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Biomedical subjects

H J Freund

Publications and source records attributed to H J Freund.

At least 127 records · Page 7Linked to original sources
PubMed1991

Acute posterior multifocal placoid pigment epitheliopathy with cerebral involvement.

In a patient with angiographically proven cerebral vasculitis five months after acute posterior multifocal placoid pigment epitheliopathy (APMPPE) neurological symptoms promptly responded to steroid treatment. Cerebrospinal fluid (CSF) showed a lymphocytic pleocytosis. Magnetic resonance imaging (MRI) revealed multifocal white matter lesions in the hemispheres and the brain stem suggesting a diffuse subcortical vasculitis.

Cerebral Arterial Diseases↗
PubMed1990

Neurophysiology of fastest voluntary muscle contraction in hereditary neuropathy.

In patients with hereditary motor and sensory neuropathy types I (demyelinative) and II (neuronal) and in normal subjects, isometric force and electromyographic activity of the first dorsal interosseous muscle were recorded during fastest voluntary contractions and during twitches evoked by nerve stimulation. The maximum voluntary force of the first dorsal interosseous muscle was also measured. In patients, fastest voluntary contraction time (i.e., time from onset of contraction to peak force) was prolonged and inversely proportional to maximum voluntary force. Maximum rate of rise of tension (i.e., slope of rise in force) was reduced and directly proportional to maximum voluntary force. In patients with hereditary motor and sensory neuropathy type I, contraction time was longer and the maximum rate of rise of tension was lower than in those with hereditary motor and sensory neuropathy type II. In patients and normal subjects, voluntary contraction time was closely correlated with the duration of electromyographic bursts. In patients, the twitch contraction time was prolonged and inversely proportional to maximum voluntary force. Twitch contraction amplitude was diminished and directly proportional to maximum voluntary force. Neither twitch contraction time nor amplitude were dependent on the type of hereditary motor and sensory neuropathy. Twitch contraction time evoked by proximal nerve stimulation was minimally longer than that evoked by distal stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Motor dysfunction in HIV-infected patients without clinically detectable central-nervous deficit.

Motor tests were performed in 50 HIV-infected patients in all stages according to the current CDC classification, but without any clinically evident central nervous system deficit, and the results compared with an age-matched control group. Patients were excluded from the study if there was alcohol or drug abuse, fever and/or opportunistic cerebral infection. The parameters tested were postural tremor of the outstretched hands, most rapid voluntary alternating index finger movements (MRAM) and rise time of most rapid index finger extensions (MRC). Whereas tremor peak frequencies did not differ significantly in the patients and controls, MRAM and rise times of MRCs showed significant slowing in the patient group. Morphologically, the motor test performance of the HIV-infected patients was similar to that of patients with manifest basal ganglia disease (Parkinson's, Huntington's and Wilson's diseases). MRI scans of all patients were normal. It is concluded that in HIV-infected patients there is a very early subclinical central nervous system affection, especially of the basal ganglia, which is detectable with appropriate, quantitative motor function tests. These functional abnormalities precede the structural alterations in the MRI scans.

Adult↗
PubMed1990

Coordination of a multi-joint movement in normal humans and in patients with cerebellar dysfunction.

The contribution of the cerebellar cortex to coordination of a multi-joint throwing movement was studied by measuring various movement and EMG parameters while normal control subjects and patients with cerebellar cortical atrophy threw a ball at a target. Although patients did not throw as accurately as controls, several coordination measurements were normal in the patients. These included parameters used by us to assess elbow-wrist coordination and the coordination of hand opening with activation of more proximal arm muscles. Postural support for the movement at the shoulder was also normal in that the shoulder was not pushed backwards by the reaction forces resulting from the rapid forward acceleration of the forearm and hand. In contrast, however, patients were unable to coordinate the muscles so as to produce the same hand direction from trial to trial when throwing at the same target. In addition, EMG onset times were abnormal in the antagonist muscles relative to agonist EMG bursts and kinematic parameters of the movement. In conclusion, our patients with cerebellar cortical atrophy showed abnormalities in visual-motor coordination, in that they were unable to consistently produce the appropriate hand direction in response to a visual target. Agonist-antagonist relationships were also impaired. Other aspects of coordination, such as the relative timing of EMG onsets of agonist muscles, even when these were active at different joints, were normal.

Adult↗
PubMed1990

Premotor cortex and conditional motor learning in man.

The role of premotor cortex (PMC) in conditional motor learning tasks in man was investigated. Patients with PMC lesions had to learn to associate 6 different visual, tactile or auditory stimuli with 6 different arm movements which were previously rehearsed (Task A). A comparative task involved an association between the same set of sensory stimuli and 6 spatial locations (Task B). Patients with PMC lesions were only impaired when they had to recall a movement from memory on the basis of a sensory cue (Task A), but not for an association involving spatial location (Task B). This indicates that the PMC plays a role in sensory conditional motor learning.

Adult↗
PubMed1990

Disturbances in human arm movement trajectory due to mild cerebellar dysfunction.

The temporal structure of arm movements was studied in nine cerebellar patients with mild impairment of the upper limbs and in six age-matched control subjects. The experimental paradigm consisted of visually guided, step tracking movements about the elbow. Movements ranged from 10 degrees to 70 degrees in amplitude and were made under different instructions (fast, fast/accurate, accurate). As in normal subjects, cerebellar patients were able to scale peak velocity with movement amplitude. This relationship was highly linear under all instruction conditions. Similar relationships existed between movement duration and amplitude. In contrast to normal subjects who produced movements with nearly symmetric velocity profiles, movements made by cerebellar patients were characterised by short acceleration and long deceleration durations. The degree of asymmetry was directly related to movement duration but was unaffected by movement peak velocity. Acceleration durations did not increase beyond 300 ms even in movements lasting up to 1s. These findings demonstrate that, despite little or no obvious impairment of the limb during routine examination, the temporal structure of voluntary movements in cerebellar patients is clearly disturbed. This supports the view that the production of an optimal movement trajectory is under cerebellar influence.

Adult↗
PubMed1990

Cerebral blood flow velocity alterations during obstructive sleep apnea syndrome.

We recorded cerebral blood flow velocity (CBFV) for the assessment of CO2-regulated alterations during apnea by means of transcranial Doppler ultrasound in a patient with obstructive sleep apnea syndrome. CBFV increased up to doubled peak flow values during obstructive apneic phases. The results provide evidence for a normal CO2 regulation of CBFV leading to periodic vascular stress during the night.

Blood Flow Velocity↗
PubMed1990

Premotor area and preparation of movement.

Clinical observations indicate that lesions of the supplementary motor area interfere with the initiation of movement, whereas damage of premotor cortex (PMC) is associated with more complex motor dysfunctions. The clinical premotor syndrome is characterized by contralateral proximal weakness and limb kinetic apraxia in particular for the adjustment of proximal limb movements on both sides. Recordings of the movement kinematics show that the postural support and the assemblage of synergies between proximodistal muscle groups, but also between the two sides, is disturbed in patients with PMC lesions. Lateral premotor lesions of the dominant hemisphere produce a motor dysgraphia or motor dysphasia or both. Special tests disclose further deficits for example in sensory cued motor learning, as well as a severe disturbance of rhythm production without difficulties in rhythm discrimination. This indicates the involvement of PMC in the acquisition of motor skills and in the temporal organization of movement. There is evidence that PMC shows a similar pattern of somatotopic organization as in the primary motor cortex, but with a larger representation for proximal muscles. The present clinical evidence in conjunction with recent PET data and from magnetic stimulation is compatible with the view that PMC represents a bilaterally organized system involved in the acquisition and performance of skilled motor acts including speech and writing.

Animals↗
PubMed1989

Altered mechanisms of muscular force generation in lower motor neuron disease.

Recruitment and firing rate modulation (FRM) of single motor units (MUs) were evaluated in the first dorsal interosseus muscle in patients with chronic lower motor neuron disorders of primarily neuroaxonal or demyelinating pathology. Residual muscle function was estimated by maximal voluntary force, twitch tension, and compound muscle action potential. The recruitment range of MUs was expanded toward higher relative force levels in all patients. Changes in firing rates per unit force increment were larger in patients with more pronounced muscle atrophy. When this effect was accounted for by calculating FRM for increments of 10% of residual maximal force, patients with subnormal motor nerve conduction velocities showed selective impairment of rate modulation. This was not due to intermittent conduction failure. We conclude that the two force-generating mechanisms, recruitment and FRM, show unspecific compensatory changes related to the loss of MUs and also alterations that are specifically related to the neuroaxonal or demyelinating nature of the neuropathy.

Action Potentials↗
PubMed1989

Invariant temporal characteristics of manipulative hand movements.

The measurement of eight manipulative serial hand movements showed a clear distribution of their temporal characteristics into two distinct groups. When the hand was used as a sense organ during active touch the finger movements across objects were restricted to a slow performance range below 2 Hz. Recordings from single mechanoreceptive afferents and calculations of their receptor densities indicated that these movements have to be slow to match the temporal requirements of the sequential sampling process from the mechanoreceptor populations. In contrast, manual skills not associated with the collection of sensory information like handwriting, typing or pencil shading, were performed rapidly. Their frequencies were close to those of fastest possible tapping. Evidence is provided that the different frequency groups are associated with distinct sensory control processes. The low frequency group represents movements involving focal sensory control (Julesz 1984). The high frequency group is not performed open-loop but monitored by preattentive sensory processes. The results indicate a dual sensory control mode operating in separate frequency domains of movement.

Action Potentials↗
PubMed1989

Sensorimotor disturbances in patients with lesions of the parietal cortex.

Somatosensory and motor disturbances of hand function were examined in 9 patients with parietal lobe lesions. A quantitative score was used for the elaboration of sensorimotor profiles displaying the relative degree of functional impairment. In patients with anterior parietal lobe lesions somaesthesis was clearly more disturbed than motor function. Simple aspects of somaesthesis (surface sensibility, two-point discrimination, position sense) were disturbed to about the same degree as complex somatosensory (tactile recognition) tasks. On the other hand, patients with lesions of the posterior parietal lobe showed preferential impairment of complex somatosensory and motor functions (exploratory and manipulative finger movements). In 4 patients, analysis of motor behaviour by means of an optoelectronic system showed that reaching, formation of hand aperture and target acquisition were less disturbed than manipulative behaviour. Finger movement trajectories during dynamic digital palpation of objects were grossly deranged in the patients with posterior parietal damage. The temporal characteristics of the finger movements during active touch were completely destroyed. This leads to a breakdown of the finely tuned digital scanning process required for the sequential sampling of mechanoreceptive information. Remarkably, these patients could produce the exploratory finger movements imitatively. The motor disability of the parietal hand does not lie in the loss of the kinetic memory to perform these movements, but in the loss of their evocation by appropriate sensory stimuli. This deficit is not due to a lack of somatosensory information because that may be relatively well preserved. It is concluded that the motor disturbance in posterior parietal lobe disease lies essentially in the conception and execution of the spatiotemporal movement patterns necessary to bring those receptors into action which would normally provide the information about tactile objects. This illustrates the intricate mutual dependence of the spatiotemporal organization of receptor activation by movement and of the formation of movement trajectories on the basis of adequate sensory processing.

Adult↗
PubMed1989

Role of the parietal cortex for sensorimotor transformation. Evidence from clinical observations.

Somatosensory and motor functions of both hands were examined in 10 patients with unilateral parietal cortex lesions as revealed by computerized tomography. Tests of elementary somatosensory functions comprised surface sensibility, vibration, and position sense. For evaluation of complex somatosensory functions, the recognition of surface textures and object forms was tested. Motor performance was examined by measuring force and position control as well as manipulative and explorative motor behaviour. All patients showed varying degrees of sensory disturbance. Although the patients had no or minor paresis, they all had motor deficits concerning force control, fine movements, and manipulation with the hand contralateral to the lesion. Patients with more posteriorly located parietal lesions revealed predominantly severe disturbances of complex sensibility, precision grip, manipulation, and explorative finger movements. The characteristic and consistent feature of the disturbed motor behaviour was the loss of the purposive nature of the motor acts which were no longer adequate for the tasks (tactile apraxia). Paresis or ataxia could not account for this deficits.

Afferent Pathways↗
PubMed1989

Motor dysfunctions in Parkinson's disease and premotor lesions.

A characteristic disturbance of hand function in Parkinson's disease lies in the performance of rapid automatized movements. Patients have difficulty in producing serial hand movements faster than 2 Hz. The only possibility to perform rapid alternating movements is to synchronize them with their tremor frequency. This mechanism underlies the so-called 'hastening' phenomenon and leads to a disturbance of skills like handwriting or typing, which are usually performed at higher frequencies. The temporal disorder in patients with lesions of premotor cortex is characterized by the difficulty in organizing higher order temporal sequences in complex motor acts.

Animals↗
PubMed1989

[New electrophysiological findings on the incidence of brain involvement in clinically and neurologically asymptomatic HIV infections].

Motor (postural tremor of the outstretched hands, most rapid voluntary alternating index finger movements and rise times of most rapid voluntary isometric index finger extensions) and psychometric tests (multiple choice vocabulary test - form b, syndrome short test, the German version of the standard progressive matrices - Raven, and the psychic and somatic findings according to the AMDP-system) as well as MRI-Scans were analysed in 100 HIV-infected patients of all stages according to the actual CDC-classification, but without any central-nervous or psychic deficit. Patients with drug, alcohol or tranquilizer abuse, opportunistic, cerebral infections or fever were excluded from the study. Tremor-peak-frequencies and reaction times did not show any significant difference to an age- and sex-matched control group; the other motor parameters revealed significant slowing in the patient group and a worsening with the CDC-stages. MRI-scans of all the patients were normal. The psychometric tests did not show significant alterations on a group statistical level, especially not in the depression scales. Morphologically, the motor performances of the HIV-infected patients resembled those of patients with basal ganglia diseases (M. Huntington, M. Wilson, M. Parkinson). Correspondingly, in some cases of clinically demented HIV-positive patients, MRI-scans showed lesions in the basal ganglia. It can be concluded, that there is an early subclinical central-nervous system affection in HIV-infected patients, especially of the basal ganglia, detectable with appropriate motor function tests sometimes considerably preceeding structural deficits seen later in the course of the disease in MRI-scans.

AIDS-Related Complex↗
PubMed1988

Post-hypoxic action (intention) myoclonus: a clinico-electroencephalographic study.

A patient with post-hypoxic action myoclonus classified as reticular reflex myoclonus was subjected to an electrophysiological investigation. The myoclonic movements involved mainly the legs but could also affect the whole body. Somatosensory evoked responses were not increased and electroencephalography (EEG) was normal when the patient was relaxed. Startle, self-paced movement or movement on command induced repetitive myoclonic jerks preceded and accompanied by repetitive small spikes in the EEG with phase reversal in the midline at the vertex or slightly posterior to it, regardless of the limb moved. The central spiking subsided considerably earlier than the myoclonic jerks as shown by polygraphic recordings. The EEG spikes were also provoked by mere imagination of movement and persisted in spite of a dramatic reduction of myoclonic activity after treatment with clonazepam. The observations suggest that the vertex spiking in post-hypoxic action myoclonus indicates synchronous cortical activation, but is not closely coupled with activation of the Betz cells of layer V where the pyramidal pathway originates.

Aorta, Abdominal↗
PubMed1988

[Successful corticoid treatment of lumbosacral plexus neuropathy in heroin abuse. Clinical aspects, electrophysiology, therapy and follow-up].

A 33 year old heroin addict developed a lumbosacral plexopathy which clinically and electrophysiologically resembled an "idiopathic lumbosacral plexus neuropathy". He complained of severe neuralgic pain, marked paresis, and distinct sensory loss in the right leg. The plexopathy was accompanied by rhabdomyolysis. He was treated with corticosteroids in high dosage. Within 3 days the disabling symptoms had almost completely disappeared. Clinical and electrophysiological findings are described in the course of the disease and are compared with the data in the literature.

Adult↗