitory system might have a role in the pathophysiology of dystonia.     

Motor representation areas in epileptic patients with focal motor seizures: a TMS study

PURPOSE: This study used TMS mapping to investigate the motor representation of the abductor pollicis brevis (APB) muscles in a group of patients with focal epilepsy originating in central or pre-central region. METHODS: Eight epileptic patients and eight control subjects participated in the study. The coil was moved in 1.5-cm steps along a grid drawn on the subject's skull over the motor cortex of both hemispheres. At each site, six APB motor responses (evoked by TMS at 1.2 times the resting motor threshold) were recorded and averaged. The peak-to-peak amplitude was measured and plotted against the mediolateral and anteroposterior coil positions. The area of each APB muscle representation was measured and the position of the optimal point was calculated. RESULTS: The resting motor threshold was increased bilaterally in epileptic patients. The maps were distorted in most patients (but not in control subjects), as evidenced by an off-centre optimal point. Interhemispheric differences in APB map areas were greater in patients than in control subjects. However, whether these increases in map area were on the epileptic side or on healthy side depended on the given subject. CONCLUSIONS: The changes in APB representation observed in epileptic patients demonstrate that reorganization occurs within the motor cortex. The heterogeneity of the present results is probably related to different locations of the epileptogenic and/or lesional areas and to a variety of compensatory phenomena that may occur, notably with respect to the disease duration.