Search PubMed⌕ Search

Biomedical subjects

M Dieterich

Publications and source records attributed to M Dieterich.

At least 73 records · Page 4Linked to original sources
PubMed1998

Horizontal or vertical optokinetic stimulation activates visual motion-sensitive, ocular motor and vestibular cortex areas with right hemispheric dominance. An fMRI study.

The differential effects of optokinetic stimulation with and without fixation suppression were analysed in an fMRI study in 10 right-handed healthy subjects. Horizontal and vertical small-field optokinetic stimulation activated the same multiple visual, ocular motor and vestibular cortical and subcortical areas in both hemispheres. The extent of activation in each hemisphere was independent of the stimulus direction. All activated areas representing cortical (occipitotemporal cortex, posterior parietal cortex, precentral and posterior median frontal gyrus, prefrontal cortex, medial part of the superior frontal gyrus) and subcortical (caudate nucleus, putamen, globus pallidus and paramedian thalamus) ocular motor structures were activated during optokinetic stimulation as well as during fixation suppression of optokinetic nystagmus. However, the activation was significantly stronger with optokinetc nystagmus compared with fixation suppression. The only relatively increased activity during fixation suppression was seen in the medial part of the superior frontal gyrus (supplementary eye field) and the anterior cingulate gyrus. The anterior insula and the posterior insula (human homologue of the parieto-insular vestibular cortex) were activated during optokinetic nystagmus but not during fixation suppression. A significant right hemispheric predominance (regardless of stimulus direction) was found under both conditions in the visual motion-sensitive and ocular motor areas of the cortex, except the supplementary eye field and anterior cingulate gyrus. This was most prominent in the occipitotemporal cortex, but did not occur in the primary visual cortex and in subcortical ocular motor structures (putamen, globus pallidus and caudate nucleus). Thus, cortical and subcortical activation patterns did not differ for horizontal and vertical optokinetic stimulation, and there was distinct right-hemisphere dominance for visual motion-sensitive and cortical ocular motor areas and the thalamus. Fixation suppression of optokinetic nystagmus yielded four different results: (i) increased activation in the supplementary eye field and anterior cingulate gyrus; (ii) unchanged activation in the visual cortex; (iii) decreased activation in most of the ocular motor areas; and (iv) suppressed activation in the anterior and posterior insula and the thalamus. Activation of the parieto-insular vestibular cortex may be related to ocular motor function rather than self-motion perception.

Adult↗
PubMed1998

Reciprocal inhibitory visual-vestibular interaction. Visual motion stimulation deactivates the parieto-insular vestibular cortex.

The vestibular system--a sensor of head accelerations--cannot detect self-motion at constant velocity and thus requires supplementary visual information. The perception of self-motion during constant velocity movement is completely dependent on visually induced vection. This can be linear vection or circular vection (CV). CV is induced by large-field visual motion stimulation during which the stationary subject perceives the moving surroundings as being stable and himself as being moved. To determine the unknown cortical visual-vestibular interaction during CV, we conducted a PET activation study on CV in 10 human volunteers. The PET images of cortical areas activated during visual motion stimulation without CV were compared with those with CV. Hitherto, CV was explained neurophysiologically by visual-vestibular convergence with activation of the vestibular nuclei, thalamic subnuclei and vestibular cortex. If CV were mediated by the vestibular cortex, one would expect that an adequate visual motion stimulus would activate both the visual and vestibular cortex. Contrary to this expectation, it was shown for the first time that visual motion stimulation with CV not only activates a medial parieto-occipital visual area bilaterally, separate from middle temporal/medial superior temporal areas, it also simultaneously deactivates the parieto-insular vestibular cortex. There was a positive correlation between the perceived intensity of CV and relative changes in regional CBF in parietal and occipital areas. These findings support a new functional interpretation: reciprocal inhibitory visual-vestibular interaction as a multisensory mechanism for self-motion perception. Inhibitory visual-vestibular interaction might protect visual perception of self-motion from potential vestibular mismatches caused by involuntary head accelerations during locomotion, and this would allow the dominant sensorial weight during self-motion perception to shift from one sensory modality to the other.

Adult↗
PubMed1998

Alternating episodes of vestibular nerve excitation and failure.

Recurrent episodes of oscillopsia, rotational vertigo, and postural imbalance were elicited and modulated by changing the horizontal head positions of a patient with an arachnoid cyst in the right cerebellopontine angle that distorted the vestibulocochlear nerve. Oculomotor analysis revealed two different types of attacks depending on the particular head position: 1) episodes of vestibular hypofunction (minutes to several hours) with normal head position and 2) paroxysmal vestibular excitation (seconds) with head rotation to the left. The most likely cause is a transition from conduction block to ectopic discharges, which occurs when various peripheral nerves are compressed. One week after resection of the cyst and decompression of the eighth cranial nerve the patient was symptom free, and the electronystagmogram was normal.

Arachnoid Cysts↗
PubMed1997

["Zurich Vertigo Meeting"--phobic postural vertigo].

Phobic postural vertigo has been described as a syndrome that is distinguishable from agoraphobia, acrophobia, and "space phobia". Closely related to locomotion, it is characterized by a combination of nonrotational vertigo with subjective postural and gait instability mainly in patients with an obsessive-compulsive personality. The monosymptomatic disturbance of balance manifests with superimposed attacks that occur with and without recognizable provoking factors in the same patient and are experienced with and without accompanying excess anxiety, misleading both patient and physician to a false diagnosis of organic disease.

Diagnosis, Differential↗
PubMed1997

Galvanic vestibular stimulation in humans: effects on otolith function in roll.

The effects of unilateral galvanic vestibular stimulation on (1) ocular torsion, (2) subjective tilt of the peripheral visual field, and (3) subjective tilt of a foveal vertical line were measured in 12 healthy subjects. A rectangular, unipolar binaural electric current was applied to the subject' s mastoid. Anodal stimulation of the right mastoid led to an ipsiversive tonic ocular torsion (0.5-3.7 degrees) and to a contralateral tilt of both the peripheral visual field (1-9 degrees), and a foveal vertical line (0.5-6.2 degrees). There was a correlation between the amount of the three measured parameters and the strength of the applied current. Static ocular torsion, central and peripheral visual tilts represent stimulus-induced tonic otolith imbalance between the two labyrinths. Thus, galvanic vestibular stimulation not only affects dynamic semicircular canal input but also static otolith input in the roll plane.

Adult↗
PubMed1997

Drug therapy for acquired pendular nystagmus in multiple sclerosis.

Acquired pendular nystagmus (APN) is regularly accompanied by oscillopsia and impairment of static visual acuity. Therapeutic approaches to APN remain controversial, and there is no generally accepted therapeutic approach. We tested 14 patients who had suffered from APN caused by multiple sclerosis for several years; 12 patients presented with fixational pendular nystagmus (increasing during fixation) and 2 with spontaneous pendular nystagmus. All 11 patients with fixational pendular nystagmus who were given memantine, a glutamate antagonist, experienced complete cessation of the nystagmus. In contrast, scopolamine caused no (6 of 8) or only a minor (10-50%) reduction of the nystagmus (2 of 8). It was concluded that memantine is a safe treatment option for APN.

Adult↗
PubMed1997

Course of illness in phobic postural vertigo.

Forty-two patients with phobic postural vertigo took part in a neurological and psychiatric follow-up study. During the follow-up time of about 2.5 years the neurological diagnosis remained stable (41 of 42 patients). PPV can be assigned to various psychiatric categories according to DSM-III-R. Although an association of PPV with anxiety disorders is evident, not all patients present with symptoms of anxiety or panic during attacks of vertigo. However most patients develop a disabling "phobic-avoidance pattern" with recurrent attacks. Important psychosocial stressors can be identified at the onset of the condition. Motives of secondary gain have also to be taken into consideration. The course of illness varies depending on the neurological syndrome of vertigo, on the one hand, and concomitant psychopathological syndromes, on the other. Despite a considerable rate of improvement in vertigo complaints (79%), the group of patients with phobic postural vertigo as a whole presented with significant psychological problems at follow-up term (74%), requiring specific psychiatric and/or psychotherapeutic interventions. Dependent or avoidant personality, and hypochondria were prognostic of a more negative course of illness.

Adult↗
PubMed1997

Sensorimotor cerebral activation during optokinetic nystagmus. A functional MRI study.

Self-motion or object motion can elicit optokinetic nystagmus (OKN), which is an integral part of dynamic spatial orientation. We used functional MR imaging during horizontal OKN to study cerebral activation patterns in sensory and ocular motor areas in 10 subjects. We found activation bilaterally in the primary visual cortex, the motion-sensitive areas in the occipitotemporal cortex (the middle temporal and medial superior temporal areas), and in areas known to control several types of saccades such as the precentral and posterior median frontal gyrus, the posterior parietal cortex, and the medial part of the superior frontal gyrus (frontal, parietal, and supplementary eye fields). Additionally, we observed cortical activation in the anterior and posterior parts of the insula and in the prefrontal cortex. Bilateral activation of subcortical structures such as the putamen, globus pallidus, caudate nucleus, and the thalamus traced the efferent pathways of OKN down to the brainstem. Functional MRI during OKN revealed a complex cerebral network of sensorimotor cortical and subcortical activation.

Adult↗
PubMed1996

Deactivation of human visual cortex during involuntary ocular oscillations. A PET activation study.

Prompted by the observation of decreased glucose metabolism in the striate and extrastriate visual cortex in a patient with opsoclonus, we studied the influence of involuntary eye movements on visual cortex activity. Repeated measurements of cerebral blood flow (CBF) by PET were performed in 12 healthy volunteers using H2(15)O-bolus technique after ear canal irrigation with ice cold or warm (44 degrees C) water with the subjects eyes closed. In addition to blood flow increases in areas involved in central vestibular processing, statistical subtraction analysis revealed a nearly symmetrical, bilateral, highly significant decrease in the occipital cortex covering Brodmann areas 17, 18, and 19 after ice water stimulation of either ears. Region of interest analysis revealed in all subjects a mean decrease in regional CBF (rCBF) of 12.8% (range 4.6-21.0%) in these areas. A similar but less pronounced effect (mean rCBF decrease in visual cortex 4.8%, range 1.1-11.5%) was observed after warm water irrigation. The observations suggest that deactivation of the visual cortex is induced by involuntary ocular oscillations. This deactivation is not dependent on changes of the retinal input (eyes closed). The physiological significance of this hitherto unknown phenomenon may be the protection from inadequate visual input (oscillopsia) during involuntary ocular oscillations.

Adult↗
PubMed1996

Torsional nystagmus during vertical pursuit.

We examined three patients with cavernous angioma within the middle cerebellar peduncle. Each patient had an unusual ocular motor finding: the appearance of a strong torsional nystagmus during vertical pursuit. The uncalled-for torsion changed direction when vertical pursuit changed direction. In one patient, we recorded eye movements with the magnetic field technique using a combined direction and torsion eye coil. The slow-phase velocity of the inappropriate torsional nystagmus was linearly related to the slow-phase velocity of vertical smooth pursuit, and changed direction when vertical pursuit changed direction. This torsional nystagmus also appeared during fixation suppression of the vertical vestibulo-ocular reflex (VOR), but was minimal during vertical head rotation when fixing a stationary target in the light. We suggest that inappropriately directed eye movements during pursuit might be another ocular motor sign of cerebellar dysfunction. Furthermore, we speculate that the signals used for vertical smooth pursuit are, at some stage, encoded in a semicircular canal VOR coordinate framework. To illustrate, for the vertical semicircular canals, vertical and torsional motion are combined on the same cells, with the anterior semicircular canals mediating upward movements and the posterior semicircular canals mediating downward movements. For the right labyrinth, however, both vertical semicircular canals produce clockwise slow phases (ipsilateral eye intorts, contralateral eye extorts). The opposite is true for the vertical semicircular canals in the left labyrinth; counterclockwise slow phases are produced. Hence, to generate a pure vertical VOR, the anterior or posterior semicircular canals on both sides of the head must be excited so that opposite-directed torsional components cancel. Thus, if pursuit were organized in a way similar to the VOR, pure vertical pursuit would require that oppositely-directed torsional components cancel in normals. If this did not happen, a residual torsional nystagmus could appear during attempted vertical pursuit.

Adult↗
PubMed1995

Vestibulo-ocular reflex.

Recent animal and clinical studies on the vestibulo-ocular reflex deal with a number of physiological and clinical aspects from which three were chosen for this review: (1) the torsional vestibulo-ocular reflex and its disorders; (2) the otolith contribution to the vestibulo-ocular reflex; and (3) neurotransmitters, neuropharmacological aspects, and medical treatment. Disorders of the vestibulo-ocular reflex can be classified according to the three major planes of action, yaw plane, pitch plane, and roll plane, which equate with horizontal nystagmus, upbeat or downbeat nystagmus, and torsional nystagmus, respectively. The particular interest in the torsional vestibulo-ocular reflex arises from new methods for measuring ocular torsion, especially the three-dimensional eye-movement recordings with scleral coils. These methods make it possible to do three-dimensional analysis of the differential effects of horizontal and vertical semicircular canal function and their individual disorders of the torsional vestibulo-ocular reflex. Otolith and semicircular canal inputs converge at the level of the vestibular nuclei to subserve static graviceptive and dynamic torsional and pitch function. The elaboration of the particular sensorial weight of the input from either the otoliths or the semicircular canal is currently a challenge for both physiologists and neurologists. Disorders of otolith function, still absent from the diagnostic repertoire of most neurologists, are increasingly being reported. The most promising developments in therapeutic measures may come from research on vestibular neurotransmitters, their agonists and antagonists. A number of pharmacological agents are effective suppressants of pathological eye movements. However, systematic prospective studies are needed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Rotational vertigo in embolic stroke of the vestibular and auditory cortices.

We describe the unique case of a woman with embolic infarction within the right middle cerebral artery territory who had nonepileptic rotational vertigo, nausea, and unsteady gait that gradually resolved within a week. A well-demarcated lesion of the posterior insula (homologous to parieto-insular vestibular cortex in monkeys) was probably the cause. This is supported by a contraversive tilt of perceived vertical and by involvement of the adjacent auditory (Heschl's) cortex. Dipole source analysis of late auditory evoked potentials revealed a decreased amplitude of a dipole source in the right insular cortex, whereas two other dipoles situated in the temporal lobe showed symmetric activity.

Acoustic Stimulation↗
PubMed1994

Vestibular cortex lesions affect the perception of verticality.

Seventy-one patients with unilateral supratentorial infarctions were evaluated with respect to static vestibular function in the roll plane, including determinations of the subjective visual vertical, skew deviation, and ocular torsion. Since animal studies have revealed at least four different areas of the parietal and temporal cortex involved in vestibular function, we tried to identify cortical areas in humans responsible for vestibular function in the roll plane. Infarcted areas, as demonstrated in magnetic resonance and computed tomography scans, were projected onto the appropriate sections of an atlas of the human brain. Infarctions in the territories of the posterior and anterior cerebral arteries did not affect static vestibular function in roll. Twenty-three of 52 patients with infarctions in the middle cerebral artery territory showed significant (p < 0.0005), mostly contraversive, pathological subjective visual vertical tilts. The overlapping area of these infarctions centered on the posterior insula, probably homologous to the parieto-insular vestibular cortex in the monkey. Although electrophysiological and cytoarchitectonic data in animals demonstrate several multisensory areas rather than a single primary vestibular cortex, the parieto-insular vestibular cortex seems to represent the integration center of the multisensory vestibular cortex areas within the parietal lobe.

Adolescent↗
PubMed1994

Vestibular syndromes in the roll plane: topographic diagnosis from brainstem to cortex.

Central vestibular syndromes may be classified according to the three major planes of action of the vestibuloocular reflex, secondary to a lesional tone imbalance in either the horizontal yaw plane or the vertical pitch or roll plane. The clinical signs, both perceptual and motor, of a vestibular tone imbalance in the roll plane are ocular tilt reaction (OTR), ocular torsion, skew deviation and tilts of the perceived visual vertical (SVV). Either complete OTR or skew torsion without head tilt indicates a unilateral peripheral deficit of otolith input or a unilateral lesion of graviceptive brainstem pathways from the vestibular nuclei (crossing midline at the pontine level) to the interstitial nucleus of Cajal (INC) in the rostral midbrain. SVV tilts are the most sensitive sign of a vestibular tone imbalance in roll and occur with peripheral or central vestibular lesions from the labyrinth to the vestibular cortex. All tilt effects, perceptual, ocular motor and postural, are ipsiversive (ipsilateral eye undermost) with unilateral peripheral or pontomedullary lesions below the crossing of the graviceptive pathways. All tilt effects are contraversive (contralateral eye undermost) with unilateral pontomesencephalic brainstem lesions and indicate involvement of the medial longitudinal fasciculus or the rostral midbrain (INC). Unilateral lesions of vestibular structures rostral to the INC typically manifest with deviations of perceived vertical without concurrent eye-head tilt. OTR in unilateral paramedian thalamic infarctions indicates simultaneous ischemia of the paramedian rostral midbrain including the INC. Unilateral lesions of the posterolateral thalamus can cause thalamic astasia and moderate ipsiversive or contraversive SVV tilts, thereby indicating involvement of the vestibular thalamic subnuclei. Unilateral lesions of the parietoinsular vestibular cortex cause moderate, mostly contraversive SVV tilts. An SVV tilt found with monocular but not with binocular viewing is typical for a trochlear or oculomotor palsy rather than a supranuclear graviceptive brainstem lesion.

Brain↗
PubMed1994

Phobic postural vertigo: a first follow-up.

Seventy-eight patients with phobic postural vertigo (PPV) and 17 patients with psychogenic disorder of stance and gait (PSG) were asked to evaluate their condition 6 months to 5.5 years after their original referral and short-term psychotherapy. Two results seem most important: (1) PPV had a favorable course with a 72% improvement rate (22% of patients becoming symptom free), whereas the majority of patients with PSG (52%) remained unchanged; (2) the majority of patients with PPV experienced complete remission or considerable improvement even if their condition had lasted between 1 and 20 years prior to diagnosis. Complete remission of PSG was observed only if the disorder has been present less than 4 months; there was no improvement if it had lasted longer than 2 years. PPV can be defined as a distinct clinical entity with a relatively benign course. It can be reliably diagnosed on the basis of typical features.

Adult↗