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Biomedical subjects

J C Kattah

Publications and source records attributed to J C Kattah.

At least 19 recordsLinked to original sources
PubMed1999

Pathologic findings in a steroid-responsive optic nerve infarct in giant-cell arteritis.

OBJECTIVE: To investigate the pathophysiologic mechanism of optic nerve infarction in giant-cell arteritis (GCA). BACKGROUND: Previous pathologic reports of optic nerve infarction in GCA involved patients who were blind at the time of death. The optic nerve infarcts were primarily retrolaminar in localization. Simultaneous short ciliary and ophthalmic artery vasculitis was found in all patients. METHODS: Clinical neurologic and ophthalmologic examination, temporal artery biopsy, and neuroimaging tests were performed in a patient with an anterior ischemic optic neuropathy secondary to GCA. Pathologic examination of the viscera, eye, and brain were performed at autopsy 1 month later. RESULTS: A prelaminar/retrolaminar infarct was found in this patient. Subsiding vasculitis was limited to the short ciliary arteries, sparing the central retinal, pial, and ophthalmic arteries. CONCLUSIONS: The authors believe that the visual improvement observed in this patient was the result of preserved, anterior optic nerve collateral circulation, as well as the neuroprotective and anti-inflammatory effect of the corticosteroids.

Aged↗
PubMed1994

Anterior ischemic optic neuropathy in Churg-Strauss syndrome.

A patient with a history of chronic rhinitis, sinusitis, and bronchial asthma developed a unilateral anterior ischemic optic neuropathy and a mild sensory motor neuropathy as the initial manifestation of systemic vasculitis. We made a probable diagnosis of Churg-Strauss syndrome. Fluorescein angiography showed delayed choroidal perfusion in both eyes. Marked eosinophilia, increased sedimentation rate, and elevated perinuclear anti-neutrophil cytoplasmic antibody and anti-myeloperoxidase antibody titers were the main laboratory abnormalities that supported this diagnosis. Therapy with high-dose methylprednisolone and cyclophosphamide may have preserved vision in the better seeing eye, improved its choroidal circulation, and reversed the laboratory abnormalities except for a mild persistent eosinophilia. The neuropathy is gradually improving.

Administration, Oral↗
PubMed1993

Side effects of glucocorticoid treatment. Experience of the Optic Neuritis Treatment Trial.

OBJECTIVE: To determine the incidence of side effects from short-term glucocorticoid therapy prescribed for treatment of optic neuritis in the Optic Neuritis Treatment Trial. DESIGN: Randomized, placebo-controlled, multicenter clinical trial. SETTING: Fifteen university- or hospital-based centers throughout the United States. PATIENTS: A total of 457 patients between the ages of 18 and 46 years with acute demyelinative optic neuritis were studied. INTERVENTIONS: (1) Intravenous methylprednisolone (250 mg every 6 hours) for 3 days while hospitalized followed by oral prednisone (1 mg/kg per day) for 11 days; (2) oral prednisone (1 mg/kg per day) for 14 days; and (3) oral placebo for 14 days. Each regimen was followed by a short taper. RESULTS: Only two patients experienced major side effects, psychotic depression in one and acute pancreatitis in the other. Both of these patients were from the intravenous methylprednisolone group and both of the side effects resolved without sequelae. Patients in both groups receiving active drugs more often reported sleep disturbances, mood change, stomach upset, and facial flushing and gained more weight during the treatment period than patients in the placebo group (P < .001 for each comparison). CONCLUSIONS: Although minor side effects are common, short-term glucocorticoid therapy in young, healthy adults is relatively safe. Because of the infrequency of serious side effects, outpatient administration of high-dose intravenous glucocorticoids may be feasible.

Acute Disease↗
PubMed1993

Metastatic prostate cancer to the optic canal.

PURPOSE: Optic neuropathies represent a common cause of blindness among patients with cancer. The authors present the clinical and imaging findings and discuss the management of optic nerve involvement from metastatic prostate cancer to the optic canal. METHODS: Five patients with advanced metastatic prostate cancer had visual loss. Neuro-ophthalmologic examination and pre- and post-gadolinium orbital and brain magnetic resonance imaging (MRI) were performed. Compressive optic neuropathy secondary to extensive optic canal involvement was demonstrated in all of the patients. Neuropathologic examination was accomplished in two cases. A combination of steroid and focal radiation therapy was used for treatment in four patients. RESULTS: Imaging and neuropathologic findings demonstrated a compressive optic neuropathy secondary to both epidural metastases and to deformity and hypertrophy of the optic canal due to metastatic cancer. Treatment was of benefit in three cases. CONCLUSION: Acute and subacute unilateral or bilateral optic neuropathy in patients with prostate cancer may be the result of optic canal metastases. Magnetic resonance imaging shows a characteristic pattern of bone hypertrophy and deformity with optic nerve compression. Early combination steroid and radiation therapy may induce long-lasting improvement.

Aged↗
PubMed1993

Recent developments in oculomotor neurophysiology.

Articles relevant to the topic of supranuclear eye-movement control including anatomy, physiology, pathology, and clinicoimaging correlates are emphasized in this review. Significant contributions in human oculomotor physiopathology were published during this review period and are discussed specifically in the sections on saccades, pursuit eye movement, and optokinetic nystagmus. A very important section is devoted to eye-to-hand coordination. Advances in the understanding of congenital nystagmus also are reviewed.

Animals↗
PubMed1991

Hemianopsia from occipital lobe abscess after dental care.

We treated four patients who developed a homonymous hemianopsia from a bacterial abscess in the occipital lobe of the brain. All four patients were treated successfully by surgical drainage of the abscess and administration of parenteral antibiotics for at least six weeks. Despite cure of the brain abscess, each patient was left with a permanent residual homonymous visual field defect. Cultures from the abscess fluid in three of the four patients grew oral flora. Moreover, each patient had a history of dental care two to four weeks before the onset of visual symptoms. A history of recent dental treatment in a patient with a new hemianoptic field defect should alert the ophthalmologist to the possibility of a bacterial abscess in the occipital lobe.

Adolescent↗
PubMed1990

Bilateral orbital involvement in fatal giant cell polymyositis.

The case of a young woman with giant cell polymyositis is described. She had bilateral, severe, midly painful proptosis and ophthalmoplegia. Extensive pharyngeal, laryngeal, and cardiac muscle involvement occurred 18 months later coincident with fatal cardiac arrhythmia. At autopsy, extensive muscle necrosis and giant cells were noted in extraocular, pharyngeal, laryngeal, and cardiac muscle with only minimal involvement of other striated muscles.

Adult↗
PubMed1990

Compensatory head tilt in upbeating nystagmus.

Upbeating nystagmus has been described in lesions of the posterior fossa. We report a case of upbeating nystagmus accompanying a focal hemorrhagic lesion of the left brachium conjunctivum, the anterior vermis, and the anterior superior left cerebellar hemisphere. The nystagmus was suppressed by a contralateral head tilt. We postulate that in this instance, acquired central nystagmus was inhibited by the otolith-ocular reflex.

Adolescent↗
PubMed1989

Primidone/phenobarbital-induced periodic alternating nystagmus.

A 37-year-old man with a history of seizures developed periodic alternating nystagmus (PAN) along with other signs of primidone/phenobarbital toxicity. The PAN gradually diminished in cycle length and intensity, finally resolving with gradual discontinuation of the drugs.

Adult↗
PubMed1987

An unusual case of central nervous system vasculitis.

A patient with CNS vasculitis limited to small vessels is described. Initial spinal cord involvement with paraparesis was followed by multifocal cerebral and cerebellar involvement, depicted by magnetic resonance imaging (MRI). She also had recurrent cerebral bleeding. A diagnosis of vasculitis was made by cerebral biopsy. Immunosuppressive therapy resulted in clinical improvement and resolution of the MRI abnormalities.

Biopsy↗
PubMed1986

Graphical analysis of two-dimensional eye movements.

Horizontal and vertical monocular movements were recorded by electronystagmography using silver plate electrodes or by the magnetic search coil system. Both horizontal and vertical monocular movements were simultaneously measured with the use of a computer-controlled testing system. The data was composed by the computer and presented as a two-dimensional graphical plot of the actual eye movement trajectories. There are three factors in eye movements, that is, slow component of eye movements--pursuit; quick component--saccades; and fixation. The two-dimensional plot of pursuit monocular movements in normal subjects indicated that the eye did not move in a perfectly straight horizontal or vertical line. The plot appeared to be a series of smooth and snaky movements. Saccades showed quick jumping movement to reach a target and fixation. During fixation, eye position was not restricted to the point of a target and the eye moved around the target. Disturbance of pursuit is known as saccadic or ataxic. A two-dimensional plot of pathological pursuit showed a series of smaller saccades and fixation. Disturbance of saccades is shown as overshoot or undershoot. Also, a two-dimensional plot of pathological saccades was made of smaller saccades and of fixation. Failure of fixation showed larger and more irregular movements around the target. Thus, the two-dimensional plot of monocular movements clearly showed normal or pathological pursuit, saccades, and fixation.

Brain Diseases↗