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Martin Tegenthoff

Publications and source records attributed to Martin Tegenthoff.

25 records · Page 2Linked to original sources
PubMed2003

Functional magnetic resonance imaging mirrors recovery of visual perception after repetitive tachistoscopic stimulation in patients with partial cortical blindness.

We investigated three patients with partial cortical blindness after brain injury by means of functional magnetic resonance imaging (fMRI) before and after the application of a daily visual stimulation-therapy over a period of 6 months. Before therapy, fMRI data showed a severely reduced blood-oxygen-level-dependent (BOLD) signal in primary visual cortex when compared to healthy volunteers. Following several months of rehabilitative therapy a neuropsychological improvement of visual functions was accompanied by an increase in BOLD signal of residual perilesional regions whereas fMRI data of the control group remained unchanged. A high capacity of functional recovery and synaptic plasticity of surviving perilesional neuronal structures of primary visual cortex followed by an increased input into post-connected visual areas can be discussed as a basis for the reoccurrence of visual functions.

Adult↗
PubMed2003

Breakdown of adenine nucleotide pool in fatiguing skeletal muscle in McArdle's disease: a noninvasive 31P-MRS and EMG study.

Energy metabolism and electrical muscle activity were studied in the calf muscles of 19 patients with proven McArdle's disease and in 25 healthy subjects. Phosphorus magnetic resonance spectroscopy and surface electromyography (S-EMG) were performed during two isometric muscle contractions of 3 min at 30% maximum voluntary contraction, one performed during normal perfusion and the other during applied ischemia. After about 1 min of ischemic muscle contraction in diseased muscle a significant acceleration in phosphocreatine breakdown was observed, along with a significant decrease in adenosine triphosphate. During both contractions the absence of glycolysis was shown by a significant alkalinization. Furthermore, in patients we observed a greater increase in the S-EMG amplitude than in control subjects. We conclude that early on during moderate exercise, a small number of muscle fibers reach metabolic depletion, indicated by a reduction in the adenine nucleotide pool. An increasing number of motor units, which are still in a high-energy state, are continuously recruited to compensate for muscle fatigue. This functional compartmentation may contribute to the pathophysiology of exercise intolerance in McArdle's disease.

Action Potentials↗
PubMed2003

Efficacy of the NMDA-receptor antagonist memantine in patients with chronic phantom limb pain--results of a randomized double-blinded, placebo-controlled trial.

Phantom limb pain (PLP) associated neuroplastic changes are partly mediated by excitatory amino acids at NMDA receptor sites. This study was undertaken to deduce if NMDA-receptor antagonists may be effective in patients with chronic PLP. Therefore a four week double-blinded, randomized placebo-controlled trial was performed to evaluate the efficacy of 30 mg memantine/day, an orally administrable NMDA receptor antagonist.Thirty-six patients, 18 per group, with a history of at least 12 months PLP and an average pain of at least 4 on the 11-point numeric rating scale (NRS) were enrolled. The patients completed a standardized questionnaire before the trial. PLP intensity and the level of eight complaints were assessed during the trial. Number needed to treat (NNT) was calculated based on the average PLP during the 3rd week (steady state). In both groups, PLP declined significantly in comparison with the baseline (verum: 5.1 (+/-2.1) to 3,8 (+/-2,3), placebo from 5.1 (+/-2.0) to 3.2 (+/-1,46) NRS) without a re-rising of the PLP during the washout period. Mean pain relief was 47% in the memantine group (10 patients reported more than 50% relief), 40% in the placebo group (6>50%): NNT were 4.5 (KI: 2.1-10.6). Analysis of covariance demonstrated a significant impact only on the prior PLP intensity, but no treatment effect. Two patients have demonstrated long-term pain relief under memantine until now (16 months). The total number of slight adverse events were comparable in both groups, but the overall number of severe events was higher in the memantine group (P<0.05). This trial failed to demonstrate a significant clinical benefit of the NMDA-receptor antagonist memantine in chronic PLP. The administration of a higher dosage is probably not tolerable.

Adult↗
PubMed2003

Repetitive visual stimulation: a neuropsychological approach to the treatment of cortical blindness.

Cortical visual disturbances can occur after traumatic or ischemic brain lesion. Patients mostly suffer from hemianopia. Different treatment approaches in patients with hemianopia are being debated with respect to their effectiveness. For more severely disabled patients with cortical blindness or residual rudimentary vision (RRV) no systematic therapeutic approaches have been reported. In a case study the positive effects of a recently developed repetitive photic stimulation therapy in a patient with RRV after a bioccipital ischemic infarction are presented. The application of this new therapy over several months, supported by treatment with amphetamines led to a statistically significant improvement of different visual functions and a reoccurrence of visual abilities important in daily life. The pathophysiological basis and possible neurorehabilitative consequences that arise from these results are discussed with respect to similar findings in animal experiments.

Blindness, Cortical↗
PubMed2002

Pharmacological suppression of plastic changes in human primary somatosensory cortex after motor learning.

The strict division between motor and somatosensory systems might be less distinct than previously thought. Many brain mapping studies have described changes of somatosensory cortex (S-I) after the execution of a motor task, which supports the idea of a profound interconnectedness in the sensorimotor system. Here we report experiments in which we investigated by means of somatosensory evoked potentials (SSEPs) mapping the reorganizational capacities in primary somatosensory cortex before and after a Hebbian repetitive co-contraction task of the thumb and arm. We investigated the susceptibility of S-I plasticity to the pharmacological modulation of the GABA-neurotransmitter system by application of the GABA(A) agonist lorazepam. We found that repetitive training induced stable motor learning characterized by a significant improvement of performance. The time differences between the onset of contraction of the deltoid muscle and the abductor pollicis brevis were progressively shortened. The process of motor learning was accompanied by plastic changes in the primary somatosensory cortex as indicated by a significant increase in the dipole strength and a significant shift of the median nerve dipole on the hemisphere contralateral to the exercised side. Moreover, the individual shifts of median nerve dipole location were correlated with the individual improvement in motor performance. After administration of lorazepam, motor learning was significantly suppressed. The behavioural effect was accompanied by an abolition of the N20 dipole shift and an unchanged dipole strength. The results imply that motor learning leads to a profound reorganization in S-I which is subject to pharmacological suppression with the GABA agonist lorazepam.

Adult↗
PubMed2002

Motor cortex activation by transcranial magnetic stimulation in ataxia patients depends on the genetic defect.

In patients with degenerative ataxia, various abnormalities in motor cortex activation by transcranial magnetic stimulation (TMS) have been observed, including a reduction of intracortical facilitation and a lengthening of the silent period. However, the groups of patients examined in previous studies were heterogeneous, involving patients with autosomal-dominant and idiopathic cerebellar ataxia, and showing different clinical features. The aim of our present study was to investigate whether differences in motor cortex activation by TMS could be observed in genetically defined subtypes of degenerative ataxia. We examined six patients with Friedreich's ataxia, three patients with spinocerebellar ataxia (SCA) type 1, seven patients with SCA2, 12 patients with SCA3, nine patients with SCA6 and 14 healthy controls. In all subjects, motor threshold, central motor conduction time, cortical silent period after TMS, and intracortical inhibition and facilitation (as assessed by TMS using a paired pulses paradigm) were determined. Additionally, F wave amplitudes evoked by electrical peripheral nerve stimulation were measured. We found a significant reduction of intracortical facilitation in SCA2 and SCA3 patients. Furthermore, motor threshold was elevated in SCA1, central motor conduction time was lengthened in patients with Friedreich's ataxia and SCA1, and F wave amplitudes were enlarged in all the genetic subgroups except for SCA6. Silent period and intracortical inhibition did not differ between patients and controls. We conclude that changes of intracortical facilitation induced by TMS and other excitability parameters of the motor system are not a common phenomenon in degenerative ataxia, but are restricted to specific subtypes. This points to differences in the underlying pathophysiological processes in genetic subtypes of ataxia.

Adolescent↗