Biomedical subjects
Publications and source records attributed to M D Sanders.
A case is reported in which recurrent episodes of visual loss occurred over a period of 26 years in a patient with bilateral optic disc drusen. Visual field loss was associated with episodes of ischaemic optic neuropathy. The possible mechanism is discussed.
The clinical, angiographic, and histopathological features of experimental posterior uveitis in the black hooded Lister rat are described. This mild form of experimental allergic uveoretinitis (EAU) is induced by sensitisation with retinal S antigen in Freund's complete adjuvant, and the inflammation produced is confined to the posterior segment of the eye. This allows for the first time precise photographic and angiographic documentation of the evolution of clinical signs, because there is minimal clouding of the vitreous by inflammatory cells. Clinically the disease is characterised by the appearance of disc oedema and periphlebitis, followed by focal infiltrates in the deep retinal layers, with eventual atrophy of the pigment epithelium. Histologically, retinal vasculitis is associated with focal mononuclear cell infiltration and necrosis of the photoreceptor layers. This model closely resembles the clinical features of idiopathic retinal vasculitis seen in man.
Five patients with isolated optic neuropathy and sarcoidosis are discussed. The spectrum of clinical disease was variable but two groups could be identified: patients with chronic progressive visual loss which was associated with thickening of the optic nerve and was refractory to steroid treatment, and patients with acute or subacute optic neuropathy in which the visual loss responded rapidly to steroids. In the latter group steroid dependence developed in all three of the patients. In none did the clinical picture resemble that of the optic neuritis associated with multiple sclerosis.
Three patients are described who presented with acute painful proptosis, ptosis and ophthalmoplegia. Orbital cellulitis was initially diagnosed in all cases, but there was no therapeutic response to antibiotics. A dramatic improvement occurred with steroids. All patients had, or developed abnormal thyroid tests and CT Scans showed thickened ocular muscles. This is an unusual presentation of thyroid ophthalmopathy.
From projected optic disk photographs we measured the size of the scleral canal in two samples of emmetropic patients: one of patients with unilateral pseudopapilledema and drusen and the other of the general normal population. Measurements on the non-drusen-containing optic disk of patients with unilateral drusen were taken to reflect the scleral canal size of the fellow, affected eye. For both trained (t = 6.642) and untrained (t = 4.274) observers, the average diameters of the non-drusen-containing optic disks of patients with unilateral drusen were significantly smaller than those of the optic disks of normal patients (P = .0005, one-tailed independent t-test). The association of a small scleral canal with vascular anomalies, frequently noted in optic disks of patients with drusen, indicates a mesodermal dysgenesis of the optic nerve head.
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In a series of 61 patients with the morphologic and histochemical features of mitochondrial myopathy, 22 (36%) had pigmentary retinopathy. Three patterns of retinopathy were identified. Eighteen patients had a "salt and pepper" type of retinal appearance, which was usually associated with good visual function. Two had many features of retinitis pigmentosa, and two others showed generalized loss, or atrophy, of the retinal pigment epithelium and choriocapillaris. These last four patients had markedly reduced visual acuities, with optic atrophy and attenuated retinal vessels. Electroretinography and electro-oculography were performed in 11 patients. Both rod and cone mediated electroretinographic functions were subnormal in eight patients, while only cone mediated functions were depressed in the remaining three. The electro-oculographic changes were variable.
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Cyclosporin A was used in nine patients with severe refractory posterior uveitis. Four patients had Behcet's disease, one had sarcoidosis, one had HLA B27 related arthritis and uveitis and three had idiopathic retinal vasculitis. The drug had beneficial ocular effects in all patients in the early stages of treatment with an improvement in the visual acuity and reduction in the severity of inflammation. The relapse rate and need for additional steroids were reduced in all patients. However, renal function deteriorated in seven patients to such an extent that the dose of Cyclosporin A had to be reduced with consequent relapse of uveitis.
This paper summarises the principal immunopathological mechanisms which may underlie ocular inflammation and draws attention to how autoimmune reactions may be regulated by idiotypic networks of the immune system. The study of autoimmunity in inflammatory eye disease is illustrated by our current investigations of retinal vasculitis in man and of experimental autoimmune uveoretinitis in rodents where three lines of evidence indicate that immune complex formation may be a compensatory host response to the development of antiretinal autoimmunity. In discussing immunological implications of these results we suggest that retinal inflammation in antiretinal autoimmunity is limited by a protective anti-idiotypic antibody response and that retinal disease arises when this compensatory response is improperly balanced. The clinical implications of this reasoning include the identification of patients at risk of relapse of ocular disease and the development of therapeutic methods for restoring an imbalanced anti-idiotypic autoimmune response towards normality.
Convergence spasm, when it is part of the near-response, is accompanied by accommodation and miosis. The differential diagnosis of bilateral sixth nerve palsy, divergence insufficiency, bilateral gaze palsy may be distinguished by clinical examination. In a review of 12 cases, 8 of whom were re-examined after a mean interval of 8.3 years, no organic disease became manifest. We suggest that extensive neurological investigation is not necessary in this group of patients. Treatment with cycloplegia and glasses gave symptomatic relief in 5 cases.
We present three patients with optic nerve drusen. On the basis of headaches, transient obscurations of vision, or visual field loss the patients underwent orbital computed tomographic (CT) scanning. This procedure confirmed the presence of buried drusen in the four optic discs that had yielded poor ophthalmoscopic and angiographic evidence of drusen; drusen had been observed in the other two discs. The indications for CT scanning in the presence of visible or buried drusen of the optic nerve head are discussed.
Two middle-aged women presented with bilateral acute painful proptosis, ptosis, ophthalmoplegia, and visual loss. In both an initial diagnosis of orbital cellulitis was made, but they did not respond to systemic antibiotics. Orbital computerised tomographic (CT) scans were thus done within 36 h of admission and they showed grossly enlarged extraocular muscles in each case suggestive of dysthyroid eye disease. Clinical examination was otherwise normal. When high doses of systemic steroids were substituted for the antibiotics the physical signs resolved rapidly, accompanied by a dramatic reduction in the size of extraocular muscles on CT scanning. One patient subsequently became clinically hypothyroid, while the other showed clinical and biochemical evidence of thyroid overactivity. These case-reports suggest that patients with bilateral acute painful proptosis should have an early CT scan to exclude atypical dysthyroid disease. Delay in giving systemic steroids may allow the development of unnecessary visual loss due to optic nerve damage.
Visual function and optic disc appearances were studied in 68 patients conforming to established criteria of benign intracranial hypertension (BIH). The clinical, radiological, and laboratory findings of those patients whose visual field or acuity deteriorated were compared with those who did not deteriorate over an average follow-up of 4.1 years. Definite loss of visual function occurred in 49% of eyes and was severe in 6%. Patients with high grade or atrophic papilledema, or peripapillary subretinal hemorrhage, were significantly more likely to have had deterioration of visual function. Transient obscurations of vision and the presence of optico-ciliary shunts were associated with severe visual loss. Anemia, older age, and high myopia were other risk factors for visual loss. Chronic papilledema may cause progressive visual loss and, for this reason, BIH is not a benign condition; fundal changes and visual function should be carefully monitored.
The aetiology of ophthalmoplegia in 15 patients with carotid-cavernous sinus fistula is discussed, and the clinical findings are correlated with angiographic and orbital CT appearances. After closure of the fistula the majority of patients with generalised ophthalmoplegia recovered full ocular movements rapidly, while patients with an isolated abduction weakness required much longer to return to normal. Orbital CT studies showed enlarged extraocular muscles in the patients with generalised ophthalmoplegia but muscles of normal size in those with abduction failure alone. After closure of the fistula repeat CT studies of patients with enlarged extraocular muscles showed a diminution in muscle size. We suggest that generalised ophthalmoplegia in carotid cavernous sinus fistula is due to hypoxic, congested extraocular muscles. Isolated abduction weakness is due to a sixth nerve palsy, which probably occurs either in the cavernous sinus or more posteriorly near the inferior petrosal sinus. A combination of these 2 mechanisms may be found in some patients.
Bilateral centrocaecal scotomata have been recognised as a sign of intrinsic optic nerve disease, usually associated with hereditary optic neuropathy, and nutritional or toxic amblyopias. This report describes four patients with central scotomata due to intracranial masses, three of whom recovered after surgical intervention. The clinician should be alerted to the association in patients with headaches, other neurological signs, and central visual loss.
We reviewed the clinical and oculomotor findings in 62 patients with downbeating nystagmus (DBN). Only those patients whose DBN was enhanced in lateral gaze were included. Apart from gait ataxia, few patients had additional neurologic signs. The two most common causes of DBN were cerebellar ectopia (25%) and cerebellar degeneration (25%) with another 10% having a variety of conditions. In about 40% the cause remained undiagnosed. In some patients with idiopathic DBN and in others with DBN due to cerebellar ectopia, the disease progressed slowly, if at all. In DBN the slow-phase velocity is dependent on vertical head position and head velocity in pitch; vertical pursuit, particularly downward pursuit, is defective and vertical vestibulo-ocular reflexes are intact. We concluded that at least some cases of DBN were due to an imbalance in otolithocular reflexes. The lesion causing DBN appears to be in the vestibulocerebellum, perhaps the nodulus, a structure that normally inhibits otolith-ocular reflexes.
Multifocal fibrosclerosis is a term used to denote a combination of similar fibrous disorders occurring at different anatomical sites and including idiopathic mediastinal and retroperitoneal fibrosis, sclerosing cholangitis, Riedel's thyroiditis, and orbital pseudotumour. This paper reports a patient, known to have retroperitoneal and testicular fibrosis, who suffered visual loss resulting from marked changes in the macular region of one eye and suprasellar extension of a mass in the pituitary fossa. These lesions appear to represent very uncommon manifestations of multifocal fibrosclerosis.