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Biomedical subjects

J W Gittinger

Publications and source records attributed to J W Gittinger.

At least 37 records · Page 2Linked to original sources
PubMed1981

Central dazzle. A thalamic syndrome?

A patient who experienced painless intolerance to light (dazzle) three months after a right posterior cerebral artery occlusion was shown by computerized tomography to have right occipital and right thalamic infarctions. His symptoms improved with amitriptyline hydrochloride and perphenazine therapy. The sensitivity to light, delayed onset, response to therapy, and presence of a thalamic lesion are analogous to the thalamic pain syndrome and suggest that central dazzle is a variant of the thalamic syndrome.

Cerebral Infarction↗
PubMed1981

Congenital adduction palsy and synergistic divergence.

Electromyography of the medial and lateral recti muscles in the right eye of a 7-year-old boy with congenital variable exotropia demonstrated cocontraction. This explained the observed simultaneous abduction on attempted levoversion. Abduction of the right eye increased intraocular pressure to 25 mm Hg from 15 mm Hg. This synergistic divergence should be considered a variant of Duane's syndrome, and, like Duane's syndrome, may occur as the result of anomalies of the peripheral oculomotor nerves or of central synaptic alterations, or of a combined central and peripheral mechanism.

Adolescent↗
PubMedDate not supplied

Giant cell (temporal) arteritis. The differential diagnosis.

A patient was referred to the neuro-ophthalmology unit with a diagnosis of Foster-Kennedy syndrome; "papilledema" had been noted in the right eye and optic atrophy in the left. Results of radiographic examinations and lumbar puncture had been normal. The considerations and procedures leading to a correct diagnosis of giant cell arteritis are discussed.

Aged↗
PubMedDate not supplied

Progressive visual loss associated with peculiar disc swelling.

A patient with progressive visual loss associated with swelling of the disc presented the classic clinical picture of Leber's optic neuropathy. The hereditary patterns, diagnostic characteristics and natural history of the disease are discussed. Although there is no efficacious treatment for Leber's optic neuropathy available at this time, correct diagnosis is important for purposes of genetic counseling and avoidance of unnecessary neuroradiologic and surgical procedures.

Adult↗
PubMedDate not supplied

Pseudotumor cerebri.

The authors evaluate the case of a 20-year-old, four-month-pregnant woman who presented with papilledema and visual field loss, and developed headache, intermittent diplopia and impairment of color vision over the next month. The procedures and considerations leading to the diagnosis of pseudotumor cerebri are discussed, as are the various modes of therapy and their indications.

Adult↗
PubMedDate not supplied

Optic neuritis--etiology?

A 44-year-old otherwise healthy woman was referred to Washington University with previous diagnoses of para planitis and retrobulbar neuritis, and with a current complaint of markedly decreased vision (light perception only) in the right eye. Among the findings at the time of this evaluation were posterior uveitis and evidence of optic neuropathy and of a disordered immune system. The patient responded to pulsed high-dose corticosteroid therapy. A subsequent similar episode in the left eye also was resolved with such treatment. Dr. Burde describes the case in detail and asks Drs. Keltner, Gittinger and Miller to offer diagnoses. Their answers vary considerably.

Adult↗
PubMedDate not supplied

Endocrinological associations of pituitary tumors.

The patient presented with poor vision (particularly OS) which had declined progressively over ten years. He had had bifrontal headaches over the past two years. Examination and visual field testing showed optic atrophy and a bitemporal hemianopia. Procedures leading to the diagnosis of pituitary adenoma are discussed, as are treatment modalities and association of pituitary adenomas with other entities.

Adenoma, Chromophobe↗
PubMedDate not supplied

Glaucomatous cupping -- sine glaucoma.

A 72-year-old man presented with transient episodes of gradually descending vision loss in either eye. Both discs showed marked cupping, but applanation tensions were normal. Carotid occlusions were present. The etiology of the transient visual disturbances, the relationship of carotid disease to low tension glaucoma, and the management of such patients are discussed.

Aged↗
PubMedDate not supplied

Central visual dysfunction with disc swelling.

A healthy 17-year-old white male suffered sudden painless onset of visual loss in the right eye. The affected eye had a cecocentral scotoma, marked disc swelling with hyperemia and flame-shaped hemorrhages, and subretinal fluid extending into the macular area. The authors each consider the differential diagnosis, indications for treatment, the natural course, and the likelihood of association with various systemic diseases.

Adolescent↗
PubMedDate not supplied

Acquired diplopia. Not always a neurologic problem.

A case is presented in which a 49-year-old man has had progressive proptosis and diplopia over a six-week period without pain, loss of vision, or history of other ophthalmic or systemic disorders. The diagnostic work-up leading to a diagnosis of thyroid ophthalmopathy in such cases is discussed. Although the orbitopathy usually has a self-limited course, major complications are corneal exposure and optic neuropathy. The several modes of therapy available to treat these complications (systemic corticosteroids, orbital radiation, and orbital decompression are described.

Diplopia↗
PubMedDate not supplied

Acquired oculomotor synkinesis.

Paradoxical patterns of pupillary, lid and eye movement may follow oculomotor nerve palsy or they can develop spontaneously in patients with no known history of oculomotor palsy. The mechanism of this condition, known variously as aberrant regeneration of the third nerve, oculomotor misdirection or acquired oculomotor synkinesis, is not known, although the prevailing opinion has held that it occurs when axons regenerating within an oculomotor nerve become misdirected and innervate muscles for which they were not intended. However, there is evidence against this hypothesis. The authors critically review the various hypotheses and elucidate the controversy concerning the pathogenesis of acquired oculomotor synkinesis.

Animals↗