PubMed HealthSearch

Biomedical subjects

V A Purvin

Publications and source records attributed to V A Purvin.

15 recordsLinked to original sources

Ocular neuromyotonia: three case reports with eye movement recordings.

The objective of this article was to evaluate the etiologies, findings, and treatment of ocular neuromyotonia (ONM) in three case reports. The etiologies of ONM were determined by the histories, neuroradiologic tests, or biopsies. Clinical observations, videotaping, and electronic eye movement recordings documented the eye movement abnormalities. Intermittent diplopia developed several years after myelography with thorium dioxide (Thorotrast), radiation treatment for a pituitary tumor, and radiotherapy for medulloblastoma of the posterior fossa. All of the patients had intermittent, variable tropias that occurred spontaneously or were induced by eccentric gaze. One patient had a partial third nerve palsy, and another had a unilateral internuclear ophthalmoplegia (INO). ONM involved the paretic third nerve, extraocular muscles, and ipsilateral lateral rectus muscle in one patient, the paretic medial rectus muscle (INO) in one patient, a lateral rectus muscle (INO) in one patient, and a lateral rectus muscle in the last patient. Eye movement recordings were consistent with spasms of the involved muscles. Carbamazepine (Tegretol) abolished the ONM in two patients. The other patient had been taking carbamazepine for seizures and developed ONM when the dose was decreased. Increasing the dose abolished the ONM. ONM is an unusual cause of intermittent diplopia and strabismus, but its distinctive history and signs identify it easily. Damage to the peripheral cranial nerves might produce segmental demyelination, axonal hyperexcitability, and a self-perpetuating, reverberating circuit that causes spasms of the extraocular muscles.

Aged

Bilateral anterior ischemic optic neuropathy following influenza vaccination.

Optic neuritis is an occasional complication of vaccination. Visual loss can be unilateral or bilateral, and most patients recover substantially without treatment. The presumptive mechanism is an immune-mediated demyelinating injury of the optic nerve. We report two patients who had permanent visual loss following influenza vaccination. Their pattern of visual loss, segmental optic disc changes, and failure of visual recovery were atypical for demyelinating optic neuritis and reminiscent of a primary ischemic injury to the optic nerve. We speculate that an immune complex-mediated vasculopathy following vaccination can cause anterior ischemic optic neuropathy. Clinicians should be aware of this entity because of the less favorable prognosis for visual recovery in these cases.

Blindness

Lumboperitoneal shunting for pseudotumor cerebri.

To clarify the appropriate role of lumboperitoneal (LP) shunting in the surgical management of pseudotumor cerebri (PTC), we retrospectively analyzed the clinical data from 30 patients who underwent this procedure. We found LP shunting to be an effective means of acutely lowering intracranial pressure. Symptoms of increased intracranial pressure improved in 82% of patients. Among 14 eyes with impaired visual acuity, 10 (71%) improved by at least two lines. Worsening of vision occurred in only one eye. Of 28 eyes with abnormal Goldmann perimetry, 18 (64%) improved and none worsened. The incidence of serious complications was low. The major drawback of LP shunting was the need for frequent revisions in a few patients. The reason for poor shunt tolerance in certain individuals is unclear. In PTC, LP shunting should be considered as the first surgical procedure for patients with severe visual loss at presentation or with intractable headache (with or without visual loss). After shunting it is important to identify patients who are shunt intolerant.

Adolescent

Intermittent diplopia and strabismus caused by ocular neuromyotonia.

PURPOSE: Two cases illustrate the symptoms, signs, etiologies, and treatment of ocular neuromyotonia (ONM). METHODS: The histories, neuroradiologic tests, and/or biopsy revealed the etiologies of ONM in both patients. Clinical observations, videotaping, and electronic eye movement recordings documented the eye movements. RESULTS: A 72-year-old man with chronic arachnoiditis following myelography with thorium dioxide (Thorotrast) developed intermittent diplopia and a partial right third nerve palsy. Left gaze induced spasm of the right medial rectus. Right gaze produced right lateral rectus spasm. A 66-year-old woman, who had radiation treatment for a pituitary tumor and acromegaly, had intermittent spasm of the left medial rectus muscle and left esotropia. The episodes occurred spontaneously and were induced by right gaze. A left internuclear ophthalmoplegia was also found. Carbamazepine (Tegretol) abolished the ONM in both patients. CONCLUSIONS: Although ONM is an unusual cause of intermittent diplopia and strabismus, its distinctive clinical features identify it. Injury to the peripheral cranial nerves probably leads to segmental demyelination, axonal hyperexcitability, and a self-perpetuating, reverberating circuit, which causes spasms of the extraocular muscles.

Aged

Neuro-ophthalmic features of cerebral venous obstruction.

OBJECTIVE: To characterize the neuro-ophthalmologic manifestations of impaired cranial venous outflow. DESIGN: A retrospective study of 20 patients who developed increased intracranial pressure as the result of impaired cerebral drainage. SETTING: Three neuro-ophthalmologic referral centers. PATIENTS: Ten patients had noncompressive thrombosis of sagittal or lateral sinuses (noncompressive group), four had compression of the sagittal sinus or jugular veins (compressive group), and six had transient sinus thrombosis following surgical procedures (iatrogenic group). INTERVENTIONS: Medical and/or surgical treatment of increased intracranial pressure and of underlying conditions predisposing to venous obstruction. MAIN OUTCOME MEASURES: Symptoms (headache and esodeviation) and signs (visual acuity, visual fields, and optic disc appearance) of increased intracranial pressure. RESULTS: Headache was more severe, esodeviation was more prevalent, and onset was more abrupt in the noncompressive group than in the compressive and iatrogenic groups. Among the 10 patients with noncompressive thrombosis, factors predisposing to thrombosis were present in seven patients but sometimes overlooked. Following treatment, visual outcome was generally favorable in all three groups. All patients had 20/30 or better visual acuity in at least one eye, and substantial visual field loss was present in both eyes of only two patients. CONCLUSIONS: The clinical manifestation of impaired cerebral venous outflow vary depending on the underlying mechanism. Although most patients maintain good vision, more aggressive treatment is sometimes indicated in patients with thrombosis or compression. The abrupt onset and marked severity of symptoms in patients with thrombosis should help to differentiate these patients from those with idiopathic intracranial hypertension.

Adult

Visual disturbance secondary to clomiphene citrate.

OBJECTIVE: To identify a distinctive constellation of persistent visual abnormalities secondary to treatment with clomiphene citrate. DESIGN: Description of the clinical findings in three patients with visual disturbance secondary to clomiphene treatment. SETTING: A neuro-ophthalmology referral center. PATIENTS: Three women aged 32 to 36 years treated for infertility with clomiphene for 4 to 15 months. RESULTS: All three patients experienced prolonged afterimages (palinopsia), shimmering of the peripheral field, and photophobia while undergoing treatment with clomiphene. The results of the neuro-ophthalmologic examination and electrophysiologic studies were normal in all three patients. Unlike previously reported cases, visual symptoms did not resolve on cessation of treatment. Patients remain symptomatic from 2 to 7 years after discontinuing treatment with the medication. CONCLUSIONS: Treatment with clomiphene can cause prolonged visual disturbance. Patients who develop such symptoms should be advised that continued administration may cause irreversible changes. Women with characteristic visual symptoms should be questioned about past use of clomiphene.

Adult

Anterior ischemic optic neuropathy secondary to interferon alfa.

OBJECTIVE: To report the occurrence of anterior ischemic optic neuropathy as a complication of treatment with interferon alfa and to consider the possible underlying mechanisms for this association. DESIGN: Description of the clinical findings in two patients with this condition. SETTING: A neuro-ophthalmology referral center. PATIENTS: Two patients, ages 40 and 51 years, undergoing treatment with interferon alfa for malignant neoplasms experienced sudden bilateral, sequential visual loss with disc-related field defects and segmental optic disc edema. INTERVENTIONS: Treatment with aspirin and prednisone in one patient. MAIN OUTCOME MEASURES: Visual acuity, color vision, Goldmann perimetry testing, and fundus photography. RESULTS: Visual loss was mild and generally nonprogressive. The interval between initiating treatment with interferon alfa and onset of anterior ischemic optic neuropathy was similar to that of interferon-associated vascular retinopathy. CONCLUSION: Anterior ischemic optic neuropathy may complicate treatment with interferon alfa. The underlying pathogenesis is probably multifactorial.

Acute Disease

Adie's tonic pupil secondary to migraine.

A 46-year-old woman observed transient unilateral mydriasis during a classic migraine attack. One week later she experienced a similar episode after which anisocoria was persistent. Subsequent examination showed the clinical and pharmacologic features of a postganglionic parasympathetic paresis (Adie's tonic pupil). This case confirms the hypothesis that transient mydriasis accompanying migraine is due to interruption of parasympathetic innervation rather than sympathetic overactivity.

Adie Syndrome

Recurrent neuroretinitis.

OBJECTIVE: To characterize a distinct disorder of the optic nerve that manifests as recurrent episodes of acute, monocular disc edema and macular star formation. DESIGN: Description of the clinical features and laboratory findings in a group of patients with this disorder. SETTING: Referral center. PATIENTS: Seven patients (average age, 27 years) who experienced from two to seven attacks of neuroretinitis at intervals ranging from 1 to 10 years (average interval, 2.7 years). INTERVENTIONS: Treatment with corticosteroids (oral in seven patients; intravenous in two patients) and azathioprine sodium (one patient). MAIN OUTCOME MEASURES: Visual acuity, color vision, Goldmann perimetry, and fundus photography. RESULTS: Visual loss manifested as disc-related field defects with variable loss of acuity. Regardless of treatment, patients did not experience significant improvement of optic nerve function following each episode. Results of tests for specific inflammatory origins were normal. CONCLUSIONS: The presence of disc-related field defects, poor recovery, and tendency to recur distinguish this disorder from the typical benign form of idiopathic neuroretinitis previously described.

Adult

Outcomes of optic nerve sheath decompression for nonarteritic ischemic optic neuropathy.

Efficacy of optic nerve sheath decompression (ONSD) in treating non-arteritic ischemic optic neuropathy (NAION) is not clear. We retrospectively analyzed the records of 91 patients with NAION, who were examined during a two-year period, and compared the final Snellen visual acuities of eyes treated with ONSD with those of eyes that did not have surgery. Seven of 18 eyes with ONSD (39%) demonstrated increased visual acuity of two or more lines; whereas 23 of 71 eyes without surgery (32%) had increased acuity. The ONSD group and no surgery group were further subdivided into eyes with progressive visual loss and nonprogressive visual loss. No statistically significant differences in visual outcome between groups were found. We did not find the high frequency of visual improvement that has been reported in some studies of ONSD for NAION.

Adult

Isolated trochlear nerve palsy secondary to dural carotid-cavernous sinus fistula.

Ophthalmoplegia associated with dural carotid-cavernous sinus fistula typically involves the third, fourth, and sixth cranial nerves. Occasionally, isolated palsy of the oculomotor or abducens nerve is noted. We report a patient with bilateral dural carotid-cavernous sinus fistulas who presented with an isolated trochlear nerve palsy.

Arteriovenous Fistula