Conjugate Eye Deviation Research Articles

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.

Wrong-way deviation: Contralateral conjugate eye deviation in acute supratentorial stroke

Supratentorial stroke can cause conjugate eye deviation directed contralateral to the affected side (wrong-way deviation). It is rare and thought to be associated exclusively with hemorrhagic stroke. We prospectively investigated the clinical features and prognostic significance of this wrong-way deviation. Subjects were 12 patients who manifested wrong-way deviation subsequent to supratentorial stroke. These patients were from a group of 968 consecutive patients hospitalized for acute supratentorial stroke during the period April 2007 through March 2010. Clinical features of wrong-way deviation were evaluated. The overall incidence of wrong-way deviation was 1.2%. The causative lesion was a huge intracranial hemorrhage (n=7) or an extensive hemispheric infarction (n=5). Left-sided lesions were most frequent (66.7% of patients). Wrong-way deviation usually appeared a few days after the initial insult and was frequently accompanied by transient downward eye deviation (58.3% of patients). Although the outcomes for patients treated conservatively were generally poor, patients who underwent surgical decompression regained consciousness. Wrong-way deviation can result not only from hemorrhagic but also ischemic stroke if the stroke is extensive. Secondary damage to the adjacent rostral brainstem where oculomotor pathways cross over from the contralateral hemisphere can explain the phenomenon, its temporal evolution, and associated eye signs. Immediate surgical decompression may be necessary to improve the prognosis in such cases.

Neuroimaging of eye position reveals spatial neglect

Conjugate eye deviation describes the tonic horizontal deviation of the eyes in acute stroke patients. Here we investigate whether measuring patients' eye-in-head position in clinical magnetic resonance imaging or computed tomography scans obtained at admission shows a specific relationship to spatial neglect. We investigated 124 continuously admitted subjects with unilateral, first-ever left- or right-sided stroke. To control for the possibility that the degree of eye deviation is related to lesion size rather than spatial neglect, overall lesion volume was used as a covariate in the statistical analysis. Horizontal eye-in-head deviation on clinical brain scans appeared to be associated with spatial neglect rather than with brain damage per se. In contrast to the subject groups without the disorder, the patients with spatial neglect showed an eye-in-head position that was significantly deviated towards the ipsilesional right. Evaluation of eye-in-head position on clinical scans thus may be an additional helpful tool for diagnosing spatial neglect, particularly in the very early period of the stroke.

51. The Utility of Conjugate Eye Deviation on Computerised Tomography of the Brain as a Marker of a Serious Neurological Condition in Patients Assessed at a Large Tertiary Emergency Department

Introduction: We aimed to identify the incidence of conjugate eye deviation on unselected Computerised Tomography (CT) brain scans in the Emergency Department (ED) and to determine its predictive value as a marker for stroke or other serious neurological condition in this setting.

Contralateral conjugate eye deviation during deep brain stimulation of the subthalamic nucleus

Deep brain stimulation of the subthalamic nucleus (STN) in patients with Parkinson disease is often very effective for treatment of debilitating motor symptoms. Nevertheless, the small size of the STN and its proximity to axonal projections results in multiple side effects during high-frequency stimulation. Contralateral eye deviation is produced in a small percentage of patients, but the precise mechanism of this side effect is at present poorly understood. Contralateral eye deviation was produced by high-frequency stimulation of 22 contact sites in nine patients undergoing deep brain stimulation of the STN. The precise locations of these contacts were calculated and compiled in order to locate the stimulated structure responsible for eye deviation. The mean x, y, and z coordinates associated with contralateral eye deviation were found to be 11.57, 2.03, and 3.83 mm lateral, posterior, and inferior to the anterior commissure-posterior commissure midpoint, respectively. The point described by these coordinates is located within the lateral anterosuperior border of the STN. Given that stimulation of frontal eye field cortical regions produces similar contralateral conjugate eye deviation, these results are best explained by electrical current spread to nearby frontal eye field axons coursing lateral to the STN within the internal capsule. Thus, placement of the implanted electrode in a more medial, posterior, and inferior position may bring resolution of these symptoms by reducing the amount of current spread to internal capsule ax-

Delayed recovery of conjugate eye deviation and head version

Delayed recovery of conjugate eye deviation and head version

Conjugate Eye Deviation in Acute Stroke

The authors studied clinical features and lesion patterns associated with conjugate eye deviation (CED) in acute stroke. Consecutive patients with supratentorial stroke (<6 hours after symptom onset) were prospectively recruited. CED was classified according to the National Institute of Health Stroke Scale (NIHSS) item "gaze palsy" as being forced, partial, or absent. Lesion patterns on diffusion-weighted images (DWI) were analyzed in 46 patients using a normalization procedure for direct comparisons between patients. Perfusion data were analyzed for a subset of patients. Partial CED was found in 7 (6%) and forced CED in 31 (26.7%) of 116 patients. Forced and partial CED were associated with higher initial NIHSS scores compared with patients without CED (16 and 10 versus 5; P<0.05). DWI lesion volume was larger in patients with CED (103.24+/-102.4 mL, mean+/-SD) as compared with patients without CED (17+/-34.98 mL, P<0.001). CED was more frequent in right hemispheric stroke (44.6% versus 23%, P<0.02). DWI pattern analysis in patients with CED with right hemispheric stroke revealed a network of affected regions, including basal ganglia and temporoparietal cortex. In left hemispheric CED, lesions were larger than in patients without CED, but no consistent pattern could be established. In a subset of selected patients with CED, a small temporoparietal perfusion deficit was sufficient to elicit CED. Selective dysfunction of cortical areas involved in spatial attention and control of eye movements is sufficient to cause CED in patients with acute stroke. However, in the majority of cases, CED is an indicator of large infarcts involving more than one area, including both cortical and subcortical structures.

Tonic eye deviation due to nonketotic hyperglycaemia induced focal seizures: Case report

We report a case of intermittent tonic conjugate eye deviation due to nonketotic hyperglycaemia induced focal seizure.

Conjugate eye deviation due to traumatic striatal-subthalamic lesion

We report the case of a 22-year-old man after severe cranial trauma, who was noted to have conjugate eye deviation (CED) to the left. A magnetic resonance imaging (MRI) scan demonstrated a lesion in the left (ipsilateral) striatal-subthalamic region. The involvement of supranuclear fibres from the left frontal eye field (FEF) traveling to the right parapontine reticular formation (PPRF) could explain this clinical finding. Alternatively, involvement of deep brain nuclei, such as the striatum and the subthalamic nucleus, could be responsible for this phenomenon. This neurological presentation is unusual after severe cranial trauma.

CT assessment of conjugate eye deviation in acute stroke.

Conjugate eye deviation seen on clinical examination helps to localize pathology in acute ischemic stroke. Eye deviation can also be assessed on a CT head scan. The authors found that CT eye deviation reliably lateralizes to the ischemic hemisphere (positive predictive value 93%) without reference to clinical examination. In an era of thrombolysis and rapid decision making in acute ischemic stroke, eye deviation on CT can help quickly direct attention to the affected hemisphere.

Conjugate Eye Deviation With Head Version due to a Cortical Infarction of the Frontal Eye Field

To the Editor: Conjugate eye deviation (CED) occurs in approximately 20% of patients with cerebrovascular disease. CED is usually caused by a certain degree of hemispheric lesion subside aphasia, hemiparesis, or coma, which indicates poor prognosis.1,2⇓ The underlying mechanism of CED is thought to be a disturbance of the cortical center or subcortical pathways involved in the control of voluntary eye movements. However, the exact site of the human frontal eye field (FEF) is still controversial. In this letter we discuss the possible location of the FEF of human response to CED in a patient with localized cortical lesion. An 82-year-old woman was admitted to the hospital for acute-onset visual disturbances. She reported the sudden appearance of visual disturbance that she felt as difficulty of fixation to her left side. General examination showed arterial blood pressure of 170/100 mm Hg and pulse rate of 72 beats/min. Neurological examination showed the eyes were deviated to the right, but there was difficulty in turning the eyes and head to the left side, although both eyes responded to horizontal oculocephalic stimulation. In addition, the neck rotated to the right. Spontaneous …

Striatocapsular haemorrhage.

Haemorrhages in the striatocapsular area, or striatocapsular haemorrhages (SCHs), have been regarded as a single entity, although the area is composed of several functionally discrete structures that receive blood supply from different arteries. We analysed the morphological and clinical presentations of 215 cases of SCHs according to a new classification method we have designed on the basis of arterial territories. SCHs were divided into six types: (i) anterior type (Heubner's artery); (ii) middle type (medial lenticulostriate artery); (iii) posteromedial type (anterior choroidal artery); (iv) posterolateral type (posteromedial branches of lateral lenticulostriate artery); (v) lateral type (most lateral branches of lateral lenticulostriate artery); and (vi) massive type. The anterior type (11%) formed small caudate haematomas, always ruptured into the lateral ventricle, causing severe headache, and mild contralateral hemiparesis developed occasionally. The outcome was excellent. The middle type (7%) involved the globus pallidus and medial putamen, frequently causing contralateral hemiparesis and transient conjugate eye deviation to the lesion side. About 50% of the patients recovered to normal. The posteromedial type (4%) formed very small haematomas in the posterior limb of the internal capsule and presented with mild dysarthria, contralateral hemiparesis and sensory deficit, with excellent outcome in general. The posterolateral type (33%) affected the posterior half of the putamen and posterior limb of the internal capsule and presented with impaired consciousness and contralateral hemiparesis with either language dysfunction or contralateral neglect. The outcome was fair to poor but there were no deaths. The lateral type (21%) formed large elliptical haematomas between the putamen and insular cortex. Contralateral hemiparesis with language dysfunction or contralateral neglect developed frequently but resolved over several weeks. The clinical outcome was relatively excellent except when the haematoma size was very large. The massive type (24%) formed huge haematomas affecting the entire striatocapsular area. Marked sensorimotor deficits and impaired consciousness, ocular movement dysfunctions including the 'wrong-way' eyes were observed quite frequently. The outcome was very poor with a case fatality rate of 81%. The clinico-radiological presentations suggested its origin was the same as the posterolateral type.

Contralateral conjugate eye deviation in acute supratentorial lesions.

Conjugate eye deviation (CED) in patients with acute supratentorial lesions is generally directed ipsilateral to the lesioned hemisphere. Incidentally, CED occurs to the contralateral side. We report five new cases and review previously published reports to elucidate the lesion responsible for and the mechanism underlying this phenomenon. In a prospective study of 133 consecutive patients with CED caused by an acute supratentorial lesion, 5 patients showed contralateral CED. This was caused by an intracerebral hemorrhage located thalamic (n = 2), frontoparietal (n = 1), and frontoparietotemporal (n = 1). In 1 patient the cause was a subdural hematoma, an association that has not been reported earlier. Four of the 5 patients died. All patients had clinical signs of rostral brain stem dysfunction and a shift of midline structures on computed tomographic scan or at autopsy. Contralateral CED is always associated with hemorrhagic lesions, most commonly in the thalamus. The prognosis of patients with this sign is generally poor. Involvement of descending oculomotor pathways from the contralateral hemisphere at midbrain level is the most probable explanation for this phenomenon.

Saccade and Smooth-Pursuit Impairment after Cerebral Hemispheric Lesions

A number of cortical and subcortical areas are involved in the control of saccades and smooth pursuit, and lesions affecting these areas result in various ocular motor syndromes. Most of these syndromes are relatively subtle and have to be ascertained using recordings, because other brain areas may largely take over the function of a damaged area. Anterior cortical, posterior cortical, large and bilateral cortical, subcortical and degenerative cerebral lesions are successively reviewed. In the anterior part of the cerebral hemisphere, the frontal eye field (FEF), supplementary eye field (SEF) and prefrontal cortex (PFC), i.e. area 46 of Brodmann, control eye movements. The FEF appears to be principally involved in the control of intentional saccades, in particular those made with a retinotopic reference system, and in smooth pursuit. The SEF could control saccades made with a spatiotopic reference system, and sequences of saccades (requiring a temporal working memory). The PFC could control the inhibition of unwanted reflexive saccades, and be involved in spatial memory used for programming all types of memory-guided saccades. In the posterior part of the cerebral hemisphere, the parietal eye field (PEF) is involved in the triggering of reflexive visually guided saccades, and the middle temporal (MT) and medial superior temporal (MST) areas in smooth pursuit. Acute and large unilateral lesions usually result in transitory ipsilateral conjugate eye deviation. Bilateral lesions affecting both the FEF and the PEF result in severe saccade and smooth-pursuit paresis, whereas bilateral posterior temporoparietal lesions result in Balint's syndrome, consisting of both eye movement and visual-attention abnormalities. Subcortical lesions also result in various eye movement abnormalities, which have been little documented to date. Lastly, degenerative cerebral diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, progressive supranuclear palsy and corticobasal degeneration result in more or less severe eye movement disturbances. Eye movement recordings may contribute to early differential diagnosis of some of these degenerative diseases.

Conjugate eye deviation after hemispheric stroke

The authors studied saccadic and smooth pursuit eye movements in patients with conjugate eye deviation (CED) due to a hemispheric stroke. This was done by clinical examination (n = 74) during the presence of CED and, if possible, by eye movement recordings (n = 10) at fixed intervals after clinical disappearance of CED during a follow-up period of six months.During CED both saccadic and smooth pursuit eye movements were equally reduced in contralateral direction. After clinical disappearance of CED disorders of saccades, contralateral more than ipsilateral, and smooth pursuit, ipsilateral more than contralateral, could stil be demonstrated for at least six months in the vast majority of patients.The eye movement disorders, both clinically and recorded, suggest a relationship with spatial neglect (in the early phase) and the structures involved in this syndrome, especially the parietal lobe.

Epileptic eye deviation

The authors describe a 12-year-old boy with attacks of leftward conjugate eye deviation due to a right occipital epileptic focus. Further examination revealed a congruous homonymous paracentral lef...

Conjugate eye deviation

Conjugate eye deviation (CED) is a well-known sign that occurs rather frequently in stroke patients. To study the lateralizing and localizing value of this sign, we investigated prospectively 78 consecutive patients presenting with CED due to a hemispheric lesion. CED occurred more frequently after right-sided hemispheral damage (64%). The lesions in the right hemisphere were located predominantly in the subcortical (fronto-) parietal region and the internal capsule; the lesions in the left hemisphere were larger, covering the entire fronto-temporo-parietal area. In the majority of patients there was no direct involvement of the frontal eye fields on either side. The results indicate that a lesion at different sites within the circuit between the inferior parietal lobule and frontal eye fields, and their projections to the superior colliculus or paramedian pontine reticular formation, can be responsible for CED. The right-left asymmetry is probably related to cerebral asymmetry for directed spatial attention.

Prognostic significance of conjugate eye deviation in stroke patients.

We prospectively studied the prognostic significance of conjugate eye deviation in 80 patients with acute stroke and compared the 3-month mortality and disability of these patients to those of the Tilburg epidemiological study of stroke. Mortality of patients with conjugate eye deviation was higher (41%) than for the general stroke population (34%), but this difference was not statistically significant (p less than 0.179). Looking at mortality and disability together, we found the outcome of patients with conjugate eye deviation to be significantly worse (p less than 0.001). Deviation of the eyes occurred more frequently to the right (65%) than to the left (35%). In the patient group with eye deviation to the left, mortality was significantly higher (64%, p less than 0.001) than in the group with eye deviation to the right (25%); only two patients of the former group (n = 28) could return home. Compared to the Tilburg epidemiological study of stroke, the group with eye deviation to the left did significantly worse, both for mortality alone (p less than 0.001) and for mortality and disability together (p less than 0.001). The group with eye deviation to the right did significantly worse only for mortality and disability together (p less than 0.01). Our results indicate that conjugate eye deviation is a prognostic factor for poor short-term mortality and disability in stroke patients, especially when the eyes are deviated to the left.

Conjugate eye deviation: Localization of hemispheric lesions

Conjugate eye deviation (CED) is generally attributed to a lesion of the frontal eye fields or its subcortical projections leading to a contralateral saccadic palsy. This theory is mainly based on experimental studies. However, clinical studies yield rather conflicting results as to the localizing value of this sign. The authors therefore performed a prospective study of 74 patients with CED caused by a hemispheric lesion. The diagnosis and site of the lesion was based on CT-scan and/or autopsy findings. In all but two patients the sign was caused by a stroke. The results of the study can be summarized as follows1. The area of the frontal eye fields is not damaged in most patients with CED, rather, the inferior parietal lobule is involved.2. One exclusive location of the lesion responsible for CED is unlikely.3. CED can probably result from a lesion at different sites within the circuit formed by inferior parietal lobule-frontal eye fields-superior colliculus and pontine reticular formation, predominantly...

Ipsiversive eye deviation and epileptic nystagmus

We studied an 11-year-old boy with focal seizures in the right temporo-occipital cortex. During the seizure, there was a 1- to 2-second period of ipsiversive (rightward) conjugate eye deviation, followed by 10 to 15 seconds of horizontal jerk nystagmus with slow phases that were directed to the right and appeared linear. The patient was conscious throughout the seizure. These findings fit the description of epileptic nystagmus. We postulate that the eye deviation and slow phases of the nystagmus in this patient were induced by epileptic activation of a cerebral smooth pursuit pathway originating from temporoccipital cortex.