Seesaw nystagmus with internuclear ophthalmoplegia from bilateral dorsomedial pons and left thalamus infarction: a case report.

BACKGROUND: We describe for the first time the clinical features and mechanisms of a bilateral dorsomedial pons and left thalamus infarction with seesaw nystagmus and internuclear ophthalmoplegia. CASE PRESENTATION: A 62-year-old Chinese man was hospitalized for sudden-onset dizziness, diplopia, and gait disturbance. A neurological examination revealed seesaw nystagmus and internuclear ophthalmoplegia. Magnetic resonance imaging disclosed an acute infarction confined to the bilateral dorsomedial pons and left thalamus. Subsequently, 2 weeks of antithrombotic therapy led to an improvement in his symptoms. CONCLUSIONS: This case illustrates that the acute onset of seesaw nystagmus and internuclear ophthalmoplegia accompanied by risk factors for cerebrovascular diseases are highly suggestive of brainstem infarction.

Nystagmus And Beyond: A Rare Ocular Motility Disorder.

Joubert syndrome is a rare autosomal recessive disorder predominantly involving the cerebellar vermis and brain stem. It is characterized clinically by global developmental delay, abnormal ocular movements, hypotonia, ataxia, intellectual disability and neonatal breathing abnormalities. Due to its uncommon and unconventional presentation, its diagnosis is usually delayed. Diagnosis of this atypical disease essentially relies upon the atypical finding of the "molar tooth" sign on Magnetic Resonance Imaging (MRI). We report a case of a 5-year-old boy who presented with abnormal eye movements, regression of milestones and developmental delay. MRI investigation revealed the distinctive molar tooth sign and bat wing shaped 4th ventricle. It requires high levels of clinical suspicion and holistic approach to such children who present with delayed milestones and abnormal eye movements, to reach at early detection and diagnosis of such rare pathologies.

Anteromedial thalamic infarct: a rare presentation.

We report a rare presentation of an anteromedial thalamic infarct in a 50-year-old woman with acute onset left eye ptosis, vertical gaze paresis and confusion. MRI identified an acute left anteromedial thalamic infarct with a severe left P1 stenosis. Thalamic infarcts are associated with marked neurobehavioural disturbances with dominant thalamic lesions causing language deficits, verbal perseveration, memory disturbances, abulia and disorientation. Ocular movement deficits can also be present and typically accompany paramedian lesions. Rarely, patients can develop an ipsilateral ptosis. We discuss these symptoms and review the literature.

A case of double depressor palsy followed by pursuit deficit due to sequential infarction in bilateral thalamus and right medial superior temporal area.

BACKGROUND: We present a unique case of a patient who suffered two rare events affecting the supranuclear control, first of the vertical and second of the horizontal eye movements. The first event involved bilateral thalamic infarcts that resulted in double depressor palsy. The second event occurred 1 year later and it involved supranuclear control of horizontal eye movements creating pursuit deficit. CASE PRESENTATION: A 47-year-old male presented with complaints of diplopia upon awakening. He had atrial fibrillation, mitral valve regurgitation, aortic valve regurgitation, and a history of spleen infarction 1 year ago. His right eye was hypertrophic and right eye downgaze was limited unilaterally of equal degree in adduction and abduction. The patient was diagnosed with double depressor palsy of the right eye. Magnetic resonance imaging (MRI) of the brain showed an old infarction of the left thalamus, and diffusion MRI showed acute infarction of the right thalamus. The patient's daily warfarin dose was 2 mg and it was increased to 5 mg with cilostazol 75 mg twice a day. Seven weeks later, the patient's ocular movement revealed near normal muscle action, and subjectively, the patient was diplopia free. At follow-up 12 months later, the patient revisited the hospital because of sudden onset of blurred vision on right gaze. He was observed to have smooth pursuit deficit to the right side, and orthophoric position of the eyes in primary gaze. MRI of the brain showed an acute infarction in the right medial superior temporal area. CONCLUSIONS: The patient experienced very rare abnormal eyeball movements twice. This case highlights the importance of evaluating vertical movement of the eyes and vascular supplies when patients present with depressor deficit and supports the theory of a supranuclear function in patients who present with pursuit deficit.

Age-related deficits in voluntary control over saccadic eye movements: consideration of electrical brain stimulation as a therapeutic strategy.

Sudden changes in our visual environment trigger reflexive eye movements, so automatically they often go unnoticed. Consequently, voluntary control over reflexive eye movements entails considerable effort. In relation to frontal-lobe deterioration, adult aging adversely impacts voluntary saccadic eye movement control in particular, which compromises effective performance of daily activities. Here, we review the nature of age-related changes in saccadic control, focusing primarily on the antisaccade task because of its assessment of 2 key age-sensitive control functions: reflexive saccade inhibition and voluntary saccade generation. With an ultimate view toward facilitating development of therapeutic strategies, we systematically review the neuroanatomy underpinning voluntary control over saccadic eye movements and natural mechanisms that kick in to compensate for age-related declines. We then explore the potential of noninvasive electrical brain stimulation to counteract aging deficits. Based on evidence that anodal transcranial direct current stimulation can confer a range of benefits specifically relevant to aging brains, we put forward this neuromodulation technique as a therapeutic strategy for improving voluntary saccadic eye movement control in older adults.

Post-traumatic Vertical Gaze Paresis in Nine Patients: Special Vulnerability of the Artery of Percheron in Trauma?

PURPOSE: The purpose was to present a case series of vertical gaze paresis in patients with a history of cranioencephalic trauma (CET). METHODS: The clinical characteristics and management are presented of nine patients with a history of CET secondary to motor vehicle accidents with associated vertical gaze paresis. RESULTS: Neuroimaging studies indicated posttraumatic contusion of the thalamic-mesencephalic region in all nine patients who corresponded to the artery of Percheron region; four patients had signs of hemorrhagic transformation. Vertical gaze paresis was present in all patients, ranging from complete paralysis of the upward and downward gaze to a slight limitation of upward gaze. DISCUSSION: Posttraumatic vertical gaze paresis is a rare phenomenon that can occur in isolation or in association with other neurological deficits and can cause a significant limitation in the quality-of-life. Studies in the literature have postulated that the unique anatomy of the angle of penetration of the thalamoperforating and lenticulostriate arteries makes these vessels more vulnerable to isolated selective damage in certain individuals and can cause-specific patterns of CET.

Impairment of saccade adaptation in a patient with a focal thalamic lesion.

The frequent jumps of the eyeballs-called saccades-imply the need for a constant correction of motor errors. If systematic errors are detected in saccade landing, the saccade amplitude adapts to compensate for the error. In the laboratory, saccade adaptation can be studied by displacing the saccade target. Functional selectivity of adaptation for different saccade types suggests that adaptation occurs at multiple sites in the oculomotor system. Saccade motor learning might be the result of a comparison between a prediction of the saccade landing position and its actual postsaccadic location. To investigate whether a thalamic feedback pathway might carry such a prediction signal, we studied a patient with a lesion in the posterior ventrolateral thalamic nucleus. Saccade adaptation was tested for reactive saccades, which are performed to suddenly appearing targets, and for scanning saccades, which are performed to stationary targets. For reactive saccades, we found a clear impairment in adaptation retention ipsilateral to the lesioned side and a larger-than-normal adaptation on the contralesional side. For scanning saccades, adaptation was intact on both sides and not different from the control group. Our results provide the first lesion evidence that adaptation of reactive and scanning saccades relies on distinct feedback pathways from cerebellum to cortex. They further demonstrate that saccade adaptation in humans is not restricted to the cerebellum but also involves cortical areas. The paradoxically strong adaptation for outward target steps can be explained by stronger reliance on visual targeting errors when prediction error signaling is impaired.

Effects of hyperbaric oxygen on eye tracking abnormalities in males after mild traumatic brain injury.

The effects of hyperbaric oxygen (HBO2) on eye movement abnormalities in 60 military servicemembers with at least one mild traumatic brain injury (TBI) from combat were examined in a single-center, randomized, double-blind, sham-controlled, prospective study at the Naval Medicine Operational Training Center. During the 10 wk of the study, each subject was delivered a series of 40, once a day, hyperbaric chamber compressions at a pressure of 2.0 atmospheres absolute (ATA). At each session, subjects breathed one of three preassigned oxygen fractions (10.5%, 75%, or 100%) for 1 h, resulting in an oxygen exposure equivalent to breathing either surface air, 100% oxygen at 1.5 ATA, or 100% oxygen at 2.0 ATA, respectively. Using a standardized, validated, computerized eye tracking protocol, fixation, saccades, and smooth pursuit eye movements were measured just prior to intervention and immediately postintervention. Between and within groups testing of pre- and postintervention means revealed no significant differences on eye movement abnormalities and no significant main effect for HBO2 at either 1.5 ATA or 2.0 ATA equivalent compared with the sham-control. This study demonstrated that neither 1.5 nor 2.0 ATA equivalent HBO2 had an effect on postconcussive eye movement abnormalities after mild TBI when compared with a sham-control.

Neurocysticercosis presenting as a vertical one-and-a-half syndrome with associated contralesional horizontal gaze paresis.

We describe a patient presenting with vertical one-and-a-half syndrome and concomitant contralesional horizontal gaze paresis as the result of a solitary neurocysticercosis (NCC) lesion in the right midbrain extending into the thalamomesencephalic junction. The patient received an albendazole-dexamethasone course which resulted in resolution of his symptoms. The neuro-ophthalmological complications of NCC are reviewed and the clinical topography of the neuro-ophthalmological findings of this unusual observation are discussed.

Dorsal midbrain syndrome from a ring-enhancing lesion.

A ring-enhancing lesion is an uncommon cause of a dorsal midbrain syndrome. Here, we describe the case of a 60-year-old man with eye movement and pupillary findings consistent with dorsal midbrain syndrome, and in whom neuroimaging showed a single ring-enhancing lesion in the right midbrain and thalamus. Further investigation revealed a longstanding right groin mass which proved to be a malignant melanoma. His intracranial lesion was presumed to be a metastatic lesion, and treated with stereotactic radiosurgery. We report the patient's clinical course, and discuss the diagnosis and management of the solitary midbrain lesion.

Contraversive shift of conjugate eye deviation in hemispheric stroke indicates emerging mass effect.

Conjugate eye deviation (CED) towards the ipsilateral or the contralateral side of the brain lesion can occur as a result of acute hemispheric stroke. To our knowledge, there have been no reports of CED shifting from the lesional side to the contralateral side in acute hemispheric stroke in the literature. We present four patients with right hemispheric stroke with a forced CED shift from the right to the left side during the acute stage with corresponding mass effect on the right internal capsule and right thalamus, as shown on brain imaging. Mass effect on thalamic mediated circuits and the corticopontine projection within the internal capsule probably underlies this CED shift via the dynamic balance of oculomotor control between the two hemispheres. Contraversive CED shift is a potentially useful early predictor of emerging mass effect in acute hemispheric stroke.

An unusual cause of head drops.

The presence of vertical ocular motor apraxia should prompt a careful assessment to detect an underlying neurometabolic condition. But congenital vertical ocular motor apraxia is a rare entity that may be attributed to perinatal stroke, hypoxia or kernicterus. We report a case of a 5-year old girl with congenital vertical ocular motor apraxia. Her magnetic resonance imaging (MRI) brain showed symmetrical high signal in the inferomedial thalamic nuclei in the distribution of the vessel of Percheron, a rare posterior cerebral artery variant. Awareness of this rare cause of childhood stroke may obviate unnecessary investigation.