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Biomedical subjects

N J Newman

Publications and source records attributed to N J Newman.

At least 37 records · Page 2Linked to original sources
PubMed2001

Hereditary optic neuropathies.

The hereditary optic neuropathies comprise a group of disorders in which the cause of optic nerve dysfunction seems to be heritable as demonstrated or suggested by familial expression or genetic analysis. Clinical variability, both within and among families with the same disease, often makes recognition and classification difficult. Genetic analysis now permits diagnosis of some of the hereditary optic neuropathies in the absence of family history or in the setting of unusual clinical presentations. The hereditary optic neuropathies are classified into three major groups: those that occur primarily without associated neurologic or systemic signs, those that frequently have associated neurologic or systemic signs, and those where the optic neuropathy is secondary in the overall disease process. This article reviewed the different hereditary optic neuropathies and emphasized the most common types.

Humans↗
PubMed2001

Neuro-ophthalmology of mitochondrial diseases.

The afferent and efferent visual pathways within the central nervous system are frequently involved in mitochondrial diseases. Neuro-ophthalmic signs figure prominently and may be the presenting or even sole manifestation of these disorders. The four most common neuro-ophthalmic abnormalities seen in mitochondrial disorders are bilateral optic neuropathy, ophthalmoplegia with ptosis, pigmentary retinopathy, and retrochiasmal visual loss.

Education, Medical, Continuing↗
PubMed2001

Neuro-ophthalmic manifestations of head trauma.

OBJECTIVE: To describe the neuro-ophthalmic findings in a group of patients with head trauma. MATERIALS AND METHODS: A retrospective chart review of all patients given a diagnosis code of head trauma in the neuroophthalmology unit at Emory University between 1991 and 1999. RESULTS: A total of 326 consecutive patients were reviewed (203 [63%] men and 123 [37.0%] women). Age ranged from 2 to 86 years, with a mean of 30 years. Motor vehicle accident was the most common cause of head trauma, occurring in 195 (59.8%) patients. An abnormal neuro-ophthalmic examination was noted in 185 of 326 patients (56.7%). Loss of consciousness was not associated with any outcome, but the presence of a neuroimaging abnormality, particularly intracranial hemorrhage, was significantly associated with specific neuroophthalmic deficits. CONCLUSIONS: Head trauma causes a number of neuroophthalmic manifestations. The afferent and efferent pathways are vulnerable to traumatic injury, although the efferent system is more commonly affected. Loss of consciousness may not be a reliable predictor of specific neuro-ophthalmic outcomes, but neuroimaging abnormalities may.

Adolescent↗
PubMed2001

Paraneoplastic optic neuropathy and cerebellar ataxia with small cell carcinoma of the lung.

Bilateral optic neuropathy and subacute cerebellar ataxia were manifestations of a paraneoplastic neurologic disorder in a woman found to have small cell carcinoma of the lung. Serologic tests revealed a neuronal autoantibody specific for CRMP-5, a 62-kd member of the collapsin response-mediating protein family. Unexplained optic neuropathy in the setting of subacute cerebellar ataxia should cause suspicion of a paraneoplastic disorder and prompt testing for this autoantibody, especially in patients at risk for lung carcinoma.

Aged↗
PubMed2001

Precipitating factors in pituitary apoplexy.

Pituitary apoplexy is a rare but life threatening condition caused by sudden haemorrhage or infarction of the pituitary gland. Potential precipitating factors in the occurrence of acute pituitary apoplexy in 30 consecutive patients were identified and compared with the clinical characteristics and outcome of patients with and without associated factors. Six patients had a previously known pituitary adenoma. All patients complained of severe headaches, associated with neuro-ophthalmological symptoms and signs in 83% and altered mental status in 30%. Potential risk factors were identified in nine patients (30%). When there was an associated factor, the clinical presentation was no different than in patients without such factors although altered mental status may be more frequent in patients with associated diseases. In these patients, the visual prognosis was worse and the diagnosis was more difficult to establish. Acute pituitary apoplexy is unpredictable and should be considered in any patient with abrupt neuro-ophthalmological deterioration associated with headache. Patients with pituitary apoplexy often have an associated disease that confounds recognition and treatment despite a typical presentation.

Adenoma↗
PubMed2001

Intracranial vascular abnormalities.

Intracranial vascular abnormalities such as intracranial aneurysms, carotid-cavernous fistulas, AVMs, and cavernous malformations commonly produce neuro-ophthalmologic symptoms and signs. Unruptured aneurysms can compress the third cranial nerve and anterior visual pathways. Subarachnoid hemorrhage from ruptured aneurysms can result in Terson's syndrome and papilledema. Direct and indirect carotid-cavernous fistulas most commonly cause the classic triad of proptosis, conjunctival chemosis, and cranial bruit but can masquerade as chronic conjunctivitis. AVMs, with or without hemorrhage, may compress portions of the retrochiasmal pathways, causing visual field loss. Cavernous malformations, when in the brainstem, commonly cause abnormalities of supranuclear, nuclear, and fascicular ocular motility. The ophthalmologist may be the first physician to encounter clinical manifestations of intracranial vascular abnormalities that may herald devastating neurologic complications. Prompt diagnosis facilitates appropriate management and therapy.

Eye Diseases↗
PubMed2001

Retinal masqueraders of optic nerve disease.

Electrophysiologic testing of the visual system and ancillary imaging investigations may be crucial aids for correctly diagnosing patients with unexplained visual loss or isolated disc pallor. These patients may harbor a retinal disease process and not an optic neuropathy. A diverse range of retinal conditions may present in this manner, and misdiagnosis may lead to unnecessary neurologic investigation and subsequent delay in therapeutic intervention.

Diagnosis, Differential↗
PubMed2001

Optic neuropathies. An overview.

A diverse group of pathologic processes may affect the optic nerve. Clinical manifestations allow localization of pathology to the optic nerve and suggest possible etiologies. Optic disc edema and optic atrophy are fundoscopically visible signs of optic nerve pathology and may provide clues to the underlying process. Hereditary, toxic, nutritional, and compressive optic neuropathies often have characteristic clinical findings that may provide clues to a possible diagnosis.

Humans↗
PubMed2001

Ocular pathology in mitochondrial superoxide dismutase (Sod2)-deficient mice.

PURPOSE: To characterize the pathologic features in retina, optic nerve, and extraocular muscle of mitochondrial superoxide dismutase (Sod2)-deficient mice, a model of increased mitochondrial production of reactive oxygen species. METHODS: Morphometric and ultrastructural study of eyes of 43 homozygous sod2(tm1Cje-/-) mice and wild-type control animals. For retinal morphometric analysis, 32 manganese 5,10,15,20-tetrakis (4-benzoic acid) porphyrin (MnTBAP)-treated animals aged either 9 to 10 days or 20 to 21 days were studied. Ultrastructural examination was performed on tissue from the treated animals, and 11 additional untreated mutant and control animals. RESULTS: In treated Sod2-deficient animals, the photoreceptor layer was thinner centrally at 9 to 10 days than in control animals (mean 8.8 vs. 14.7 microm). By 20 to 21 days, all retinal layers apart from the outer nuclear layer and retinal pigment epithelium (RPE) were thinner centrally in mutant animals (total retinal thickness, 233.2 vs. 272.6 microm; combined nerve fiber layer, ganglion cell layer, and inner plexiform layer, 86.2 vs. 103.4 microm; inner nuclear layer, 51.8 vs. 60.3 microm; photoreceptors, 26.7 vs. 35.6 microm). Optic nerve cross-sectional area was less in 20- to 21-day-old treated Sod2-deficient animals than in control animals. Mitochondrial morphologic abnormalities (swelling, pale matrix, and disorganized cristae) were found predominantly in older mutant animals' (16 and 20 to 21 days) RPE and in extraocular muscle of a 16-day-old untreated mutant. CONCLUSIONS: In sod2(tm1Cje-/-) mice, there is relative progressive retinal thinning, with particular involvement of the inner retinal layers and an early effect on the photoreceptor layer, as well as mitochondrial morphologic abnormalities, all consistent with mitochondrial disease.

Animals↗
PubMed2000

Isolated comitant esotropia and Chiari I malformation.

PURPOSE: To report four patients with isolated comitant esotropia and Chiari I malformation and discuss the most appropriate management. METHODS: Case reports and literature review. RESULTS: All four patients (5, 14, 16, and 37 years of age) presented with an isolated comitant esotropia that led to the diagnosis of Chiari I malformation. The first two patients underwent uncomplicated neurosurgical decompression of their malformation, followed by complete resolution of their esotropia. The third patient underwent strabismus surgery and experienced initial resolution of the esotropia, but eventual recurrence resulted in the strabismus surgery being repeated 5 years later. The fourth patient had strabismus surgery with resolution of the esotropia but only 2 months of follow-up. CONCLUSION: Although management of patients with Chiari I malformation and severe neurologic findings typically includes surgical decompression, management is less straightforward in cases with subtle findings or in which ocular findings are isolated. The decision to perform neurosurgical decompression or strabismus surgery should still be made on a case-by-case basis, with the understanding that strabismus surgery may provide only temporary ocular alignment.

Adolescent↗
PubMed2000

Stages of improvement in visual fields after pituitary tumor resection.

PURPOSE: To use static threshold perimetry to examine the stages of improvement and the potential for late improvement of visual fields after surgical resection of pituitary adenomas causing visual loss from compression of the anterior visual pathways. METHODS: Retrospective review of charts of patients with pituitary tumors and abnormal static threshold perimetry before or soon after treatment who had subsequent visual fields. Quantification of the visual field mean deviation overall, superotemporally, and inferotemporally was performed and compared between visits. Postoperative visits were considered in five time periods: visit 1 (surgery to 1 week), visit 2 (1 month to 4 months), visit 3 (6 months to 1 year), visit 4 (2 years), and visit 5 (3 or more years). RESULTS: Sixty-two patients were included (33 men and 29 women; mean age 54 years [SD +/- 15 years; range, 22 to 83 years]). At visit 1, the relative improvement of the overall mean deviation for the right eye was 30.8% (P =.01) and for the left eye was 13.7% (P =.3067). At visit 2, the relative improvement of the overall mean deviation for the right eye was 30. 4% (P =.0142) and for the left eye was 32.6% (P =.0092). At visits 1 and 2, the inferotemporal quadrants were the quadrants with greatest improvement (visit 1, right eye, 37.8% [P =.0082]; visit 2, left eye, 30.8% [P =.0074]). At visits 3, 4, and 5, an overall trend toward mild improvement was observed with statistical significance only for the inferotemporal quadrant of the left eye from visit 2 to visit 3, which improved 19.7% (P =.0270). CONCLUSION: The pattern of recovery of visual function after decompression of the anterior visual pathways suggests at least three phases of improvement. The early fast phase (surgery to 1 week) of improvement may lead to normalization of visual fields in some individuals. The early slow phase (1 month to 4 months) is the period of most notable improvement. A late phase (6 months to 3 years) of mild improvement does not appear significant overall but may be marked in some individuals. Each of these phases may have one or more mechanisms underlying the observed improvement.

Adenoma↗
PubMed2000

A case-control study of tobacco and alcohol consumption in Leber hereditary optic neuropathy.

PURPOSE: To determine if tobacco or alcohol consumption is associated with vision loss among sibships harboring pathogenic mitochondrial mutations associated with Leber hereditary optic neuropathy. METHODS: Retrospective case-control study with questionnaires obtained from both affected and unaffected siblings from 80 sibships with Leber hereditary optic neuropathy. Sibships harbored molecularly confirmed mitochondrial DNA mutations at nucleotide positions 11778 (63), 14484 (10), and 3460 (7). Exposure in affected individuals was calculated based on reported consumption before vision loss. RESULTS: For male probands (67 sibships), the recurrence risk within a sibship was 10.3% (eight of 78) for males and 3.1% (three of 98) for females. For female probands (13 sibships), the recurrence risk within a sibship was 17.6% (three of 17) for males and 0% (zero of 22) for females. Greater risk of vision loss was associated with male sex (odds ratio [OR] = 6.63; 95% confidence interval [CI] = 2.96 to 14.84; P =.00001) and harboring a 3460 or 14484 in comparison with the 11778 mutation (OR = 2.071; 95% CI = 1.19 to 3.58; P =.0095). No significant association of maximal intensity of smoking or cumulative smoking, whether light or heavy, with vision loss was observed. Light (OR = 0. 31; 95% CI = 0.17 to 0.56; P =.0001) and heavy alcohol consumers (OR = 0.25; 95% CI = 0.11 to 0.58; P =.0011) were less likely to be affected than individuals who did not consume alcohol after adjusting for age, sex, and mutation. In a categorical analysis of sibships with the 3460 or 14484 mutation, no relationship of vision loss with tobacco or alcohol consumption was observed. CONCLUSION: Unlike previous studies, the present study calculated exposure based on self-reported consumption of tobacco or alcohol before vision loss. No significant deleterious association between tobacco or alcohol consumption and vision loss among individuals harboring Leber hereditary optic neuropathy mutations was observed. Tobacco and alcohol do not appear to promote vision loss in Leber hereditary optic neuropathy.

Adolescent↗
PubMed2000

Third nerve palsies.

The diagnosis and management of third nerve dysfunction varies according to the age of the patient, characteristics of the third nerve palsy, and presence of associated symptoms and signs. Indeed, third nerve palsies may be partial or complete, congenital or acquired, isolated or accompanied by signs of more extensive neurological involvement. They can result from lesions located anywhere from the oculomotor nucleus to the termination of the third nerve in the extra-ocular muscles within the orbit. Recent advances in noninvasive neuroimaging facilitate early diagnosis; however, management of a patient presenting with an isolated third nerve palsy remains a challenge.

Humans↗
PubMed2000

Coffee and doughnut maculopathy: a cause of acute central ring scotomas.

AIMS: To report the clinical features of five patients with non-progressive central ring scotomas of acute onset associated with excellent retained visual acuity. METHODS: Complete neuro-ophthalmological examinations were performed. Visual fields were performed by tangent screen, Goldmann, or Humphrey perimetry. In some cases further testing was carried out including fundus photography, fluorescein angiography, ERG, VEP, and neuroimaging. RESULTS: The patients were three women and two men whose ages ranged from 25 to 57 years. Four patients were heavy caffeine consumers while the fifth patient experienced an episode of hypotension. Vision loss was acute in all cases. The onset of vision loss was bilateral/simultaneous in three cases, bilateral/sequential in one case, and unilateral in one case. All affected eyes retained visual acuities of 20/25 or better. Colour vision was subnormal in three of four cases. Visual field defects were characterised by a central ring scotoma having an outer diameter less than 10 degrees. Fundus examination demonstrated temporal optic nerve pallor in three patients (five of 10 affected eyes) and reddish, petaloid macular lesions in one patient. Good visual acuity was maintained for the duration of follow up in all five patients. CONCLUSION: Central ring scotomas with excellent retained visual acuity may present as an acute, bilateral syndrome in patients who are heavy caffeine consumers. The configuration of visual field loss and its location, combined with the presence of temporal pallor in five eyes, suggest that the defect localises to the inner layers of the macula. While these cases could be considered an expansion of the clinical spectrum of acute macular neuroretinopathy, some may represent a distinct entity.

Adult↗
PubMed2000

Isolated Horner's syndrome and syringomyelia.

Although syringomyelia has been associated with Horner's syndrome, it is typically associated with other neurological findings such as upper limb weakness or numbness. A patient is described who had an isolated Horner's syndrome as the only manifestation of syringomyelia. A 76 year old woman was discovered to have right upper lid ptosis and right pupillary miosis. Neurological examination was unremarkable, and pharmacological testing was consistent with localisation of the lesion to a first or second order sympathetic neuron. Neuroimaging disclosed a Chiari I malformation with a syrinx extending to the C2 to C4 level. An isolated Horner's syndrome may be the presenting manifestation of syringomyelia.

Aged↗