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Biomedical subjects

M Strupp

Publications and source records attributed to M Strupp.

At least 37 records · Page 2Linked to original sources
PubMed2003

[The most common form of dizziness in middle age: phobic postural vertigo].

Up to now, there have been only a few valid epidemiological investigations of dizziness or vertigo as key symptoms. According to an analysis of 4,214 patients examined between 1989 and 2002 in an outpatient dizziness unit, benign peripheral paroxysmal positional vertigo (BPPV) and phobic postural vertigo (PPV) constitute the two most frequent syndromes. In this study, the relative age and sex distribution of both disorders was analysed. In the age group from 20 to 50 years, PPV was comparatively the most frequent form of dizziness, with a share of 22% to 26%. When left untreated, PPV becomes chronic in most cases and leads to considerable impairments, also at work. However, when diagnosed correctly, it can be treated successfully in more than 70% of cases. Thus, it takes on considerable medical and socioeconomic significance and should be part of the diagnostic repertoire of every doctor.

Adult↗
PubMed2003

Anterior canal failure: ocular torsion without perceptual tilt due to preserved otolith function.

A patient with anterior semicircular canal dehiscence syndrome underwent surgical patching that caused an isolated dysfunction of the left anterior semicircular canal postoperatively. He exhibited significant ocular torsion toward the side of the affected labyrinth (17 degrees excyclotropia of the ipsilateral eye), but no displacement of the subjective visual vertical. This dissociation suggests that an isolated ocular torsion may occur after an anterior semicircular canal lesion. A combined ocular torsion and subjective visual vertical tilt, which is usually seen with vestibular lesions, requires an associated otolith dysfunction.

Eye Diseases↗
PubMed2002

[External ophthalmoplegia caused by amitriptyline poisoning].

Drug-induced ocular motor disorders occurring during coma may be difficult to distinguish from structural cerebral lesions. We recently encountered a case of reversible amitriptyline-induced external ophthalmoplegia, which was first described by Mladinich and Carlow in 1977. We suggest that the mechanism for gaze paresis and loss of vestibulo-ocular reflex due to amitriptyline overdose involves the modulation of neurons of the pontine paramedian reticular formation, the rostral fasciculus longitudinalis medialis, and the vestibulo-ocular reflex. Clinical features that might be useful when distinguishing amitriptyline-induced ophthalmoplegia from structural brain lesions--such as basilar thrombosis--include the preservation of corneal response, purposeful withdrawal from noxious stimuli, rapid recovery within 24 hours, and the reversal of symptoms by physostigmine.

Adult↗
PubMed2001

"Atraumatic" Sprotte needle reduces the incidence of post-lumbar puncture headaches.

Post-lumbar puncture headache (PLPH) is best explained by spinal fluid leakage due to delayed closure of a dural defect. In a prospective, randomized, double-blind study, taking into consideration all known methodological problems, the authors compared the incidence of PLPH using the "atraumatic" Sprotte needle vs the "traumatic" Quincke needle. Of the 230 patients included in the final analysis, 24.4% of patients in the "traumatic" group developed PLPH, whereas only 12.2% of patients in the "atraumatic" group did (p < 0.05). Therefore, use of the "atraumatic" Sprotte needle for lumbar puncture is recommended.

Adult↗
PubMed2001

Smoking and balance: correlation of nicotine-induced nystagmus and postural body sway.

Unaccustomed smoking may elicit transient nystagmus, dizziness, unsteadiness, and nausea. Infrared videonystagmography and posturography were performed simultaneously to study the differential effects of nicotine on the association of ocular motor and postural disturbances in 25 non- or occasional smokers. Sixteen showed nicotine-induced nystagmus (NIN) of various directions (mainly horizontal or upbeat) which was associated with a significant increase in postural sway after smoking a cigarette (total sway path (SP) before smoking 2.22 +/- 0.82 m/min (mean +/- s.d.), 1 min after smoking 3.83 +/- 1.41 m/min; p < 0.0004, ANOVA); nine showed neither effect. There was a high correlation between the intensity of the nystagmus (measured as peak slow phase velocity) and the increase in total SP (correlation coefficient 0.78) as well as the time courses of both. Visual fixation of an LED integrated in the mask not only caused a suppression of NIN but also a decrease in body sway. Transient ocular motor and postural effects are compatible with simultaneous nicotine-induced effects on the vestibulo-ocular and vestibulo-spinal functions.

Adult↗
PubMed2001

Visually induced gait deviations during different locomotion speeds.

Optic flow is essential for the perception of self motion and the control of path integration during locomotion. Inverting prisms oriented 15 degrees off vertical in the roll plane were used to experimentally distort optic flow during locomotion. Depending on the direction in which the prisms were rotated, optic flow was diagonally upward to the right or upward to the left. A reproducible deviation of gait toward the direction of perceived optic flow was found in ten healthy subjects. This deviation is explained to be a gait deviation that compensates for misleading perceived self motion induced by optic flow. The amount of deviation was dependent on locomotion speed. When walking slowly (about 1 m/s), mean deviation was 0.22+/-0.08 m/s to the right and -0.18+/-0.08 m/s to the left for right and left, respectively, diagonal prism orientation. Deviation was significantly less when running (about 3 m/s) with mean deviations of 0.05+/-0.03 m/s and -0.06+/-0.03 m/s, respectively (ANOVA, P<0.01). It is assumed that path integration during running is largely achieved by highly automated spinal programs operating independently of sensory control. In contrast, walking is more dependent on afferent and reafferent visual control. Thus, the experiments show that visual control of locomotion is direction specific and dependent on optic-flow-induced vection. It becomes less influential with increasing speed of locomotion, e.g., when walking in contrast to running.

Adult↗
PubMed2001

Acute vestibulopathy.

Acute vestibulopathy is characterized by the acute or subacute onset of vertigo, dizziness or imbalance with or without ocular motor, sensory, postural or autonomic symptoms and signs, and can last for seconds to up to several days. Acute vestibular lesions may result from a hypofunction or from pathological excitation of various peripheral or central vestibular structures (labyrinth, vestibular nerve, vestibular nuclei, cerebellum or ascending pathways to the thalamus and the cortex). This update focuses on new aspects of the aetiology, pathophysiology, epidemiology, and treatment of (i) acute peripheral disorders (benign paroxysmal positioning vertigo, vestibular neuritis, Menière's disease, perilymph fistula, especially 'superior canal dehiscence syndrome', vestibular paroxysmia); and (ii) acute central vestibular disorders (especially 'vestibular migraine'). Finally, the clinical relevance of recent diagnostic tools (three-dimensional analysis of eye movement, imaging techniques) is discussed.

Acute Disease↗
PubMed2001

Exercise and drug therapy alter recovery from labyrinth lesion in humans.

Acute unilateral vestibular failure is characterized by rotatory vertigo, horizontal-rotatory nystagmus, and postural imbalance, all of which last from days to weeks. These signs and symptoms are caused by a vestibular tone imbalance between the two labyrinths. Recovery results from a combination of peripheral restoration of labyrinthine function (usually incomplete) and central vestibular compensation (CVC) of the vestibular tone imbalance. Acute unilateral failure is most often caused by vestibular neuritis, which is most likely due to the reactivation of a latent HSV-1 infection. Therefore, therapeutic strategies to improve the outcome of VN are theoretically based on two principles: (a) vestibular exercises and drugs to improve CVC and (b) drug treatment of the assumed viral inflammation. The following conclusions can be drawn from studies in animals and/or humans: (1) There is strong evidence that vestibular exercises may improve vestibulo-spinal compensation. These exercises should begin as early as possible after symptom onset. Moreover, slower exercises are likely to be more effective than faster exercises because slower ones seem to depend more on the vestibular system. (2) Despite extensive data from animal experiments indicating that drugs have a favorable effect on CVC, this has not been clinically proven and thus cannot be recommended yet. (3) Preliminary results of an interim analysis from an ongoing randomized, prospective study showed that methylprednisolone (plus an antiviral agent?) may be useful for improving peripheral vestibular function in vestibular neuritis.

Acyclovir↗
PubMed2001

Prevalence of HSV-1 LAT in human trigeminal, geniculate, and vestibular ganglia and its implication for cranial nerve syndromes.

Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in allTG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG.

Adult↗
PubMed2001

Absence of nystagmus during REM sleep in patients with vestibular neuritis.

Saccades, including fast phases of nystagmus, disappear during drowsiness and non-rapid eye movement (NREM) sleep, but are present during the alert state and REM sleep. The purpose of this study was to determine whether spontaneous nystagmus is present in patients with vestibular neuritis during REM sleep. Eight patients with spontaneous nystagmus due to vestibular neuritis and eight control patients without any nystagmus underwent at least one night of polysomnography. Fast phases of nystagmus were analyzed. The number of right and left horizontal saccades were counted, first during 3-5 minute samples of the awake state before sleep onset, then during the first REM episode and the last REM episode of nocturnal sleep, and finally during the alert state in the morning after nocturnal sleep. All patients with vestibular neuritis showed significantly more saccades (fast phases) towards the side contralateral to their vestibular lesion in the awake state before and after the polysomnography. This reflects their spontaneous nystagmus. By contrast, during REM sleep the patients with vestibular neuritis showed no preponderance in saccade direction. The eye movement pattern in REM was the same for patients and controls. In conclusion, peripheral vestibular imbalance producing nystagmus in vestibular neuritis in the awake state is not active at the brain stem level during REM sleep.

Aged↗
PubMed2000

Nicotine-induced nystagmus: three-dimensional analysis and dependence on head position.

Two- and three-dimensional analyses of nicotine-induced eye movements were performed in 53 subjects to evaluate whether they were primarily of vestibular or ocular motor origin. Nicotine-induced nystagmus was detected in 27 subjects (51%); in 25 of these (93%) it was modulated by otolith input. Three-dimensional analysis of nicotine-induced nystagmus revealed that it violates Listing's law. Taken together, these findings suggest that nicotine induces an imbalance in the vestibulo-ocular reflex.

Adult↗
PubMed2000

Detection of herpes simplex virus type 1 in human vestibular nuclei.

The distribution of herpes simplex virus type 1 (HSV-1) in human geniculate, vestibular ganglia, and vestibular nuclei was determined in 10 human temporal bones and brainstems of five individuals by PCR. HSV-1 was found in 3 of 10 of each ganglia and vestibular nuclei. The various patterns of HSV-1 infection of vestibular structures are compatible with virus migration from the vestibular ganglia to the vestibular nuclei and from the ipsilateral to the contralateral vestibular nucleus via commissural fibers.

Adult↗
PubMed2000

Differential effects of vestibular stimulation on walking and running.

Prompted by our recent observation that an acute vestibular tone imbalance causes less deviation from the intended path when running than when slowly walking, we examined 10 healthy subjects when walking or running at different step frequencies during galvanic vestibular stimulation. Blindfolded subjects were asked to walk (1 Hz step frequency) or run (3 Hz step frequency) straight ahead toward a previously seen target. The mean gait deviation after 10 s was 6.0 +/- 2.4 degrees at 1 Hz and 2.8 +/- 1.8 degrees at 3 Hz step frequency (n = 10; p < 0.001, paired t-test). In a second experiment walking and running in place were investigated. There was no significant difference in body displacement. Walking and running are highly automated processes based on spinal locomotor generators that are under supraspinal control. We conclude that vestibular input is differentially regulated depending on the locomotion speed and pattern used.

Adult↗
PubMed2000

Rotational vertebral artery occlusion syndrome with vertigo due to "labyrinthine excitation".

Leftward head rotations in a patient with a rotational vertebral artery occlusion syndrome elicited recurrent uniform attacks of severe rotatory vertigo and tinnitus in the right ear. These attacks were accompanied by a mixed clockwise torsional downbeat nystagmus with a horizontal component toward the right. A transient ischemia of the right labyrinth probably induced the attacks and led to a combined transient excitation of the right anterior and horizontal semicircular canals as well as the cochlea.

Angiography, Digital Subtraction↗