PubMed Health⌕ Search

Biomedical subjects

M Dieterich

Publications and source records attributed to M Dieterich.

At least 19 recordsLinked to original sources
PubMed1999

Increased body sway at 3.5-8 Hz in patients with phobic postural vertigo.

Postural sway during upright stance was analyzed in 12 patients with phobic postural vertigo (PPV) and in 12 age-matched healthy volunteers. Recordings were made under different conditions (with the eyes open or closed): when standing on a foam rubber pad with the head upright, turned 30 degrees to the right or left, or during 1 Hz horizontal head oscillations. Sway analysis included calculation of sway path, of root mean square values of sway and of the power spectrum of sway in fore/aft and lateral directions. There was a significant increase in sway activity in the 3.53-8 Hz frequency band in patients with PPV. This did not impair objective postural stability. Increase in higher frequency sway activity may simply reflect a change in postural strategy rather than a sensorimotor dysfunction. The patients' conscious control of stance may augment co-activation of anti-gravity muscles, a strategy applied by normal subjects when performing demanding balancing tasks.

Adult↗
PubMed1999

Sympathetic contralateral vestibulopathy after unilateral zoster oticus.

A unique case of initially right sided varicella zoster induced Ramsay-Hunt syndrome with complete vestibular loss is reported. The patient subsequently developed deficits of the left vestibule 5 months later. An autoimmune pathogenesis of the left vestibular failure rather than bilateral varicella zoster infection was suggested by the following data: (1) no evidence of vesicular eruptions on the left auricle and the virtual absence of antiviral antibodies after onset of bilateral vestibulopathy; (2) prompt response of the left vestibule to immunosuppressive therapy with corticosteroids; and (3) presence of atypical nervous tissue specific autoantibodies against a 45 kDa protein.

Adult↗
PubMed1998

Three-dimensional modeling of static vestibulo-ocular brain stem syndromes.

Static vestibulo-ocular brain stem syndromes characterized by skew deviation, a vertical disconjugacy of the eyes, and ocular torsion are the result of a vestibular tone imbalance in the frontal (roll) plane. Similar physiological changes in static eye position, ocular counter-roll and conjugated deviations of vertical eye position, are caused by the influence of gravity mediated by the utricles. These observations prompted our approach with the model described here: based on the known deviations of static eye position, we devised a three-dimensional mathematical model of otolith-ocular function including detailed brain stem anatomy. This model is able to explain and predict the differential effects of unilateral and bilateral peripheral or central vestibular lesions on static eye position in roll, pitch, and yaw planes.

Animals↗
PubMed1998

Highly variable distribution of HSV-1-specific DNA in human geniculate, vestibular and spiral ganglia.

Viral reactivation in temporal ganglia is the suspected cause of Bell's palsy, vestibular neuritis and sudden hearing loss. Since the distribution of latent herpes simplex type 1 (HSV-1) in geniculate, vestibular and spiral ganglia of individual human temporal bones could have implications for the explanation of isolated as well as combined disorders of these three cranial nerves, we examined these ganglia in 18 human temporal bones of adults by nested polymerase chain reaction. In all of the temporal bones HSV-1 specific DNA was detected: 10/18 (56%) of the geniculate, 11/18 (61%) of the vestibular and 9/18 (50%) of the spiral ganglia samples were positive. All combinations of positive and negative ganglia were found in individual temporal bones at roughly equal frequencies. These data support a viral etiology of all three conditions, especially their occasional combinations.

Adult↗
PubMed1998

Bilateral vestibular failure impairs visual motion perception even with the head still.

Visual motion perception of a single object, moving with a constant angular velocity of 40 min of arc/s in four orthogonal directions, was measured in eight patients with chronic bilateral vestibular failure (BVF) with the head stationary. Perception of object motion was more severely impaired for horizontal than for vertical directions and the impairment was more pronounced in the dominant eye than the nondominant eye. Impaired motion perception in patients with BVF is best explained by a central visual mechanism that suppresses oscillopsia due to the involuntary retinal slip caused by the defective vestibulo-ocular reflex (VOR). This mechanism cannot be switched off with the head stationary (inactive VOR) and thus causes a measurable deficit of motion perception.

Adult↗
PubMed1998

Direction-specific impairment of motion perception and spatial orientation in downbeat and upbeat nystagmus in humans.

Downbeat and upbeat nystagmus can be classified as central vestibular syndromes in the vertical (pitch) plane of the vestibulo-ocular reflex (VOR) which are defined by ocular motor, perceptual, and postural manifestations. While the ocular motor syndrome was often studied investigations on the perceptual consequences for spatial orientation and motion perception are rare. Subjective visual straight ahead (SVA) and perception of object motion were measured in 11 patients with downbeat (n=6) and upbeat (n=5) nystagmus. Upward deviations of SVA (median +5.2 degrees) were found in downbeat nystagmus, and downward deviations (median -7.8 degrees) in upbeat nystagmus. SVA was deviated toward the slow phase of the vertical nystagmus in the pitch plane and associated with increased fore-aft body sway. Perception of object motion was more severely impaired for vertical (particularly for motion in the direction of slow nystagmus phases) than for horizontal directions in both downbeat and upbeat nystagmus. Impairment of motion perception in the vertical pitch plane of the VOR is beneficial to the extent that it alleviates disturbing oscillopsia due to the involuntary retinal slip. Thus, our findings confirm the hypothesis that downbeat and upbeat nystagmus reflect a central tone imbalance of the VOR in the vertical pitch plane with ocular motor, postural, and perceptual manifestations.

Adult↗
PubMed1998

Bilateral functional MRI activation of the basal ganglia and middle temporal/medial superior temporal motion-sensitive areas: optokinetic stimulation in homonymous hemianopia.

OBJECTIVE: To determine to what extent sensorimotor control is achieved for each hemisphere separately or interactively during small-field optokinetic stimulation in patients with complete homonymous hemianopia. DESIGN: Functional and structural neuroimaging using high-resolution magnetic resonance imaging. SETTING: University medical center research facility. PATIENTS: Three patients with complete homonymous hemianopia after acute infarction of the right posterior cerebral artery. MAIN OUTCOME MEASURES: Anatomical location of activated structures during horizontal optokinetic stimulation and T2-weighted anatomical magnetic resonance imaging. RESULTS: Occipitotemporal cortical areas (Brodmann areas 39 and 40) were the only activated cortical structures that showed statistically significant (P<.01) activation on the affected hemisphere. Of the subcortical areas, activation of thalamic nuclei appeared to be missing on the affected side, whereas the basal ganglia (putamen, globus pallidus, and caudate nucleus) were bilaterally activated. CONCLUSIONS: Bilateral activation of the basal ganglia confirms the concept of the basal ganglia-thalamocortical motor loop and of the efference copy of oculomotor pathways from each hemisphere. Our findings suggest 2 possible explanations for the activation of occipitotemporal areas (the human homolog of middle temporal/medial superior temporal areas) on the infarcted hemisphere: involvement of direct extrastriatal visual pathways or interhemispheric callosal connections between right and left middle temporal/medial superior temporal areas.

Aged↗
PubMed1998

Cerebral functional magnetic resonance imaging of vestibular, auditory, and nociceptive areas during galvanic stimulation.

Cerebral activation was investigated with functional magnetic resonance imaging (fMRI) during galvanic stimulation of the mastoid in 6 normal volunteers. Cutaneous stimulation at the neck C4-5 level served as a control. During mastoid stimulation, bilateral vestibular activation occurred in the posterior insula (parietoinsular vestibular cortex, PIVC), the transverse temporal (Heschl's) gyrus, and thalamic pulvinar. The cutaneous pain elicited by galvanic stimulation caused bilateral activity of the medial part of the insula and the anterior median thalamus. Thus, galvanic stimulation at the mastoid level activates cortical areas of three different sensory systems in the insulathalamic region, the vestibular, the auditory, and the nociceptive systems.

Adult↗
PubMed1998

Serum antibodies against membranous labyrinth in patients with "idiopathic" bilateral vestibulopathy.

To investigate the possibility of an autoimmune mechanism in idiopathic bilateral vestibulopathy (IBV), we screened patients' sera for antibodies against inner ear structures. IgG antibodies against membranous labyrinth (ampulla, semicircular canals, saccule and utricle) were detected in 8 of 12 patients by immunofluorescence on rat inner ear cryosections. All but one serum of 22 healthy controls and the sera of 6 patients with known autoimmune disorders showed only background staining. Low-titre anti-nuclear IgM antibodies were present in three control sera and one IBV serum. High-titre anti-nuclear IgM was found in a patient with lupus erythematosus and in one with scleroderma. Anti-nuclear IgM was not organ-specific. No human serum used contained detectable anti-vascular preformed antibodies. Cross-reactivity to sections of liver, kidney, cornea, brain and skeletal muscle was absent. Double-staining for IgG and F-actin, the primary constituent of hair cell cilia, did not show predominant Ig-coating of sensory hair cells. Immunosuppressive therapy in 3 IBV patients did not improve the disorder, probably owing to irreversible loss of sensory and neural structures. These data suggest that the bulk of anti-labyrinthine autoantibodies may be an epiphenomenon, yet a small subgroup of organ-specific autoantibodies may synergize with a cellular response in the development of vestibular lesions.

Autoantibodies↗
PubMed1998

Effects of galvanic vestibular stimulation on otolithic and semicircular canal eye movements and perceived vertical.

OBJECTIVE: The aim of this study was to determine the otolithic and semicircular canal effects of galvanic vestibular stimulation with increasing current strengths on eye movements and the perception of verticality. METHODS: We measured (1) 3-dimensional eye movements, (2) subjective tilt of the peripheral visual field, and (3) subjective tilt of a central vertical line in 12 healthy subjects during galvanic vestibular stimulation. A rectangular, unipolar binaural electric current was applied to each subject's mastoid. RESULTS: Anodal stimulation of the right mastoid led to an ipsiversive tonic ocular torsion of up to 5.4 degrees, to a contralateral tilt of both the peripheral visual field (1-9 degrees), and a central vertical line (0.5-6.2 degrees) increasing in amplitude with increasing current strengths applied. This reflects otolith stimulation. In most subjects, current strengths of 3 mA or more elicited a slight (horizontal-) torsional nystagmus (amplitude 1-2 degrees) that was superimposed on static torsion. This reflects horizontal and vertical semicircular canal stimulation. A correlation was found in the amount of the 3 measured parameters and the strength of the applied current. CONCLUSIONS: Thus, galvanic vestibular stimulation at low current intensities (1-3 mA) preferably excites otolith responses, which increase with increasing current intensity. With higher current intensity above 3 mA, additional semicircular canal responses are elicited in the form of horizontal-rotatory nystagmus superimposed on static torsional deviations. The lack of a vertical deviation and nystagmus can be explained by the counterdirected vertical components of the anterior and posterior semicircular canal.

Adult↗
PubMed1998

Perceptual and oculomotor effects of neck muscle vibration in vestibular neuritis. Ipsilateral somatosensory substitution of vestibular function.

Afferent cervical somatosensory input may substitute for absent vestibular information as part of central vestibular compensation after unilateral peripheral vestibular deficit. In order to determine the particular contribution of neck muscle spindles to the perception of body orientation and to the oculomotor system, we measured (i) the subjective visual straight ahead (SVA) by psychophysical tests and (ii) the changes in eye position by video-nystagmography during unilateral stimulation of the posterior neck muscles by vibration (100 Hz). Twenty-five patients with subacute unilateral vestibular lesion (vestibular neuritis) and 25 controls participated in the study. Vibration elicited a horizontal displacement of SVA towards the side of stimulation in all subjects. Mean displacement (+/- SD) was 3.28 +/- 2.96 degrees for right-side and 3.45 +/- 2.93 degrees for left-side stimulation in controls. Muscle stimulation on the patients' lesion side induced a significantly higher displacement (11.51 +/- 6.63 degrees) than contralateral stimulation (3.04 +/- 2.95 degrees, P < 0.01, paired Student's t test). The mean difference during stimulation between the two sides in the patients was 8.02 +/- 5.52 degrees; in the controls, however, it was only 0.74 +/- 0.47 degree (P < 0.001, Student's t test). This asymmetry increased gradually in patients over a period of weeks, reaching a maximum at days 60-80 and declining thereafter. Videonystagmography revealed that ipsilateral stimulation in patients induced large horizontal eye deviations of up to 25 degrees towards the side of the lesion (9.1 +/- 7.6 degrees, n = 18). Contralateral stimulation induced only small shifts, which were within the range of controls. The correlation coefficient between displacement of the SVA and change in eye position was high (r = 0.94, P < 0.0001), indicating that the shift of SVA is the perceptual correlate of the directional change of gaze in space. This interpretation was supported by two control experiments in which the subject was required to (i) indicate the subjective straight ahead by finger-pointing with the eyes closed and (ii) adjust SVA when looking through horizontally reversing prisms. Vibration of neck muscles caused almost no displacement of the SVA when it was indicated by pointing with the eyes closed, but reversed the direction of the displacement if the subject wore reversing prisms. In summary, our data showed: (i) an increase in muscle spindle input following unilateral vestibular lesion; (ii) this increase is asymmetrical, restricted to the affected side, and gradually builds up over weeks; and (iii) the perceived effects during vibration are secondary to changes in eye position rather than changes in cortical representation of body orientation. This is the first study to demonstrate a unilateral increase in somatosensory weight, which substitutes for missing vestibular input.

Adolescent↗
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↗