[Visually induced pseudocoriolis-effects and circularvection. A contribution to opto-vestibular interaction].
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Coriolis Force↗
Biomedical subjects
T Brandt
Publications and source records attributed to T Brandt.
[Comparative study on intramuscular and intraarticular administration of the depot steroid Triamcinolone acetonide].
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Adrenal Glands↗
[Neuroleptic effect of premedication with dehydrobenzperidol].
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Adult↗
[Comparison of acute blood pressure reducing effects of parenterally administered antihypertensive agents in normotonics and hypertonics].
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Aniline Compounds↗
A new method for accurate dental measurement.
Using digital dividers (analogue-digital transformer, Brandt-Hermanussen device), it has become possible to measure distances between human teeth with a technical error of 0.04 mm. The technique implies a small preparation (trough) into the respective teeth. The ball-shaped metal probes of the instrument fit into these troughs and enable the determination of this distance directly in the patient. It does not require the use of casts. The present method was compared with two conventional and popular techniques of tooth arch determination, using the natural retentions of the deepest points of the central fossa of the respective teeth without the preparation of an artificial trough (manual caliper rule with nonius, digital caliper rule). The technical error of these techniques ranged between 0.46 mm and 0.52 mm. In order to investigate whether the preparation of an artificial trough could be avoided, the digital measuring dividers were modified and equipped with sharp probes for the determination of the natural distance between the deepest points of the central fossa, in analogy to the conventional techniques. Under these circumstances however, the technical error increased up to 0.27 mm (observer 1), and 0.21 mm (observer 2). It is concluded that dental marking is necessary for accurate dental measurement.
Child↗
Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature.
Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.
Cerebral Infarction↗
Can short-latency vestibulospinal reflexes in lower leg muscles be elicited by tapping the head?
A gentle tap on the forehead evoked short-latency motor responses in the sternocleidomastoid muscle, which may be vestibulocollic reflexes with characteristics similar to those elicited by clicks. We tested this paradigm in subjects standing upright, in order to determine the differential effects of taps on the forehead on the patterns and latencies of spinal stretch and vestibulospinal reflexes, which are important for postural control. Taps on the forehead elicited short-latency inhibitory electromyographic responses in both gastrocnemius muscles with a mean latency of 48.3 +/- 3.1 ms (onset) to 98.3 +/- 6.3 ms (end). Taps on the sternum elicited similar responses from the gastrocnemius muscles, indicating that vestibular stimulation is not essential for eliciting these responses. Both responses may play a role in predetermining the strategy for correcting body perturbations. The actual reflex is probably elicited by somatosensory input from the neck, which converges with vestibular input for the multisensory control of posture.
Acceleration↗
HSV-1 not only in human vestibular ganglia but also in the vestibular labyrinth.
Reactivation of herpes simplex virus type 1 (HSV-1) in the vestibular ganglion (VG) is the suspected cause of vestibular neuritis (VN). Recent studies reported the presence of HSV-1 DNA not only in human VGs but also in vestibular nuclei, a finding that indicates the possibility of viral migration to the human vestibular labyrinth. Distribution of HSV-1 DNA was determined in geniculate ganglia, VGs, semicircular canals, and macula organs of 21 randomly obtained human temporal bones by nested PCR. Viral DNA was detected in 48% of the labyrinths, 62% of the VGs, and 57% of the geniculate ganglia. The potential significance of this finding is twofold: (1) Inflammation in VN could also involve the labyrinth and thereby cause acute unilateral vestibular deafferentation. (2) As benign paroxysmal positional vertigo often occurs in patients who have had VN, it could also be a sequel of viral labyrinthitis.
Adult↗
Cervical vertigo--reality or fiction?
Neck afferents not only assist the coordination of eye, head, and body, but they also affect spatial orientation and control of posture. This implies that stimulation of, or lesions in, these structures can produce cervical vertigo. In fact, unilateral local anesthesia of the upper dorsal cervical roots induces ataxia and nystagmus in animals, and ataxia without nystagmus in humans. If cervical vertigo exists outside these experimental conditions, it is obviously characterized by ataxia and unsteadiness of gait, and not by a clear rotational or linear vertigo. Neurological, vestibular, and psychosomatic disorders must first be excluded before the dizziness and unsteadiness in cervical pain syndromes can be attributed to a cervical origin. To date, however, the syndrome remains only a theoretical possibility awaiting a reliable clinical test to demonstrate its independent existence.
Afferent Pathways↗
Episodic ataxia type 1 and 2 (familial periodic ataxia/vertigo).
Episodic ataxia (EA) is a rare, disabling condition of autosomal dominant inheritance, but it is not a distinct clinical entity. Synonyms are familial periodic ataxia or hereditary paroxysmal cerebellar ataxia. Family members have a similar clinical syndrome; however, the syndrome varies considerably from family to family. At least two groups of disorders have been separated clinically: (1) episodic ataxia type 1 (EA-1), which manifests without vertigo and is associated with 'interictal' myokymia, and (2) episodic ataxia type 2 (EA-2), which often manifests with vertigo and is associated with 'interictal' nystagmus. EA-1 and EA-2 have been identified as channelopathies. EA-1 is due to different heterozygous missense point mutations in a voltage-gated (delayed rectifier) potassium channel gene (KCNA1/Kv1.1) on chromosome 12p13, whereas EA-2 is caused by mutations of the cerebral P/Q-type calcium channel alpha 1 subunit gene CACNL1A4 localized on chromosome 19p, which is highly expressed in the cerebellum. The diagnosis of EA-1 and EA-2 is important, since they can be easily treated and are often mislabeled. As effective as acetazolamide is in preventing attacks, prospective studies still have to prove whether it can prevent progressive ataxia in EA-2 or even improve chronic cerebellar deficits.
Acetazolamide↗
Optokinetic-graviceptive interaction in different head positions.
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Gravitation↗
Computer analysis of optokinetic nystagmus in patients with spontaneous nystagmus of peripheral vestibular origin.
The bias of slow phase velocity (SPV) of optokinetic nystagmus (OKN) caused by an acute labyrinthine lesion was examined in 8 patients using differnet optokinetic stimulus velocities. In all patients a directional preponderance of OKN-SPV was found corresponding to spontaneous nystagmus. This was due to enhancement of nystagmus SPV to the side of the lesion and depression of SPV in the opposite horizontal direction. The preponderance of OKN on the average increased with the intensity of spontaneous nystagmus and decreased along with recovery. These vestibularly induced differences in OKN-SPV range up to 70%. A differentiation is discussed between OKN preponderances caused by labyrinthine lesions and brain stem lesions.
Acute Disease↗
The mechanism of physiological height vertigo. I. Theoretical approach and psychophysics.
A theory is presented supporting a geometrical explanation of physiological height vertigo as a 'distance vertigo' created by visual destabilization of posture when the distance between the observer and visible stationary contrasts becomes critically large. Though height vertigo is generally regarded as a psychopathological process, we hypothesize that it might instead result from an intersensory mismatch when visual information is at variance with vestibular and proprioceptive inputs. Psychophysical experiments confirming the hypothesis revealed that: 1) height vertigo is clearly related to body position, being the greatest in the upright stance; 2) it is the eye-object distance rather than the direction of gaze which is critical; 3) there is a saturation of height vertigo magnitude. Subjective vertigo increases with increasing altitude only below 20 metres. Physiological 'distance vertigo' must be distinguished from psychological 'acrophobia'. Its postural consequences may be ameliorated by strategies gleaned from knowledge of its mechanism such as providing nearby stationary contrasts in the peripheral visual field.
Adult↗
The mechanism of physiological height vertigo. II. Posturography.
In order to validate the hypothesis that height vertigo is based on visual destabilization of free stance when the distance between eye and object becomes critically large, several of its consequences were demonstrated in posturographic experiments: (1) Visual signals conflicting with simultaneous vestibular and somatosensory inputs provided by sinusoidally tilting rooms may destabilize postural sway in the fore-aft as well as in the lateral direction. (2) In natural surrounding sway amplitudes increase with increasing eye-object distance up to 5 meters. Thus, teleologically, subjective height vertigo serves as an appropriate warning signal to withdraw the body from a stimulus situation inducing postural imbalance. (3) Postural height vertigo problems can be alleviated (a) by adjusting the head relative to the gravitational vector, and (b) by the presence of nearby stationary contrasts in the visual periphery according to the dominance of retinal periphery for dynamic spatial orientation.
Adult↗
Prolonged survival with isolated levocardia and situs inversus.
Isolated levocardia with situs inversus, or ILSI, is a rare anomaly with a reported incidence of 1:22,000 in the general population and from 0.4% to 1.2% of all patients with congenital heart diseases. It is commonly associated with both congenital heart disease and splenic abnormalities, either asplenia or polysplenia. The prognosis is poor, and only about 5% to 13% of patients survive more than 5 years. The case described here, which had computed tomographic findings, is the first case reported with multiple malignancies associated with ILSI. This patient, at 73 years of age, is the second longest survivor reported in the literature.
Abnormalities, Multiple↗
Cogan's Syndrome. High resolution MRI indicators of activity.
In the chronic-relapsing form of Cogan's syndrome, it can be difficult to evaluate the activity of the disease. In contrast to the initial stage, routine diagnostic techniques sometimes fail to indicate progression in the chronic stage. To determine whether high-resolution magnetic resonance imaging (HR-MRI) can be used to differentiate between active and inactive stages, we examined three patients with Cogan's syndrome (one during an acute relapse, two with chronic audiovestibular deficits), all of whom had antibodies to inner ear tissue (cochlea, vestibular labyrinth). Unenhanced T1-, T2, gadolinium-enhanced T1-weighted, and three-dimensional constructive interference in steady stage (CISS) images were used. Abnormal MRI signals of the inner ear were related to the activity of the disease. The patient studied during an acute exacerbation showed abnormal MRI signals in the vestibule, semicircular canals, vestibular nerve, and cochlea, which disappeared after the relapse. These abnormalities included high signal in the membranous labyrinth, the vestibule, and cochlea, with enhancement on T1-weighted images, indicating gadolinium leakage through the abnormal labyrinthine membrane into the perilymphatic spaces. In contrast, the other two patients with chronic audiovestibular deficits but no clinical signs of an acute relapse, had narrowing or occlusion of semicircular canals of the cochlea on the 3D-CISS images, but no high signal lesions (T1) and no enhancement. We conclude that sequential gadolinium-enhanced MRI can identify the active stage of Cogan's syndrome. The combination of HR-MRI and antibodies to inner ear antigens are helpful in the diagnosis of acute, sequential, bilateral audiovestibular impairment of autoimmune origin.
Acute Disease↗
High resolution Gd-DTPA MR imaging of the inner ear in 60 patients with idiopathic vestibular neuritis: no evidence for contrast enhancement of the labyrinth or vestibular nerve.
Sixty patients with acute idiopathic vestibular neuritis (confirmed by clinical examination and caloric irrigation) were evaluated in a prospective study by high resolution magnetic resonance imaging (hr-MRI) between days 3 and 30 after onset of symptoms. We used a 1.5 Tesla imager with an axial and coronal T1-weighted 2D-fast low angle shot-, T2-weighted turbo spin echo-, and an axial T2-weighted 3D-constructive interference in steady-state sequence for MRI. None of the patients' MRIs exhibited contrast enhancement of the labyrinth, vestibulocochlear nerve, or vestibular ganglion, even when high doses of gadolinium (0.2 mmol/kg) were used. In contrast, several previous studies demonstrated contrast enhancement of the vestibulocochlear nerve/labyrinth in herpes zoster oticus, labyrinthitis, and Cogan's syndrome or of the facial nerve in Bell's palsy. On the basis of our MRI findings, we speculate that idiopathic vestibular neuritis is neither a viral infection directly affecting the nerve (such as herpes zoster) nor a labyrinthitis. An autoimmunological disease of the labyrinth, which should involve only the anterior and horizontal semicircular canals, is also unlikely. A subacute reactivation of a latent viral infection--as discussed for Bell's palsy--is compatible with our MRI findings. The observed differences between contrast enhancement of the facial nerve in Bell's palsy and the vestibulocochlear nerve in vestibular neuritis may be due to their dissimilar anatomy: contrary to the vestibular nerve, the facial nerve has very prominent circumneural arteriovenous structures. Hyperemia within these vascular structures may cause the contrast enhancement seen in Bell's palsy.
Acute Disease↗