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Spasm of accommodation is the sudden development of a considerable degree of myopia which disappears after cycloplegia, usually functional in origin.1 Bohlmann and France2 reported a patient with persistent spasm of accommodation 9 years after head trauma and suggested that a possible lesion in the upper brainstem might be responsible for the dysfunction. We report two similar cases in which magnetic resonance imaging (MRI) failed to show abnormalities in the mid-brain and revealed cerebellar and supratentorial traumatic lesions.
A 34 year old female patient came to the refractive surgery service for correction of myopia and astigmatism. She had been comatose for 45 days after suffering severe head injury at the age of 24, and 3 months later noticed difficulties in her distant vision and was prescribed corrective lenses.
Dynamic refraction revealed in the right eye −3.75 sph −1.50 cyl × 5 and in the left eye −3.50 sph −1.00 cyl × 170. Visual acuity was 20/25 in each eye with this correction. Pupils were equal in size and measured 5 mm in normal room light, with normal reactions. Cycloplegic refraction after instillation of two drops of 1% cyclopentolate and one drop of 1% tropicamide revealed −1.25 sph −1.50 cyl × 5 right eye and −0.75 sph −1.25 cyl × 165 left eye, obtaining 20/20 in each eye. She had attention and memory deficits, left cerebellar ataxia, left pyramidal syndrome, and speech difficulties due to vocal cord paresis. The MRI scan showed multiple lesions in the periventricular and subcortical white matter involving the left temporal lobe (Fig 1) and in the frontal and parieto-occipital regions bilaterally on FLAIR sequences. High signal intensity was observed in the cerebellar vermis as well as in the dorsal pons (Fig 1). No abnormalities was observed in the mid-brain. Images with 3 mm thickness T2 weighted spin echo sequences also did not reveal abnormalities in the mid-brain (Fig 2).
The cycloplegic refraction was prescribed but she returned 2 months later complaining of blurred vision. She was prescribed −2.50 sph −1.50 cyl × 5 right eye and −2.00 sph −1.25 cyl × 165 left eye which she has been wearing for 6 years, despite still having difficulties with distance vision. Multiple repeat examinations confirm that she needs −1.25 sph over her glasses in order to reach 20/20 vision in each eye. Cycloplegic refraction remain unchanged from the first examination.
A 24 year old male patient had blurred distant vision soon after he recovered from head injury including a 2 months period in a coma. He had not worn glasses in the past.
On examination visual acuity was 20/200 both eyes without correction and 20/25 with −3.00 sph in each eye. Pupils measured 4 mm each with normal reactions. The rest of the ophthalmic examination was normal. Cycloplegic refraction, after instillation of two drops of 1% cyclopentolate and one drop of 1% tropicamide, revealed 20/20 vision both eyes (+0.25 sph in each eye). He had recent memory and gait deficits. MRI scan revealed a heterogeneous area, hypointense on T1 and hyperintense on T2 weighted images, affecting the left temporal lobe, compatible with gliotic reaction. There were no abnormalities in the dorsal mid-brain.
The patient was prescribed 1% atropine every 12 hours, which he took for 6 months with normal distance vision but he complained of difficulties reading and photophobia. Atropine was discontinued and blurred distant vision recurred. He then took atropine every other day for 2.5 years associated with reading glasses. When it was discontinued however, accommodative spasm again recurred and a −3.00 sph correction in both eyes was prescribed.
In our patients, a relation of accommodative spasm and the head trauma seems well established because it appeared soon after they have recovered from severe head injury, persisted for several years despite the prolonged use of cycloplegic drops, and the patients were not trying to obtain any benefit by complaining of blurred vision.
The supranuclear control of accommodation is poorly understood. In cats, neurons that discharge in temporal correlation with accommodation were found in the lateral suprasylvian area.3 Electrical stimulation on ipsilateral interpositus nuclei and on contralateral interpositus and fastigial nuclei in the cerebellum are known to induce accommodation.4 These nuclei are connected to parasympathetic oculomotor neurons in the mid-brain.3,4
Very little accommodative dysfunction resulting from central lesions has been reported in humans. Ohtsuka et al5 studied a patient with left middle cerebral artery occlusion who had reduced accommodative responses and markedly lowered accommodation velocity. Their patient had low density lesions on computed tomograph (CT) scan involving the left temporal lobe, near the sylvian fissure. Kawasaki et al6 reported a patient with normal accommodation amplitude but increased accommodation and relaxation times. Their patient recovered normal accommodation 10 days after removal of a large subtentorial arachnoid cyst and the authors suggested that the cerebellum might have a role in the organisation of the human central control system of accommodation.
Bohlmann and France described a patient with persistent spasm of accommodation after head trauma.2 CT scan revealed a skull base fracture without intracranial abnormalities and the authors suggested that a possible mesencephalic lesion might be responsible for the spasm. Chan and Trobe7 reported a retrospective review of six patients with post-traumatic pseudomyopia but did not include MRI studies. In our patients, MRI scan failed to show abnormalities in the mid-brain. Both of them had lesions in the left temporal lobe and the first patient also had abnormalities in the frontal and parieto-occipital lobes bilaterally and the cerebellum. Although it is possible that they have small mesencephalic lesions, not detected by MRI scan, the findings is our cases suggest a higher origin for accommodative dysfunction in some patients with closed head trauma.
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