Biomed Res Int. 2013;2013:719096.

Profile of gaze dysfunction following cerebro-vascular accident

Fiona J Rowe1, on behalf of the Vision In Stroke (VIS) Group [David Wright, Darren Brand, Carole Jackson, Shirley Harrison, Tallat Maan, Claire Scott, Linda Vogwell, Sarah Peel, Nicola Akerman, Caroline Dodridge, Claire Howard, Tracey Shipman, Una Sperring, Sonia MacDiarmid, Cicely Freeman]

1 University of Liverpool, Liverpool L69 3GB, UK



Aim: To evaluate the profile of ocular gaze abnormalities occurring following stroke.

Methods: Prospective multi-centre 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%) 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) or 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, lid or pupil abnormalities. Area of brain stroke was 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 complain of visual symptoms. Two thirds show some improvement in ocular motility.



The gaze abnormalities reported in 207 of 915 patients in this study included horizontal gaze palsy, vertical gaze palsy, complete gaze palsy, internuclear ophthalmoplegia, one and a half syndrome, dorsal midbrain (Parinaud’s) syndrome, saccadic palsy, smooth pursuit palsy and impaired gaze holding.

Saccadic palsy involves a loss of voluntary movement to the contralateral side and is due to cortical damage or a lesion of the paramedian pontine reticular formation in the brainstem pons. An object may be followed slowly using smooth pursuit movements if foveal fixation is maintained into the affected field. Smooth pursuit palsy is due to cortical damage and involves loss of slow eye movements to the ipsilateral side. Normal smooth-pursuit movements are replaced by series of small saccades termed “cog-wheeling”.

In gaze palsies, whether horizontal, vertical or combined, there is an inability to move the eyes either by saccades or smooth pursuit in a given direction. Horizontal gaze palsies result from lesions involving the sixth nerve nucleus (Bronstein et al. 1990, Pierrot-Deseilligny & Goasguen 1984) and result in loss of horizontal side gaze to the ipsilateral side. A complete vertical gaze palsy involving both up and down gaze is typically due to midbrain and/or thalamic infarctions involving the rostral interstitial nucleus of the medial longitudinal fasciculus, interstitial nucleus of Cajal and/or posterior commissure midbrain (Bender 1980, Green et al. 1993, Lagreze et al. 1996). A vertical gaze palsy is possible with a unilateral lesion but in which there is involvement of decussating pathways giving a functionally bilateral palsy (Alemdar et al 2006).

In dorsal midbrain syndrome, the lesion affects the dorsal aspect of the upper midbrain. There is bilateral upgaze paresis (Gregory et al 2011) and when the patient attempts to look up, both eyes are seen to converge and retract into the orbit (convergence retraction nystagmus). The pupils may be mid dilated with light-near dissociation and there may be lid retraction on downgaze. With light-near dissociation, there is an absent pupil response to a light stimulus but normal pupil constriction occurs to an accommodative target.

Internuclear ophthalmoplegia (INO) is due to a lesion within the medial longitudinal fasciculus which prevents innervation transferring to the medial rectus muscle. This causes a horizontal deviation on conjugate gaze to the affected side with an ataxic nystagmus of the abducted eye. One and a half syndrome is produced where there is a unilateral pontine lesion which affects both the horizontal gaze centre in the abducens nucleus and the ipsilateral medial longitudinal fasciculus, causing a combined ipsilateral horizontal gaze palsy and ipsilateral INO.

In many gaze palsies, the impairment of gaze in both eyes is symmetrical and therefore does not cause diplopia. However, as seen from table 1, it is clear that many patients with gaze palsies did complain of diplopia indicating an asymmetrical gaze palsy or additional cortical strabismus or cranial nerve palsy strabismus which are outlined in table 2. Symptoms of diplopia and blurred vision were present in 35%. The gaze palsies were isolated impairments in 50% of cases but were in association with other ocular abnormalities in 50% including impaired convergence, nystagmus, lid or pupil abnormalities. Those with nystagmus frequently were aware of their moving eyes and complained of oscillopsia.

Conversely, not all patients with asymmetrical gaze palsies complained of diplopia as might be expected. For example, only twelve of twenty patients with INO complained of diplopia. It is possible that the impairment to ocular alignment when looking straight ahead is mild and in these cases, the patient’s natural reserves of binocular function are sufficient to control the ocular deviation so that straight eyes are maintained. Alternatively patients may have coexistent impairment of vision, visual field or attention which prevents appreciation of diplopia (Rowe et al 2013) or patients are unable to verbalise their visual symptoms due to cognitive and/or communication issues. Furthermore, some patients complain of blurred or altered vision rather than diplopia as they see images as more jumbled or confused rather than clear double images (figure 1).

Fiona Rowe-picture1Figure 1         Illustration of blurred and jumbled vision


Why is this important? The visual symptoms and presence of these gaze abnormalities have considerable impact to activities of daily living and quality of life. Clearly if an individual has double vision, blurred vision, unstable vision and/or is unable to move their eyes to look around, this impairs aspects such as navigation, mobility, driving, self-care and reading. Thus it is important to identify these individuals and ensure referral for accurate assessment and tailored management. Our past work has shown that screening assessments by non-eye trained staff are inaccurate if detection of visual problems is based on identifying visible (to the observer) signs of ocular problems (Rowe et al 2011). It is easier to detect visual problems where the patient is able to verbalise whether vision-related symptoms are present. Thus to improve detection, further research is required to validate better screening methods and careful observations are required such as noting the presence of a deviated eye, head posture, closing one eye, pupil size, lid position and odd eye movements.



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Dr. Fiona Rowe

Department of Health Services Research

Thompson Yates Building

University of Liverpool

Brownlow Hill

Liverpool L69 3GB

T:   0151 7945732



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