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Biomedical subjects

W Waespe

Publications and source records attributed to W Waespe.

At least 55 records · Page 3Linked to original sources
PubMed1990

Oculomotor disturbances during visual-vestibular interaction in Wallenberg's lateral medullary syndrome.

Transient and lasting oculomotor disturbances during visual-vestibular interaction are described in 9 patients with Wallenberg's lateral medullary syndrome. In all patients magnetic resonance imaging (MRI) demonstrated a single focal area of pathological signal intensity in the (dorso)-lateral medulla suggesting infarction. In 2 of these 9 patients and in 3 further patients with no medullary signs, the infarction involved the cerebellar territory of the posterior inferior cerebellar artery (PICA). Acutely, all patients with Wallenberg's syndrome (except 1) had saccadic lateropulsion and spontaneous nystagmus in light with the horizontal fast component beating to the contralateral normal side. The velocity of the slow drift to the side of the lesion was dependent on eye position and induced a characteristic asymmetry of the visually and vestibularly elicited slow eye movements. In most patients smooth pursuit, optokinetic nystagmus and visual suppression of the vestibulo-ocular reflex were still impaired when this spontaneous drift was minimal or absent. The oculomotor disturbances in patients with and without cerebellar infarction are compared. The following conclusions are made. (1) The spontaneous drift that is dependent on eye position is mostly created by 'ocular lateropulsion', that is, a tonic bias within the oculomotor system which may have several sources. (2) The abnormalities and asymmetries of oculomotor responses during visual-vestibular stimulation cannot solely be explained by this spontaneous drift and its interaction with otherwise normal eye movements. Instead, structures and pathways are damaged in Wallenberg's syndrome which mediate visual and/or motor signals important for the cerebellar control of visually-guided slow eye movements. (3) Damage to these pathways occurs in the lateral medulla, as the MRI findings show that in most patients the cerebellum is rarely involved, but no definite conclusion can be made as to which of the fibres travelling in the inferior peduncle to the cerebellum may be interrupted.

Adult↗
PubMed1989

[Neurological gait changes in old age: basic principles, senile gait].

Gait abnormalities and falls often occur in the elderly, and it is often difficult for the practitioner to distinguish between a specific disease causing disordered gait and gradual changes due to "normal" involution. Based on the biomechanics and the neural control mechanisms of normal adult gait, characteristics of the "senile gait" are described. The senile gait abnormality is regarded as a clinical entity ascribed to age alone and its many cerebellar, extrapyramidal and cerebrofrontal changes, all of which may give rise to disordered central programming of upright stance and gait. The need for a careful evaluation of the elderly patient's station and gait is stressed.

Aged↗
PubMed1989

Oculomotor functions of the flocculus and the vestibular nuclei after bilateral vestibular neurectomy.

Ito's hypothesis of an important role of the flocculus of the vestibulocerebellum in the immediate visual control of the VOR during visual-vestibular interaction has received substantial support. Nevertheless, several parts in this hypothesis are unclear, at least in primates. In normal monkey, vestibularly driven neurones in the vestibular nuclei do not carry signals which are adequate to account for the full range of eye movement responses during optokinetic tracking (OKN) and different situations of visual-vestibular interaction (especially VOR-suppression). Thus these neurones seem not to be located at the final stage where floccular "gaze-velocity" Purkinje cells (PCs) exert their control function on the three-neurone-reflex arc. The signals of these "central" vestibular neurones (if relevant for the oculomotor output) must further be processed. After bilateral vestibular neurectomy (BVN) only a small number of vestibular nuclei neurones were found with eye velocity sensitivities during smooth pursuit tracking (SP) and OKN in the range of those of floccular PCs (also after BVN), and with the appropriate polarity of modulation. Our difficulties in finding neurones in the vestibular nuclei which, according to their neurophysiological behaviour, could be main target cells of floccular PCs, either in normal or in BVN monkeys, are discussed.

Action Potentials↗
PubMed1989

[The physiologic and anatomic principles of rapid eye movements (saccades) and their clinical significance].

Our understanding of the organisation of eye movements has been greatly expanded in recent years, mainly due to studies in animals. A review of the clinically important neurophysiological and anatomical aspects of the generation of rapid eye movements (saccades) will be presented. A knowledge of these basic aspects will assist the clinician's investigation and understanding of pathological eye movements in patients.

Brain↗
PubMed1988

[Carotid artery dissection. Case examples and review].

"Spontaneous" dissection of the internal carotid artery is a not unusual cause of stroke, particularly in younger subjects. Initial signs are typical, whereas the spectrum of neurological deficits is wide. Three selected case records are presented which demonstrate the spectrum of symptoms and the management of this disease.

Adult↗
PubMed1988

[Olivopontocerebellar atrophy as an important differential diagnosis in atactic gait disorders in elderly patients].

The sporadic form of olivo-ponto-cerebellar atrophy (OPCA) is described in 5 patients. The diagnosis was confirmed by autopsy in one patient. The OPCA can be suspected from the history and symptoms if neuroradiologic examination also demonstrates atrophy of the cerebellum and pons. OPCA is a rare but important cause of a progressive gait disturbance in the elderly patient. The differential diagnosis of atactic gait is discussed.

Brain↗
PubMed1988

[Rapid eye movements (saccades): review of their physiological and anatomical basis and their clinical significance].

Our understanding of the organization of eye movements has been greatly expanded in recent years, mainly due to studies in animals. A review of the clinically important neurophysiological and anatomical aspects of the organization of rapid eye movements (saccades) is presented. A knowledge of these basic aspects will assist the clinician's investigation and understanding of pathologic eye movements in patients.

Action Potentials↗
PubMed1988

Neurotoxicity of antituberculous drugs in a patient without active tuberculosis.

A 56-year old patient presented 3 months after initiation of an antituberculous regimen with Isoniacid (INH, 5 mg/kg daily), Ethambutol (20 mg/kg daily) and Rifampicin (675 mg daily) a mild sensory polyneuropathy and a bilateral retrobulbar neuritis which progressed to a severe optic atrophy. Multiple hyperintense foci were detected with NMR-imaging in the cerebral white matter suggestive of demyelination. INH and Ethambutol are known for their neurotoxic effects but suggestion was made that neurologic signs may not be due to drug neurotoxicity but could be induced by immunological processes initiated by the tubercle bacillus. In the reported patient the suspected tuberculosis of the urogenital tract was never proved histologically. Most likely his neurological symptoms were therefore cause by the administration of INH and Ethambutol. Patients with a low serum zinc level and a slow acetylation of INH are reported to be at special risk; both factors were present in our patient.

Antitubercular Agents↗
PubMed1988

Lower cranial nerve palsies due to internal carotid dissection.

A 41-year-old man experienced intense headache and neck pain, bruits, and a complete unilateral cranial nerve palsy IX-XII (Collet-Sicard syndrome) after a trivial back trauma. Magnetic resonance imaging and angiography demonstrated features of bilateral internal carotid artery dissection with aneurysm formation at the base of the skull compressing the nerves at the level of the jugular foramen. Severe dysphagia persisted for 1 month but rapidly improved after occlusion of the carotid aneurysm with a detachable balloon.

Adult↗
PubMed1988

[Epidural anesthesia in a patient with Friedreich's ataxia].

Friedreich's ataxia (FA), a hereditary disease with degenerative changes localized chiefly in the spinal cord and cerebellum, is characterized clinically by ataxia, absence of tendon reflexes, loss of proprioceptive sensation, and extensor plantar responses. There are only a few reports on anesthesia for patients with FA. General but not regional anesthesia is usually recommended because a persistent aggravation of symptoms is feared with regional anesthesia. We report a 31-year-old gravida 1 para 0 patient with FA who was admitted at the 20th week of gestation for induced abortion, curettage and tubal ligation. Familial FA was diagnosed at the age of 15, and since the age of 23 the patient had been confined to a wheelchair. As she strictly declined general anesthesia, epidural analgesia with 0.125% bupivacaine and morphine was used for 14 h, during which period induced abortion by prostaglandin was performed. This was followed by epidural anesthesia with 2% lidocaine for curettage and laparoscopic tubal ligation. A reduced dosage of local anesthetics, as commonly recommended during pregnancy, was used. Neurological consultation before and 1 day, 6 weeks, and 7 months after operation revealed no undue exacerbation of symptoms. Our case report suggests that epidural anesthesia can safely be administered to a patient with FA.

Abortion, Induced↗
PubMed1987

Slow eye movements induced by apparent target motion in monkey.

Slow eye movements were observed while the monkey fixated on a subject-stationary, small target light in front of a moving optokinetic drum in an attempt to suppress optokinetic nystagmus (OKN). These slow eye movements of low amplitude were directed opposite to the moving optokinetic stimulus and, hence, were not identical to slow phases of incompletely suppressed OKN. It is assumed, based on comparable findings in humans, that these slow eye movements are induced by a perceived target motion, i.e. by the perception of an apparent motion of the subject-stationary fixation light opposite to the actual motion of the optokinetic drum.

Animals↗
PubMed1986

Characteristics of eye velocity storage during periods of suppression and reversal of eye velocity in monkeys.

An eye velocity storage mechanism has been postulated in the vestibulo-optokinetic system to account for the prolongation of vestibular nystagmus (VN) and the occurrence of optokinetic after-nystagmus (OKAN). Presentation of a subject-stationary full-field surround during VN and OKAN (= full-field fixation) rapidly reduces activity related to eye velocity of the storage mechanism. If the subject-stationary full-field surround is presented for short periods during VN or OKAN, nystagmus resumes when the animal is again in darkness, but at a lesser velocity than would be predicted from a control response. This reduction in peak eye velocity after fixation reflects a decrease in activity of the storage mechanism due to full-field fixation. This decrease in activity occurs with a shorter time constant compared to that in control trials, it has been called "dumping". We demonstrate that a subject-stationary small target light presented during VN or OKAN (= target fixation) also reduces activity of the storage mechanism with a time constant slightly greater than that for full-field fixation, but still considerably smaller than that in control trials. In 3 monkeys the time constant of discharge was reduced during the post-rotatory period from 20 s in control trials to 4.6 s by fixation of a single target light and to 2.9 s by fixation of a full-field. The time constant of discharge was reduced during OKAN from 13.2 s in control trials to 3.8 s by target fixation and to 2.6 s by full-field fixation. We report a second experimental paradigm with which the dynamics of visual-vestibular interaction involving the eye velocity storage mechanism is analysed by means of transient step responses. In this paradigm eye velocity due to activation of the storage mechanism (OKAN) is forced to reverse by a short exposure to a full-field moving in the opposite direction of the slow phases of nystagmus. Short periods of eye velocity reversal did not reduce activity of the storage mechanism more rapidly than fixation, i.e. suppression of eye velocity alone. Fixation of a full-field or of a single target light during vestibular or optokinetic stimulation reduces peak nystagmus velocity after stimulation when monkeys are in darkness. Suppression of OKN by target fixation during full-field stimulation reduces the initial eye velocity of OKAN to 15-20% compared to the OKAN velocity when OKN is allowed to occur.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Dynamic modification of the vestibulo-ocular reflex by the nodulus and uvula.

The time constant of the decay of slow-phase eye velocity of postrotatory nystagmus or optokinetic after-nystagmus is reduced during exposure to a stationary visual surround (visual suppression). It is also reduced after tilting the head (tilt suppression). A "dump" mechanism in the vestibulo-ocular reflex has been proposed to rapidly discharge activity from the central vestibular system during both types of suppression. Monkeys lost this mechanism after lesions of the nodulus and uvula. They also lost the ability to habituate the time constant of nystagmus on repeated exposure to optokinetic and vestibular stimuli. Periodic alternating nystagmus, which is believed to represent an instability in the vestibulo-ocular reflex, was observed in two of three monkeys. These data indicate that the nodulus and uvula play an important role in suppressing, habituating, and stabilizing the vestibulo-ocular reflex.

Animals↗
PubMed1985

Purkinje cell activity in the flocculus of vestibular neurectomized and normal monkeys during optokinetic nystagmus (OKN) and smooth pursuit eye movements.

Single unit activity was recorded in the primate flocculus after the vestibular nerves were cut (bilateral vestibular neurectomy) during optokinetic nystagmus (OKN), smooth pursuit eye movements (SP) and whole field visual stimulation with gaze fixed on a stationary target light (OKN-suppression). Following vestibular neurectomy monkeys had no vestibular responses and no optokinetic after-nystagmus (OKAN) in the horizontal plane. However, OKN slow phases still reached steady state velocities of up to 100 deg/s. After neurectomy, simple spike (SS) activity of Purkinje cells (P-cells) was modulated in relation to eye velocity, regardless of whether eye velocity was induced by a small target light moving in darkness (SP) or by a moving visual surround (OKN). In over 90% of the P-cells firing rate increased with eye velocity to the ipsilateral side and decreased with velocities to the contralateral side. Modulation in firing rate increased monotonically with increasing eye velocity. The strength of modulation was similar during SP and OKN for the same eye velocity. The change in firing rate of P-cells in response to a sudden change in optokinetic stimulus velocity contained a component related to eye velocity and a component related to eye acceleration. Only a few P-cells were also modulated with image slip velocity during OKN-suppression. The modulation of P-cells during SP and OKN was compared in normal and vestibular neurectomized monkeys. The sensitivity of floccular P-cells to eye velocity during SP was 1.14 imp X s-1/deg X s-1 in normal monkey and 1.28 imp X s-1/deg X s-1 after neurectomy. The similarity of eye velocity sensitivities demonstrates that neurectomy does not change the characteristics of floccular P-cell modulation during SP. In contrast, during OKN modulation of P-cells is quite different in normal and neurectomized monkey. In normal monkey, P-cells are modulated during steady state OKN for eye velocities above 40-60 deg/s only. This threshold velocity corresponds approximately to the maximal initial OKAN velocity (i.e. OKAN saturation velocity). After neurectomy, the threshold velocity is 0 deg/s and P-cells are modulated during steady state OKN also over ranges of eye velocities that do not cause a response in normal monkey. Sensitivities of P-cells to eye velocity during OKN for eye velocities above the threshold velocity are 1.0 imp X s-1/deg X s-1 in neurectomized monkey and 1.43 imp X s-1/deg X s-1 in normal monkey.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

Optokinetic nystagmus (OKN) and optokinetic after-responses after bilateral vestibular neurectomy in the monkey.

The superior branch of the vestibular nerve containing peripheral axons of primary afferents originating in the lateral and anterior semicircular canals was cut bilaterally in three monkeys (vestibular neurectomy). Vertical and horizontal components of eye position were monitored by electro-oculography (EOG) during different stimulus and behavioral paradigms. Postoperatively, monkeys were unable to hold their eyes in eccentric lateral positions in complete darkness. The eyes drifted slowly back to the primary position where eye drift was minimal (null-zone). After vestibular neurectomy the time constant of the eye position integrator in darkness was 4-8 s. Constant velocity optokinetic stimuli produced peak velocities of horizontal OKN that were similar to those before operation. Consistent optokinetic after-responses could not be observed after neurectomy for stimulus durations of less than 60 s. However, with stimulus periods greater than 60-120 s a drift near the primary position of the eyes appeared in darkness which had the same direction as the slow phases of the preceding OKN. Drift velocity was too high to be explained by drift due to the imperfect eye position integrator alone. We assume that drift after prolonged optokinetic stimulation is a combination of an after-response similar as it can be observed after smooth pursuit and of drift due to an imperfect eye position integrator. Secondary optokinetic after-nystagmus was not observed after neurectomy.

Animals↗
PubMed1984

Purkinje cell activity in the primate flocculus during optokinetic stimulation, smooth pursuit eye movements and VOR-suppression.

Purkinje cell (PC) activity in the flocculus of trained monkeys was recorded during: 1) Vestibular stimulation in darkness. 2) Suppression of the vestibulo-ocular reflex (VOR-supp) by fixation of a small light spot stationary with respect to the monkey. 3) Visual-vestibular conflict (i.e. the visual surround moves together with the monkey during vestibular stimulation), which leads to attenuation or suppression of vestibular nystagmus. 4) Smooth pursuit eye movements. 5) Optokinetic nystagmus (OKN). 6) Suppression of nystagmus during optokinetic stimulation (OKN-supp) by fixation of a small light spot; whereby stimulus velocity corresponds then to image slip velocity. Results were obtained from PCs, which were activated with VOR-supp during rotation to the ipsilateral side. The same PCs were also modulated during smooth pursuit and visual-vestibular conflict. No tonic modulation during constant velocity OKN occurred with slow-phase nystagmus velocities below 40-60 deg/s. Tonic responses were only seen at higher nystagmus velocities. Transient activity changes appeared at the beginning and end of optokinetic stimulation. PCs were not modulated by image slip velocity during OKN-supp. The results show that in primates the same population of floccular PCs is involved in different mechanisms of visual-vestibular interaction and that smooth pursuit and certain components of OKN slow-phase velocity share the same neural pathway. It is argued that the activity of these neurons can neither be related strictly to gaze, eye or image slip velocity; instead, their activity pattern can be best interpreted by assuming a modulation, which is complementary to that of central vestibular neurons of the vestibular nuclei, in the control of slow eye movements.

Animals↗