The spectrum of vertical gaze palsy following unilateral brainstem stroke

A single unilateral lesion, near the midline, may interrupt the pathways involved in vertical gaze just before and after they decussate, inducing an anatomically unilateral, but functionally bilateral, lesion. We report 11 patients with supranuclear vertical gaze palsies (two with conjugate upgaze palsy, four with combined up- and downgaze palsies, two with monocular elevation palsy, and three with vertical "one-and-a-half" syndrome) due to unilateral midbrain strokes.     

Reflex vertical gaze and the medial longitudinal fasciculus

Extraocular movements were investigated in a patient with bilateral vascular lesions of the medial longitudinal fasciculus. The patient showed voluntary and reflex horizontal gaze consistent with his lesion, but had absent reflex vertical gaze. Voluntary vertical gaze was present. Necropsy was performed, and the findings suggest that the medial longitudinal fasciculi in the pons conveys impulses for reflex vertical gaze, but are not required for voluntary vertical gaze.     

Convergence nystagmus and vertical gaze palsy of vascular origin

A case of convergence-retraction nystagmus with upward vertical gaze paralysis and skew deviation (right hypotropia), without any other neurological signs, is reported. The probably vascular lesion was located at the mesodiencephalic junction, lying between the right border of the posterior commissure, the right interstitial nucleus of Cajal and the periaqueductal grey matter, accounting for the three ocular motor signs. The particular interest of this case is due to the relative smallness of the lesion.     

Cerebellar control of ocular gaze stability

The ability to hold an eccentric position of gaze has been attributed to a brainstem network termed the ocular motor neural integrator. For this integrator to function properly, an intact cerebellum is necessary. This report describes a patient with cerebellar dysfunction who showed an unusual form of nystagmus: each slow phase had a waveform of increasing velocity. This contrasts with gaze paretic nystagmus, the more typical manifestation of cerebellar disorder, in which each slow phase has a waveform of decreasing velocity. Based on these observations and results from basic research, we propose that (1) the cerebellum controls neural integration in the brainstem by a positive feedback loop, and (2) pathological alterations in the strength of transmission (or gain) through the feedback loop cause the eyes to drift off target, with either an exponentially increasing (gain too high) or decreasing (gain too low) velocity.     

Paralysis of vertical gaze as a sequela of Wernicke's encephalopathy

In the acute phase of Wernicke's encephalopathy the treatment with thiamine results quickly in a normal ocular motor function. In a patient with severe and long-time alcoholism, and poor nutrition, an acute Wernicke's disease is reported in which a complete gaze palsy was associated with cerebellar symptoms, desorientation and anterograde amnesia. The treatment by thiamine, pyridoxine and folic acid resulted in the disappearance, in 1 week, of the extra-ocular symptoms. Lateral gaze palsy disappeared in 3 weeks, but vertical gaze palsy was unchanged after 8 months. Eye movement disorders rarely persist more than 1 week in well-treated patients. In this case, clinical signs and course, computed tomography have excluded another disease of the midbrain (i.e.: tumor, infarct, centro-pontine myelinolysis.) Hypotheses are considered to account for this fact: first, subclinical lesions persisting after a similar episode three years before; second, an abnormality of the transcetolase enzyme system: third, the association of the thiamine deficiency with a possible toxicity of very odd fooding habits. This patient, since several months, ate nothing but spoiled food with an admixture of strong alcoholic beverages.     

A hypothetical immunemediated unifying mechanism for the Holmes-Adie syndrome

The Holmes-Adie syndrome consists of pupillotonia, arreflexia and autonomic dysfunction. Some explanations for these different symptoms have been attempted, centred upon neuropathological and electrophysiological findings. A hypothetical immunemediated mechanism, as in the Guillain Barré syndrome, is presented in this paper for explaining the three chief symptoms of the syndrome.     

The strategic control of gaze direction in the Tower-of-London task

In this paper, we describe a novel approach to the study of problem solving involving the detailed analysis of natural scanning eye movements during the "one-touch" Tower-of-London (TOL) task. We showed subjects a series of pictures depicting two arrangements of colored balls in pockets within the upper and lower halves of a computer display. The task was to plan (but not to execute) the shortest movement sequence required to rearrange the balls in one half of the display (the Workspace) to match the arrangement in the opposite half (the Goalspace) and indicate the minimum number of moves required for problem solution. We report that subjects are more likely to look towards the Goalspace in the initial period after picture presentation, but bias gaze towards the Workspace during the middle of trials. Towards the end of a trial, subjects are once again more likely to fixate the Goalspace. This pattern is found regardless of whether the subjects solve problems by rearranging the balls in the lower or upper visual fields, demonstrating that this strategy correlates with discrete phases in problem solving. A second experiment showed that efficient planners direct their gaze selectively towards the problem critical balls in the Workspace. In contrast, individuals who make errors spend more time looking at irrelevant items and are strongly influenced by the movement strategy needed to solve the preceding problem. We conclude that efficient solution of the TOL requires the capacity to generate and flexibly shift between control sets, including those underlying ocular scanning. The role of working memory and the prefrontal cerebral cortex in the task are discussed.     

A case of left third nerve palsy and contralateral vertical gaze palsy with medial midbrain infarction]

An 81-year-old man developed oculomotor nerve palsy of the left eye and vertical gaze palsy of the right eye due to left medial midbrain infarction. His left eyelid was ptotic and the pupil was dilated. His right eye showed normal horizontal movement and Bell's phenomenon was preserved although the oculocephalic reflex was incomplete. There were no other abnormal neurological findings. The brain MRI revealed a high-intensity lesion in left medial midbrain on T2 weighted image. This lesion involved the oculomotor nerve nucleus, the interstitial nucleus of Cajal, and the rostral intersititial nucleus of the medial longitudinal fasciculus (riMLF). We thought that upward gaze palsy of the right eye was resulted from the infarction of the left riMLF or disruption of the axonal collateral of upward gaze fibers in the left oculomotor nucleus. Downward gaze palsy was resulted from the damage of the downward gaze fibers before their decussation, or the damage of the left interstitial nucleus of Cajal. This case provides evidence that unilateral lesion of the midbrain could cause contralateral vertical gaze palsy.     

Preview control of gaze saccades: Efficacy of prediction modulates eye-head interaction during human gaze saccades

Abstract

Healthy human subjects made orienting saccades towards visual target stimuli, either with the head fixed or during intended time optimal head movements. Four experimental paradigms were used to study the influence of target predictability on eye-head coordination. They represented different sequences of horizontal target steps; that were varied in amplitude, direction and frequency. In some subjects midflight perturbations of the active head movements were applied to examine the intrasaccadic vestibulo-ocular reflex (VOR). In coordinated gaze saccades, latencies and dynamics of the eye saccade and the additional head trajectory demonstrated specific task-related changes with respect to the head fixed condition. Highly predictable target steps result in the relatively earlier onset of the head movement and an increase of the intrasaccadic head contribution to the overall gaze displacement. Differences in the level of VOR suppression became significant when gaze amplitudes exceeded 60°. Consequently, an effective speed up of large gaze saccades was found with increased target predictability. We concluded’ that eye—head coordination during human gaze saccades underlies high level preview control mechanisms. A parametric modulation of the intrasaccadic VOR maintains gaze accuracy, although the actual contribution of the more flexible head motor system varied, depending on gaze amplitude and prediction. The efficacy of preview control depends on interaction of these factors. [Neurol Res 1993; 15: 417-432]     

Locomotor control by the brainstem and spinal cord

One of the fundamental characteristics of animal is locomotion. Although not visually apparent, goal-directed locomotor movements are always accompanied by automatic adjustment of muscle tone and postural reactions. Because the basic and essential mechanisms that control postural muscle tone and locomotion are located in the brainstem and spinal cord, a variety of locomotor behaviors are achieved by the projections from the forebrain structures (cerebral cortex, basal ganglia, and limbic-hypothalamic systems) and cerebellum to the brainstem-spinal cord. In this short review, we particularly focus on the role of the brainstem and spinal cord in the control of postural muscle tone and generation of locomotor rhythm. Abnormalities in the convergence inputs from the forebrain structures to the brainstem-spinal cord are further discussed in relation to the pathogenesis of disturbances in locomotor control.     

Clinicopathological study of atypical motor neuron disease with vertical gaze palsy and ballism

The case of a 38-year-old patient with rapidly progressing motor neuron disease, complicated by major dysfunction of the extrapyramidal system and of vertical gaze is described. Neuropathological examination revealed a degenerative process that severely affected the lower motor neurons, as well as the neurons of the pars compacta of the substantia nigra, the nucleus of Darkschewitsch, the nucleus interstitialis of Cajal, the colliculi superiores, and the pallidum. The long tracts were unaffected at all levels of the brain stem and spinal cord. There was no convincing evidence for the presence of a multiple system atrophy or progressive supranuclear palsy; the results rather revealed a pattern of vulnerability characteristic of a variant of motor neuron disease. Received: 9 November 1999 / Revised, accepted: 10 December 1999     

Maturation of otolith-related brainstem neurons in the detection of vertical linear acceleration in rats

To investigate the critical maturation time of otolith-related neurons in processing vertical orientations, rats (postnatal day 4 to adults) were studied for functional activation of c-fos expression in brainstem neurons by immuno-/hybridization histochemistry. Conscious rats were subjected to sinusoidal linear acceleration along the vertical plane. Labyrinthectomized and/or stationary controls showed only sporadically scattered Fos-labeled neurons in the vestibular nuclei, confirming an otolithic origin of c-fos expression. Functionally activated Fos expression in neurons of the medial and spinal vestibular nuclei and group x were identifiable by P7 and those in group y by P9. A small number of Fos-labeled neurons characterized by small soma size were found in the ventral part of lateral vestibular nucleus by P9. Other vestibular-related areas such as prepostitus hypoglossal nucleus, gigantocellular reticular nucleus and locus coeruleus of normal experimental rats showed functionally activated c-fos expression at P7. Neurons in dorsal medial cell column and beta subnucleus of the inferior olive only showed functionally activated c-fos expression by the second postnatal week. These findings revealed a unique critical maturation time for each of the vestibular-related brainstem areas in the recognition of gravity-related vertical head orientations. By mapping the three-dimensional distribution of Fos-immunoreactive neurons, we found an even distribution of otolith-related neurons within the spinal vestibular nucleus in groups x and y but a clustered distribution in the middle-lateral-ventral part of the medial vestibular nucleus. Taken together, our findings reveal the developmental profile of neuronal subpopulations within the vertical otolith system, thereby providing an anatomical basis for postnatal coding of gravity-related vertical head movements.     

Feedback in the brainstem: An excitatory disynaptic pathway for control of whisking

Sensorimotor processing relies on hierarchical neuronal circuits to mediate sensory‐driven behaviors. In the mouse vibrissa system, trigeminal brainstem circuits are thought to mediate the first stage of vibrissa scanning control via sensory feedback that provides reflexive protraction in response to stimulation. However, these circuits are not well defined. Here we describe a complete disynaptic sensory receptor‐to‐muscle circuit for positive feedback in vibrissa movement. We identified a novel region of trigeminal brainstem, spinal trigeminal nucleus pars muralis, which contains a class of vGluT2+ excitatory projection neurons involved in vibrissa motor control. Complementary single‐ and dual‐labeling with traditional and virus tracers demonstrate that these neurons both receive primary inputs from vibrissa sensory afferent fibers and send monosynaptic connections to facial nucleus motoneurons that directly innervate vibrissa musculature. These anatomical results suggest a general role of disynaptic architecture in fast positive feedback for motor output that drives active sensation. J. Comp. Neurol. 523:921–942, 2015. © 2014 Wiley Periodicals, Inc.     

Midbrain ischemia presenting as vertical gaze palsy: value of diffusion-weighted magnetic resonance imaging

BACKGROUND: Conventional magnetic resonance imaging may fail to identify very small but clinically relevant acute subcortical brain infarcts. Diffusion-weighted magnetic resonance imaging (DWI) is very sensitive and specific for acute cerebral ischemia and should contribute to the early detection of such lesions. METHODS: We analyzed 6 patients who presented with acute vertical gaze palsy and in whom DWI was performed within 1-6 days from symptom onset. RESULTS: DWI accurately identified ischemia in an area supplied by the posterior thalamosubthalamic paramedian artery in all patients. T(2)-weighted and FLAIR imaging failed to identify the clinically relevant lesion in 2 and 3 patients, respectively. CONCLUSION: DWI improves the clinicoanatomical correlation in patients presenting with supranuclear oculomotor disturbances.     

Cholinergic brainstem sites for gain control of vestibulospinal reflexes in cats

Decerebrate cats were injected with carbachol into the locus coeruleus (LC) or with carbachol or bethanechol into the dorsal pontine reticular formation (pRF) of one side; recordings were made of the tonic contraction of forelimb extensor muscles of both sides and of their responses to sinusoidal roll tilt of the animal. Both drugs had similar effects when injected into the pRF: a decrease in the tonic contraction of limb extensors and a greatly enhanced amplitude and gain with slightly decreased phase lead in the responses to animal tilt of the forelimb extensor, triceps brachii, ipsilateral to the side of injection. Injected into the LC, carbachol produced a response opposite to the above: it increased the tonic contraction of limb extensors ipsilateral to the side of injection, but decreased the amplitude and gain of the EMG responses of limb extensor muscles to labyrinth stimulation induced by sinusoidal tilt. These findings did not depend on changes in posture since they were still observed when postural EMG activity was maintained constant by appropriate changes in static stretch of the muscle. Moreover, the magnitude of the effects increased in a dose-dependent manner. Results suggest that cholinergic activation of dorsal pRF neurons through muscarinic receptors increases the background discharge of medullary inhibitory reticulospinal (RS) system neurons, thus increasing their modulatory influence. Further, it is postulated that cholinergic activation of LC neurons would cause them to inhibit this tonic facilitatory drive by the pRF. Common to both sites of carbachol injection is the increase in phase lag of the EMG response of limb extensors to animal tilt.(ABSTRACT TRUNCATED AT 250 WORDS)     

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

Deviations of the position of the ey in the roll plance, ocular trosion (OT), and the subjective visual vertical (SVV) wre systematically studied in 111 patients with acure vascular brainstem lesions. Of the 111 partents, 104 (94%) showed a direction-specific pathological tilt of the static SVV in our series, Sevenry-one (83%) of 86 partients exhibited pathological static OT of one (47%) or both (36%) eyes. OT and SVV tilts are therefore sensitive signs in acture unilateral brainstem disorders. Measurements of SVV and OT may prove to be useful components of the neuroophthalmological evaluation. With respect to the directions of pathological tilt, SVV an OT are generally in the same direction. Based on neuroimaging, we conclude that all unilateral brainstem lesion 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 tills of OT and SVV. Evidence is presented that pathological tilts of OT and SVV are secondary to a dysfunction of the tonic bilateral vestibular imputs that stabilize the eyes and head in normal upright position in the roll plance and dominate our perception of verticality.