[On acute reversible disorders of the ocular motility. On the question of isolated ocular myositis].
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Head-eye coordination subserves the rapid transference of gaze and between gaze shifts stabilizes fixation on stationary or smoothly moving targets. The coordination involves various combinations of the components of head movement, saccadic eye movements and visual and vestibular slow phase eye movement whose fine tuning may be adjusted, to an extent currently debated, by higher order mechanisms. Disorders of head-eye coordination may result in loss of acuity when slow phases are impaired or difficulty with reorientation if there is difficulty with saccades or head movement. Pathophysiology in the brain stem affecting individual components of eye movement may often be identified with success, particularly for the horizontal system, but the organization of other functions, notably pursuit suppression and vertical movements, are little understood. Similarly little is known about the disorders of the overall pattern of coordination--'gaze types'--including the apraxias, which have been attributed to cortical, basal ganglia or even cerebellar dysfunction and are reported in an almost bewildering variety of diseases. The development of coordination in infancy is a rich field in which there have been few studies with adequate observational techniques. The differentiation between congenital disorders whose severity may subsequently wax or wane, variants on normal development and acquired disorders poses a clinical problem which could largely be resolved with adequate recording techniques. For the future there is the tantalizing promise that once the principles of coordination are understood, we can move on to the more intriguing questions of how a certain 'toss of the head' and 'look in the eye' not only transfer gaze but can also be so meaningful.
Fifty patients suffering from Graves' disease underwent CT examination of the orbit. The medical rectus width was measured, together with the degree of proptosis and the value of the preseptal area, in order to evaluate the volumetric increase in both the muscle and the fatty tissue. The three parameters were correlated with disorders of ocular motility and with optic neuropathy. The results indicate the presence of 3 classes of patients; a) with main or exclusive increase of muscular tissue; b) with main or exclusive increase of fatty tissue; c) with increase of both muscular and fatty tissues. Only in patients from class c) disorders of ocular motility and optic neuropathy were seen to occur.
We present three cases of the adult opsoclonus-myoclonus syndrome in patients with systemic carcinoma. In addition to opsoclonus and myoclonus, other clinical components of the syndrome can include ataxia, tremor, gait and stance dysfunction, altered mental status, and head and face dyskinesias. The most common etiologies are idiopathic, paraneoplastic, and infectious encephalitis. Radiographic and pathological studies suggest brain-stem dysfunction with associated cerebellar and/or cerebellar pathway dysfunction. In many cases, there is evidence for the involvement of immunologic and/or inflammatory processes in the pathogenesis of this syndrome. The timely recognition of this syndrome is important because of its implications for the underlying etiology and prognosis. The appearance of this syndrome should prompt the search for an occult malignancy.
In recent years there has been renewed interest in the role of autoimmunity in many neurological disorders such as multiple sclerosis and neurodegenerative diseases. Research advances in this field have led to the discovery of new potential therapeutic strategies. There are, however, only a few neurological disorders in which an autoimmune origin has been adequately documented and definitely confirmed. The most important neurological diseases causing movement disorders in which an autoimmune basis has been demonstrated are summarized in this review. The possible role of immunity with the most frequent movement disorders such as parkinsonism or dystonia is also commented.
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Two instances of successful treatment of the rare ocular dyskinesia, opsoclonus, with chlormethiazole are reported. A 65-year-old woman had the opsoclonus-myoclonus syndrome associated with carcinoma of the breast; her myoclonia and opsoclonus did not respond to intravenous diazepam or phenytoin. Treatment with intravenous chlormethiazole resulted in rapid control of her myoclonic attacks, followed by slower but complete resolution of the opsoclonus. Following control of the acute symptoms the patient was transferred to an oral chlormethiazole maintenance dose which was further reduced and subsequently discontinued after 5 months, when the patient's overall clinical status had improved. A 53-year-old man with opsoclonia, myoclonia, ataxia and encephalopathy, not associated with neoplasia, was given immunosuppressor drugs to establish basal control, and oral chlormethiazole for symptomatic treatment. Almost immediately after the initial dose of chlormethiazole the patient became more orientated; he was sedated and the agitation and myoclonic fits were brought under control quite quickly. The opsoclonus responded progressively and was completely resolved after a few days. The initial oral dose of chlormethiazole was gradually reduced and was discontinued after 5-6 months. Chlormethiazole was well tolerated; it may have an important role in the management of the rare opsoclonus-myoclonus syndrome.
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BACKGROUND: Many clinicians have noted that patients demonstrate a myopic refractive change following Traumatic Brain Injury (TBI). This apparent myopic shift disappears with cycloplegia, yet stubbornly reappears as soon as the pharmaceutical effect wears off. We propose that this shift is secondary to an irritative lesion that affects the parasympathetic innervation, resulting in ciliary body contracture. The dilemma for the clinician is whether to provide the immediate relief of clear distance vision by prescribing additional minus lenses, or to work toward attempting to re-establish the baseline refractive error. CASE REPORTS: The natural history of post-traumatic pseudomyopia in our experience involves one of the following three courses: (1) a transient condition that will occasionally resolve; (2) the typical case, a recalcitrant condition that will resolve under cycloplegic intervention, but immediately return as the cycloplegic wears off; or (3) a less-common subgroup of patients who continue to show an increase in myopia over time. Our description of these cases demonstrates management strategies (including atropinization) to relax accommodative spasm, traditional vision therapy techniques aimed at loosening the accommodative system, and refractive corrections. CONCLUSIONS: Pseudomyopia is one of many ocular and behavioral sequelae following TBI. By understanding the natural course and potential management options for post-traumatic pseudomyopia, the clinician will be better prepared to deal with these challenging cases. Flexibility is required, since options that work with one patient may prove ineffective with another. Counseling the patient as to potential outcomes given the natural history of this condition helps establish more-realistic expectations by the patients being treated.
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