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Biomedical subjects

D Kömpf

Publications and source records attributed to D Kömpf.

At least 37 records · Page 2Linked to original sources
PubMed1998

Visually induced reactivity in posterior cerebral artery blood flow.

To evaluate visually induced reactivity (VIR) in the posterior cerebral artery (PCA), mean flow velocities in the PCA were measured bilaterally in 35 normal subjects and in 17 patients with PCA territory infarctions, by means of transcranial Doppler ultrasound. After the individual PCA baseline flow was estimated, different visual stimuli were applied: on-off light, colored light, complex scene, and visual imagery task, and the CO2 test was administered. A sampling rate of 20 Hz was used, and the raw data were transferred to a computer. The baseline flow and the maximum flow increase were calculated with a specially designed program. In control subjects, the on-off light stimulus induced a mean increase in PCA flow velocities of 21.5+/-6.4%, and colored light induced an increase of 22.3+/-6.3%. Complex scenes significantly elevated VIR more than light and colored light, with a mean increase of 28.8+/-6.8% (p < 0.05). Mental imagery had no significant effect on PCA flow velocities. There was no significant difference in flow between the right and left PCA in healthy subjects. In patients with PCA territory infarctions with homonymous hemianopsia or quadrantanopsia, there was a marked decrease of VIR and CO2 reactivity on the affected side corresponding to the extent of PCA territory infarction. Visual stimuli increased blood flow velocity bilaterally in the PCA, which supply the visual cortex and visual association area. This noninvasive test seems to be well suited to normal subjects and to patients with vascular disorders affecting the PCA.

Adult↗
PubMed1997

Double-blind crossover study with physostigmine in patients with degenerative cerebellar diseases.

OBJECTIVE: To determine whether treatment with physostigmine can improve the conditions of patients with ataxia. DESIGN: A double-blind crossover study with physostigmine was performed in 19 patients with degenerative cerebellar diseases. SETTING: Patients were selected from an ongoing prospective follow-up study at the university hospital in Lübeck, Germany. PATIENTS: Eleven patients with autosomal dominant cerebellar ataxia and 8 patients with idiopathic cerebellar ataxia. INTERVENTION: Physostigmine was administered by using a transdermal system (patch) containing 30 mg of physostigmine as a base, of which about 6 mg is released during 24 hours along a diffusion gradient. Each treatment phase with the physostigmine patch or the placebo lasted 4 weeks, after which the treatment of patients was crossed over to the other phase. MAIN OUTCOME MEASURES: Ataxia was documented and quantified by using a clinical score and posturographic measures. RESULTS: Physostigmine patches had no significant effect on cerebellar symptoms. CONCLUSION: Treatment with physostigmine does not improve the conditions of patients with ataxia.

Cerebellar Ataxia↗
PubMed1997

Slow saccades and other eye movement disorders in spinocerebellar atrophy type 1.

In order to study the relation between genotype and phenotype, a detailed study of the course of oculomotor deficits was performed in three patients with autosomal-dominant cerebellar ataxia, subtype spinocerebellar atrophy type 1 (SCA 1) using clinical testing and electrooculography. DNA analysis revealed a CAG repeat expansion of 65 in the SCA 1 gene on chromosome 6p in all patients. A progressive disorder of the saccadic system became obvious, leading to a marked slowing of saccadic eye movements and loss of pathological and physiological nystagmus. An upward gaze palsy developed early, followed by horizontal and downward gaze palsy at a later state of the disease. Smooth pursuit eye movements were disturbed to a lesser extent; the vestibulo-ocular reflex was reduced. As an additional feature, severe loss of visual acuity developed due to progressive optic nerve atrophy. The oculomotor deficits can be explained by progressive damage to the brain stem rather than to the cerebellum. Each combination of oculomotor deficits with or without optic atrophy may occur irrespective of the gene locus of the disease, making a correlation between clinical signs and genetic findings difficult.

Adult↗
PubMed1997

A study of visual hallucinations in patients with Parkinson's disease.

In a hospital-based case-control study 29 patients with idiopathic Parkinson's disease (PD) and visual hallucinations (VH) were compared with 58 PD patients matched for age and disease duration, but without VH. VH patients had more frequently sleep disturbances and dementia, higher PD-related disability (Schwab-England scale), and took selegiline more frequently as an anti-Parkinsonian drug. The patient groups did not differ in age at PD onset, Webster score, treatment duration, dosage of any anti-Parkinsonian drug, frequency of levodopa-associated movement disorders, or measures on brain CT. After a median follow-up period of 27 months more VH patients had developed wearing-off and freezing phenomena, while their scores in the Mini Mental State Examination were lower. Nursing home placement during the follow-up period was associated with higher PD-related disability in VH patients.

Aged↗
PubMed1997

Event-related potentials suggest slowing of brain processes in generalized epilepsy and alterations of visual processing in patients with partial seizures.

Event-related potentials were recorded in two auditory tasks and in one visual task from 13 patients with partial seizures (PS), 12 patients with idiopathic generalized epilepsy (IGE), and healthy age-matched participants. IGE patients had delayed latencies in the auditory tasks, with the delay being reliable already at N1, and continuously increasing at N2b and at P3. The P3 delay correlated with duration of epilepsy both in IGE and in PS patients. In the visual task, the posterior N2 was delayed in PS patients, in particular in PS patients with temporal focus. Resembling the delays as found in healthy elderly adults, the delays with auditory stimuli might reflect a slowing of brain processes as it occurs in healthy aging. The isolated delay of posterior N2 in temporal PS patients might indicate a specific impairment of the occipito-temporal visual pathway. Taken together, event-related potentials prove to be a very sensitive instrument for measuring altered brain functioning in epileptic patients, when compared to measurement of overtly visible responses.

Adult↗
PubMed1997

[CADASIL: 2 case reports of hereditary multi-infarct dementia].

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary stroke disease linked to chromosome 19 q 12. We report on two families affected by this disease, which is characterised by recurrent subcortical ischaemic strokes, progressive pseudobulbar palsy, and presenile dementia. Neuroimaging revealed multiple deep infarcts and diffuse leukoencephalopathy. Diagnosis of CADASIL based on the typical clinical feature without vascular risk factors, the neuroradiological signs of extensive leukoencephalopathy, and the autosomal dominant pattern of inheritance. CADASIL might be an underestimated cause of familial stroke and should be considered in the differential diagnosis of hereditary stroke.

Brain↗
PubMed1997

Responses to cued signals in Parkinson's disease. Distinguishing between disorders of cognition and of activation.

Impairment of movement execution in Parkinson's disease could be due to disorders of cognition and/or of activation. These two factors are hard to separate by measuring response times only. Therefore, in this study response force and event-related EEG potentials were measured continuously during tasks in which subjects had to respond to cued signals. Fifteen patients with Parkinson's disease and 15 healthy subjects were studied during two tasks: (i) the 'clock task', in which the signal's identity was fully precued but its presentation time was uncertain and (ii) the 'validity task' in which the cue did not always predict the response validly. Thus, the clock task required more sustained attention, and the validity task sometimes required fast switching. The patients generally responded slower than control subjects. In the clock task, the response times of both groups changed to the same extent with presentation time, whereas in the validity task the patients were additionally slower than the control group with invalidly cued signals. The patients generally had a weaker response force and a lower rate of force production. In the clock task, both force measures changed with presentation time in the control group only, whereas in the validity task, the two measures increased in both groups to the same extent with invalidly cued signals. The contingent negative variation amplitudes in the patients' event-related EEG potentials were reduced, reflecting reduced activation of movement preparation, whereas lateralization of the motor cortices (i.e. the lateralized readiness potential) did not differ significantly between groups, reflecting unimpaired response selection. Force and contingent negative variation were generally reduced in the patients showing that their general slowing is at least partially due to impaired activation. Task-specific problems added to the general activation deficit; the lack of modulation of response force by presentation time revealed pronounced deficits of activation in the monotonous clock task. The specific delay of responses with invalidly cued signals, unparalleled by activation measures, might suggest a problem of cognition. The task-specific deficits may reflect a basic dilemma for patients with Parkinson's disease: cognitive problems may arise in complex tasks but disorders of activation may become pronounced in more simple, monotonous tasks.

Adult↗
PubMed1997

The diagnosis of 'essential palatal tremor'.

We report a patient with a 30-year history of progressive, involuntary movements of the left ear and clicking sounds in both ears for 2 years. The patient had rhythmic contractions of the tensor veli palatini muscle and could relieve palatal movements and ear clicks, but not ear movements, by pressing a pillow against the left ear or by finger pressure on the tragus or the retroauricular region. We discuss the significance of these sensory tricks and the nosology of the long-standing ear movements within a classification of essential and symptomatic palatal tremor. Current diagnostic criteria for both types of palatal tremor may not cover some atypical cases such as ours.

Aged↗
PubMed1997

Apraxia of eyelid opening after bilateral stereotaxic subthalamotomy.

The case of a patient with apraxia of eyelid opening and blepharospasm occurring during the course of idiopathic torsion dystonia and previously treated with stereotaxic subthalamotomy is presented. The anatomic basis of this lid movement disorder is suggested to be located in the rostral brain stem. There was a considerable amelioration after treatment with trihexyphenidyl.

Adult↗
PubMed1996

Salsolinol, catecholamine metabolites, and visual hallucinations in L-dopa treated patients with Parkinson's disease.

We could quantify the tetrahydroisoquinoline derivative salsolinol in urine of patients with Parkinson's disease and normal control subjects by means of high performance liquid chromatography and electrochemical detection. Urine levels of salsolinol were positively related to the homovanillic acid/3-O-methyl-dopa ratio in the cerebrospinal fluid that reflects dopamine metabolism. In the patient group with visual hallucinations, mean salsolinol level was significantly increased to almost the 3-fold of those found in patients without hallucinations. Since the daily L-dopa doses of both patient groups were nearly identical this result is not due to different L-dopa medications. Additionally, either high values of the main serotonin metabolite, 5-hydroxyindole acetic acid (HIAA) or the L-dopa/3-O-methyl-dopa ratio were found in cerebrospinal fluid of patients with hallucinations. The enhanced salsolinol levels in patients with visual hallucinations seem to be due to an overloaded dopaminergic pathway with an imbalance between dopaminergic and serotonergic systems. Thus, salsolinol appears as a predictor for hallucinosis in Parkinson's disease.

Aged↗
PubMed1996

On-line brain potential correlates of right parietal patients' attentional deficit.

EEG potentials evoked by cues and targets were recorded in Posner's visual cueing task from 10 patients with lesions of the right parietal cortex and from age-matched healthy subjects. The patients' N1 component evoked by left-side cues was reduced at the right-parietal recording site, suggesting a general impairment in processing left-side visual input. As usual, patients' keypress responses were delayed when left targets were preceded by right cues. There were two correlates of this delay in the patients' EEG potentials evoked by the critical combination of right cue/left target: their mean amplitude 160-280 ms after target onset ('Nd') was less negative than with other combinations of cue and target, and the following frontal P300 was enhanced. The Nd reduction seems to be an on-line measure of patients' momentary decrease of attention for the left hemifield, while the frontal P300 might reflect the patients' attempts at reorienting. In conclusion, different components were sensitive to different aspects of the patients' disorder, suggesting the utility of this approach for developing detailed hypotheses on the mechanisms of attentional deficits involved in visual extinction and neglect.

Aged↗
PubMed1996

Deficits of smooth pursuit eye movements after frontal and parietal lesions.

To assess the contribution of the human frontal and parietal cortices to smooth pursuit (SP) eye movements, we recorded ocular motor responses to predictable (periodic) and unpredictable (step-ramp) foveal pursuit stimuli and to constant-velocity optokinetic full-field motion in 31 patients with chronic focal unilateral hemispheric lesions and in 50 age-related healthy adults, using infrared reflection oculography. Lesions were located either in the posterior parietal cortex (PPC), leaving the visual fields largely intact, or in the region of the frontal eye fields (FEF), the dorsolateral prefrontal cortex (PFC) or the supplementary motor area (SMA). We found (i) directional deficits in terms of lower pursuit velocities with ipsiversive target motion, more pronounced with predictable than with step-ramp stimuli, in patients with FEF lesions more frequently (in each of the four cases) than in patients with PPC lesions (in four out of 13 cases with foveal and in eight out of 13 cases with optokinetic stimulation); (ii) a relatively prolonged latency of direction reversal with periodic constant-velocity stimuli after SMA lesions (three cases), implying impaired anticipation of the target trajectory; (iii) no SP deficits following selective prefrontal lesions (eight cases); (iv) in some patients with PPC lesions (four out of 13) retinotopic deficits of SP initiation in both horizontal directions when step-ramp stimuli started in the contralesional hemifield, including prolonged pursuit latencies, which were independent of contralateral visual hemineglect. Directional and retinotopic SP deficits in patients with PPC lesions corresponded to SP deficits after unilateral lesions of middle temporal (MT) and medial superior temporal (MST) cortex in the monkey, and occurred only when lesions included the junction of Brodmann areas 19, 37 and 39, where the human homologues of MT and MST are assumed to lie. In conclusion, human SP eye movements are controlled, as in non-human primates, by a network of frontal and posterior cortical areas. Selective damage to each of these areas impairs specific SP subfunctions, reflecting subsequent stages of cortical processing from visual motion input to SP-related motor output.

Adult↗
PubMed1996

Basilar artery blood flow during head rotation in vertebrobasilar ischemia.

PATIENTS AND METHODS: Forty-six patients with vertebrobasilar ischemia and 40 control subjects were examined during head rotation using transcranial Doppler ultrasonography. RESULTS: In the control group, no difference in blood flow velocity through the BA was found between the neutral and rotated positions. Based on these data, a blood flow reduction in the BA of more than 20% was considered to be significantly abnormal (p < 0.01). In three of 46 patients no signal was detectable in the BA using TCD. The reduction in blood flow velocity through the BA during head rotation was strongly dependent on the condition of the VA; none of 23 patients without atherosclerotic lesions or hypoplasia of the VA developed a significant reduction in blood flow through the BA. Two of 11 patients with unilateral VA lesions had significantly reduced blood flow in the BA (27% and 31%), although both were asymptomatic. Five of nine patients with bilateral VA lesions showed a significant reduction in blood flow through the BA (mean = 52%, minimum = 30%), and four of these developed clinical symptoms such as vertigo or diplopia during the rotation maneuver. CONCLUSION: These data suggest that patients with uni- or bilateral lesions of the VA are at risk for developing clinically relevant reductions in blood flow through the BA during head rotation. Because not all patients with VA lesions developed reduced blood flow velocity, we conclude that individual vascular mechanisms must play an important compensatory role.

Adult↗