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Biomedical subjects

J W Gittinger

Publications and source records attributed to J W Gittinger.

At least 19 recordsLinked to original sources
PubMed1992

Selective immunohistochemical staining in the paraneoplastic retinopathy syndrome.

BACKGROUND: The mechanism leading to visual loss in paraneoplastic retinopathy is not known. An autoimmune process has been imputed based on immunologic investigations of several patients and by analogy to certain other paraneoplastic syndromes. METHODS: Two patients with documented small cell carcinoma of the lung who had clinical evidence of paraneoplastic retinopathy are described. Histopathologic examination of the retina from one patient and immunohistochemical staining of human retina with serum from control subjects and both patients were performed. RESULTS: Electroretinograms demonstrated dysfunction of photoreceptors in both patients, with predominant loss of rod function in one patient. Post mortem examination showed patchy loss of photoreceptors of the extramacular retina and relative sparing of cones, findings consistent with the clinical and electrophysiologic test results. Serum from both patients stained the retina in an identical manner, with restriction of the stain to the outer retina. Stain was present over the outer plexiform layer, the outer nuclear layer, and the inner and outer segments of most photoreceptors. A sharp demarcation was present between those areas that did and did not stain. All rod inner and outer segments appeared to stain, and many cone inner segments were not stained. Immunologic tests obtained elsewhere did not show serum antibody to the 23 kD protein. CONCLUSION: These findings support the concept of an autoimmune pathogenesis by showing selectivity of the immune response and correlation between the apparent target of the immune response and the clinical and pathologic findings. The mechanism by which cell loss occurs in the retina is not answered by this study. The absence of antibody to the 23 kD protein does not exclude the diagnosis of paraneoplastic retinopathy.

Aged↗
PubMed1989

Ocular involvement in Castleman's disease. Response to radiotherapy.

A 21-year-old man with known Castleman's disease, a lymphoproliferative disorder with both local and systemic manifestations, presented with decreased vision in the left eye and chromatopsia. He had infiltration of the left disc and choroid with elevation of the retina, multiple bilateral depigmented areas at the level of the choroid or retinal pigment epithelium (RPE) (also thought to represent infiltrates), and left exophthalmos. A serious retinal detachment (RD) evolved, but then responded to radiotherapy, with recovery of good vision. Occult leptomeningeal involvement resolved during a period of observation. There was no systemic evidence of malignant lymphoma.

Adult↗
PubMed1989

Macular abnormalities in papilledema from pseudotumor cerebri.

Three young women with papilledema secondary to pseudotumor cerebri evolved mottled macular pigmentation with preservation of normal visual acuity. Choroidal folds or macular star figures were observed. These macular changes could represent the sequelae of either macular edema or a mechanical disruption of the retinal pigment epithelium. The mechanism of choroidal folds in papilledema remains uncertain.

Adolescent↗
PubMed1987

Papillopathy caused by amiodarone.

Disc swelling and hemorrhages appeared in three eyes of two men receiving amiodarone hydrochloride for cardiac arrhythmias. The initial diagnosis was ischemic optic neuropathy, but visual acuity was preserved, and visual field changes were present in only one eye. Amiodarone is a cationic amphiphilic compound, and other drugs with this property have keratopathy, retinopathy, and optic neuropathy as side effects. We believe our patients had an amiodarone-induced papillopathy.

Amiodarone↗
PubMed1986

Functional monocular temporal hemianopsia.

Four patients, two men 25 and 43 years old and two women 20 and 40 years old, had complete monocular temporal hemianopsias, suggesting that it may be a more common functional deficit than has been recognized. The initial symptoms were visual loss and headache, and eye pain also occurred. Correct diagnosis is possible if the absence of a relative afferent pupillary defect and the persistence of a hemianopsia on binocular testing are demonstrated.

Adult↗
PubMed1986

Medial orbital wall blow-out fracture producing an acquired retraction syndrome.

Trauma in an 8-year-old Black-Vietnamese boy caused a medial wall blow-out fracture, which presented as an acquired retraction syndrome. Computed tomography demonstrated both the fracture and entrapment of the medial rectus and surrounding tissues. Surgical relief of the entrapment resulted in improvement of ocular motility, but retraction persisted. This is the sixth young black male reported with a medial wall blow-out fracture, which suggests that this group may have an orbital structure vulnerable to this relatively uncommon fracture.

Child↗
PubMed1986

Occipital infarction following chiropractic cervical manipulation.

A 44-year-old man developed a complete homonymous hemianopia 2 days after undergoing chiropractic cervical manipulation. Thromboembolism from the vertebrobasilar circulation--as the consequence of trauma to the vertebral arteries by adjacent bones, muscles, and ligaments during twisting and extension of the neck--is the probable mechanism for occipital infarction and other strokes in this and previous cases. Other neuroophthalmic manifestations reported include Horner's syndrome and sixth nerve and gaze palsies.

Adult↗
PubMed1984

Ischemic optic neuropathy associated with optic disc drusen.

Ischemic optic neuropathy developed in five eyes of four patients with optic nerve drusen. Two of the patients were in their 20s, a decade when idiopathic ischemic optic neuropathy is rare. This argues against a chance concurrence of drusen and idiopathic ischemic optic neuropathy. Infarction of the distal portion of the optic nerve in patients with drusen may result from mechanical distortion of blood vessels in the laminar and prelaminar regions.

Adult↗
PubMed1983

Cavernous sinus syndrome due to prolactinoma: resolution with bromocriptine.

Cavernous sinus syndrome due to a pituitary tumor is quite rare. Our patient had a large prolacinoma that extended superiorly, causing bitemporal visual field defects, and laterally into the right cavernous sinus, causing tearing, dysesthesia in the distribution of the fifth cranial nerve, a loss of the corneal reflex, and a sixth cranial nerve palsy. Prolactin levels ranged between 800 and 1000 ng/mL. Treatment with 7.5 mg of bromocriptine daily caused a marked reduction in the size of the tumor and resolution of her visual field defects and cranial nerve dysfunction over 6 months. We feel that bromocriptine should be considered as initial therapy for patients with prolactinomas extending into the middle or posterior cranial fossae.

Bromocriptine↗
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↗