Disorders of Ocular Motility Due to Disease of the Brainstem, Cerebellum, and Diencephalon

2015 ◽  
pp. 836-915
Author(s):  
R. John Leigh ◽  
David S. Zee
Keyword(s):  
Developmental Disorders ◽  
Medial Longitudinal Fasciculus ◽  
Ocular Motility ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Abducens Nucleus ◽  
Cerebellar Syndromes ◽  
Vertical Gaze ◽  
Dorsal Midbrain Syndrome ◽  
Gaze Palsy

This chapter reviews clinical features (with illustrative video cases) and pathophysiology of medullary lesions, including Wallenberg’s syndrome and oculopalatal tremor. Manifestations and pathophysiology of three cerebellar syndromes are described (flocculus and paraflocculus, nodulus and ventral uvula, dorsal vermis and fastigial nucleus), applying these principles to interpret the effects of developmental disorders (e.g., Chiari malformation), hereditary ataxia, paraneoplastic cerebellar degeneration, cerebellar stroke, and cerebellar tumors. Characteristics of pontine lesions are discussed, including lesions of the abducens nucleus, paramedian pontine reticular formation (PPRF), internuclear ophthalmoplegia (INO), one-and-a-half syndrome, slow horizontal saccades, and saccadic oscillations. The effects of midbrain lesions are summarized, including lesions affecting the rostral interstitial nucleus of the medial longitudinal fasciculus (RIMLF), interstitial nucleus of Cajal, posterior commissure, and more diffuse processes causing slow vertical saccades or vertical gaze palsy (dorsal midbrain syndrome), including Whipple’s disease. Effects of lesions affecting the superior colliculus, thalamus, and pulvinar are also discussed.

scholarly journals Wall-eyed bilateral internuclear ophthalmoplegia in posterior circulation stroke-a case report

2021 ◽  
Vol 8 (11) ◽  
pp. 1752
Author(s):  
Mary Stephen A. ◽  
Jayasri P. ◽  
Harigaravelu P. J.
Keyword(s):  
Case Report ◽  
Neurological Impairment ◽  
Artery Occlusion ◽  
Basilar Artery Occlusion ◽  
Medial Longitudinal Fasciculus ◽  
Ocular Motility ◽  
Internuclear Ophthalmoplegia ◽  
Headache Patient ◽  
Vertical Gaze ◽  
Gaze Palsy

Internuclear ophthalmoplegia is characterised by restricted ocular motility in lateral gaze in which the affected eye shows impairment of adduction and it results from damage to medial longitudinal fasciculus (MLF). Wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) is an extremely rare neurological manifestation which has typical signs including primary gaze exotropia, vertical gaze palsy, ptosis, abducting nystagmus. The common and serious etiological factor is cerebrovascular accident involving the vessels supplying MLF and many cases have life threatening associated neurological impairment. In this case report we have discussed about a gentleman who presented with bilateral ptosis, primary gaze exotropia and headache. Patient found to have vertical gaze palsy and abducting nystagmus on examination. Computed tomography (CT) imaging shows infarct in pontine region and CT angiography revealed basilar artery occlusion supplying region of pons with involvement of posterior cerebral artery. Patient treated with antiplatelet and diplopia managed. Patient showed improvement on subsequent follow-up visits.

Structure of the primate oculomotor burst generator. I. Medium-lead burst neurons with upward on-directions

1991 ◽  
Vol 65 (2) ◽  
pp. 203-217 ◽  
Author(s):  
A. K. Moschovakis ◽  
C. A. Scudder ◽  
S. M. Highstein
Keyword(s):  
Eye Movements ◽  
Mesencephalic Reticular Formation ◽  
Medial Longitudinal Fasciculus ◽  
Posterior Commissure ◽  
Inferior Rectus ◽  
Interstitial Nucleus Of Cajal ◽  
Burst Neurons ◽  
Physiological Characterization ◽  
Highly Correlated ◽  
Oculomotor Complex

1. To investigate the structure of the primate burst generator for vertical saccades, we obtained intra-axonal records from vertical medium-lead burst neurons with upward on-directions (UMLBs) in alert, behaving squirrel monkeys, while monitoring their spontaneous eye movements. After physiological characterization, these UMLBs were injected with horseradish peroxidase. 2. UMLBs (n = 14) had no spontaneous activity and emitted bursts of action potentials that preceded rapid eye movements by approximately 6 ms. Parameters of the burst (duration and number of spikes) were highly correlated with parameters of the rapid eye movement (duration and amplitude of the upward displacement of the eyes). 3. The axons of six UMLBs projected to the oculomotor complex. Their somata (4 were recovered) were all in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). Their axons traveled caudally in the medial longitudinal fasciculus (MLF) and ramified in the interstitial nucleus of Cajal (NIC) before entering the oculomotor nucleus. Five axons terminated bilaterally in the subdivisions innervating the superior rectus and inferior oblique muscles and therefore were presumed to be excitatory. One axon terminated in the ipsilateral inferior rectus and superior oblique subdivisions of the oculomotor complex and was presumed to be inhibitory. 4. Additionally, our data demonstrate that the nucleus of the posterior commissure (nPC) may also contain UMLBs. The axon of one such neuron crossed the midline within the posterior commissure and provided terminal fields to the contralateral nPC, riMLF, NIC, and the mesencephalic reticular formation but not to the oculomotor complex. 5. In conclusion, our data demonstrate that the rostral mesencephalon of the monkey contains neurons that have both the activity and the connections that are necessary either to provide motoneurons innervating extraocular muscles of both eyes with the pulse of activity they display during upward saccades or to inhibit their antagonists. Furthermore, our data demonstrate that some UMLBs are better suited for closing the feedback path of the local feedback loop rather than for providing direct input to extraocular motoneurons.

scholarly journals Profile of Gaze Dysfunction following Cerebrovascular Accident

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Fiona J. Rowe ◽  
David Wright ◽  
Darren Brand ◽  
Carole Jackson ◽  
Shirley Harrison ◽  
...  
Keyword(s):  
Ocular Motility ◽  
Blurred Vision ◽  
Temporal Lobes ◽  
Cortical Areas ◽  
Gaze Holding ◽  
Brain Stroke ◽  
Horizontal Gaze ◽  
Vertical Gaze ◽  
Multicentre Cohort ◽  
Gaze Palsy

Aim. To evaluate the profile of ocular gaze abnormalities occurring following stroke. Methods. Prospective multicentre cohort trial. Standardised referral and investigation protocol including assessment of visual acuity, ocular alignment and motility, visual field, and visual perception. Results. 915 patients recruited: mean age 69.18 years (SD 14.19). 498 patients (54%) were diagnosed with ocular motility abnormalities. 207 patients had gaze abnormalities including impaired gaze holding (46), complete gaze palsy (23), horizontal gaze palsy (16), vertical gaze palsy (17), Parinaud’s syndrome (8), INO (20), one and half syndrome (3), saccadic palsy (28), and smooth pursuit palsy (46). These were isolated impairments in 50% of cases and in association with other ocular abnormalities in 50% including impaired convergence, nystagmus, and lid or pupil abnormalities. Areas of brain stroke were frequently the cerebellum, brainstem, and diencephalic areas. Strokes causing gaze dysfunction also involved cortical areas including occipital, parietal, and temporal lobes. Symptoms of diplopia and blurred vision were present in 35%. 37 patients were discharged, 29 referred, and 141 offered review appointments. 107 reviewed patients showed full recovery (4%), partial improvement (66%), and static gaze dysfunction (30%). Conclusions. Gaze dysfunction is common following stroke. Approximately one-third of patients complain of visual symptoms, two thirds show some improvement in ocular motility.

Anatomy and physiology of the primate interstitial nucleus of Cajal I. efferent projections

1996 ◽  
Vol 75 (2) ◽  
pp. 725-739 ◽  
Author(s):  
T. Kokkoroyannis ◽  
C. A. Scudder ◽  
C. D. Balaban ◽  
S. M. Highstein ◽  
A. K. Moschovakis
Keyword(s):  
Superior Colliculus ◽  
Reticular Formation ◽  
Mesencephalic Reticular Formation ◽  
Head Movements ◽  
Zona Incerta ◽  
Medial Longitudinal Fasciculus ◽  
Thalamic Nuclei ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Efferent Projections

1. The efferent projections of the interstitial nucleus of Cajal (NIC) were studied in the squirrel monkey after iontophoretic injections of biocytin and Phaseolus Vulgaris leucoagglutinin into the NIC. To ensure the proper placement of the tracer, the same pipettes were used to extracellularly record the discharge pattern of NIC neurons. 2. Three projection systems of the NIC were distinguished: commissural (through the posterior commissure), descending, and ascending. 3. The posterior commissure system gave rise to dense terminal fields in the contralateral NIC, the oculomotor nucleus, and the trochlear nucleus. 4. The descending system of NIC projections deployed dense terminal fields in the ipsilateral gigantocellular reticular formation and the paramedian reticular formation of the pons, as well as in the ventromedial and commissural nuclei of the first two spinal cervical segments. It also gave rise to moderate or weak terminal fields in the vestibular complex, the nucleus prepositus hypoglossi, the inferior olive, and the magnocellular reticular formation, as well as cell groups scattered along the paramedian tracts in the pons and the pontine and medullary raphe. 5. The ascending system of NIC projections gave rise to dense terminal fields in the ipsilateral mesencephalic reticular formation and the zona incerta as well as moderate or weak terminal fields in the ipsilateral centromedian and parafascicular thalamic nuclei. It also provided dense bilateral labeling of the rostral interstitial nucleus of the medial longitudinal fasciculus and the fields of Forel, and moderate or weak bilateral labeling of the mediodorsal, central medial, and central lateral nuclei of the thalamus. 6. Models of saccade generation that rely on feedback from the velocity-to-position integrators and include the superior colliculus in their local feedback loop are contradicted because no fibers originating from the NIC traveled to the superior colliculus to deploy terminal fields. 7. Consistent with its morphological and functional diversity, these data indicate that the primate NIC sends signals to a multitude of targets implicated in the control of eye and head movements.

The Neural Basis for Conjugate Eye Movements

2015 ◽  
pp. 386-473
Author(s):  
R. John Leigh ◽  
David S. Zee
Keyword(s):  
Posterior Parietal Cortex ◽  
Visual Area ◽  
Medial Longitudinal Fasciculus ◽  
Descending Pathways ◽  
Adaptive Optimization ◽  
Focal Lesions ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Medial Superior Temporal ◽  
Dorsolateral Prefrontal

This chapter draws on a range of studies of macaque and humans to forge an anatomical scheme for the control of gaze. At each stage, this scheme is used to predict effects of focal lesions on the control of gaze, with video examples. Contributions include the abducens nucleus, medial longitudinal fasciculus (MLF), and paramedian pontine reticular formation (PPRF) to horizontal gaze; the rostral interstitial nucleus of the medial longitudinal fasciculus (RIMLF), interstitial nucleus of Cajal, and posterior commissure to vertical gaze; cerebellar flocculus, paraflocculus, dorsal vermis, fastigial nucleus, and inferior olive to adaptive optimization of gaze. Cortical control of gaze by structures including primary visual cortex (V1), middle temporal visual area (MT, V5), medial superior temporal visual area (MST), posterior parietal cortex, frontal eye fields, supplementary eye fields, dorsolateral prefrontal cortex, cingulate cortex, descending pathways, thalamus, pulvinar, caudate, substantia nigra pars reticulata, subthalamic nucleus, and superior colliculus are each discussed.

VERTICAL GAZE PALSY AFTER THALAMIC STIMULATION FOR TOURETTE SYNDROME

Neurosurgery ◽  
2007 ◽  
Vol 61 (5) ◽  
pp. E1100-E1100 ◽  
Author(s):  
◽  
Linda Ackermans ◽  
Yasin Temel ◽  
Noel J.C. Bauer ◽  
Veerle Visser-Vandewalle
Keyword(s):  
Deep Brain Stimulation ◽  
Eye Movements ◽  
Tourette Syndrome ◽  
Brain Stimulation ◽  
Medial Longitudinal Fasciculus ◽  
Thalamic Stimulation ◽  
Pretectal Area ◽  
Vertical Gaze ◽  
Gaze Palsy ◽  
Deep Brain

Abstract OBJECTIVE We describe a patient who developed a vertical gaze paralysis after deep brain stimulation performed for intractable Tourette syndrome due to a small deep bleeding in the upper mesencephalon. CLINICAL PRESENTATION A 39-year-old man underwent thalamic deep brain stimulation for intractable Tourette syndrome. Immediately postoperatively, he had diplopia and dizziness. The neurological examination revealed vertical gaze palsy with preserved vertical oculocephalic movements. A postoperative computed tomography scan revealed a discrete high-density lesion across the midline at the distal end of the left electrode. This area corresponds with the pretectal area, including the rostral interstitial nucleus of the medial longitudinal fasciculus, with sparing of the oculomotor and rubral nuclei. INTERVENTION Six months postoperatively, maximal upward and downward smooth pursuit eye movements were achieved. Upward saccadic velocities were still reduced by 20 to 25 degrees. CONCLUSION This case report describes a complication that might demand special attention during the planning of thalamic deep brain stimulation for the treatment of Tourette syndrome. Examination of both horizontal and vertical eye movements during deep brain stimulation surgery is recommended.

scholarly journals Understanding Parinaud’s Syndrome

2021 ◽  
Vol 11 (11) ◽  
pp. 1469
Author(s):  
Juan Fernando Ortiz ◽  
Ahmed Eissa-Garces ◽  
Samir Ruxmohan ◽  
Victor Cuenca ◽  
Mandeep Kaur ◽  
...  
Keyword(s):  
Visual Field ◽  
Light Stimulus ◽  
Medial Longitudinal Fasciculus ◽  
Visual Field Defects ◽  
Superior Cerebellar Peduncle ◽  
Eyelid Retraction ◽  
Posterior Commissure ◽  
Interstitial Nucleus Of Cajal ◽  
Parinaud’S Syndrome ◽  
Field Defects

Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’s main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. In Parinaud’s syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. We did not find a reasonable explanation for squint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.

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