[Unilateral optic neuritis and Miller Fisher syndrome]. / Neuropathie optique unilatérale et syndrome de Miller Fisher.

INTRODUCTION: Miller Fisher syndrome is an autoimmune neuropathy characterized by the clinical triad of ataxia, areflexia and external ophthalmoplegia. Ophthalmologic involvement in this syndrome is most often represented by motility disorders. The diagnosis is confirmed by the presence of anti-GQ1b antibodies. OBSERVATION: We report the case of a 65-year-old patient referred by his treating physician to the emergency department for ataxia, dizziness and decreased visual acuity in the left eye. In addition, the patient presented with clinical signs of subacute appendicitis for 2 weeks. After treatment with intravenous immunoglobulin, the patient complained of further decreased visual acuity and oculomotor disorders. On ophthalmological follow-up, he quickly recovered his initial visual acuity and more gradually his ocular motility. DISCUSSION: Unilateral optical neuropathy does not preclude the diagnosis of Miller Fisher syndrome. On the contrary, in the case of any rapidly progressive ophthalmologic involvement associated with peripheral neurological signs of ataxia, the diagnosis of Miller Fisher syndrome must be considered. CONCLUSION: Miller Fisher is a rare syndrome for which the diagnosis must be made quickly, so that the patient may benefit from urgent intravenous immunoglobulin therapy. In most cases, ophthalmologic recovery precedes peripheral neurologic recovery by 6 months to 1 year.

[A case of primary herpetic eye disease]. / Un cas de primo-infection herpétique oculaire.

Herpetic eye disease is very common. However, primary infections are most frequently asymptomatic. We report herein a case of a 15-year-old male whose diagnosis of primary herpetic infection was delayed and who initially had unsuitable treatment that aggravated the symptoms. This case highlights the importance of early diagnosis of primary herpetic infection, which allows an adapted therapeutic care.

[Superior oblique myokymia: a report of three cases]. / Myokimie de l'oblique supérieur : à propos de trois cas.

INTRODUCTION: Superior oblique myokymia (SOM/MOS) is an under-recognised and probably under-diagnosed disorder. We describe the clinical signs of this condition among three patients. Next, from review of the literature, we suggest an algorithm for diagnosis and treatment. OBSERVATION: Retrospective study of three patients aged 40 to 55 presenting with brief, intermittent monocular episodes of oscillopsia. DISCUSSION: The acute symptomatology of superior oblique myokymia follows a recognizable pattern: it always presents with brief, intermittent monocular vertical oscillopsia and/or vertical diplopia with torsion. The clinical signs are related to a neurogenic hyperexcitability of the superior oblique muscle. Treatment may be medical (carbamazepine, gabapentin, beta-blocker) or surgical. Recent publications report that superior oblique myokymia may result from vascular compression of the trochlear nerve (fourth cranial nerve), which controls the action of the superior oblique muscle, placing this condition in the category of vasculonervous conflicts. CONCLUSION: Superior oblique myokymia is a relatively poorly known disorder, despite classic pathognomonic symptoms. It is a benign condition, which can nonetheless become incapacitating. It occasionally portends an intracranial pathologic process, which must then be addressed with specific treatment.