Biomedical subjects
Publications and source records attributed to N R Miller.
Recent articles in the scientific literature have described major advances in our understanding of the anatomy and vascular relationships of the three ocular motor nerves (cranial nerves III, IV, and VI) and of the diagnosis and treatment of a variety of pathologic processes that damage these nerves, including ischemia, inflammation, and compression.
We conducted a retrospective study of 27 patients with pseudotumor cerebri (PTC) treated with at least one lumboperitoneal shunt (LPS) to ascertain the efficacy of this treatment. The average duration of follow-up for this population was 77 months (median, 47 months), with a range of 21 to 278 months. A functioning LPS was successful in alleviating symptoms in all patients studied, and no patient with a functioning shunt complained of shunt-related symptoms, such as low-pressure headache or abdominal pain, within 2 months after the shunt was performed. Twelve patients (44%) required no revisions. The number of revisions among the 15 patients (56%) who required them ranged from 1 (5 patients) to 13 (1 patient). Three of these patients required 35 of the 66 total shunt revisions (53%). There were no major complications from LPS, other than failure of the shunt, even in patients who required multiple shunts. We conclude that placement of a lumboperitoneal shunt is satisfactory treatment for the majority of patients with PTC who require surgical therapy for the disorder, even though some patients ultimately require multiple shunt revisions.
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The treatment of optic nerve sheath meningiomas (ONSM) is controversial. Radiation therapy has been used with some success in patients with progressive visual loss. We report a case of visual improvement in a patient with an optic nerve sheath meningioma and progressive visual field loss, treated with conformal radiotherapy.
OBJECTIVE: To determine the ability of the Hardy-Rand-Rittler (HRR) and Ishihara colour plates to detect acquired colour vision defects in patients with nonglaucomatous optic neuropathy (NGON). DESIGN: Prospective study. SETTING: Neuro-Ophthalmology Unit of the Wilmer Eye Institute, Baltimore. PATIENTS: A total of 178 consecutive patients (349 eyes) referred to the Neuro-Ophthalmology Unit and the General Eye Service of the Wilmer Eye Institute and examined by two of the authors were enrolled from July 1992 to June 1993. OUTCOME MEASURES: Results of testing with HRR and Ishihara plates. RESULTS: Among the 202 eyes that were found to have no ocular disease on neuro-ophthalmologic testing, the HRR plates gave a normal result in 168 (83.2%), compared with 196 (97.0%) with the Ishihara plates (p < 0.0001). The HRR plates detected an acquired colour vision deficit in 48 (87.3%) of the 55 eyes with NGON, compared with 38 (69.1%) for Ishihara plates (p = 0.001). The values for the eyes with NGON with a visual acuity of 20/25 or better were 76.5% (13/17) and 35.3% (6/17) respectively (p = 0.008) and with a visual acuity less than 20/25, 92.1% (35/38) and 84.2% (32/38) respectively. CONCLUSIONS: For patients with unilateral or bilateral NGON, HRR plates are more likely than Ishihara plates to detect a colour vision defect, particularly when the visual acuity is 20/25 or better. However, neither test is sensitive enough to be used as the sole criterion for the diagnosis of NGON. The results of comparison of colour perception of the two eyes may be more useful than absolute colour vision responses, particularly in patients with unilateral disease.
OBJECTIVE: To evaluate the clinical significance of V- or tongue-shaped infrapapillary retinochoroidal depigmentation in association with dysplastic optic discs. METHODS: Clinical data from all patients with V- or tongue-shaped infrapapillary retinochoroidal depigmentation and dysplastic optic discs were evaluated retrospectively. RESULTS: Five patients with this atypical colobomatous anomaly had transsphenoidal encephalocele. A sixth patient had an ectopic midline pharyngeal mass with no skull-base defect. CONCLUSION: In patients with optic disc dysplasias, the finding of this V- or tongue-shaped retinochoroidal pigmentary anomaly should prompt neuroimaging to look for transsphenoidal encephalocele.
Ocular alignment and saccades were studied in seven patients with trochlear nerve pareses, before and after strabismus surgery. Prior to surgery, a position-dependent vertical ocular misalignment was present, and downward saccades were hypometric in the paretic eye. Strabismus surgery reduced the magnitude and position-dependence of the static misalignment. Saccade conjugacy improved in the patients with congenital pareses, and in the patient with a gradual-onset acquired paresis, but less improvement occurred in subjects with traumatic pareses. The post-operative change in saccade conjugacy relative to the change in static alignment correlated with pre-operative vertical vergence, suggesting that changes in saccade yoking depend on an interaction between saccades and vertical vergence.
BACKGROUND: Leber hereditary optic neuropathy (LHON) is a mitochondrial genetic disorder characterized by bilateral central visual loss typically in early adulthood. Few histopathologic studies, including ultrastructural and molecular genetic analysis, have been reported. METHODS: Ocular tissue was obtained postmortem from an 81-year-old woman with LHON from the Queensland 1 pedigree characterized by mutations at nucleotide positions 4160 and 14484. Routine histopathologic studies, electron microscopy, electron-probe analysis, and molecular genetic analysis were performed. RESULTS: Marked atrophy of the nerve fiber and retinal ganglion cell layers and optic nerves was present. Results of electron microscopic examination demonstrated 1.2 microns electron-dense, double-membrane-bound inclusions, consisting of calcium by electron-probe analysis, in retinal ganglion cells. The optic nerve was homoplasmic for mutations 4160 and 14484. CONCLUSION: Optic nerve and inner retinal atrophy in LHON may be a result of metabolic mitochondrial dysfunction leading to intramitochondrial calcification. Homoplasmy for mitochondrial mutations 4160 and 14484 in the leukocyte/platelet fraction of whole blood may correlate with homoplasmy in the optic nerve.
Ameloblastomas are histologically benign tumors derived from the odontogenic apparatus. Although these tumors are locally invasive, they rarely invade the paranasal sinuses, orbits, or intracranial cavity, and, thus, they rarely produce ophthalmologic signs and symptoms. In this report, we describe the neuro-ophthalmologic features of three patients with chronically aggressive ameloblastoma. Two of the patients developed a progressive and recurrent orbital apex and cavernous sinus syndromes. One of these patients is, to our knowledge, the first patient described with orbital and cavernous simus involvement by an ameloblastoma initially arising in the mandible. The other is only the second case described with bilateral orbital involvement. The third patient in this series developed a trigeminal sensory neuropathy as the only sign of the tumor. Although ameloblastomas are benign, slowly growing tumors, they may, often over a long period of time, cause significant neuro-ophthalmologic and orbital manifestutions that can only be partially ameliorated by surgery.
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The authors describe the method and results of treatment of 12 consecutive patients with carotid-cavernous sinus fistulas (CCFs). Treatment was by embolization via a transvenous approach through the superior ophthalmic vein (SOV). The CCFs (two direct and 10 dural) had previously been treated unsuccessfully or, for mechanical reasons, could not be treated by the standard techniques of endoarterial balloon occlusion, particle or glue embolization of feeding vessels from one or both external carotid arteries, or transvenous occlusion of the fistula via the ipsilateral inferior petrosal sinus. All 12 patients were successfully treated either by advancement of a detachable balloon catheter through the ipsilateral SOV into the cavernous sinus with subsequent inflation and detachment of the balloon (11 patients) or by introduction of multiple thrombogenic coils into the fistula via the ipsilateral SOV (one patient). All patients had complete resolution of symptoms and signs after successful occlusion of the CCF. There were no intraoperative complications; however, one patient required postoperative embolization of a residual posteriorly draining fistula via the ipsilateral external carotid artery, and another developed a persistent abducens nerve paresis that eventually required surgical correction. Ten (83.3%) of the 12 patients underwent cerebral angiography 3 to 6 months after surgery, and none showed evidence of a recurrent fistula. Similarly, none of the 12 patients developed recurrent symptoms and signs suggesting recurrence of the fistula during a follow-up period that ranged from 6 months to 10 years (mean 64 months). It is concluded that the transvenous approach to the cavernous sinus through the SOV is a safe and effective treatment of both direct and dural CCFs that are not amenable to transarterial or other transvenous approaches.
We describe a 31-year-old man who developed sudden painful loss of vision in the right eye and was found to have a retrobulbar optic neuropathy. Magnetic resonance (MR) imaging gave normal results, and a diagnosis of retrobulbar optic neuritis was made. The patient was treated with oral prednisone, but he continued to lose vision in the right eye and then began to lose vision in the left eye. Repeat MR imaging performed eight weeks after the initial study showed a giant intracranial aneurysm compressing the right and left optic nerves. Cerebral angiography revealed that the aneurysm arose from the origin of the right ophthalmic artery. Treatment of the aneurysm by a trapping procedure resulted in improvement in vision in the left eye but no change in vision in the right eye. This report emphasizes the difficulty in imaging intracranial aneurysms of various sizes, the rapidity with which intracranial aneurysms can enlarge, and the importance of continued follow-up examinations in patients thought to have idiopathic optic neuritis.
A patient presented with an isolated left sixth nerve palsy. Magnetic resonance imaging revealed a sharply marginated 3 cm lesion in the left cavernous sinus, which was isointense to gray matter on T1-weighted images, hyperintense on T2-weighted images, and enhanced with paramagnetic contrast material. Cerebral angiography showed a homogeneous blush fed by an enlarged meningohypophyseal artery. The neuroimaging findings were thought to be most consistent with the diagnosis of a cavernous sinus meningioma. At the time of surgery, a vascular mass was encountered, and a biopsy was consistent with a cavernous hemangioma. This report describes the clinical and neuroimaging features of cavernous sinus hemangiomas that may help to differentiate them from other cavernous sinus lesions.
Primary oculomotor nerve synkinesis is almost always caused by an intracavernous meningioma or aneurysm. We treated a patient who had signs of primary oculomotor nerve synkinesis from an unruptured extracavernous aneurysm located at the junction of the internal carotid artery and the posterior communicating artery. The aneurysm was successfully clipped, resulting in some improvement in ocular motility and alignment. Although most aneurysms affecting the subarachnoid portion of the oculomotor nerve cause an acute, painful oculomotor nerve paresis, such aneurysms may rarely produce painless primary oculomotor synkinesis and therefore should be considered in the differential diagnosis of this phenomenon.
OBJECTIVE: To investigate the clinical presentations and long-term course of patients with superior oblique myokymia (SOM). METHODS: The medical records of all 16 patients with the diagnosis of SOM seen in the Neuro-Ophthalmology Unit of The Wilmer Ophthalmological Institute, The Johns Hopkins Hospital, Baltimore, Md, between 1976 and 1993 were reviewed. Follow-up information was obtained for 14 (88%) of the 16 patients. RESULTS: Of the 16 patients with SOM, nine (56%) were male and seven (44%) were female. The age of onset of symptoms ranged from 22 to 50 years (mean age, 34 years). All patients were otherwise healthy with no history of neurologic illness. Seven (44%) of the 16 patients complained of paroxysms of uniocular "shimmering," "fluttering," or oscillopsia lasting seconds, three (19%) complained of vertical and torsional diplopia, and six (38%) had both types of symptoms. Five (31%) of the 16 patients underwent neuroimaging studies within 1 year of onset of symptoms. All imaging study results were normal. Follow-up information was obtained for 14 patients (88%). The time from onset of symptoms to our most recent contact was 3 to 29 years. Of the seven patients who received no treatment, five (71%) continue to have symptoms to date. Three patients received medical treatment only; one of the three has experienced lasting benefit with carbamazepine. Four patients underwent superior oblique tenectomy combined with inferior oblique myectomy after not responding to medical treatment. All four patients experienced resolution of all ocular symptoms after surgery. CONCLUSIONS: Because SOM is a much more chronic disease than formerly realized and because of the poor long-term effects and potential side effects of the medications used, medical treatment of SOM is not the optimum way to manage the disease. Extraocular muscle surgery is the treatment of choice when symptoms of SOM are intolerable to the patient.
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