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Biomedical subjects

H J Freund

Publications and source records attributed to H J Freund.

At least 19 recordsLinked to original sources
PubMed1996

Thalamic metbolism and corticospinal tract integrity determine motor recovery in stroke.

We studied the role of remote metabolic depressions and pyramidal tract involvement regarding motor recovery following a first hemiparetic ischemic stroke. In 23 patients the regional cerebral glucose metabolism (rCMRGlu) was measured with positron emission tomography and the location and spatial extent of the stroke lesions were assessed by magnetic resonance imaging. Motor impairment during the acute and chronic stages (4 weeks after stroke) was determined by a motor score and recordings of magnetic evoked motor potentials. Twelve patients recovered significantly, whereas 11 patients retained a disabling hemiparesis. In contrast to patients with good motor recovery, rCMRGlu was severely depressed in the thalamus on the lesion side in patients with poor motor recovery. This patient group also showed more severe damage to the pyramidal tract on magnetic resonance images and a more pronounced reduction of the magnetic evoked motor potential amplitude. Neither the size of the stroke lesions nor the spatial extent of the lesional and remote rCMRGlu depressions outside the thalamus correlated with the thalamic hypometabolism and the improvement of the motor score. We conclude that preservation both of parts of the pyramidal tract and of the thalamic circuitry is a major determinant for the quality of hand motor recovery following acute brain ischemia in the adult.

Adult↗
PubMed1996

Basal ganglia and cerebellar impairment differentially affect the amplitude and time scaling during the performance of forearm step tracking movements.

Forearm step tracking movements of different amplitudes were analysed in nine patients with cerebellar and five patients with parkinsonian symptoms in comparison to six normal subjects. Movements were made under two instructions: 1) track "as fast as possible" and 2) "as precisely as possible". Movement duration, acceleration duration and peak velocity increased with increasing amplitude. The ratio between acceleration and deceleration duration was independent of movement amplitude in the parkinsonian patients and the normal subjects. In the cerebellar patients, however, this ratio decreased with increasing amplitude. This impairment of the relative timing between acceleration and deceleration duration implies that, in contrast to parkinsonian patients, cerebellar patients cannot anymore utilize physiological scaling mechanisms when performing movements of different amplitudes.

Adult↗
PubMed1995

Modulation of somatosensory evoked magnetic fields by sensory and motor interferences.

Modulatory influences of skilled exploratory finger movements on somatosensory evoked magnetic fields evoked by median nerve stimulation were investigated in six healthy subjects using a whole head magnetometer (MEG) system. The exploratory finger movements caused major changes in the somatosensory evoked fields. The most prominent effect was a reversal of the dipolar magnetic field around 30 ms after median nerve stimulation. Similar but less pronounced effects were exerted by repetitive finger movements and tactile stimulation of the hand. A dipole analysis and super-imposition of resulting sources on individual MRI scans showed that all somatosensory evoked fields up to 60 ms after stimulation, and the modulation of these responses were located in the primary somatosensory cortex (SI).

Adult↗
PubMed1995

Ataxic breathing during alternating forearm movements of various frequencies in cerebellar patients.

Breathing was analyzed at rest and during sinusoidal tracking movements of the forearm of the dominant side at various frequencies in 11 patients with a cerebellar impairment and in 9 healthy subjects. In the patients, breathing movements were always rhythmical as in normal subjects during rest, but sometimes were interrupted by intermittent breathing-arrests during tracking (breathing ataxia). In 9 of the 11 cerebellar patients, the normal phase relationships between breathing and forearm movements at target frequencies in the spontaneous breathing rate range were absent. Thus patients with cerebellar lesions not only show disturbed skeletomotor movements, but also show an impaired coordination between breathing and limb movements.

Adult↗
PubMed1995

Large-scale plasticity of the human motor cortex.

The adult primate brain is capable of modifying rapidly the size of cortical receptive fields or motor output modules in response to altered synaptic input. We used positron emission tomography (PET) to map the regional cerebral blood flow changes related to voluntary finger movements in patients with tumours occupying the hand area of motor cortex. All patients showed activations solely outside the tumour. Compared with the unaffected side, the activations were shifted by 9-43 mm either along the mediolateral body representation of motor cortex or into premotor or parietal somatosensory cortex. These results provide evidence that slowly developing lesions can induce large-scale reorganization that is not confined to changes within the somatotopic body representation in motor cortex.

Adult↗
PubMed1995

Subcortical origin of visuomotor apraxia.

Visuomotor apraxia (VMA) is a clinical syndrome characterized by a failure to make use of visual information when performing a target-directed movement. Visuomotor apraxia has traditionally been assumed to result from a disconnection of cortico-cortical fibres between visual and motor areas following occipito-parietal lesions. We describe a patient who developed a permanent contralesional and a temporary ipsilesional visuomotor apraxia as part of a complex neurological syndrome after a right [corrected] thalamic haemorrhage. MRI showed that the suprathalamic white matter was not involved but the most caudal fibres of the internal capsule appeared to be interrupted. To our knowledge this is the first case of a VMA with a lesion restricted to a deep subcortical area indicating that VMA can result from damage to subcortical projections rather than interruption of cortico-cortical fibres.

Aged↗
PubMed1995

Somatosensory evoked potentials elicited by intraneural microstimulation of afferent nerve fibers.

Cortical somatosensory evoked potentials (SEPs) after intraneural microstimulation (IMS) of cutaneous and afferent muscle nerve fibers in the median nerve were recorded to study the contribution of different afferent fiber groups to the SEP. Thirty-seven cutaneous fiber bundles, 10 afferent muscle nerve fiber bundles, and 45 single mechanoreceptive afferents of FA I- (n = 12), FA II- (n = 8), SA I- (n = 13), and SA II-type (n = 12) were studied in 29 healthy subjects. IMS of cutaneous fiber bundles evoked cortical responses corresponding to the N20 component after median nerve stimulation in 86% of the fascicles studied, whereas IMS of muscle nerve fiber bundles elicited responses only in 20%. After IMS of single mechanoreceptive afferents of FA I-, FA II-, and SA I-type cortical responses were obtained in all groups in approximately 80% of the stimulated units. The latencies of the SEPs evoked by IMS were comparable to that after compound median nerve stimulation (mean difference 0.58 ms). The N20 amplitudes of SEPs after IMS of cutaneous fiber bundles were on average 28% (n = 32) and for single afferents 22% (n = 30) of that after compound nerve stimulation. It is concluded that the median nerve SEPs evoked by compound median nerve stimulation of the resting hand are dominated by cutaneous rather than muscle afferent input. Furthermore, the fact that selective stimulation of only a few cutaneous afferents produces cortical SEPs of rather high amplitude is compatible with the view that sensory information produced by selective afferent stimulation is differentially gated into the somatosensory cortex.

Adult↗
PubMed1995

Late diagnosis of Wilson's disease in a case without onset of symptoms.

Wilson's disease (WD) was diagnosed on the basis of a liver biopsy, blood investigations and a radio copper test in a 60-year-old, neurologically normal female with uncharacteristic gastrointestinal complaints. Since this patient never developed symptoms indicative for WD this case suggests the possibility of a subclinical course of untreated WD.

Biopsy↗
PubMed1995

The pattern of motor deficits in relation to the site of stroke lesions.

Thirty-two patients with hemispheric stroke lesions of distinct cortical functional zones (premotor, precentral, parietal) or of striatocapsular or striatothalamic subcortical territories were scored at the acute and chronic stage for the following sensorimotor arm-hand functions: force, praxis, motor attention, sensation and dexterity. The selection criterion was that in spite of the wide variation of lesion sites all patients had hemiparesis as the presenting clinical sign. Analysis of the scores showed that most patients showed apraxia, motor neglect or disturbed sensation in addition to hemiparesis. The distribution and severity of these deficits varied, so that different lesion groups showed different patterns. The actual functional impairment of arm-hand function was determined by the combined effect of these different sensorimotor dysfunctions.

Adult↗
PubMed1994

Motor analysis predicts progression in HIV-associated brain disease.

One hundred HIV-positive individuals without clinically evident central nervous system (CNS) deficits entered this follow-up study and were examined clinically and with a well-defined motor test battery every 3 months over 2 years or until they decreased. They underwent magnetic resonance tomography once a year. None received any form of therapy at onset of the study. Three groups were analyzed: (A) patients without electrophysiologically detectable motor impairment (n = 23), (B) patients with electrophysiologically detectable motor impairment but no virostatic medication (n = 33), and (C) patients with motor deficits undergoing AZT treatment (n = 44) after study onset. Group A patients, although slightly deteriorating over time, had the best clinical and electrophysiological outcome compared to the other groups, whereas group B patients deteriorated markedly in both clinical and electrophysiological tests, even though the majority did not develop cerebral complications during the observation period. Those group C patients belonging to early CDC stages (II and III) improved electrophysiologically under AZT therapy, while 76% of the patients in more advanced stages (CDC IVA-D) died of cerebral AIDS manifestations. Four patients of this group, being alive at the end of the study, were completely demented. It is suggested that early detectable motor impairment predicts future cerebral involvement in AIDS. Late onset of virostatic treatment did not influence the clinical outcome.

AIDS Dementia Complex↗
PubMed1994

Cerebral network underlying unilateral motor neglect: evidence from positron emission tomography.

In 4 male patients (age range 50-73 years) with unilateral motor hemineglect as a sequelae of circumscribed cerebral infarction, depressions of the regional cerebral glucose metabolism (rCMRGlu) were mapped to identify the metabolically affected cerebral structures. Motor neglect was defined according to Castaigne by lack of spontaneous and pain-induced motor activity on one side of the body in the absence of paresis, pyramidal signs, and sensory loss. The depressions of the rCMRGlu as determined by positron emission tomography (PET) were found to exceed the areas of structural damage but to be restricted to the affected cerebral hemisphere. Significant mean rCMRGlu depressions followed a focal pattern involving the premotor, prefrontal, parietal and cingulate cortex, as well as the thalamus. In correspondence to the lack of significant mean rCMRGlu depressions in primary sensorimotor cortex, basal ganglia, and cerebellum the cortico-spinal pathway was spared as indicated by preserved magnetic evoked motor potentials. Our data provide evidence suggesting that motor hemineglect is a disturbance in a cerebral network of higher order cortical areas subserving motor activity in the presence of an intact motor cortical output system.

Aged↗