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Biomedical subjects

Michael Strupp

Publications and source records attributed to Michael Strupp.

35 records · Page 2Linked to original sources
PubMed2004

Methylprednisolone, valacyclovir, or the combination for vestibular neuritis.

BACKGROUND: Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. Its assumed cause is a reactivation of herpes simplex virus type 1 infection. Therefore, corticosteroids, antiviral agents, or a combination of the two might improve the outcome in patients with vestibular neuritis. METHODS: We performed a prospective, randomized, double-blind, two-by-two factorial trial in which patients with acute vestibular neuritis were randomly assigned to treatment with placebo, methylprednisolone, valacyclovir, or methylprednisolone plus valacyclovir. Vestibular function was determined by caloric irrigation, with the use of the vestibular paresis formula (to measure the extent of unilateral caloric paresis) within 3 days after the onset of symptoms and 12 months afterward. RESULTS: Of a total of 141 patients who underwent randomization, 38 received placebo, 35 methylprednisolone, 33 valacyclovir, and 35 methylprednisolone plus valacyclovir. At the onset of symptoms there was no difference among the groups in the severity of vestibular paresis. The mean (+/-SD) improvement in peripheral vestibular function at the 12-month follow-up was 39.6+/-28.1 percentage points in the placebo group, 62.4+/-16.9 percentage points in the methylprednisolone group, 36.0+/-26.7 percentage points in the valacyclovir group, and 59.2+/-24.1 percentage points in the methylprednisolone-plus-valacyclovir group. Analysis of variance showed a significant effect of methylprednisolone (P<0.001) but not of valacyclovir (P=0.43). The combination of methylprednisolone and valacyclovir was not superior to corticosteroid monotherapy. CONCLUSIONS: Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir does not.

Acyclovir↗
PubMed2004

Prevalence and distribution of HSV-1, VZV, and HHV-6 in human cranial nerve nuclei III, IV, VI, VII, and XII.

The etiology of idiopathic cranial nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) nuclei] and in nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) nuclei] of five human brainstems. Samples of the cranial nerve nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic cranial nerve palsies. HSV-1 was distributed at random in all cranial nerve nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic cranial nerve palsies result from viral reactivation in the brainstem nuclei.

Abducens Nerve↗
PubMed2004

Brain activation patterns during imagined stance and locomotion in functional magnetic resonance imaging.

Posture and gait are sensorimotor actions that involve peripheral, spinal, and supraspinal structures. To investigate brain activity during stance and locomotion, 13 healthy subjects were asked to stand, walk, run, and lie down; subsequently, they were trained to imagine standing, walking, running, and lying [imagined lying as rest condition in functional magnetic resonance imaging (fMRI)]. Separate and distinct activation/deactivation patterns were found for the three imagined conditions: (1) standing imagery was associated with activation in the thalamus, basal ganglia, and cerebellar vermis; (2) walking imagery was associated with activation in the parahippocampal and fusiform gyri (areas involved in visuospatial navigation), occipital visual areas, and in the cerebellum; (3) running imagery caused a predominantly cerebellar activation in the vermis and adjacent hemispheres (six times larger than during imagination of walking or standing), but activations in the parahippocampal and fusiform gyri were smaller than during walking. Deactivations were found for walking and running, but not for standing imagery. They were located in the vestibular (posterior insula, superior temporal gyrus, supramarginal gyrus) and somatosensory (postcentral gyrus) cortex with right-hemispheric dominance. These findings support the concept of a hierarchical organization of posture and locomotion. Automated locomotion, for example, running, is based on spinal generators whose pace is driven by the cerebellar locomotor region. Deactivation in the vestibular and somatosensory cortex prevents adverse interactions with the optimized spinal pattern and sensory signals; this confirms earlier findings of a multisensory inhibition during unhindered locomotion. During slow walking, spatial navigation, mediated by the parahippocampal cortex, becomes more important. Postural control during standing involves a low intensity cerebellar activity and sensorimotor control via the thalamus and basal ganglia.

Adult↗
PubMed2004

Mitoxantrone therapy in multiple sclerosis and acute leukaemia: a case report out of 644 treated patients.

As a rare complication of mitoxantrone (MITOX) therapy in multiple sclerosis (MS), a therapy-related acute leukaemia (TRAL) may develop. The incidence is difficult to estimate, as frequently single cases are reported, up to now a total of eight MS patients. Here we report a new case out of 644 patients. This is a 45-year-old female patient with secondary progressive MS who developed TRAL after a total dose of 48 mg/m2 MITOX. The TRAL was classified as acute myeloblastic leukaemia (AML) M4eo and showed an inversion of chromosome 16 and a partial trisomy 11. Her TRAL was treated with chemotherapy followed by allogeneic bone marrow transplantation. It responded well to the transplantation, whereas the MS symptoms initially worsened but have nearly returned to the pretransplantation level. This report brings the currently published frequency of MITOX-associated TRAL in MS therapy to five in a total of 2336 treated MS patients, representing an incidence of 0.21%.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2003

Inverse U-shaped curve for age dependency of torsional eye movement responses to galvanic vestibular stimulation.

To investigate age dependent changes we analysed torsional eye movement responses to binaural and monaural galvanic vestibular stimulation (GVS) in 57 healthy subjects (20-69 years old). GVS (1-3 mA) induced torsional eye movements consisting of static torsion toward the anode (amplitude 1-6 degrees ) and superimposed torsional nystagmus (slow phase velocity 0.5-3 degrees /s, quick phase amplitude 0.5-2 degrees, nystagmus frequency 0.75-1.5 s-1). Static ocular torsion and torsional nystagmus increased from the third to the sixth decade and decreased in older subjects, e.g. slow phase velocity increased from 1.5 degrees /s (20-29 years) to 2.9 degrees /s (50-59 years) and decreased to 2.5 degrees /s for the seventh decade (60-69 years). Thus, an inverse U-shaped curve was found for the dependence of torsional eye movement responses on age. All structures relevant for vestibular function degenerate with age, but at varying times. Since hair cell loss precedes those seen in the vestibular nerve and Scarpa's ganglion, the decrease in hair cell counts could be compensated for by increased sensitivity of afferent nerve fibres or central mechanisms. Increased sensitivity could thus maintain normal function despite reduced peripheral input. As GVS acts at the vestibular nerve (thereby bypassing the hair cells), electrical stimulation should be more efficient in subjects with the beginning of hair cell degeneration, as seen in our data up to the sixth decade. The degeneration of nerve fibres, ganglion cells and central neurons becomes evident at older ages. Thus, the compensatory increase in sensitivity breaks down and GVS-induced eye movements decline-a finding that is reflected by the inverse U-shaped curve for age dependency presented in this study.

Adult↗
PubMed2003

Dually infected (HSV-1/VZV) single neurons in human trigeminal ganglia.

Human trigeminal ganglia were tested by double fluorescence in situ hybridization for the presence and distribution of herpes simplex virus type 1 (HSV-1) and varicella-zoster virus (VZV) latency. Latency transcripts of both viruses were detected in common areas within the ganglia. Also, a few single neurons were shown to harbor HSV-1 and VZV together.

Adolescent↗
PubMed2003

Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response.

The majority of trigeminal ganglia (TGs) are latently infected with alpha-herpesviruses [herpes simplex virus type-1 (HSV-1) and varicella-zoster virus (VZV)]. Whereas HSV-1 periodically reactivates in the TGs, VZV reactivates very rarely. The goal of this study was to determine whether herpesvirus latency is linked to a local immune cell infiltration in human TGs. T cells positive for the CD3 and CD8 markers, and CD68-positive macrophages were found in 30 of 42 examined TGs from 21 healthy individuals. The presence of immune cells correlated constantly with the occurrence of the HSV-1 latency-associated transcript (LAT) and only irregularly with the presence of latent VZV protein. In contrast, uninfected TGs showed no immune cell infiltration. Quantitative RT-PCR revealed that CD8, interferon-gamma, tumor necrosis factor-alpha, IP-10, and RANTES transcripts were significantly induced in TGs latently infected with HSV-1 but not in uninfected TGs. The persisting lymphocytic cell infiltration and the elevated CD8 and cytokine/chemokine expression in the TGs demonstrate for the first time that latent herpesviral infection in humans is accompanied by a chronic inflammatory process at an immunoprivileged site but without any neuronal destruction. The chronic immune response seems to maintain viral latency and influence viral reactivation.

Adolescent↗
PubMed2003

Spatial memory deficits in patients with chronic bilateral vestibular failure.

The role of the vestibular system for navigation and spatial memory has been demonstrated in animals but not in humans. Vestibular signals are necessary for location-specific "place cell" activity in the hippocampus which provides a putative neural substrate for the spatial representation involved in navigation. To investigate the spatial memory in patients with bilateral vestibular failure due to NF2 with bilateral neurectomy, a virtual variant (on a PC) of the Morris water task adapted to humans was used. Significant spatial learning and memory deficits were shown in 12 patients as compared to 10 healthy controls. These data suggest that functional hippocampal deficits manifest due to a chronic lack of vestibular input in these patients. These deficits can even be demonstrated with the subjects stationary, i.e., without any actual vestibular or somatosensory stimulation.

Adult↗
PubMed2003

Expression of neuronal markers in differentiated marrow stromal cells and CD133+ stem-like cells.

Bone marrow stromal cells, which normally give rise to bone, cartilage, adipose tissue, and hematopoiesis-supporting cells, have been shown to differentiate in vitro and in vivo into neural-like cells. In this study, we examined the expression of neuronal and glial markers in human marrow stromal cells under culture conditions appropriate for neural stem cells, and compared the unsorted cell population to bone marrow CD133+ stem-like cells using immunofluorescence, Western blot, and functional patch-clamp analysis. Overall, the expression of the early neuronal marker beta3-tubulin was most pronounced in the presence of DMEM/F12 and neurotrophin 3 (NT3) or brain-derived neurotrophic factor (BDNF), when marrow stromal cells were cultured onto fibronectin. Electrophysiological examination, however, could not show fast sodium currents or functional neurotransmitter receptors in differentiated marrow stromal cells. CD133+ mesenchymal stem-like cells, but not CD34+/CD133- cells, generally showed a higher expression of neuronal markers than did unsorted marrow stromal cells, and differentiated CD133+ cells more resembled neuron-like cells.

AC133 Antigen↗
PubMed2003

Torsional eye movement responses to monaural and binaural galvanic vestibular stimulation: side-to-side asymmetries.

Vestibular stimulation by head accelerations always involves multisensory activation of the vestibular, somatosensory, and visual systems. Over the past few years, galvanic vestibular stimulation (GVS) has become increasingly popular for testing vestibular function for clinical and research purposes. Although GVS provides a nonphysiological stimulation, it is more selective than natural head accelerations and is thus an attractive tool for such tests. Eye movement responses elicited by GVS mainly consist of torsional and horizontal components, as first described by Hitzig in 1871. Animal experiments have shown that GVS increases the vestibular afferent spike frequency at the cathodal site and decreases it at the anodal site of stimulation. As a continuation of a study on age-dependency of eye movement responses to GVS, we analyzed side-to-side asymmetries in healthy subjects. It is necessary to know the normal range of asymmetry between left- and right-sided stimulation to interpret GVS responses in patients with vestibular diseases.

Adult↗
PubMed2002

Both actual and imagined locomotion suppress spontaneous vestibular nystagmus.

Acute unilateral vestibulopathy is characterized by a combination of signs and symptoms including spontaneous nystagmus, postural imbalance and gait disturbance. A functional link between these vestibulo-ocular and vestibulo-spinal motor responses has been demonstrated. These responses use common vestibular input and partially overlapping neuronal networks, but it is not known if and to what extent they are linked or operate separately. We found that slow phase velocity of spontaneous vestibular nystagmus in patients with acute vestibulopathy was suppressed by 26% during actual walking (ANOVA p< 0.02, = 6). It was also suppressed by imagined locomotion: by 26% during the imagination of walking and by 42% during the imagination of running ( p< 0.003, = 10). The suppression of vestibular nystagmus might be beneficial for patients, for it alleviates the disturbing impression of movement of the visual scene (oscillopsia) caused by involuntary eye movements.

Adult↗
PubMed2002

Suppression of eye movements improves balance.

The aim of this study was to investigate the possible interaction of vestibulo-ocular and vestibulo-spinal functions. Spontaneous eye movements and anterior-posterior and lateral body sway were recorded simultaneously in 10 patients with vestibular neuritis (Experiment 1) and in 11 healthy subjects (Experiment 2) while all subjects wore a mask that allowed fixation of a head-fixed target. For the healthy subjects, there was no significant difference in postural sway for the conditions of eyes open in darkness and fixation of the head-fixed target. For the patients, the question was whether transient suppression of the spontaneous nystagmus by fixating the target affected excessive body sway or whether modulation of nystagmus and postural sway were largely independent. The mean peak slow-phase velocity of the spontaneous nystagmus decreased from 13.5 +/- 5.6 to 4.3 +/- 2.4 degrees /s during fixation. The suppression of nystagmus also reduced postural sway while standing on foam rubber. Mean value decreased from 25.2 +/- 7.6 to 16.2 +/- 7.7 mm (right-left root mean square values; ANOVA, P = 0.003). Since a head-fixed target was used to suppress spontaneous eye movements, the data cannot be explained by any stabilizing effect of afferent visual cues. Instead, ocular motor efference copy signals or reafferences may have contributed to the postural instability of patients with vestibular neuritis, which would explain the reduction of postural sway during fixation suppression of the nystagmus. Thus, ocular motor signals rather than afferent visual cues about retinal slip are used for visual control of postural sway, at least in this experimental paradigm.

Adult↗