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Biomedical subjects

N J Schatz

Publications and source records attributed to N J Schatz.

At least 19 recordsLinked to original sources
PubMed1995

Optic disk swelling and abducens palsies associated with OKT3.

PURPOSE/METHODS: Orthoclone OKT3 is a monoclonal murine IgG immunoglobulin used to treat acute cellular rejection of allografted organs. Aseptic meningitis and meningoencephalopathy are known adverse side effects from the drug. OKT3 caused additional ophthalmologic and neurologic complications in an 18-year-old woman who was treated for transplanted kidney graft rejection. Papilledema and bilateral abduction deficits developed. RESULTS/CONCLUSIONS: Results of magnetic resonance imaging and magnetic resonance angiography were unremarkable. Lumbar puncture disclosed increased intracranial pressure and sterile meningeal inflammation. Most of the symptoms resolved by one week after discontinuation of OKT3. Ophthalmologists and neurologists should be aware that optic disk swelling and abducens palsies can be associated with OKT3 when used in the treatment of transplanted kidney graft rejection.

Abducens Nerve↗
PubMed1995

Persistent positive visual phenomena in migraine.

Ten patients with migraine developed persistent positive visual phenomena lasting months to years. The complaints were similar in their simplicity and involvement of the entire visual field and usually consisted of diffuse small particles such as TV static, snow, lines of ants, dots, and rain. Neurologic and ophthalmologic examinations were normal, and EEGs were normal in eight of eight patients tested. MRI was normal in all patients except one who had nonspecific biparietal white matter lesions and another with a small venous angioma. Treatment of this unusual complication of migraine was unsuccessful.

Adult↗
PubMed1994

High-dose methylprednisolone and acetazolamide for visual loss in pseudotumor cerebri.

We treated four patients who had acute, severe visual loss associated with pseudotumor cerebri with intravenous methylprednisolone (250 mg four times per day) for five days followed by an oral taper, in combination with acetazolamide and ranitidine. In addition to high-grade disk edema, one patient had serous detachment of both maculas and lipid deposition, one had a unilateral macular star, and one had a monocular branch retinal artery occlusion. These three patients experienced rapid and lasting improvement in visual acuity, visual field, papilledema, and symptoms. Vision of the fourth patient did not improve, requiring optic nerve sheath fenestration for chronic papilledema. Transient acne developed in one patient. This regimen is a safe, effective treatment of acute, severe visual loss associated with florid papilledema of pseudotumor cerebri. Lack of immediate improvement is an indication for optic nerve sheath decompression.

Acetazolamide↗
PubMed1994

Pseudotumor cerebri associated with corticosteroid withdrawal in inflammatory bowel disease.

We treated two patients with Crohn's disease and one patient with ulcerative colitis who developed headache, papilledema, and intracranial hypertension (pseudotumor cerebri) during corticosteroid withdrawal. One had four separate episodes with corticosteroid withdrawal, which suggested a causal relationship. This association between pseudotumor cerebri and corticosteroid withdrawal has been documented in children, but is rare in adults with inflammatory bowel disease.

Adolescent↗
PubMed1994

Optic nerve sheath fenestration for progressive ischemic optic neuropathy. Results in second series consisting of 21 eyes.

OBJECTIVE: To determine the efficacy of optic nerve sheath fenestration in eyes with the progressive form of common anterior ischemic optic neuropathy. This investigation complements a previously reported initial series of 26 similar patients. PATIENTS AND METHODS: Optic nerve sheath fenestrations were performed in 21 eyes for treatment of common (nonarteritic) ischemic optic neuropathy with documented progressive deterioration of visual function. All patients underwent thorough preoperative and postoperative ocular evaluations by the Neuro-Ophthalmology Service at the Bascom Palmer Eye Institute, Miami, Fla. RESULTS: During a mean follow-up of 22.5 weeks (range, 3 to 104 weeks), results were as follows: visual acuity increased by 2 or more lines on the Snellen chart in two eyes (9.5%; the combined improvement rate for the two series was 14.9%); visual acuity decreased by 2 more lines in two eyes (9.5%). CONCLUSIONS: Data from this series of 21 surgical procedures indicate no beneficial effect on visual morbidity in cases of common ischemic optic neuropathy and confirm the generally poor visual outcome implied from the results of optic nerve sheath decompression in our initial series. Based on this experience with a total of 47 eyes, we have discontinued optic nerve sheath decompression as a form of therapy for ischemic optic neuropathy.

Aged↗
PubMed1994

Visual morbidity in giant cell arteritis. Clinical characteristics and prognosis for vision.

PURPOSE: To characterize visual morbidity in giant cell arteritis and to assess prognosis with respect to treatment. METHODS: Record review of 185 patients with coded diagnosis of giant cell (cranial) arteritis examined at the Bascom Palmer Eye Institute from January 1, 1980, to January 31, 1993. RESULTS: Forty-five patients with biopsy-proven giant cell arteritis had visual symptoms, and 41 individuals (63 eyes) lost vision. The visual loss was unilateral in 19 patients (46%), sequential in 15 (37%), and simultaneous in 7 (17%). Anterior ischemic optic neuropathy developed in 88% of eyes, visual acuity was 20/200 or worse in 70%, 21% had no light perception, and the majority of field defects in testable eyes, aside from central scotomas associated with loss, showed altitudinal or arcuate patterns. Six patients lost vision during corticosteroid therapy for systemic symptoms of giant cell arteritis, whereas in 39 patients visual symptoms prompted steroid treatment. For visual symptoms, 25 patients received intravenous methylprednisolone, whereas 20 received oral prednisone alone. In the 41 patients with visual loss, vision was unchanged in 20 (49%), it worsened in 7 (17%), and it improved in 14 (34%). Subsequent fellow eye involvement was observed only with oral therapy, and a greater percentage of patients (9/23 [39%] versus 5/18 [28%]) improved after intravenous treatment. CONCLUSIONS: In the authors' series, patients with visual loss due to giant cell arteritis had a 34% chance for some improvement in visual function after corticosteroid treatment. Intravenous therapy may diminish the likelihood of fellow eye involvement and was associated with a slightly better prognosis for visual improvement.

Administration, Oral↗
PubMed1994

[Neuro-ophthalmologic complications of disseminated lupus erythematosus].

BACKGROUND: Systemic lupus erythematosus (SLE) is a multisystemic inflammatory disease of unknown etiology. Physiopathology includes small vessel occlusion and auto-antibody production. Neuro-ophthalmic complications can be detected in 10-30% of SLE cases. Further, some patients can present with neuro-ophthalmic complications prior to diagnosis of SLE. PATIENTS AND METHODS: We report seven cases of neuro-ophthalmic complications of SLE demonstrating lesions from the retina to the brain. The other possible manifestations of SLE will be reviewed. RESULTS: Two cases were not yet diagnosed with SLE when neuro-ophthalmic disease occurred. Anti-double stranded DNA antibodies were detected at a very high titer, suggesting SLE, later confirmed by rheumatologists. CONCLUSIONS: Ophthalmologists should be aware of the unusual patient presenting with a neuroophthalmic disorder prior to the diagnosis of SLE. In such cases, autoantibodies should be sought. Antinuclear antibodies are very sensitive but non specific for SLE. Anti-double stranded DNA antibodies are specific for SLE and elevated titer should raise the suspicion of undiagnosed SLE.

Adult↗
PubMed1994

Visual loss from idiopathic intracranial pachymeningitis.

We report three patients with chronic headaches and optic neuropathy due to widespread meningeal thickening shown on enhanced MRI; all had biopsy-proven intracranial pachymeningitis (fibrosclerosis of the meninges). Two patients had bilateral optic neuropathy, elevated CSF protein, and polyclonal serum hypergammaglobulinemia. They developed temporal lobe cortical necrosis or sagittal sinus thrombosis, presumably due to compromised dural venous drainage from extensive meningeal fibrosis. The other patient had multiple cranial nerve palsies and unilateral optic neuropathy with normal CSF. Corticosteroid therapy improved visual function in all three patients, although all had persisting visual deficits. Gadolinium-enhanced MRI was essential in identifying meningeal inflammation and locating suitable biopsy sites.

Adult↗
PubMed1993

Chiasmal compression from fat packing after transsphenoidal resection of intrasellar tumor in two patients.

After transsphenoidal resection of a pituitary (or other) tumor, the remaining intrasellar cavity, and sphenoid sinus are usually packed with exogenous fat or muscle to prevent cerebrospinal leak and prolapse of the optic chiasm into an empty sella. We treated two patients in whom chiasmal compression occurred postoperatively because of packing of fat. In one patient, the expected visual improvement in the postoperative period was suboptimal. The subsequent removal of fat resulted in total visual recovery. In the other patient, chiasmal compression persisted from intrasellar fat and residual tumor. Iatrogenic compression of the optic nerves or chiasm should be considered in all patients in whom visual recovery is incomplete.

Adipose Tissue↗
PubMed1993

Optic nerve sheath fenestration for treatment of progressive ischemic optic neuropathy. Results in 26 patients.

Optic nerve sheath fenestration was performed in 26 eyes for treatment of the progressive type of common (nonarteritic) anterior ischemic optic neuropathy. During a mean follow-up period of 21 weeks (range, 6 to 52 weeks), results were as follows: visual acuity increased by two or more lines on the Snellen chart in 7 eyes; visual acuity decreased by two or more lines in four eyes; some regression of visual field defects occurred in six eyes, including two eyes in which acuity also improved. These results, attributed to surgical decompression, do not exceed the spontaneous recovery rates reported in the literature pertaining to nonarteritic anterior ischemic optic neuropathy and fail to substantiate the sanguine visual outcome in recently reported series of patients undergoing optic nerve sheath decompression.

Aged↗
PubMed1993

Pretectal eyelid retraction and lag.

We report 2 patients who had eyelid retraction and eyelid lag with minimal impairment of vertical gaze. In both patients, magnetic resonance imaging demonstrated a circumscribed unilateral lesion immediately rostral and dorsal to the red nucleus involving the lateral periaqueductal gray area. Our clinical and radiological findings support the existence of a premotor eyelid control center in the region of the nucleus of the posterior commissure.

Adult↗
PubMed1993

Fluorescein angiography in the diagnosis of giant cell arteritis.

Clinical data and fundus fluorescein angiograms were analyzed from 35 patients with acute (onset less than four weeks) anterior ischemic optic neuropathy. Nineteen of the 35 patients (54%) had nonarteritic disease, and 16 patients (46%) had giant cell arteritis confirmed by biopsy. Patients with arteritis had higher erythrocyte sedimentation rates, larger cup/disk ratios, and delayed fluorescein dye appearance and choroidal filling times. Three additional patients with cranial arteritis confirmed by biopsy, but without visual loss, had angiographic characteristics similar to patients with arteritic ischemic neuropathy. We consider fluorescein angiography a valuable diagnostic adjunct in identifying patients with giant cell arteritis.

Adrenal Cortex Hormones↗
PubMed1993

Orbital infarction syndrome.

BACKGROUND: The authors define orbital infarction as ischemia of all intraorbital and intraocular structures. It is a rare disorder due to the rich anastomotic vascularization of the orbit. PATIENTS: The authors report three patients with orbital infarction with similar clinical presentations: acute blindness, orbital pain, total ophthalmoplegia, and anterior and posterior segment ischemia. RESULTS: Etiologies of orbital infraction syndrome include occlusion of the common carotid artery (case 1), giant-cell arteritis (case 2), and mucormycosis (case 3). CONCLUSION: Three cases discussed in this article illustrate that orbital infarction is a disorder that can occur secondary to different mechanisms such as (1) acute perfusion failure (e.g., common carotid artery occlusion [possibly combined with anomalous orbital anastomotic channels]), 2) systemic vasculitis (e.g., giant-cell arteritis), and (3) orbital cellulitis with vasculitis (mucormycosis). The blindness and retinal and optic nerve damage were permanent, whereas the other signs of orbital ischemia (ophthalmoplegia and anterior segment ischemia) resolved. Therefore, diagnosis of orbital infarction can best be made during the acute phase.

Aged↗
PubMed1993

Congruous quadrantanopia and optic radiation lesion.

Homonymous visual field defects are rare in patients with MS and are usually caused by large lesions in the white matter of the posterior optic radiations and visual cortex. The postulate of Holmes and others, early this century, that optic radiation lesions could produce quadrantic defects has recently been questioned. We report the full recovery of a patient with probable MS who presented with congruous quadrantanopia from a small white matter lesion in the contralateral trigone area.

Brain Diseases↗
PubMed1993

Pulseless (Takayasu) disease with ophthalmic manifestations.

Pulseless disease (PD) is a rare disorder in which inflammation of the aorta and its major branches leads to stenosis or occlusion of these arteries. It mainly affects young Oriental women, who suffer chronic ischemic injury to tissues of the brain, orbits, upper limbs, myocardium, and kidneys. The ophthalmologic features of pulseless disease tend to be late manifestations, and can include ischemia of the retina, choroid, and anterior segment. The inflammatory process may be reversed in early stages with systemic corticosteroids, but, more frequently, significant arterial stenosis necessitates arterial bypass surgery. A 59-year-old Caucasian woman with stenosis of all four major cervical arteries presented with recurrent blurred vision, syncope, mental obtundation, and a remarkable funduscopic appearance due to bilateral orbital hypoperfusion. Her acute symptoms improved slightly on high-dose systemic corticosteroids, and then resolved completely following arterial bypass surgery.

Arterial Occlusive Diseases↗
PubMed1993

Do thalamic lesions really cause vertical gaze palsies?

Two patients with thalamic infarctions presented with vertical gaze palsies. Magnetic resonance imaging (MRI) demonstrated extension of the lesions into the upper midbrain. A common vascular supply to both areas, and the inability of computed tomography (CT) scans to adequately assess posterior fossa structures, necessitate MRI of the mesencephalon in the assessment of all patients with vertical gaze dysfunction. These cases shed further doubt regarding a specific role of the thalamus in control of vertical eye movements.

Adult↗