Journal Contents
| |||
Neuro-OphthalmologyObjective Detection of Hemifield and Quandrantic Field Defects by Visual Evoked Cortical Potentials Bradnam MS, Montgomery DMI, Evans AL, Keating D, Mcclure EA, Damato BE, Mcfadzean R. British Journal of Ophthalmology, 80(4):297-303, 1996 Apr. Aims/Background An objective method for detecting hemifield and quadrantic visual field defects has been developed using steady state visual evoked cortical potentials (VECPs), an adaptive noise canceller (ANC), and Hotelling's t(2) statistic. The purpose of this study was to determine the sensitivity and specificity of the technique. Methods Nine subjects (mean age 44 years) were investigated with field loss due to a variety of causes including both anterior and posterior visual pathway lesions. Dynamic perimetry was performed by means of a Goldmann or Tubingen perimeter. VECP recordings were made from each visual field quadrant (23 degrees X23 degrees) by means of a steady state reversing checkerboard (7 . 7 rev/s). The central 5 degrees of the visual field and the vertical and horizontal meridians were masked during these measurements. Recordings were made from three electrode sites, positioned over the visual cortex, relative to a mid frontal electrode. Each recording lasted 2 minutes, during which time fixation was monitored. The data from each recording were divided into 4 second segments, and the amplitude and phase of the VECP signal measured using the ANC. Hotelling's t(2) statistic was applied to determine the probability of signal detection. Receiver operating characteristic curves were used to find the optimum signal detection threshold for identification of the visual field defects. Results The results of the study confirmed patterns of subjective visual field loss. The technique had a sensitivity and a specificity of 81% and 85%, respectively, for detecting 'non-seeing' areas in the inferior visual field, and 82% and 89%, respectively, for detecting 'non-seeing' areas in the superior visual field. Conclusion These results demonstrate that the technique is of potential clinical value to ophthalmologists and neurologists when subjective perimetry is not possible.
Neuro-OphthalmologyMagnetic resonance Imaging in Patients with Unexplained Optic Neuropathy Golnik, K., Hund, P., Stroman, G. and Stewart, W. Ophthalmology, 1996;103:515-520 Optic atrophy of uncertain etiology is a recurrent clinical dilemna. The authors investigate a theory based on the neurosurgical idea that a normal intracranial blood vessel can compress an adjacent nerve causing damage and potential atrophy. They seek to discover the anatomical relationship between the intracranial portion of the internal carotid artery (ICA) and the optic nerve as it exits the optic canal on its way to the optic chiasm.
Records were reviewed and 48 patients were identified as having gradual optic atrophy of uncertain etiology. All patients had optic disk pallor, visual field abnormalities, afferent defect (unless condition was bilateral - 3 patients), normal MRI scans and a negative work-up. They could not have any evidence of optic nerve swelling, progressive cupping, temporal arteritis, multiple scelerosis, loss of vision less than 46 years of age or a history of acute visual loss. Each patient was age matched with an otherwise healthy indiviual to form a control group.
MRI scans including coronal images were performed within three months of the initial exam. Measurements for each were recorded in a masked fashion:
Results:
Comparing the affected optic nerves to the same patient's unaffected nerve and to the control group, the following was reported:
The authors prudent point out "these results do not prove a cause and effect relation". They suggest that if visual function is severely decreased and is progressive with no apparent etiology, decompression should be considered.
Neuro-OphthalmologyCranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery Bakram Mokri, MD et al Neurology 1996; 46:356-359 Internal carotid artery dissections are usually thought of in terms of headaches, oculosympathetic palsy and focal ischaemic cerebral episodes in a middle-aged individual. This article points out that a painful extra ocular palsy may be signaling a spontaneous internal carotid artery dissection. In a Mayo clinic consecutive series of 190 cases of spontaneous dissection of the extracranial internal carotid artery, cranial nerve palsy was present in 23. An upper cranial nerve palsy syndrome could be seen in which the 3, 4, 5 and 6th nerves were affected. Patients presented with single and combination of palsies. A lower cranial nerve palsy syndrome was also seen in which the cranial nerves 7 through 12 were affected. The mechanism of cranial nerve involvement was felt to be due in part to compression or stretching of the nerve by an expanded artery. However, since the dissections mainly start in the neck and do not extend intracranially, other mechanisms must be operative. It was suggested that there was impairment to the cranial nerve blood supply that could have been mechanical, embolic, or hemodynamic. When faced with painful extra ocular muscle palsies, carotid artery dissections should be included in the list of considerations.
Neuro-OphthalmologyPrevalence of Intracranial Lesions in Children Initially diagnosed With Disconjugate Nystagmus (Spasmus Nutans) K.A. Arnoldi and L.Tychsen J Pediatr Ophthalmol Strabismus , 1995;32;296-301 How frequently do children with spasmus nutans develop optic pathway gliomas and what and the warning signs? The authors address these problems with a study of 67 consecutive cases of spasmus nutans [defined as asymetric high frequency small amplitude pendular nystagmus with a history of head nodding and or torticollis. Optic pathway gliomas were rare and not felt to be present in any of the 67 cases. The mean age at onset of spasms nutans was 5.2 months while approximately one half developed strabismus or had non ocular developmental abnormalities. The nystagmus was horizontal in 94% and vertical in only 6%. The literature reports that in cases of spasmus nutans with optic glioma the incidence of vertical nystagmus was 38%. The following indications were offered as signs and symptoms that would suggest that an immediate neuro imaging study should be obtained:
An abnormal neurological exam might well be another indication.
Neuro-OphthalmologyAnterior Ischemic Optic Neuropathy Secondary to Interferon Alfa. Purvin VA. Arch Ophthal , 1995; 113:1041-1044 and Tang RA. Editorial pg 987. Dr Purvin describes 2 patients who developed non-arteritic anterior ischemic optic neuropathy (AION) as a complication of interferon alfa therapy. This is a newly reported side effect which may have several contributing factors as causation. The suggestion is made to advise patients of this possibility as well as limit other confounding risk factors for AION where possible. The two patients were middle-aged, 40 and 51 years, and had classic signs of optic nerve dysfunction, with segmental disc edema, acuity loss, color loss, relative Afferent Pupil Defect, field loss and subsequent disc pallor. Symptoms began within weeks of initiating therapy. Therapy was discontinued but restarted for systemic reasons and AION developed in the fellow eyes. These patients had sudden, non-progressive, mild visual loss. The article reviews the possible pathogenesis of interferon-induced AION including hypotension, papilledema, hyperviscosity syndrome, immune complex deposition and associated risk factors (crowded disc, tobacco use). The most interesting hypothesis is the relationship to interferon-associated retinopathy described by Guyer, et al Arch Ophthal 1993;111:350-6. Purvin suggests involvement of the posterior ciliary arteries rather than the retinal vessels may be the etiology. Recognition of new side effects from agents, like interferons, which are finding broader indications for treatment and wider clinical use is important for all clinicians.
Neuro-OphthalmologySuperior Oblique Luxation and Trochlear Luxation as New Concepts in Superior Oblique Muscle Weakening Surgery Mombaerts I, Koornneff L, Everhard-Halm, YS, Hughes DS, Maillette LJJ. Am J Ophthalmol 1995; 120:83-91 (July) The authors propose a new procedure involving anterior orbital surgery on the trochlear to provide superior oblique (SO) weakening without surgery on the tendon itself. In a series of patients with acquired Brown's syndrome (4) and patients with superior oblique overaction (2 with A-pattern and 3 with secondary overaction due to contralateral inferior rectus restriction), they produced SO weakening by displacing the trochlea towards the center of the orbit or by incising the trochlea and displacing the SO out of the pulley. The effect is to lengthen the tendon by changing the functional origin (the trochlea) without altering the tendon's posterior-temporal insertion and function (depression, abductor, and incyclotorter). 8/9 pts had objective improvement with no cases of superior oblique palsy. The trochlea luxation is created by a periosteal incision and avoids the potential risks of supratrochlear nerve/artery damage of the SO luxation procedure which requires additional maneuvers in the anterior orbit. The authors credit Hughes and Bogart (AJO 1942;25:911-5) for describing this procedure which they wish to restore to the superior oblique weakening armamentarium. They do not report intraoperative forced duction testing which is recommended for Brown's syndrome to verify elimination of restriction. Past reports have indicated self-grading of response to SO recession and tenotomy and the authors propose a similar response to trochlear luxation. A prospective study comparing muscle origin (trochlear) and insertional (SO tenotomy, recession or silicone expander) procedures would be interesting.
|