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Biomedical subjects

R L Tomsak

Publications and source records attributed to R L Tomsak.

At least 19 recordsLinked to original sources
PubMed1995

Dynamic properties of the human vestibulo-ocular reflex during head rotations in roll.

We investigated the dynamic properties of the human vestibulo-ocular reflex (VOR) during roll head rotations in three human subjects using the magnetic search coil technique. In the first of two experiments, we quantify the behavior of the ocular motor plant in the torsional plane. The subject's eye was mechanically displaced into intorsion, extorsion or abduction, and the dynamic course of return of the eye to its resting position was measured. The mean predominant time constants of return were 210 msec from intorsion, 83 msec from extorsion, and 217 msec from abduction, although there was considerable variability of results from different trials and subjects. In the second experiment, we quantify the efficacy of velocity-to-position integration of the vestibular signal. Position-step stimuli were used to test the torsional or horizontal VOR, being applied with subjects heads erect or supine. After a torsional position-step, the eye drifted back to its resting position, but after a horizontal position-step the eye held its new horizontal position. To interpret these responses we used a simple model of the VOR with parameters of the ocular motor plant set to values determined during Exp 1. The time constant of the velocity-to-position neural integrator was smaller (typically 2 sec) in the torsional plane than in the horizontal plane (> 20 sec). No disconjugacy of torsional eye movements was observed. Thus, the dynamic properties of the VOR in roll differ significantly from those of the VOR in yaw, reflecting different visual demands placed on this reflex in these two planes.

Adult↗
PubMed1995

Unsatisfactory treatment of acquired nystagmus with retrobulbar injection of botulinum toxin.

PURPOSE: We quantified the effects of botulinum toxin injected into the retrobulbar space of patients with acquired nystagmus with prominent vertical or torsional components. METHODS: We measured binocular eye rotations in three planes before and after injection of botulinum toxin (10, 12.5, or 25 units) into the retrobulbar space of one eye of each of three patients, ages 28 to 37 years, with acquired pendular nystagmus. RESULTS: Retrobulbar injection of botulinum toxin abolished or reduced all components of the nystagmus in the treated eye in all three patients for about two to three months. The patient who received 25 units developed complete external ophthalmoplegia and blepharoptosis. The other two patients retained some voluntary movements but developed diplopia. In one patient, visual acuity improved from Jaeger 5 to Jaeger 1. In a second patient, filamentary keratitis developed, and visual acuity declined from Jaeger 2 to Jaeger 7; keratitis was a recurrent problem one year after the botulinum toxin injection. In the third patient with predominantly torsional nystagmus, visual acuity was unchanged at Jaeger 2. No patient was pleased with the results, because of blepharoptosis, diplopia, or discomfort (from keratitis), and none elected to repeat the procedure. CONCLUSIONS: The side effects of botulinum toxin administered by retrobulbar injection limit its therapeutic value in the treatment of acquired nystagmus. Even smaller doses that do not abolish nystagmus may produce troublesome diplopia.

Adult↗
PubMed1994

Treatment of abnormal eye movements that impair vision: strategies based on current concepts of physiology and pharmacology.

Certain abnormal eye movements, especially pathological nystagmus, degrade vision and cause illusory motion of the seen environment. These symptoms are due to excessive movement of images of stationary objects on the retina. Recently, the pathophysiology underlying several types of nystagmus and saccadic oscillations was better defined by the development of animal models and by experimental pharmacological studies. Despite this, few reliable therapies are currently available for these abnormal eye movements. In clinical studies, a number of drugs reportedly helped individual patients, but few drugs have been subjected to double-blind trials. An alternative approach to pharmacological suppression of abnormal eye movements is optical stabilization of images on the retina, which is helpful in selected patients. Weakening of the extraocular muscles, using botulinum toxin or surgery, is prone to cause diplopia and may induce plastic-adaptive changes that render the effect temporary. In some patients, treatment of an underlying condition, such as the Arnold-Chiari malformation, reduces nystagmus and improves vision. There is a need for multicenter trials to evaluate systematically potential treatments of abnormal eye movements that impair vision.

Animals↗
PubMed1992

Effectiveness of botulinum toxin administered to abolish acquired nystagmus.

We injected botulinum toxin into the horizontal rectus muscles of the right eyes of 2 patients who had acquired pendular nystagmus with horizontal, vertical, and torsional components. This treatment successfully abolished the horizontal component of the nystagmus in the injected eye in both patients for approximately 2 months. Both patients showed a small but measurable improvement of vision in the injected eye that may have been limited by coexistent disease of the visual pathways. The vertical and torsional components of the nystagmus persisted in both patients. In 1 patient, the horizontal component of nystagmus in the noninjected eye increased; we ascribe this finding to plastic-adaptive changes in response to paresis caused by the botulinum toxin. Such plastic-adaptive changes and direct side effects of the injections--such as diplopia and ptosis--may limit the effectiveness of botulinum toxin in the treatment of acquired nystagmus. Neither patient elected to repeat the botulinum treatment.

Adult↗
PubMed1992

Absence of the relative afferent pupillary defect with monocular temporal visual field loss.

We report five patients with monocular temporal visual field abnormalities who did not have clinically detectable relative afferent pupillary defects. The causes for the field defects were posterior ischemic optic neuropathy, craniopharyngioma, pituitary adenoma, pseudotumor cerebri, and traumatic optic neuropathy. We discuss the possible explanations for our observations, considering the known anatomy of the pregeniculate visual pathways and the afferent pupillary pathways.

Adenoma↗
PubMed1992

Rapid response of syphilitic optic neuritis to posterior sub-tenon's steroid injection.

An HIV-positive man with subacute syphilitic meningitis developed severe bilateral visual loss from optic neuritis. His visual acuity improved remarkably within 24 hours after single posterior sub-Tenon's injections of triamcinolone (Kenalog) were given. Periocular steroid injections should be considered as an adjunctive treatment of syphilitic optic neuritis.

HIV Seropositivity↗
PubMed1991

Alternating sequential intracarotid BCNU and cisplatin in recurrent malignant glioma.

The authors entered 43 patients with recurrent malignant glioma in a trial of alternating sequential intracarotid BCNU and cisplatin. Protocol design was alternating courses of BCNU (2 doses, 300 to 400 mg each) and cisplatin (2 doses, 150 to 200 mg each) each at 4-week to 6-week intervals. Eight of 40 patients (20%) evaluable after the first course of BCNU showed partial or minor response. Only 18 patients were evaluable after the first course of cisplatin, and 5 were evaluable after the second course of BCNU. Median survival was 9 months (range, 2 weeks to 6 years). Cerebral or ocular toxicity unique to this method of chemotherapy administration and failure to show clinical improvement were the most common reasons for removal from study. Because of the high attrition rate, the authors were unable to determine a meaningful response to alternating sequential BCNU and cisplatin or to test the clinical degree of cross-resistance to these agents in human malignant glioma.

Adult↗
PubMed1991

Superior oblique myokymia. Quantitative characteristics of the eye movements in three patients.

Using the magnetic search coil technique, we measured horizontal, vertical, and torsional rotations of both eyes of two patients with idiopathic superior oblique myokymia, and of the affected eye in a third patient. Superior oblique myokymia was strictly monocular and consisted of an initial intorsion and depression of the affected eye and subsequent oscillations with torsional and vertical components. The peak-to-peak torsional and vertical amplitudes of the oscillations were less than 1 degree, but peak velocities frequently exceeded 4 degrees/sec in both planes. Fourier analysis indicated two features: (1) a broad range of frequencies up to about 50 Hz, indicating irregular oscillations; and (2) a superimposed larger-amplitude oscillation in the range from 1.5 to 6 Hz. Taken with electromyographic data from other studies, these results indicate that superior oblique myokymia reflects spontaneous discharge of trochlear motor neurons that have undergone regenerative changes.

Adult↗
PubMed1991

Ophthalmologic aspects of headache.

Pain around the eye can be caused by local ophthalmic disorders or by disease of other structures sharing trigeminal nerve sensory innervation. In general, most ocular causes for pain also cause the eye to be red, thus alerting the examiner to the focality of the problem. However, conditions like eyestrain, intermittent angleclosure glaucoma or neovascular glaucoma, and low-grade intraocular inflammation can be painful and not be associated with obvious redness. Ocular signs and symptoms also occur with numerous other causes of headache. Double vision in association with periocular pain can result from orbital lesions, isolated cranial neuropathies, and cavernous sinus lesions. Pupillary abnormalities like Horner's syndrome may result from a variety of painful conditions, including cluster headache, parasellar neoplasms or aneurysms, internal carotid dissection or occlusion, and Tolosa-Hunt syndrome. Pain with a dilated and unreactive pupil may reflect a benign condition like Adie's syndrome or ophthalmoplegic migraine, or it may herald the presence of a life-threatening posterior communicating artery aneurysm. Headache and transient visual loss can be manifestations of classic migraine, or be symptoms of ocular hypoperfusion from ipsilateral internal carotid occlusion or increased intracranial pressure from pseudotumor cerebri. In a young patient, head pain with a fixed visual deficit may result from optic neuritis, in an older adult, temporal arteritis may be the culprit. Ophthalmologic aspects of headache thus encompass problems that range from simple and benign to complex and formidable.

Eye Diseases↗
PubMed1991

Superficial temporal artery biopsy. A simplified technique.

A simplification of the method for superficial temporal artery biopsy is presented. The main trunk of the artery is taken preferentially because of its more constant anatomic location. An improvement in the technique for performing the subcutaneous dissection is also discussed.

Biopsy↗
PubMed1990

The characteristics and mechanisms of visual disturbance associated with anticonvulsant therapy.

Eight epileptic patients receiving anticonvulsants had recurrent visual disturbances in the form of diplopia and oscillopsia in the horizontal or vertical planes. The symptoms could be ascribed to impaired vergence mechanisms, vertical nystagmus, or abnormalities of the vestibulo-ocular reflex. Other eye movements, such as pursuit and gaze-holding, were also affected, but did not lead to complaints. Episodes of visual disturbance were often preceded by prodromes of ocular or systemic discomfort, after which oscillopsia or diplopia evolve rapidly. The symptomatology was stereotyped but unique for each patient and may reflect idiosyncratic susceptibility to the ocular motor side effects of anticonvulsants. Six of the 8 patients were taking carbamazepine and phenytoin in combination, which have similar effects on the ocular motor system.

Adult↗
PubMed1990

Balint's syndrome in Alzheimer's disease: visuospatial functions.

A subgroup of patients with Alzheimer's disease (AD) developed Balint's syndrome, an uncommon and incompletely understood disorder of visuospatial processing. We characterized the visuospatial features of three AD patients with Balint's syndrome and compared them to three comparably demented AD patients without this syndrome. On visuospatial tasks, the Balint patients were unable to integrate visual stimuli over space. On contrast sensitivity testing, the Balint patients had significantly decreased contrast sensitivities for low spatial frequency gratings (0.5, 1.0 and 2.0 cpd) alternated at 7.5 Hz. Furthermore, the Balint patients had left visual field attentional deficits and normal hemifield P100 visual evoked potentials. In AD, Balint's syndrome involved decreased sensitivity to low spatial frequencies necessary for global visuospatial analysis, a disturbance suggesting damage to the magnocellular visual system in the occipitoparietal association cortex and, possibly, in the optic nerves.

Aged↗
PubMed1990

Disorders of the visual system in Alzheimer's disease.

Alzheimer's disease (AD) is associated with disturbances in basic visual, complex visual, and oculomotor functions. The broad range of visual system disorders in AD may result from the concentration of neuropathology in visual association cortex and optic nerves in this disease. AD patients and their caregivers frequently report visuospatial difficulties in these patients. Examination of the visual system in AD may reveal visual field deficits, prolonged visual evoked potentials, depressed contrast sensitivities, and abnormal eye movement recordings. Complex visual disturbances include constructional and visuoperceptual abnormalities, spatial agnosia and Balint's syndrome, environmental disorientation, visual agnosia, facial identification problems, and visual hallucinations. The purpose of this article is to review the spectrum of visual system disturbances found in AD and, in particular, to describe the methods used to screen for complex visual abnormalities in these patients.

Alzheimer Disease↗
PubMed1989

Herniation of the suprasellar visual system and third ventricle into empty sellae: morphologic and clinical considerations.

Intrasellar herniation of the optic nerve, optic chiasm, optic tract (suprasellar visual system, SVS), and anteroinferior third ventricle can occur into primary or secondary empty sellae. The anatomic part of this study evaluated the appearance of the SVS in subjects with normal sellae (n = 52), the patterns and prevalence of SVS herniation in enlarged primary empty sellae (n = 24), and the patterns of intrasellar herniation of the SVS in secondary empty sellae (n = 8). The clinical part of this study was to correlate the visual status with the anatomic patterns of the intrasellar herniated SVS. High-resolution MR and CT were used to define the anatomy. MR was superior to CT in all groups in defining accurately the SVS relationship to the sella turcica. In the normal group, the SVS invariably had a straight-line appearance formed by the optic nerve, optic chiasm, and floor of the third ventricle and was above the sella. The SVS was herniated in three of 24 enlarged primary empty sellae. A difference in the appearance of the hypothalamic and infundibular recesses in the primary empty sella group with SVS herniation (dilated recesses and formation of an obtuse angle) and in the secondary empty sella group with SVS herniation (nondilated recesses and formation of an acute angle) was observed. Visual disturbances in primary empty sellae with SVS herniation were present in two of three subjects. Visual disturbances may be absent or minimal in primary empty sellae and secondary empty sellae with herniation of the SVS. Progression of the symptoms--visual field defects, optic atrophy, and loss of vision--is not inevitable. There was no correlation between the severity of visual symptoms and the degree of herniation of the SVS in either the primary or secondary sellae. We found that intrasellar herniation of the SVS into a primary or secondary empty sella is well delineated with MR, and MR should facilitate decisions concerning surgery or therapy. Visual disturbances proved to be an unreliable indicator of herniation.

Adult↗
PubMed1989

High-signal periventricular lesions in patients with sarcoidosis: neurosarcoidosis or multiple sclerosis?

The vast majority of periventricular abnormalities visualized with MR imaging in patients less than 50 years old represents multiple sclerosis (MS) lesions. There are many other causes of periventricular lesions, most of which can be differentiated from MS on the basis of history and physical or MR findings. Five cases of biopsy- or Kveim test-proved sarcoidosis with MR findings consistent with MS are reported. Each of these patients, diagnosed as having sarcoidosis, had symptoms identical to those seen in MS. Although these patients have not had histologic characterization of the intraparenchymal lesions seen on MR, they illustrate the difficulty of differentiating sarcoidosis with CNS involvement from MS in some patients on the basis of clinical, radiographic, electrodiagnostic, or CSF testing. This series contributes to a growing body of evidence that neurosarcoidosis probably should be included in the differential diagnosis of isolated periventricular lesions in patients less than 50 years old.

Adult↗
PubMed1989

Anterior ischemic optic neuropathy and increased intraocular pressure.

Five patients were noted to have increased intraocular pressure (IOP) during evaluation for acute nonarteritic anterior ischemic optic neuropathy (AION). Three of the five had no prior record of IOP elevation; all five had small cup-to-disc ratios. Elevated IOP may be a risk factor for developing AION, especially in eyes with structurally congested optic discs.

Aged↗