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 ocular nystagmus was observed, however, there was no facial palsy, dysarthria, or dysphagia. The patient did not complain of any muscle weakness, and neurological examination revealed no motor signs and no abnormal reflexes. The Mini-Mental State Examination score was 21, and neuropsychological examination revealed no hemispatial agnosia. CED diminished on day 2, although persistence of left horizontal gaze palsy was noted. All symptoms disappeared 4 days after commencement of treatment.
MRI was performed on a 1.5-T Magnetom Vision system (Siemens Medical Systems) 16 hours after onset of symptoms. T2-weighted images of the brain did not detect any specific lesions in suspected areas including the brain stem, although right-sided CED was identified (FigureA–C). However, diffusion-weighted images successfully identified a localized cortical lesion in the caudal part of the right middle frontal gyrus (Figure D). Further examination of the affected lesion with fast fluid-attenuated inversion recovery on day 19 showed the lesion extended from the junction between the superior frontal sulcus and precentral sulcus (Figure F).
The clinical features and response to therapy in our patient are consistent with a transient ipsilateral CED with right-sided head version due to a localized cortical infarction in the right middle frontal gyrus. A sudden imbalance between the left and right tonic frontal inputs on the superior colliculus and/or premotor reticular formations of the brain stem is the probable mechanism of the initial eye deviation observed after an acute frontal lesion.3 A rapid adaptation involving both the opposite frontal lobe and the cerebellar or brain stem structures may explain the relatively brief nature of eye deviation.3 Tijssen et al1 postulated the ocular motor centers are asymmetrically organized in the two hemispheres: diffuse on the left and focal on the right. Our case suggests that a localized lesion resulted in CED because of the involvement of the right hemisphere.
The anatomic area responsible for the symptoms has been traditionally believed to be Brodmann’s area (BA) 8. This assumption is based on experimental findings that electrical stimulation of the FEF evokes contralateral eye movements. Paus4 evaluated the location and possible function of the human FEF by reviewing the results of cerebral blood flow (CBF) and lesion studies with positron emission tomography and MRI and challenged the commonly held view of the FEF being located in BA 8. The medial cluster of CBF-defined FEF peaks were detected at the junction of the superior frontal sulcus and precentral sulcus, and thus, the eye movement field proper lies in BA 6. Subsequent studies using functional MRI5 and transcranial magnetic stimulation6 supported these findings (Figure E). The affected lesion in our patient also corresponded to BA 6, which is the junction of the superior frontal sulcus and the precentral sulcus (Figure F).
Our patient presented with simple right CED with right-sided head version. Goodwin and Kansu7 reported deviation of the eyes was also occasionally accompanied by deviation of the whole head, which rotates to a greater or lesser degree around the axis of the neck such that the face is turned toward the shoulder of the nonparalyzed side. Furthermore, Godoy et al8 showed head version was accompanied by eye deviation during electrical stimulation of the FEF in more than half of their subjects. This finding suggests that the FEF is likely to be located close to the areas that control head movement or is part of the same functional area. The relationship between the direction of eye deviation and head version suggests that the sternocleidomastoid muscle receives bilateral hemispheric innervation and that the maximal input originates from the ipsilateral hemisphere.9
- ↵Tijssen CC, van Gisbergen JAM, Schulte BPM. Conjugate eye deviation: side, site, and size of the hemispheric lesion. Neurology. 1991; 41: 846–850.
- ↵Petit L, Haxby JV. Functional anatomy of pursuit eye movements in humans as revealed by fMRI. J Neurophysiol. 1999; 82: 463–471.
- ↵Paus T, Jech R, Thompson CJ, Comeau R, Peters T, Evans AC. Transcranial magnetic stimulation during positron emission tomography: a new method for studying connectivity of the human cerebral cortex. J Neurosci. 1997; 17: 3178–3184.
- ↵Goodwin JA, Kansu T. Vulpian’s sign: conjugate eye deviation in acute cerebral hemisphere lesions. Neurology. 1986; 36: 711–712.
- ↵Godoy J, Luders H, Dinner DS, Morris HH, Wyllie E. Versive eye movements elicited by cortical stimulation of the human brain. Neurology. 1990; 40: 296–299.
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