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Biomedical subjects

J Liepert

Publications and source records attributed to J Liepert.

At least 19 recordsLinked to original sources

Transcranial magnetic stimulation in neurorehabilitation.

In neurorehabilitation, transcranial magnetic stimulation (TMS) offers information regarding prognosis and pathophysiology and could also be useful for therapeutic purposes. Numerous studies have indicated that, after stroke, the absence of motor evoked potentials is associated with a poor motor recovery. In contrast, MEPs obtained in the paretic muscle with low stimulus intensities suggest a good restitution of motor function. TMS studies have shown that the location of a brain lesion determines motor cortex excitability changes: Patients with central somatosensory lesions show a disinhibition in the ipsilesional motor cortex. Lesions in the territory of the superior cerebellar artery are associated with a loss of motor cortex excitability. Stroke patients participating in a Constraint-induced movement therapy show an enlargement of the motor output area in the affected hemisphere after therapy. This enhancement of motor excitability is associated with an improvement of motor function. Some evidence is emerging that the application of low frequency repetitive TMS over the non-lesioned hemisphere improves neglect phenomena by down-regulation of the excitability of the non-lesioned hemisphere.

Brain↗

Motor cortex excitability after thalamic infarction.

OBJECTIVE: We examined 8 patients with hemihypesthesia due to an ischemic thalamic lesion to explore the effects of a central sensory dysfunction on motor cortex excitability. METHODS: Motor excitability was assessed using transcranial magnetic stimulation techniques and electrical peripheral nerve stimulation. Motor function was evaluated by the Nine-Hole-Peg Test and measurement of hand grip strength. The affected side was compared with the non-lesioned side and with an age-matched control group. RESULTS: Patients had a loss of inhibition and an increase of facilitation in the motor cortex of the affected side. The silent period was prolonged and motor function was impaired on the affected side. CONCLUSIONS: A thalamic lesion can modulate motor cortical excitability. SIGNIFICANCE: This study suggests that, under normal conditions, somatosensory afferents influence inhibitory and excitatory properties in the motor cortex.

Adult↗

Motor cortex excitability and fatigue in multiple sclerosis: a transcranial magnetic stimulation study.

We investigated electrophysiological correlates of fatigue in patients with multiple sclerosis (MS). Transcranial magnetic stimulation (TMS) was used to explore motor excitability in three groups of subjects: MS patients with fatigue (MS-F), MS patients without fatigue (MS-NF) and healthy control subjects. All participants had to perform a fatiguing hand-grip exercise. TMS was performed prior to and after the exercise. Prior to the motor task, MS-F patients had less inhibition in the primary motor cortex compared to both other groups. Postexercise, intracortical inhibition was still reduced in the MS-F patients compared to the MS-NF patients. In MS-F patients the postexercise time interval for normalization of the motor threshold was correlated with the fatigue severity. We conclude that MS patients with fatigue have an impairment of inhibitory circuits in their primary motor cortex. The results also indicate that fatigue severity is associated with an exercise-induced reduction of membrane excitability.

Adult↗

Motor cortex excitability after cerebellar infarction.

BACKGROUND AND PURPOSE: The cerebellum has an influence on motor excitability. We investigated if the location of a cerebellar infarction was crucial for changes of motor cortex excitability and if the electrophysiological findings were correlated with motor performance. METHODS: Transcranial magnetic stimulation was applied to study intracortical inhibition (ICI), intracortical facilitation (ICF), motor thresholds, and corticospinal excitability. Dexterity as a measure of motor performance was tested with the Nine-Hole-Peg Test (9HPT). Ratios (affected/unaffected) were also calculated. RESULTS: ICI and ICF ratios were negatively correlated with 9HPT ratios in all patients (n=9). Compared with an age-matched control group, patients with lesions in the territory of the superior cerebellar artery (SCA) (n=3) or a lesion rostral of the dentate nucleus (n=1) had abnormally enhanced ICI and a loss of ICF (3 patients). Dexterity was impaired in all 4 patients. Motor excitability and motor performance normalized over the subsequent weeks. Patients with an infarct either in the territory of the anterior inferior cerebellar artery (n=2) or in the territory of the posterior inferior cerebellar artery (n=3) displayed motor excitability and motor performance within the normal range. CONCLUSIONS: The superior part of the cerebellum has a strong influence on motor cortex excitability. We suggest that the enhancement of motor inhibition and reduction of motor facilitation is mediated by an impairment of the deep cerebellar nuclei.

Adult↗

Modulation of motor cortex excitability induced by pinch grip repetition.

UNLABELLED: We examined the influence of right handed pinch grips and the effect of a motor training on motor cortex excitability of the left first dorsal interosseus muscle (FDI). TMS single and paired pulses were applied over the right human motor cortex (M1) during and after right handed pinch grips with low force. In another experiment, these stimulations were performed before and after a 30-minute right handed pinch grip training. RESULTS: MEP amplitudes in left FDI were reduced when TMS single pulses were applied during the pinch grip. Simultaneously, motor cortex excitability was enhanced but returned to baseline after the training period. CONCLUSION: Phasic pinch grips of the right hand exert an inhibiting effect on the corticospinal excitability of the ipsilateral motor cortex and lead to an increase of intracortical excitability. These changes are distinct and independent of each other. Motor training has an interhemispheric effect on intracortical excitability.

Adult↗

Motor excitability and motor behaviour after modafinil ingestion--a double-blind placebo-controlled cross-over trial.

Modafinil is a novel vigilance-enhancing agent. We were interested if modafinil would also enhance motor excitability and improve motor performance and attention in healthy subjects. Ten volunteers received either a single oral dose of placebo or 200 mg modafinil. A randomized double-blind crossover design was used. Transcranial magnetic stimulation was employed to test intracortical inhibition, intracortical facilitation, the cortical silent period and to obtain stimulus-response curves. In addition, M responses and F waves were recorded. Reaction time tasks, the nine-hole-peg test and the d2 attention test were also applied. These studies were performed prior to and 3 and 24 hours after drug ingestion. Modafinil did not change excitatory or inhibitory properties in the motor cortex. It did not alter corticospinal excitability and alpha motoneuronal excitability. In the modafinil group and in the placebo group, performance of the nine-hole-peg test and the d2 test improved to a similar extend over time. Thus, this study does not demonstrate significant differences between a single dose of modafinil and placebo in healthy subjects.

Adult↗

Lesion-induced and training-induced brain reorganization.

INTRODUCTION: A stroke may modulate motor cortex excitability. We examined if distinct ischemic brain lesions are associated with a specific pattern of excitability changes. We also investigated the effects of a rehabilitative therapy on motor excitability. METHODS: In stroke patients, the consequences of a) a lesion in the central somatosensory system, b) a cerebellar lesion and c) a two week period of Constraint-induced movement therapy (CIMT), on motor cortex excitability were studied. Transcranial magnetic stimulation techniques and functional magnetic resonance imaging (fMRI) were employed. RESULTS: Patients with a lesion in the primary somatosensory cortex or in the ventroposterolateral nucleus of the thalamus had a decreased intracortical inhibition on the affected side. Patients with lesions in the territory of the superior cerebellar artery had a loss of intracortical facilitation and an increase of intracortical inhibition. Patients with cortical lesions undergoing CIMT had a loss of intracortical inhibition prior to therapy. After CIMT, changes of ICI were stronger in the lesioned than in the non-lesioned hemisphere but could result either in an increase of ICI or a reduction of ICI. In three patients fMRI results showed that cortical activation was less post CIMT as compared to pre-treatment activation. In parallel, ICI was reduced after treatment. CONCLUSIONS: Our results suggest that, physiologically, central somatosensory influence on the motor cortex is inhibitory. In contrast, the cerebellum normally exerts a facilitatory influence on the motor cortex. CIMT induces changes of intracortical excitability mainly in the affected hemisphere.

Brain↗

Pre-movement motor excitability is reduced ipsilateral to low force pinch grips.

Motor excitability ipsilateral to pinch grips was investigated during the pre-movement period. Subjects performed right-handed phasic pinch grips with 2% or 20% maximum voluntary contraction (MVC) in response to a visual go-signal. Transcranial magnetic stimulation (TMS) was applied over the right motor cortex at various intervals before the go-signal and 100 msec after movement onset. Motor evoked potentials were recorded from the relaxed left first dorsal interosseous muscle. Immediately prior to and during 2% MVC pinch grips, MEP amplitudes were reduced. In contrast, MEPs obtained by transcranial electrical stimulation tended to be increased, indicating that MEP decreases are mediated at a cortical level. Before and during 20% MVC pinch grips MEP amplitudes were enhanced. TMS delayed reaction time if applied close to the go-signal. We conclude that the motor cortex ipsilateral to low force movements is inhibited prior to and during movement.

Adult↗

Interhemispheric effects of high and low frequency rTMS in healthy humans.

OBJECTIVE: We investigated whether repetitive transcranial magnetic stimulation (rTMS) applied to the right motor cortex modified the excitability of the unstimulated left motor cortex. METHODS: Interhemispheric effects of 0.5 and 5 Hz subthreshold rTMS over the right motor cortex were examined by single pulse and paired pulse TMS and by transcranial electrical stimulation (TES) applied to the unstimulated left motor cortex. The effects of (a) 1800 pulses real and sham rTMS with 5 Hz, (b) 180 pulses real and sham rTMS with 0.5 Hz and (c) 1800 pulses real rTMS with 0.5 Hz were studied. RESULTS: Following 5 Hz right motor rTMS motor evoked potential (MEP) amplitudes induced by single pulse TMS over the left motor cortex increased significantly. Intracortical inhibition (ICI) and facilitation (ICF) and MEP amplitudes evoked by TES were unchanged. Sham stimulation had no influence on motor cortex excitability. After 180 pulses right motor cortex rTMS with 0.5 Hz a significant decrease of left motor ICF, but no change in single pulse MEP amplitudes was found. A similar trend was observed with 1800 pulses rTMS with 0.5 Hz. CONCLUSIONS: High frequency right motor rTMS can increase left motor cortex excitability whereas low frequency right motor rTMS can decrease it. These effects outlast the rTMS by several minutes. The underlying mechanisms mediating interhemispheric excitability changes are likely to be frequency dependent.

Adult↗

Motor system abnormalities in hereditary spastic paraparesis type 4 (SPG4) depend on the type of mutation in the spastin gene.

BACKGROUND: Hereditary spastic paraparesis (HSP) denotes a group of inherited neurological disorders with progressive lower limb spasticity as their clinical hallmark; a large proportion of autosomal dominant HSP belongs to HSP type 4, which has been linked to the SPG4 locus on chromosome 2. A variety of mutations have been identified within the SPG4 gene product, spastin. OBJECTIVE: Correlation of genotype and electrophysiological phenotype. MATERIAL: Two large families with HSP linked to the SPG4 locus with a very similar disease with respect to age of onset, progression, and severity of symptoms. METHODS: Mutation analysis was performed by PCR from genomic DNA and cDNA, and direct sequencing. The motor system was evaluated using transcranial magnetic stimulation. RESULTS: Patients differ in several categories depending on the type of mutation present. CONCLUSIONS: For the first time in hereditary spastic paraparesis, a phenotypic correlate of a given genetic change in the spastin gene has been shown.

Adenosine Triphosphatases↗

Fatigue suppresses ipsilateral intracortical facilitation.

Experimental data in animals and humans have demonstrated connections between right and left motor cortices. Interactions between these cortical areas can be explored with electrical or magnetic stimulation. In the present study we examined the interhemispheric effect of fatigue on intracortical facilitation (ICF) and inhibition (ICI) using a paired-pulse transcranial magnetic stimulation (TMS) paradigm. Ten healthy subjects performed pinch grips with their left hand with 50% maximum voluntary contraction (MVC) until fatigue occurred. In the control experiment, the same number of pinch grips was performed with 5% MVC without inducing fatigue. Motor evoked potentials (MEP) produced by single and paired pulse TMS over the left motor cortex were recorded from right first dorsal interosseous muscle (FDI) and right abductor digiti minimi muscle (ADM) before and after the tasks. ICF of the right FDI was significantly reduced after fatigue ( P=0.0008). Fifteen minutes after finishing the task ICF had returned to baseline values. There was no change of ICF of right FDI in the control experiment without inducing fatigue. In both experiments the right ADM did not show significant MEP changes. Additional control experiments showed that M-responses and F-waves were unchanged in right FDI after performing the fatigue task with left FDI, and TMS test pulse amplitudes were significantly reduced in left FDI after fatigue. Fatigue caused by pinch grips induces a short-lasting and task-specific suppression of intracortical facilitation in the motor cortex of an homologous contralateral hand muscle. These results indicate interhemispheric interactions between the two motor cortices that are still effective after cessation of movements.

Adult↗

Structural and functional cortical abnormalities after upper limb amputation during childhood.

Functional reorganization has been well documented in the human adult brain after amputation of the arm. To assess the effects of amputation on the developing brain, we investigated six patients with upper limb amputation in early childhood and one with right dysmelia. Transcranial magnetic stimulation indicated contralateral cortical disinhibition and enlargement of the excitable area of the stump. FMRI data corroborated these plastic changes and also showed an ipsilateral functional reorganization. In the T1-weighted MRI, we found structural deformities of the contralateral and ipsilateral central sulcus in three patients and a contralateral atrophic parietal lobule in two patients. Therefore, arm amputation in childhood affects functional organization as well as anatomical structure in both hemispheres.

Adolescent↗

Orally administered atropine enhances motor cortex excitability: a transcranial magnetic stimulation study in human subjects.

Oral application of atropine was used to test if a modulation of cholinergic neurotransmission changed motor excitability. Healthy volunteers received either 1 or 2 mg atropine. Paired transcranial magnetic stimulation was used to study intracortical inhibition and intracortical facilitation before, 1 h and 24 h after ingestion of atropine. In addition, the silent period, motor threshold, F wave and motor response amplitudes were measured. The 1 mg dose of atropine induced a loss of intracortical inhibition, the 2 mg dose produced an intracortical disinhibition and enhanced intracortical facilitation. These changes returned to baseline after 24 h. Other electrophysiological parameters remained unchanged. Thus, an antagonist of pre- and postsynaptic muscarinic receptors increased excitability in the human motor cortex in a dose-dependent manner, indicating an influence of the cholinergic system on motor cortex excitation.

Administration, Oral↗

[Repetitive transcranial magnetic stimulation (rTMS) in the acute and long-term therapy of refractory depression--a case report].

We report on a patient with therapy-resistant major depression according to DSM-IV criteria who has been hospitalized for 60 months during the last 7 years. Not even five electroconvulsive therapy (ECT) series (61 single applications) brought lasting remission of symptoms. As cognitive deficits developed and prolonged postnarcotic recovery times were observed, further ECT was contraindicated. The left frontal cortex was chosen as the target site for repetitive transcranial magnetic stimulation (rTMS) treatment. For identification, a neuronavigational system was used that allows online monitoring of the position of the magnetic coil in relation to the individual cortex. The therapeutic progress was monitored by standardized psychiatric ratings (HAMD, BDI). In addition, cognitive performance was tested during the course of treatment. Only a few rTMS applications already caused an obvious brightening in mood, remission of depressive delusional symptoms, and an increase in personal interests and activities. After 4 weeks of daily treatment, the patient was discharged from the ward. The rTMS treatments and psychotherapeutic counseling have been continued on an outpatient basis. Thus, pharmaco- and psychotherapeutic interventions combined with rTMS led to persistent symptom remission and social reintegration.

Adult↗

Motor cortex plasticity during forced-use therapy in stroke patients: a preliminary study.

Treatment-induced plastic changes were investigated in the brains of stroke patients in the subacute stage of illness. Nine patients participated in 1 week of conventional physiotherapy. In the subsequent week conventional physiotherapy was combined with forced-use therapy. Focal transcranial magnetic stimulation was used to determine the motor output areas of the abductor pollicis brevis muscles prior to the treatment and after the first and after the second week. Motor performance was evaluated using the Nine Hole Peg Test, the Frenchay Arm Test and vigorometry to measure the grip strength. Before treatment the cortical representation area of the paretic hand muscle was significantly smaller than the contralateral side. This difference persisted after the first week of physiotherapy. In contrast, the motor output map in the affected hemisphere was significantly enlarged after forced-use therapy. This increase in motor cortex excitability was accompanied by a significant improvement in dexterity. Across the two treatment weeks the centres of the motor output maps shifted significantly stronger in the affected hemisphere than in unaffected hemisphere, suggesting the recruitment of adjacent brain areas. We conclude that the combination of forced-use therapy and conventional physiotherapy enhances motor cortex excitability and improves motor performance compared to a preceding conventional physiotherapy alone. Due to the small number of patients and the lack of a control group, these results are preliminary observations and require replication in a larger sample.

Aged↗

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.

Adult↗

Disinhibition of somatosensory and motor cortex in mitochondriopathy without myoclonus.

OBJECTIVE: To test electrophysiologically, if patients with mitochondriopathy but without evidence of myocloni have subclinical signs of disinhibition in motor and somatosensory cortices. METHODS: Two patients were studied and compared with age-matched control groups. RESULTS: In both patients, giant somatosensory evoked potentials after median nerve stimulation and a reduced intracortical inhibition tested by transcranial magnetic stimulation in a paired pulse paradigm indicated a dysfunction of inhibitory circuits in the motor as well as the somatosensory cortex. In addition, the somatosensory evoked 600 Hz activity recorded by magnetoencephalography was abolished. CONCLUSIONS: Patients with mitochondriopathy may suffer from a subclinical disturbance of inhibition in the sensorimotor cortex. The loss of 600 Hz activity indicates that these high-frequency oscillations could reflect the activity of inhibitory neurons in the somatosensory cortex.

Adult↗