Isolated optic neuritis from an identified Gnathostoma spinigerum.

PURPOSE: To describe a patient with isolated monocular optic neuritis caused by an identified Gnathostoma spinigerum infestation. CASE REPORT: A 21-year-old man developed a swollen eyelid and painful monocular visual loss of his left eye which did not improve after treatment by intravenous steroid and albendazole. A remarkable eosinophilia in his peripheral blood count was demonstrated. The patient subsequently found a live parasite emerged from his lower eyelid and it was successfully removed by himself. Gross and histopathology examinations of the obtained parasite was undertaken. The parasite was identified as Gnathostoma spinigerum. His blood test for Gnathostoma antibody was positive. DISCUSSION: The etiology of isolated optic neuritis in this patient was Gnathostoma spinigerum which was confirmed by the histopathology of the obtained parasite and the positive serologic test. CONCLUSIONS: We could identify the exact parasite that was proven to cause an isolated optic neuritis. The immediate removal of a causative parasite maynot result in an improvement of the injured tissue but is beneficial in preventing further destruction as well as future complications.

An unusual family with Leber's hereditary optic neuropathy and facioscapulohumeral muscular dystrophy.

We performed an observational prospective analysis to study the clinical characteristics as well as a molecular genetic analysis of 17 members of a Thai family who had visual loss and/or muscle weakness. Their blood mitochondrial DNA were examined for the presence of the G11778A Leber's hereditary optic neuropathy (LHON) mutation. Facioscapulohumeral muscular dystrophy (FSHD) DNA analysis was performed in four members who had visual loss. Of 17 family members, the eight members who had the 11778 LHON mutation were all from branch 'a'. Three of these eight members had FSHD with a 17-27-kb deletion of a tandem repeat in the 4q35 subtelomere, and two had been clinically diagnosed as FSHD. Four of six examined members in branch 'b' showed muscular dystrophy clinically diagnosed as FSHD. No correlation of blood DNA analysis between LHON and FSHD in affected members was found. We describe the first family with FSHD and G11778A LHON in which a mutation in mitochondrial DNA at nucleotide position 11778 of branch 'a' was found to be the origin of the mutation.

Ethambutol and optic neuropathy.

PURPOSE: To demonstrate the association between ethambutol and optic neuropathy. METHOD: Thirteen patients who developed optic neuropathy after being treated with ethambutol for tuberculosis of the lung or lymph node at Siriraj Hospital between 1997 and 2001 were retrospectively reviewed. The clinical characteristics and initial and final visual acuity were analyzed to determine visual outcome. RESULTS: All patients had optic neuropathy between 1 to 6 months (mean = 2.9 months) after starting ethambutol therapy at a dosage ranging from 13 to 20 mg/kg/day (mean = 17 mg/kg/day). Seven (54%) of the 13 patients experienced visual recovery after stopping the drug. Of 6 patients with irreversible visual impairment, 4 patients had diabetes mellitus, glaucoma and a history of heavy smoking. CONCLUSION: Early recognition of optic neuropathy should be considered in patients with ethambutol therapy. A low dose and prompt discontinuation of the drug is recommended particularly in individuals with diabetes mellitus, glaucoma or who are heavy smokers.

Botulinum toxin treatment of the sixth nerve palsy: an experience of 5-year duration in Thailand.

Forty-five patients (48 eyes) with sixth nerve palsy were treated with botulinum toxin injection to antagonist medial rectus muscle at Siriraj Hospital from October 1995 to September 2000. The common causes of palsy were ischemia, trauma and inflammation. Thirty-eight patients (group I) had an interval to treatment of less than 24 weeks (average, 8.7 weeks) and seven patients (group II), longer than 24 weeks. The mean pre-injection esodeviation and extent of abduction in group I were 28.1 prism diopters (PD) and 28.4 per cent, and in group II were 38 PD and 8.1 per cent respectively. After a mean follow-up of 12.2 months, twenty-seven (71.1%) patients in group I recovered completely after the first injection and three (7.9%), after the second injection with a mean interval to recovery of 8.1 weeks. One (14.3%) of 7 patients of group II obtained complete recovery without fusion. Twenty-six (83.9%) of 31 patients with complete resolution achieved binocular function. We conclude that botulinum toxin treatment is a safe and effective alternative to traditional surgery of acute onset sixth nerve palsy.

Leber's hereditary optic neuropathy in Thailand.

PURPOSE: To study the clinical features of Leber's hereditary optic neuropathy (LHON) in Thai patients as compared with patients in the United States, Europe, and other Asian countries. METHODS: The blood mitochondrial DNA of patients from 19 Thai pedigree families was studied for LHON mutation by restriction enzyme analysis. RESULTS: Mitochondrial mutation at nucleotide position 11778 was detected in 37 affected patients and 21 unaffected maternal relatives. Ten of the 19 families were sporadic in transmission. The male preponderance in affected patients was 76%. The onset of visual loss ranged from 6 to 53 years of age (mean = 21.5 years). Of the 31 patients whose eyes were affected bilaterally, 48.4% developed visual loss simultaneously. Unilateral visual loss was found in 2 patients but 1 already had a blind eye resulting from trauma. Onset interval between eyes was up to 12 months (mean = 2.3 months). No associated heart disease or neurological disorder was detected in our pedigrees. Hyperemic disc, retinal telangiectasia, and tortuosity of vessels appeared on ophthalmoscopy in 29% of the patients. Final visual outcome was 0.1, or worse in 82.3%, with a mean follow-up period of 19.5 months. CONCLUSION: The clinical features of LHON in Thai patients are similar to those found in patients harboring the 11778 mutation in the United States, Europe, and Japan. However, although there is a male predominance in all populations studied, this is not so marked in the European and Thai populations.

Minocycline treatment and pseudotumor cerebri syndrome.

PURPOSE: To demonstrate the association between minocycline treatment and development of the pseudotumor cerebri syndrome. METHODS: A retrospective study was conducted of 12 patients from five neuro-ophthalmic referral centers who developed pseudotumor cerebri syndrome after being treated with standard doses of minocycline for refractory acne vulgaris. The main outcome measures included resolution of headaches, transient visual obscurations, diplopia, papilledema, and visual fields static thresholds after withdrawal of minocycline and treatment for increased intracranial pressure. RESULTS: Nine (75%) of the 12 patients developed symptoms of the pseudotumor cerebri syndrome syndrome within 8 weeks of starting minocycline therapy; six were not obese. Two patients developed symptoms only after a year had elapsed because of commencement of treatment with minocycline. One patient was asymptomatic, and pseudotumor cerebri syndrome was diagnosed by finding papilledema on routine examination 1 year after minocycline was started. None of the patients developed recurrences for at least 1 year after the discontinuation of minocycline and treatment for increased intracranial pressure, but three (25%) of the 12 patients had substantial residual visual field loss. CONCLUSION: Minocycline is a cause or precipitating factor in pseudotumor cerebri syndrome. Although most patients have prominent symptoms and are diagnosed promptly, others are asymptomatic and may have optic disk edema for a long period of time before diagnosis. Withdrawal of minocycline and treatment for increased intracranial pressure lead to resolution of the pseudotumor cerebri syndrome, but visual field loss may persist.

Retinal detachment with macular hole.

Retinal detachment with macular hole was treated by different methods. Intravitreal SF6 injection was helpful to seal the macular hole and reattach the retina. In cases of retinal detachment with macular hole and peripheral retinal tear, the retinal reattachment could be achieved by scleral buckling procedure. When vitreous traction adjacent to the macular hole or proliferative vitreoretinopathy was present, vitrectomy combined with internal temponade by SF6 gas injection was indicated. Failure of the operation was caused by inadequate removal of the vitreous traction and post-operative vitreoretinopathy. In a successful operation, visual acuity of 6/60 or better was found in eight of thirty-one patients. (25.8%)