Wall-eyed Bilateral Internuclear Ophthalmoplegia Syndrome Research Articles

WEBINO (Wall-eyed bilateral internuclear ophthalmoplegia) syndrome due to mesencephalon infarction

WEBINO (Wall-eyed bilateral internuclear ophthalmoplegia) syndrome due to mesencephalon infarction

A case of cardioembloic stroke with wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome

Here, we report a case of an 85-year-old man who presented sudden onset of diplopia, dysarthria, and gait disturbance. On admission, he exhibited bilateral adduction palsy, convergence palsy, and binocular exotropia in the forward gaze showing wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome. He had a history of chronic nonvalvular atrial fibrillation. DWI-MRI revealed acute ischemic lesions in the paramedian pontine tegmentum, lower midbrain, both cerebellar hemispheres, and left frontal cortex. He was thus diagnosed with an acute phase of cardioembolic stroke. Subsequently, the right eye adduction palsy in the forward gaze was slightly improved, but other eye movement disorders persisted during discharge from the hospital. The pathology was suspected to involve bilateral damages to both medial longitudinal fasciculus and the paramedian pontine reticular formation. WEBINO syndrome was not only ascribed to lacunar infarction and large artery atherosclerosis but also cardioembolic stroke. The presence of other non-eye symptoms and multiple ischemic lesions could be the characteristics of WEBINO syndrome following cardioembolic stroke.

WEBINO syndrome (wall-eyed bilateral internuclear ophthalmoplegia) secondary to ischemic stroke, about a case

WEBINO (wall-eyed bilateral internuclear ophthalmoplegia) syndrome is characterized by bilateral adduction impairment, nystagmus of the abducting eye, and primary gaze exotropia. We present the case of a 68 year-old man who was initially attended in emergency department with sudden onset diplopia. Neurological exploration revealed WEBINO and gait ataxia. Relevant medical history included liver transplantation and subsequent tacrolimus prescription. Complementary exams revealed ischemic lesion in mesencephalic tegmentum, involving medial longitudinal fasciculus and pretectal area. WEBINO syndrome is unfrequent. Among its etiologies, ischemic and demyelinating are the most frequent. In our case, iatrogenic etiology was also considered. Clinical recognition of this syndrome is required to perform adequate exams in order to reach diagnosis.

Síndrome de WEBINO (wall-eyed bilateral internuclear ophthalmoplegia) secundario a ictus isquémico, a propósito de un caso

WEBINO (wall-eyed bilateral internuclear ophthalmoplegia) syndrome is characterized by bilateral adduction impairment, nystagmus of the abducting eye, and primary gaze exotropia. We present the case of a 68 year-old man who was initially attended in emergency department with sudden onset diplopia. Neurological exploration revealed WEBINO and gait ataxia. Relevant medical history included liver transplantation and subsequent tacrolimus prescription. Complementary exams revealed ischemic lesion in mesencephalic tegmentum, involving medial longitudinal fasciculus and pretectal area. WEBINO syndrome is unfrequent. Among its etiologies, ischemic and demyelinating are the most frequent. In our case, iatrogenic etiology was also considered. Clinical recognition of this syndrome is required to perform adequate exams in order to reach diagnosis.

Unusual Clinical Presentations and Mechanism of Bilateral Thalamic Infarcts: A Case Series (P06.250)

Objective: To highlight the breadth of clinical syndromes and mechanisms of artery of Percheron territory strokes. Background Simultaneous bilateral thalamic infarction represents a relatively rare stroke syndrome. The underlying vascular anatomy often suspected in these cases is a variant of the posterior circulation first described by Percheron in 1975, wherein the paramedian thalami as well as rostral midbrain structures are supplied by a single arterial branch of the proximal posterior cerebral artery. The artery of Percheron, though difficult to visualize even with conventional angiography, may be present in as many as one third of patients. Pathophysiologically, these strokes can be attributed to athero- or thromboembolic phenomena, or result from hypoperfusion due to poor cardiac output. The classical clinical presentation is described as a triad of hypersomnolence, amnesia, and vertical gaze paresis. However, in practice, presentations can be far more variable, with a myriad of cognitive and behavioral changes in addition to eye findings, representing a challenge to the clinician in terms of both lesion localization and determination of etiology. Design/Methods: Case series. Data collected from chart review, serial neurologic examinations. Results: We present a series of three cases of bilateral paramedian thalamic infarcts. In one, we report for the first time an association with WEBINO (wall-eyed bilateral internuclear ophthalmoplegia) syndrome, itself a rare phenomenon with fewer than 20 cases reported in the English literature.We describe another patient with unilateral oculomotor nerve palsy, an unusual stroke presentation. Finally, we present a patient with amnesia and behavioral changes whose stroke occurred in the setting of atrial myxoma. Conclusions: Patients with artery of Percheron territory strokes may present with unusual clinical findings that can confound the diagnosis and potentially delay treatment. The protean clinical presentation represents a challenge to the clinician with respect to lesion localization and etiology. Disclosure: Dr. Manchak has nothing to disclose. Dr. Odrzywolski has nothing to disclose. Dr. Kelly has nothing to disclose. Dr. Benesch has nothing to disclose.

WEBINO and the Return of the King's Speech

We present a 69year-old man with hypertension who developed the sudden onset of horizontal binocular diplopia and stuttering of speech. On examination, bilateral exotropia (i.e. ‘wall-eyed’) was observed in the primary position. Attempted horizontal saccades revealed bilateral internuclear ophthalmoplegia; all consistent with the wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome. Convergence, vertical saccades and vestibular ocular reflexes were likewise impaired. Pupillary and levator palpebrae superioris functions were intact. Mild left-sided dysmetria, intention tremor and dysdiadochokinesia were elicited. Conspicuously, further characterization of the patient's history revealed that he had stuttered as a child, but it had resolved in adolescence. Brain MRI revealed an acute infarction of the mesencephalic and upper pontine tegmentum involving the periaqueductal gray region and the medial longitudinal fasciculus bilaterally with greater involvement of the left. Like the WEBINO syndrome, re-emergent developmental stuttering is a rare neurologic phenomenon. To our knowledge, this is the first case report of a mesencephalic and upper pontine infarction causing both syndromes. We discuss the pathobiological underpinnings of the WEBINO syndrome and neurogenic stuttering and in relationship to this unusual case.

A small pontine infarct on DWI as a lesion responsible for wall-eyed bilateral internuclear ophthalmoplegia syndrome

A 64-year-old man presented with alternating exotropia and bilateral medial longitudinal fasciculus (MLF) syndrome known as wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome. Diffusion-weighted imaging showed a small localized lesion in the median dorsal pons, and high-resolution T2-weighted imaging revealed slight left deviation of the lesion. A small penetrating artery was assumed to be occluded at the level of the MLF decussation. The median dorsal pons appears to be a location for the lesions causing WEBINO syndrome.

Wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome in a patient with neuromyelitis optica spectrum disorder and anti-aquaporin-4 antibody

This report describes, for the first time, an occurrence of wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) in a 19-year-old female with neuromyelitis optica (NMO) spectrum disorder, who had anti-aquaporin-4 (AQP4) antibody. A high signal intensity lesion on T2-weighted MRI was detected in the midbrain tegmentum adjacent to the aqueduct, and presumably involved the medial longitudinal fasciculus bilaterally at the caudal levels. Plasma exchange resolved both WEBINO syndrome and the midbrain lesion. Although WEBINO syndrome is occasionally reported in multiple sclerosis patients, diagnosis of NMO should not be excluded in patients with WEBINO syndrome, because AQP4 is expressed abundantly around the periaqueductal region.

A variant of WEBINO syndrome after top of the basilar artery stroke

Wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) is an uncommon neuro-ophthalmologic syndrome consisting of both eyes primary position exotropia and bilateral internuclear ophthalmoplegia. It is thought to be caused by medial midbrain lesions involving both bilateral medial longitudinal fasciculi and medial rectus subnuclei. We report the clinical and neuroimaging findings of a WEBINO syndrome associated to bilateral ptosis, non-reactive mydriasis and complete vertical gaze palsy in a 55-year-old man who suffered a top of the basilar artery stroke causing tegmental midbrain infarction.

Progressive Supranuclear Palsy With Walleyed Bilateral Internuclear Ophthalmoplegia Syndrome

Walleyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome has mainly been reported in patients with cerebrovascular diseases and multiple sclerosis, but has never been described in patients with neurodegenerative diseases. To describe a patient with progressive supranuclear palsy (PSP) who presented with WEBINO syndrome. Case report and review of literature. A university hospital. A 72-year-old man began to display akinesia, freezing of gait, postural instability, mild rigidity of the neck, and vertical supranuclear palsy, including downward gaze limitation, at 66 years of age. At 68 years, he started to develop diplopia. At 70 years, he had bilateral medial longitudinal fasciculus syndrome. Later, his eye positions gradually showed alternating exotropia. A diagnosis of probable PSP was made based on the National Institute of Neurological Disorders and Stroke and the Society for Progressive Supranuclear Palsy criteria. He showed alternating exotropia in the forward gaze, and adduction paresis and monocular nystagmus of the abducted eye in the horizontal gaze, 2 clinical symptoms of WEBINO syndrome. This is the first reported case of a patient with PSP presenting with WEBINO syndrome. Because bilateral medial longitudinal fasciculus lesions are commonly observed in PSP as clinical and pathological findings, particular attention should be given to WEBINO syndrome in patients with PSP.

Internuclear ophthalmoplegia and contralateral exotropia Nonparalytic pontine exotropia and WEBINO syndrome

To examine whether nonparalytic pontine exotropia, i.e., contralateral exotropia with internuclear ophthalmoplegia (INO), is caused by conjugate deviation by an ipsilateral paramedian pontine reticular formation (PPRF) lesion, we retrospectively reviewed seven patients with this disorder and two with wall-eyed bilateral INO (WEBINO) syndrome. In agreement with a hypothesis that this conjugate deviation is involved, one patient showed a transition from the paralytic to the nonparalytic form as the gaze palsy was resolved. Slowing of saccades toward the lesion was detected in another three patients. Unexpectedly, a milder outward deviation of the eye on the INO side was discovered during eye closure in three patients, implying the participation of a secondary deviation by fixating with the exotropic paretic eye. The presence of abduction nystagmus during fixation with the paretic eye supports this concept. In the two patients with WEBINO syndrome, deprivation of visual fixation with Frenzel goggles and eye closure similarly diminished exotropia, while one eye fixation elicited the marked outward deviation of the other eye with abduction nystagmus. In addition to conjugate deviation, therefore, our results show that secondary deviation induced by over-excitation of contralateral PPRF under fixation with the paretic eye is also involved in the development or aggravation of pontine exotropia.