Search PubMed⌕ Search

Biomedical subjects

G Deuschl

Publications and source records attributed to G Deuschl.

At least 91 records · Page 5Linked to original sources

Movement-related electroencephalographic desynchronization in patients with hand cramps: evidence for motor cortical involvement in focal dystonia.

We studied the dynamic changes in the amplitude of scalp electroencephalographic (EEG) oscillations to self-paced simple index finger abduction movements in patients with writer's cramp and compared them with those of normal aged-matched controls. The changes in EEG oscillations were measured in predefined frequency bands (8-10, 10-12, 12-20, and 20-30 Hz) by using the event-related desynchronization technique. Movements of the affected and unaffected hand in patients with writer's cramp showed significantly less reduction in 20- to 30-Hz power compared with controls. The differences in movement-related EEG power decline were apparent over the contralateral central and midline regions before and after electromyographic onset. Because EEG beta rhythm in the sensorimotor region likely emanates from the motor cortex and is related to ongoing muscle activity, this abnormality could be a manifestation of the abnormal motor command at the cortical level.

Adult↗

The pathophysiology of essential tremor.

The pathophysiologic abnormalities that underlie essential tremor (ET) are difficult to decipher because autopsy studies reveal no gross or microscopic abnormalities. Electrophysiologic studies are consistent with a central source of tremorogenic oscillation. The inferior olive and cerebellum are implicated by PET studies. Harmaline tremor in animals shares many features with ET, and the inferior olive has been identified as the source of oscillation in this animal model. Therefore, a disturbance of olivocerebellar rhythmicity is at present the most popular hypothesis for the etiology of ET. Although electrophysiologic tests are available that are helpful in the diagnosis of ET, a gold-standard test or biologic marker for ET is still lacking.

Animals↗

Classical conditioning of the electrically elicited blink reflex in humans: a new method of data analysis.

The eyeblink conditioning paradigm is a well-established model to study learning processes in humans and animals. Especially results from animal studies have supplied new insight into physiological pathways and brain structures involved in associative motor learning and memory. An important role of the cerebellum and its afferent fiber systems could be shown. Recent studies in humans have given evidence that results of animal experiments can be applied directly to the human condition. A high variation of baseline EMG activity and/or spontaneous blinks may influence the analysis of classical conditioning of the electrically elicited blink reflex in humans. To optimize differentiation between real conditioned responses and stimulus-independent EMG activity, we developed an algorithm which is fully automated and independent of a possible bias of an examiner. In a first step the algorithm decides whether a subject fulfills the criteria of a successful learning process or not. The second step quantifies the learning process. For quantification of the learning process, the following parameters were calculated: number of conditioned responses, onset of conditioning, time and amount of maximal conditioning, speed of conditioning and speed of habituation. According to our criteria, 80% of the healthy volunteers acquired conditioned responses. There is an age-related decline in eyeblink classical conditioning. Analysis of patient groups with different types of lesions will further improve our knowledge and understanding of pathways involved in learning processes in humans. The proposed new algorithm of data analysis takes less than 10 s on a standard computer, is more sensitive and more specific in detecting conditioned responses and, therefore, may further improve the value and reliability of the eyeblink conditioning paradigm in clinical research.

Adult↗

Involvement of cranial muscles and high intermuscular coherence in orthostatic tremor.

Electromyographic recordings were conducted from limb, trunk, and cranial muscles in 6 patients with orthostatic tremor. Spectral analysis revealed a high-frequency tremor not only in the muscles of the limbs and trunk, but also in cranial muscles. The cross spectra were analyzed between various pairs of muscles that displayed a high-frequency tremor pattern. The resulting peak correlations were uniformly very high (near one) suggesting a high level of coherence. The involvement of cranial muscles suggests that supraspinal mechanisms are involved in the generation of orthostatic tremor. The high intermuscular coherence between all muscles indicates the existence of either a unique oscillator that generates tremor in all involved muscles on both sides of the body or a linking mechanism probably at a supraspinal level. The high-frequency tremor was only found when the muscles were contracted isometrically, irrespective of body posture. Thus, tremor generation might be more closely linked to mechanisms responsible for isometric force control than to those involved in stance regulation.

Aged↗

Function of the cerebellum in Parkinsonian rest tremor and Holmes' tremor.

We describe a patient who developed Parkinson's disease (PD) 17 years after resection of his right cerebellum because of a Lindau tumor. He showed a classic 4.3-Hz resting tremor on the left side but a 3.1-Hz resting, postural, and intention tremor on the right side compatible with midbrain tremor (Holmes' tremor). We conclude that the generator of the tremor in PD cannot be located within the olivocerebellar loop. The cerebellum, however, seems to modulate the tremor frequency of parkinsonian rest tremor and may prevent the rest tremor from transforming into a postural and goal-directed tremor.

Adult↗

Pathophysiology of chorea and bradykinesia in Huntington's disease.

This article reviews the neurophysiological abnormalities described in Huntington's disease. Among the typical features of choreic movements are variable and random patterns of electromyographic (EMG) activity, including cocontraction of agonist and antagonist muscles. Studies of premotor potentials show that choreic movements are not preceded by a Bereitschaftspotential, therefore demonstrating that choreic movement is involuntary. Early cortical median-nerve somatosensory-evoked potentials have reduced amplitudes and the reduction correlates with reduced glucose consumption in the caudate nucleus. Long-latency stretch reflexes evoked in the small hand muscles are depressed. These findings may reflect failed thalamocortical relay of sensory information. In Huntington's disease, the R2 response of the blink reflex has prolonged latencies, diminished amplitudes, and greater habituation than normal. These abnormalities correlate with the severity of chorea in the face. Patients with Huntington's disease perform simple voluntary movements more slowly than normal subjects and with an abnormal triphasic EMG pattern. Bradykinesia is also present during their performance of simultaneous and sequential movements. Eye movements show abnormalities similar to those seen in arm movements. In Huntington's disease, arm movement execution is associated with reduced PET activation of cortical frontal areas. Studies using transcranial magnetic stimulation show that patients with Huntington's disease have normal corticospinal conduction but some patients have a prolonged cortical silent period. Bradykinesia results from degeneration of the basal ganglia output to the supplementary motor areas concerned with the initiation and maintenance of sequential movements. The coexisting hyperkinetic and hypokinetic movement disorders in patients with Huntington's disease probably reflect the involvement of direct and indirect pathways in the basal ganglia-thalamus-cortical motor circuit.

Basal Ganglia↗

Animal models of tremor.

Animal models of tremor have been widely used in experimental neurology, because they are an indispensable requirement for understanding the pathophysiology of human tremor disorders and the development of new therapeutic agents. This review focuses on three approaches to produce tremor in animals (application of tremorgenic drugs, experimental central nervous system lesions, study of genetic mutants) and their use in simulating tremor syndromes of humans. Whereas harmaline induces a postural/kinetic tremor in animals that shares some features with human essential tremor/enhanced physiological tremor, MPTP tremor is the best model available for rest tremor in people. The tremor following experimental lesion of the ventromedial tegmentum in primates closely resembles Holmes tremor in humans, whereas cerebellar intention tremor is mimicked by cooling of the lateral cerebellar nuclei. The "campus syndrome," discovered in a breed of Pietrain pigs, might be a useful model of human orthostatic tremor. However, no animal model has yet been generated that exactly recreates all features of any of the known tremor disorders in humans. Problems encountered when comparing tremor in animals and humans include differing tremor frequencies and the uncertainty, if specific transmitter abnormalities/central nervous system lesions seen in animal tremor models are characteristic for their human counterparts. The search for adequate tremor models continues.

Animals↗

Differential diagnosis of tremor.

The differential diagnosis of tremor is based on the clinical distinction of rest, postural and intention tremor and the presence of additional clinical signs and data from the medical history. The most common pathological tremors are essential tremor and the tremors of Parkinson's disease. Among the patients with essential tremor those with intention tremor are often misdiagnosed as cerebellar tremors. Patients with monosymptomatic resting tremors represent a special subgroup of Parkinson's disease. Primary orthostatic tremor and dystonic tremor are rare clinical syndromes which have recently been well defined. Holmes' tremors are defined by their low frequency and the occurrence of resting and intention tremor. Palatal tremor can be separated into two subgroups. Psychogenic tremor can be diagnosed on the basis of clinical criteria. The gold standard of tremor differential diagnosis is still based on clinical criteria.

Diagnosis, Differential↗

A software for recording and analysis of human tremor.

For many diseases various methods for the diagnosis and treatment monitoring are available. Presently, such methods are not established for an investigation of tremor diseases, although the different forms of tremor are common neurological symptoms and occur frequently in various neurological diseases and also other conditions. We developed an easy-to-use application for tremor-analysis and recording, running under MS-Windows, that allows us to investigate different forms of tremor by advanced mathematical methods of time series analysis. The application is also applicable for users who are not familiar with these kind of advanced data analysis methods. It provides tools for the diagnosis and treatment monitoring under laboratory conditions, based on previously developed and established methods of spectral and cross spectral analysis of tremor and electromyographic time series.

Electronic Data Processing↗

Side-to-side correlation of muscle activity in physiological and pathological human tremors.

OBJECTIVE: Many tremors occur always or often bilaterally. The question arises whether this could be explained by a common source or commonly transmitting pathways or by bilaterally represented, independent structures with the same oscillatory properties. A similar tremor frequency does not provide sufficient information to clarify this question. METHODS: We analyze coherencies between surface electromyographies (EMG) to investigate if bilateral physiologic (PT), essential (ET), Parkinsonian (PD) and orthostatic (OT) tremors originate from a common source for both sides of the body. We show that commonly used techniques to test whether coherencies are significant could lead to false positive results for tremor EMGs. A new estimation procedure is proposed to test EMG tremor time series on their linear independence. We apply this test to bilateral tremors. RESULTS: All measured EMG-pairs in OT (n = 7) were highly coherent between both sides with reproducible coherency values of up to 0.99. All other investigated tremors, i.e. PT and enhanced physiological tremors (EPT, n = 117), ET (n = 76) and PD resting and postural tremors (n = 70) do not show a significant side-to-side correlation. CONCLUSIONS: This finding shows that the pathophysiologies of OT and other pathological tremors are definitely different. Either they have different origins or different kinds of transmitting pathways. The proposed method might also be used to investigate other electrophysiological data and is a helpful, easy to use investigation for a daily clinical routine.

Computer Simulation↗

Spontaneous oscillations of arterial blood pressure, cerebral and peripheral blood flow in healthy and comatose subjects.

Slow and rhythmic spontaneous oscillations of cerebral and peripheral blood flow occur within frequencies of 0.5-3 min-1 (0.008-0.05 Hz, B-waves) and 3-9 min-1 (0.05-0.15 Hz, M-waves). The generators and pathways of such oscillations are not fully understood. We compared the coefficient of variance (CoV), which serves as an indicator for the amplitude of oscillations and is calculated as the percent standard deviation of oscillations within a particular frequency band from the mean, to study the impairment of generators or pathways of such oscillations in normal subjects and comatose patients in a controlled fashion. With local ethic committee approval, data were collected from 19 healthy volunteers and nine comatose patients suffering from severe traumatic brain injury (n = 3), severe subarachnoid hemorrhage (n = 3), and intracerebral hemorrhage (n = 3). Cerebral blood flow velocities were measured by transcranial Doppler ultrasound (TCD), peripheral vasomotion by finger tip laser Doppler flowmetry (LDF), and ABP by either non-invasive continuous blood pressure recordings (Finapres method) in control subjects, or by direct radial artery recordings in comatose patients. Each recording session lasted approximately 20-30 min. Data were stored in the TCD device for offline analysis of CoV. For CoV in the cerebral B-wave frequency range there was no difference between coma patients and controls, however there was a highly significant reduction in the amplitude of peripheral B-wave LDF and ABP vasomotion (3.8 +/- 2.1 vs. 28.2 +/- 16.1 for LDF, p < 0.001; and 1.2 +/- 0.7 vs. 4.6 +/- 2.8 for ABP, p < 0.001). This observation was confirmed for spontaneous cerebral and peripheral oscillations in the M-wave frequency range. The CoV reduction in peripheral LDF and ABP oscillations suggest a severe impairment of the proposed sympathetic pathway in comatose patients. The preservation of central TCD oscillations argues in favor of different pathways and/or generators of cerebral and peripheral B- and M-waves.

Adult↗

From off-period dystonia to peak-dose chorea. The clinical spectrum of varying subthalamic nucleus activity.

The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's Disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons.

Adult↗

Surgical treatment of Parkinson's disease.

Ablative surgery and deep brain stimulation for Parkinson's disease can be performed in the thalamus, the pallidum and the subthalamic nucleus. The efficacy and safety of unilateral pallidotomy is well established. Deep brain stimulation has a lower morbidity and is preferred for bilateral surgery. The subthalamic nucleus presently seems to be the most promising target in advanced stage Parkinson's disease.

Electric Stimulation↗