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Biomedical subjects

T Lempert

Publications and source records attributed to T Lempert.

At least 19 recordsLinked to original sources
PubMed1998

Horizontal otolith-ocular responses in humans after unilateral vestibular deafferentation.

We studied horizontal eye movements evoked by lateral whole body translation in nine patients who underwent vestibular nerve section. Preoperatively, all had preserved caloric function on both sides. Testing was performed before, 1 week and 6-10 weeks after surgery. Patients were seated upright in an electrically powered car running on a linear track. The car executed acceleration steps of 0.24 g, randomly to the left and right in the dark. The normal response consisted of a bidirectionally symmetrical nystagmus with compensatory slow phases. Response asymmetry of the slow-phase velocity of the desaccaded and averaged eye position signal was less than 13% in normals (n = 21). Before surgery, patients' responses were mostly symmetrical. Postoperatively, responses were diminished or absent with head acceleration towards the operated ear in all patients, causing a marked asymmetry which averaged 56% after correction for spontaneous nystagmus. On follow-up, responses regained symmetry. Thus, early after vestibular nerve section, a single utricle produces a normal LVOR only with ipsilateral head translation. Therefore, afferents for the LVOR seem to originate from the mid-lateral area of the macula, where hair cells are stimulated in their on-direction during ipsilateral head translation. Compensation may depend on recovery of the off-directional responses from lateral hair cells of the remaining utricle.

Acceleration↗
PubMed1998

Vertigo.

Insight into the pathomechanisms of the benign positional vertigo syndromes has led to quick and effective treatment with positional manoeuvres. Our understanding of other causes of vertigo is progressing at a slower pace, but several recent findings regarding vestibular neuritis, vascular compression of the eighth nerve and psychogenic vertigo are of immediate clinical relevance.

Animals↗
PubMed1997

Selective vestibular damage in neurosarcoidosis.

We report a patient with neurosarcoidosis who developed bilateral benign paroxysmal positional vertigo (BPPV) of the posterior canals, deafness, and absent responses to conventional caloric and rotational vestibular testing. Additional rotation in the planes of the vertical semicircular canals revealed relative sparing of vertical canal function. This vertical-horizontal canal dissociation explains the presence of BPPV and suggests that the vestibular damage in this patient is secondary to a vasculitic neuropathy.

Adult↗
PubMed1997

[Syncope. Phenomenology and differentiation from epileptic seizures].

Confusion between syncope and epileptic seizures is a common problem in clinical practice. Recently, new insights into the phenomenology of transient cerebral hypoxia have been gained from video analysis of experimentally induced syncope. Common elements of syncope include multifocal and generalized myoclonus, tonic body extension, automatisms, vocalizations, eye deviations and hallucinations. Thus, it is not the presence or absence of these features but their specific character that distinguishes syncope from epileptic seizures. Other clues for differential diagnosis include precipitating factors, premonitory symptoms and postictal events, such as tongue bites and postictal confusion, which has been identified as the single most powerful factor discriminating syncope from epileptic seizures. In contrast, incontinence and head injury are common in both conditions. Investigations such as electroencephalogram, tilt testing and postictal prolactin or creatine kinase levels may aid diagnosis but are never diagnostic in isolation. In rare cases, hypoxic and epileptic mechanisms may interact within one attack.

Adult↗
PubMed1997

Effect of otolith dysfunction. Impairment of visual acuity during linear head motion in labyrinthine defective subjects.

Visual symptoms emerging after the loss of vestibular function are usually attributed to the dysfunction of semicircular canal vestibulo-ocular reflexes, as they have been shown to stabilize vision during angular head movements. However, natural head displacements involve both angular and linear motion, and therefore visual instability may occur because of defective otolith-ocular reflexes (OORs) which are the eye movements evoked by linear head acceleration. In this paper, the relationship between OORs and visual acuity during linear head motion was studied in normal subjects and 14 patients with bilateral loss of caloric responses. OORs were elicited in darkness by step acceleration (0.24 g) of the whole body along the interaural axis. Latency, slow phase velocity and asymmetry of the OOR were measured from the desaccaded and averaged electrooculographic trace. Visual acuity was assessed during sinusoidal lateral oscillation of the subject viewing an earth-fixed target, and vice versa with the subject stationary and the target moving at 0.5, 1.0 and 1.5 Hz. The task was to recognize numbers flashing up on a three digit light-emitting diode visual display. Normal subjects had symmetrical OORs with short latencies (< 130 ms). In patients, OORs were either absent (n = 2) or abnormal with asymmetries (n = 8), diminished velocities (n = 4) or prolonged latencies (n = 6). At high frequency oscillation (1.5 Hz), normal subjects invariably recognized more numbers during self-motion compared with target motion, whereas most patients did not. In patients, abnormal dynamic visual acuity was correlated with absent or delayed OOR responses. This is the first demonstration of a functional role of the OORs in that they contribute to visual stabilization during high frequency linear head motion. Bilateral vestibular failure commonly affects the OORs and thereby compromises dynamic visual acuity.

Acceleration↗
PubMed1997

Three hundred sixty-degree rotation of the posterior semicircular canal for treatment of benign positional vertigo: a placebo-controlled trial.

The canalithiasis hypothesis proposes that benign positional vertigo (BPV) is caused by dislodged otoconia that settle in the posterior semicircular canal (PSC). When head position is changed these particles move within the canal and induce abnormal endolymph flow. To clear the PSC from debris we developed a procedure that consists of a full circle of backward head rotation in the exact plane of the canal. Patients were seated in a three-dimensional motion device that rotated in steps of 110 degrees every 30 seconds. The first part of the study was conducted as an open trial; the second part followed a single-blinded, placebo-controlled design: Forward rotation (placebo) was applied first and backward rotation was applied 1 week later if BPV persisted. All patients were assessed with a symptom diary and, in the controlled trial, also with the Dix-Hallpike maneuver. In the open study 10 of 15 patients became asymptomatic after one treatment session. In the controlled trial all 15 patients remained symptomatic after forward rotation while 10 of 14 undergoing backward rotation were relieved from positional vertigo immediately (p = 0.004). The presence of secondary nystagmus during the procedure indicated a favorable outcome. Our findings provide evidence for the efficacy of canal-clearing procedures that validate the canalithiasis hypothesis of BPV.

Calculi↗
PubMed1997

Horizontal otolith-ocular responses to lateral translation in benign paroxysmal positional vertigo.

Benign paroxysmal positional vertigo (BPPV) is assumed to result from utricular damage, but it is controversial if patients have manifest utricular dysfunction. Therefore, we investigated linear vestibulo-ocular reflexes (LVORs) during lateral whole-body translation in 14 patients with unilateral BPPV. Patients were subjected to linear acceleration steps of 0.24 g along the interaural axis, which were applied randomly to the left and right, both in the dark and in the light with a visual target at a distance of 60 cm. The LVOR was measured by EOG from the slow phase velocity of the averaged and desaccaded compensatory eye movement. In normal cases, maximum asymmetry of LVOR velocity was 13% in the dark and 10% in the light. In patients, LVOR velocities were normal in the dark but mildly reduced in the light (p < 0.05). Five patients had mild LVOR asymmetries in the dark (range 18-38%) and two in the light (11 and 13%), but there was no consistent relationship to the affected side. The absence of gross changes of the LVOR may be explained either by minor utricular damage that is functionally irrelevant or by central compensation of a chronic unilateral deficit.

Adult↗
PubMed1996

Transaural linear vestibulo-ocular reflexes from a single utricle.

To clarify the directional sensitivity of a single utricle with respect to the transaural linear vestibulo-ocular reflex (L-VOR) we studied seven patients before and after vestibular neurectomy. Patients were seated upright in an electrically powered car running on a linear track. Transaural acceleration steps of 0.24 g were applied randomly to the left and right in the dark. The slow phase velocity of the L-VOR was measured from the average of the induced compensatory eye movements. L-VOR asymmetry was calculated as (R-L/R + L x 100) and is < 13% in normals. Before surgery, responses were mostly symmetrical. One week after surgery, however, all patients had diminished or absent responses with medial acceleration of the remaining utricle. Asymmetries averaged 65% after correction for spontaneous nystagmus. Our findings indicate that afferents for the L-VOR originate from the lateral region of the macula where hair cells with ipsilateral on-directions are located.

Eye↗
PubMed1996

A positional maneuver for treatment of horizontal-canal benign positional vertigo.

Horizontal-canal benign positional vertigo (HC-BPV) is characterized by brief attacks of intense vertigo that are induced by mainly rolling over in bed. Examination shows a burst of purely horizontal nystagmus beating toward the undermost ear when the head is turned from supine to either lateral position. Two patients with typical HC-BPV were treated by a new positional procedure that aims to clear particles from the affected canal. The maneuver starts with the patient in the supine position and consists of three 90-degree head rotations toward the unaffected ear. Both patients had immediate and sustained relief of their attacks. No positional nystagmus could be elicited after the maneuver. The rapid cessation of positional vertigo and nystagmus adds evidence that HC-BPV is caused by dense particles that move within the canal whenever its orientation toward gravity is changed.

Female↗
PubMed1996

Recognizing syncope: pitfalls and surprises.

Loss of consciousness and falling are the key features of syncope. Common accompaniments include tonic and myoclonic muscle activity, eye deviations, automatisms, vocalizations and hallucinations which may render the distinction from epileptic seizures difficult. Differential diagnosis is based on the specific features and not the mere presence of these phenomena. Recognition of syncope depends also on accurate information about precipitants, premonitory symptoms and postictal events: the absence of postictal confusion has been identified as the single most powerful factor discriminating syncope from epileptic seizures whereas incontinence and head injury are common in both conditions. Investigations such as electroencephalogram, tilt testing and postictal prolactin or creatine kinase levels may be helpful but are never diagnostic in isolation. Exceptionally, hypoxic and epileptic mechanisms interact within a single attack.

Automatism↗
PubMed1996

The eye movements of syncope.

We videotaped the eye movements of syncope in 25 healthy volunteers who induced fainting by hyperventilation and Valsalva maneuver on a tilt table. In an additional three subjects, syncope was similarly induced during horizontal sinusoidal oscillation on a rotating chair while eye movements were recorded by electro-oculogram. Fourteen of 25 subjects experienced syncope on the tilt table. Six had downbeat nystagmus (DBN) at the onset that evolved into upward eye deviation, whereas seven showed isolated tonic upward deviation. In one subject the eyes remained in primary position. The gain of the vestibulo-ocular reflex (VOR) increased by 65% on average during syncope with concurrent vestibular stimulation. DBN, upward eye deviation, and increased VOR gain may all be caused by vestibular disinhibition caused by cerebellar hypoperfusion.

Adult↗
PubMed1995

[Clinical variants of pseudotumor cerebri syndrome].

Increased cerebrospinal fluid pressure of usually unknown etiology is called pseudotumor cerebri. The key symptoms are headache, papilledema and fluctuating visual disturbances. Six cases are presented to illustrate the clinical variability of this syndrome. Headache or papilledema may be missing in individual cases. The clinical diagnosis can be facilitated by the recognition of accessory signs and symptoms, such as VIth nerve palsy, tinnitus and other cranial nerve disorders or neck stiffness. For the therapeutic outcome it is essential to detect and monitor visual disturbances early in the course of the disease.

Adult↗