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Biomedical subjects

T Brandt

Publications and source records attributed to T Brandt.

At least 181 records · Page 10Linked to original sources
PubMed1994

Unilateral mimicking bilateral benign paroxysmal positioning vertigo.

BACKGROUND: Unilateral benign paroxysmal positioning vertigo (BPPV) may mimic bilateral BPPV if the diagnostic positioning maneuver is executed without appropriate alignment of the head and neck with the trunk. OBSERVATIONS: Appropriate alignment is achieved by adjusting the plane of the affected posterior semicircular canal so that it is parallel to the plane of diagnostic head tilt, ie, 45 degrees horizontal head rotation to the left before a head tilt to the right in suspected right-sided BPPV. With inappropriate head alignment and head tilt to the side of the unaffected ear, a free-floating clot within the long arm of the uppermost posterior canal may gravitate toward the cupula and become settled on it. This causes ampullopetal cupulolithiasis, evoking geotropic nystagmus, which may mimic BPPV of the unaffected ear. CONCLUSION: This hypothesis explains the seemingly paradoxical observation of immediate relief from "bilateral BPPV" following unilateral surgical canal occlusion on the "more symptomatic" side.

Calculi↗
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

The sequence of a 32,420 bp segment located on the right arm of chromosome II from Saccharomyces cerevisiae.

The sequence of a 32,420 bp segment of Saccharomyces cerevisiae chromosome II has been deduced. The sequence data revealed 19 potential new genes covering 83.5% of the sequence. Four genes had already been cloned and sequenced: part of RIF1, DPB3, MRP-L27 and SNF5. Besides these four genes, 15 open reading frames (ORFs) of at least 100 amino acids encoding potential new genes were identified. Two of these ORFs are overlapping and a third is located within another ORF. The putative gene product of ORF YBR2039 was homologous to the group of uncoupling proteins involved in the mitochondrial energy transfer system. We propose a remapping of the MRP-L27 gene encoding the mitoribosomal protein YmL27 as it previously has been mapped on chromosome X. The ORF YBR2020 has a strong homology with a 31.9% identity in a 473 amino acid region to the yeast gene SEC61, suggesting that YBR2020 is a new gene encoding a protein involved in translocation of proteins in the yeast cell. Six of the potential genes do not exhibit any significant homology to previously sequenced genes as predicted in the Fast A analysis.

Amino Acid Sequence↗
PubMed1994

Dependence of visual stabilization of postural sway on the cortical magnification factor of restricted visual fields.

Monocular visual stabilization of fore-aft and lateral body sway was tested posturographically in normal subjects (wearing visual field blinds) as a function of visual field size and location of the visual field on the central or peripheral retina. Body sway applied to a force- measuring platform is less with central (foveal) vision when central and peripheral visual fields have the same area. If, however, the peripheral field size is corrected by the cortical magnification factor of the retina in the primary cortex, body sway is stabilized by the peripheral retina to the same extent. Thus, there is no functional specialization of central and peripheral retina with respect to balance control. Visual stabilization of upright stance is a function of field size and cortical representation of the retina. The central and the peripheral retina have different thresholds to detect motion; this was surprisingly not reflected in measurements of normal fore-aft and lateral body sway.

Adult↗
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↗
PubMed1994

VIIIth nerve vascular compression syndrome: vestibular paroxysmia.

Neurovascular cross-compression of the root entry zone of the Vth, VIIth and IXth cranial nerves causes symptoms of trigeminal neuralgia, hemifacial spasm and glossopharyngeal neuralgia. It is reasonable to search for a group of patients presenting with typical paroxysmal vestibular and/or cochlear symptoms, analogously caused by neurovascular compression of the VIIIth cranial nerve. Since no pathognomonic sign or test has yet been established, the diagnosis of 'vestibular paroxysmia' secondary to neurovascular cross-compression is based on four characteristic features: (1) short attacks of rotational to-and-fro vertigo lasting seconds to minutes; (2) attacks frequently dependent on particular head positions and modification of the duration of the attack by changing head position ('disabling positional vertigo'); (3) hyperacusis or tinnitus permanently or during the attack; and (4) measurable auditory or vestibular deficits by neurophysiological methods. Carbamazepine is a most effective drug. In medically intractable cases, retromastoid craniotomy and microvascular decompression is a recommended procedure once the side of disorder has been identified.

Arteriovenous Malformations↗
PubMed1994

[Mechanical dynamic ankle passive motion for physical prevention of thrombosis? Changes in hemodynamics in the lower pressure system with new dynamic splints].

The use of mechanical ankle exercise devices with continuous passive motion (CPM) of the ankle joint can improve venous reflow in the lower limbs after operations. Duplex ultrasonography allows the observations of blood flow velocity and flow volume during continuous movement of the devices. We tested two different CPM devices for ankle movement in a preclinical study on 10 healthy, uninjured people and saw the following changes in the deep venous system in the common femoral vein: after 5 min of motion the velocity of the venous reflow was increased to 112.5% and the flow volume passing the femoral vein to 123% of the initial mean values. After 15 min of motion the devices led to an increase of the venous reflow velocity to 125% and of flow volume to 143% of the baseline values in the femoral vein. These positive effects were still evident even 15 min after the devices have been turned off.

Adult↗
PubMed1994

[Benign paroxysmal positional vertigo. Differential diagnosis of posterior, horizontal and anterior canalolithiasis].

Evidence is presented that all typical features of benign paroxysmal positioning vertigo can be explained by canalolithiasis rather than by cupulolithiasis. A free floating clot of "heavy" inorganic particles gravitates to the most dependent part of the canal as soon as the patient's head is moved in a way that alters the angle between the canal's plane and the gravity vector. Based on the canalolithiasis mechanism we describe how characteristics of the thus elicited nystagmus differ if the posterior, the horizontal or the anterior semicircular canal is causative.

Calculi↗
PubMed1993

Ocular torsion and tilt of subjective visual vertical are sensitive brainstem signs.

Deviations of the position of the eye in the roll plane, ocular torsion (OT), and the subjective visual vertical (SVV) were systematically studied in 111 patients with acute vascular brainstem lesions. Of the 111 patients, 104 (94%) showed a direction-specific pathological tilt of the static SVV in our series. Seventy-one (83%) of 86 patients exhibited pathological static OT of one (47%) or both (36%) eyes. OT and SVV tilts are therefore sensitive signs in acute unilateral brainstem disorders. Measurements of SVV and OT may prove to be useful components of the neuro-ophthalmological evaluation. With respect to the directions of pathological tilt, SVV and OT are generally in the same direction. Based on neuroimaging, we conclude that all unilateral brainstem lesions caudal to the upper pons cause ipsiversive OT of one or both eyes, with concurrent ipsiversive tilts of SVV adjustments; all lesions rostral to this pontine level cause contraversive tilts of OT and SVV. Evidence is presented that pathological tilts of OT and SVV are secondary to a dysfunction of the tonic bilateral vestibular inputs that stabilize the eyes and head in normal upright position in the roll plane and dominate our perception of verticality.

Accommodation, Ocular↗
PubMed1993

Skew deviation with ocular torsion: a vestibular brainstem sign of topographic diagnostic value.

Fifty-six patients with unilateral brainstem infarctions presenting with skew deviation of the eyes were analyzed for static vestibular function in the roll plane. Ischemic lesions were allocated to the level and side of the brainstem by the clinical syndrome and neuroimaging. Two findings of clinical relevance were obtained: (1) All skew deviations were ipsiversive (ipsilateral eye was undermost) with caudal pontomedullary lesions and contraversive (contralateral eye was lowermost) with rostral pontomesencephalic lesions. (2) All skew deviations were associated with concomitant ocular torsion and tilts of subjective visual vertical toward the undermost eye. Thus, skew deviation or more correctly, ocular skew torsion is a sensitive brainstem sign of localizing and lateralizing value. Evidence is presented that the ocular skew torsion sign indicates a vestibular tone imbalance in the roll plane secondary to graviceptive pathway lesions.

Adolescent↗
PubMed1993

Detection and localization of triadin in rat ventricular muscle.

Dyads (transverse tubule--junctional sarcoplasmic reticulum complexes) were enriched from rat ventricle microsomes by continuous sucrose gradients. The major vesicle peak at 36% sucrose contained up to 90% of those membranes which possessed dihydropyridine (DHP) binding sites (markers for transverse tubules) and all membranes which possessed ryanodine receptors and the putative junctional foot protein (markers for junctional sarcoplasmic reticulum). In addition, the 36% sucrose peak contained half of the vesicles with muscarine receptors. Vesicles derived from the nonjunctional plasma membrane as defined by a low content of dihydropyridine binding sites per muscarine receptor and from the free sarcoplasmic reticulum as defined by the M(r) 102K Ca2+ ATPase were associated with a diffuse protein band (22-30% sucrose) in the lighter region of the gradient. These organelles were recovered in low yield. Putative dyads were not broken by French press treatment at 8,000 psi and only partially disrupted at 14,000 psi. The monoclonal antibody GE4.90 against skeletal muscle triadin, a protein which links the DHP receptor to the junctional foot protein in skeletal muscle triad junctions, cross-reacted with a protein in rat dyads of the same M(r) as triadin. Western blots of muscle microsomes from preparations which had been treated with 100 mM iodoacetamide throughout the isolation procedure showed that cardiac triadin consisted predominantly of a band of M(r) 95 kD. Higher molecular weight polymers were detectable but low in content, in contrast with the ladder of oligomeric forms in rat psoas muscle microsomes. Cardiac triadin was not dissolved from the microsomes by hypertonic salt or Triton X-100, indicating that it, as well as skeletal muscle triadin, was an integral protein of the junctional SR. The cardiac epitope was localized to the junctional SR by comparison of its distribution with that of organelle markers in both total microsome and in French press disrupted dyad preparations. Immunofluorescence localization of triadin using mAb GE4.90 revealed that intact rat ventricular muscle tissue was stained following a well-defined pattern of bands every sarcomere. This spacing of bands was consistent with the interpretation that triadin was present in the dyadic junctional regions.

Animals↗
PubMed1993

Ocular torsion and perceived vertical in oculomotor, trochlear and abducens nerve palsies.

Ocular torsion (OT) and subjective visual vertical (SVV) were determined in acute and chronic oculomotor (n = 6), trochlear (n = 21) and abducens (n = 7) palsies separately for each eye in the primary position with the head upright. Ocular torsion measured by fundus photographs was not only within normal range in all abducens palsies, but unexpectedly also in 68% of third and fourth nerve palsies which involve oblique eye muscles. Pathological OT, when measurable, was slight (2 degrees - 8 degrees), monocular and occurred either in the paretic or in the nonparetic eye. Subjective visual vertical tilts were more frequent (67% of third and fourth nerve palsies) although mostly small in amplitude (1 degree - 6 degrees). They were confined either to the paretic or the nonparetic eye depending on the duration of the palsy. Determinations of SVV were always normal under binocular viewing conditions. The dissociated occurrence of OT and SVV tilts in the paretic or the nonparetic eye was dependent on the acuteness of the palsy and reflected sensory and/or motor compensation mechanisms. Third and fourth nerve palsies cause only minor and unpredictable monocular OT and SVV tilts as distinct from the frequent binocular and conjugate tilts seen in patients with acute unilateral brainstem lesions.

Abducens Nerve↗
PubMed1993

A reevaluation of the vestibulo-ocular reflex: new ideas of its purpose, properties, neural substrate, and disorders.

Conventional views of the vestibulo-ocular reflex (VOR) have emphasized testing with caloric stimuli and by passively rotating patients at low frequencies in a chair. The properties of the VOR tested under these conditions differ from the performance of this reflex during the natural function for which it evolved--locomotion. Only the VOR (and not visually mediated eye movements) can cope with the high-frequency angular and linear perturbations of the head that occur during locomotion; this is achieved by generating eye movements at short latency (< 16 msec). Interpretation of vestibular testing is enhanced by the realization that, although the di- and trisynaptic components of the VOR are essential for this short-latency response, the overall accuracy and plasticity of the VOR depend upon a distributed, parallel network of neurons involving the vestibular nuclei. Neurons in this network variously upon a distributed, parallel network of neurons involving the vestibular nuclei. Neurons in this network variously encode inputs from the labyrinthine semicircular canals and otoliths, as well as from the visual and somatosensory systems. The central vestibular pathways branch to contact vestibular cortex (for perception) and the spinal cord (for control of posture). Thus, the vestibular nuclei basically coordinate the stabilization of gaze and posture, and contribute to the perception of verticality and self-motion. Consequently, brainstem disorders that disrupt the VOR cause not just only nystagmus, but also instability of posture (eg, increased fore-aft sway in patients with downbeat nystagmus) and disturbance of spatial orientation (eg, tilt of the subjective visual vertical in Wallenberg's syndrome).

Brain Diseases↗