1/69. Fresnel membrane prisms: clinical experience.BACKGROUND: There are few published reports on the clinical application of Fresnel membrane prisms in the treatment of diplopia in adults. The authors describe the use of these prisms in patients with fourth and sixth cranial nerve palsies, restrictive motility caused by thyroid-related orbital disease, and convergence insufficiency. methods: Of 209 patients who had been treated with Fresnel prisms, 141 were selected. The database included patients from a private practice in Montreal, seen from 1988 to 1996, and patients seen by orthoptists in the ophthalmology department of a children's hospital in Montreal between 1992 and 1996. All the patients had diplopia associated with fourth (48 patients) or sixth (43 patients) cranial nerve palsy, thyroid-related orbitopathy (18 patients) or convergence insufficiency (32 patients). After qualitative and quantitative assessment of the ocular misalignment, a Fresnel prism was selected for power and axis and for appropriate location on the spectacle lens. Ocular dominance and side of paresis or restriction were also considered in the placement of the prism. The patient's response to treatment was documented. RESULTS: The Fresnel prisms were oriented horizontally in 72 patients (51%), vertically in 55 (39%) and obliquely in 14 (10%). They were placed on the spectacle lens before the nondominant eye in 127 cases (90%), either covering the entire lens, or on the upper or lower segment or both. The patients were followed for an average of 15 (range 2 to 96) months. Of the 141 patients 113 (80%) had a successful outcome, with relief of their diplopia. Twenty-seven patients (19%) eventually had the prismatic correction ground into the lens, 70 (50%) chose to wear the Fresnel prism on a permanent basis because incorporation into the lens was not possible or because of cost, and 17 (12%) used the Fresnel prism as a temporary device before or after surgery. Most patients who converted to incorporated prisms did so when the prismatic power became stable, usually after 6 to 8 months. Eight patients (6%) stopped using the prism because of associated side effects, such as blurred vision, persistent diplopia, torsion or optical aberrations. INTERPRETATION: The Fresnel prism is an excellent device in treating diplopia in adult patients. It is a reasonable permanent option when incorporating the prism into the spectacle lens is not possible. A fused blurred image caused by a Fresnel prism placed in front of the nondominant eye is preferable to double but clear images.- - - - - - - - - - ranking = 1keywords = palsy (Clic here for more details about this article) |
2/69. Lagophthalmos: an unusual manifestation of oculomotor nerve aberrant regeneration.PURPOSE: To describe a patient with unusual findings after regeneration of the oculomotor nerve. methods: Case report. RESULTS: A 35-year-old woman developed complete right third nerve paralysis after neurosurgical ligation of internal carotid-posterior communicating and internal carotid-ophthalmic artery aneurysms. Permanent ipsilateral lagophthalmos appeared as third nerve function spontaneously recovered. CONCLUSION: Lagophthalmos may rarely develop after aberrant regeneration of the oculomotor nerve, presumably caused by co-contraction of the levator and superior rectus muscles during the Bell's phenomenon.- - - - - - - - - - ranking = 0.20687778709395keywords = paralysis (Clic here for more details about this article) |
3/69. Unilateral thalamic infarction and vertical gaze palsy: cause or coincidence?Although vertical gaze palsy (VGP) is commonly associated with lesions of the rostral mesencephalon, there is some evidence that VGP may also be caused by a unilateral thalamic lesion. The case of a 68-year-old man with persistent upward gaze palsy after a unilateral thalamic infarction, demonstrated on computed tomography and magnetic resonance imaging scans, is presented. Subsequent high-resolution magnetic resonance scanning, however, showed involvement of the rostral mesencephalon as well. The authors suggest that in previous patients with VGP ascribed to a unilateral thalamic infarction, a coexisting mesencephalic involvement may have been missed because of inappropriate imaging techniques. Strong evidence of unilateral thalamic infarction as a cause of VGP is still lacking.- - - - - - - - - - ranking = 6keywords = palsy (Clic here for more details about this article) |
4/69. Clinicopathological study of atypical motor neuron disease with vertical gaze palsy and ballism.The case of a 38-year-old patient with rapidly progressing motor neuron disease, complicated by major dysfunction of the extrapyramidal system and of vertical gaze is described. Neuropathological examination revealed a degenerative process that severely affected the lower motor neurons, as well as the neurons of the pars compacta of the substantia nigra, the nucleus of Darkschewitsch, the nucleus interstitialis of Cajal, the colliculi superiores, and the pallidum. The long tracts were unaffected at all levels of the brain stem and spinal cord. There was no convincing evidence for the presence of a multiple system atrophy or progressive supranuclear palsy; the results rather revealed a pattern of vulnerability characteristic of a variant of motor neuron disease.- - - - - - - - - - ranking = 5keywords = palsy (Clic here for more details about this article) |
5/69. Case report: one-and-a-half-syndrome and tuberculosis of the pons in a patient with AIDS.A patient with advanced AIDS presented with right conjugate gaze palsy and impaired adduction on left gaze (the one-and-a-half syndrome). The responsible pontine lesion involved the ipsilateral abducens nucleus and the adjacent medial longitudinal fasiculus (MLF), as demonstrated by magnetic resonance imaging (MRI). tuberculosis (TB) was the etiology of the brainstem lesion. The patient had complete recovery after anti-tuberculosis treatment. The nuclear location of the tuberculoma is unusual and the reversal of this neuro-ophthalmologic syndrome is noteworthy.- - - - - - - - - - ranking = 1keywords = palsy (Clic here for more details about this article) |
6/69. Remission of superior oblique myokymia after microvascular decompression.Superior oblique myokymia (SOM) is an ocular motility disorder characterized by oscillopsia, vertical or torsional diplopia, sometimes combined with pressure sensation. Although the pathophysiological basis is unclear, isolated case reports have documented its association with intracranial pathological processes. We present a case of SOM associated with a vascular compression of the fourth nerve at the root exit zone. Following microneurosurgical decompression, SOM completely resolved and paralysis of the fourth nerve occurred. This was less disturbing.- - - - - - - - - - ranking = 0.20687778709395keywords = paralysis (Clic here for more details about this article) |
7/69. Eye deviation in patients with one-and-a-half syndrome.To understand malalignments of the visual axes in one-and-a-half syndrome, we measured eye positions in 4 patients with this syndrome under two conditions: with Frenzel goggles to prevent eye fixation and without Frenzel goggles. When fixation was prevented with the Frenzel goggles, all patients showed mild outward deviation in both eyes. Removal of the Frenzel goggles elicited adduction of the eye ipsilateral to the side of the lesion for fixation, with greater outward deviation of the contralateral eye (acute stage), or adduction of both eyes to midposition for biocular fixation (convalescent stage). In 3 patients whose outward eye deviation with Frenzel goggles was greater on the ipsilateral side, a transition from one-and-a-half syndrome to ipsilateral internuclear ophthalmoplegia was noted, whereas a transition to ipsilateral gaze palsy was seen in the one patient whose deviation was greater on the contralateral side. These findings suggest that in one-and-a-half syndrome patients, the eyes tend to be in divergent positions when fixation is prevented; ipsilateral eye deviation may result from medial longitudinal fasciculus involvement, and contralateral eye deviation may result from paramedian pontine reticular formation involvement. Viewing a target may lead to a secondary deviation or adaptation of eye positions for fixation.- - - - - - - - - - ranking = 1keywords = palsy (Clic here for more details about this article) |
8/69. Total recovery after bilateral paramedian thalamic infarct.Bilateral paramedian thalamic infarcts are characterised initially by the association of acute vigilance disorders and vertical gaze palsy, followed by persisting dementia with severe mnemic disturbance, global aspontaneity and apathy. We describe a patient with a dramatic neuropsychological recovery, confirmed by testing examination and completed by a cerebral metabolism study. The pathophysiology of this type of cognitive deficit is discussed.- - - - - - - - - - ranking = 1keywords = palsy (Clic here for more details about this article) |
9/69. July 2000: A 70 year old with rigidity, decreased ocular movements, and dementia.The July Case of the Month (COM): A 70 year old male presented with a four year history of cognitive decline, difficulty expressing himself, and an increasingly unsteady gait with numerous falls. At presentation he was wheel-chair bound. Examination showed some slowing of speech, mild memory impairment, but normal cranial nerves. Spastic weakness and brisk reflexes were also noted, with bilateral ankle clonus. MRI scans were normal. Four years later he was admitted with a urinary tract infection and was mute with severely impaired ocular motility. He died 18 months later and autopsy showed the classic neuropathological findings of typical Progressive supranuclear palsy, including tau-positive glial inclusions.- - - - - - - - - - ranking = 1keywords = palsy (Clic here for more details about this article) |
10/69. Complete bilateral horizontal gaze paralysis disclosing multiple sclerosis.Two women presented with bilateral internuclear ophthalmoplegia evolving in a few days to complete bilateral horizontal gaze paralysis. Convergence and vertical eye movements were normal. Cerebral MRI showed a few small white matter lesions in the lateral ventricle regions, and, at the brainstem level, a single, small, bilateral lesion affecting the posterior part of the medial pontine tegmentum and responsible for the clinical syndrome. The condition gradually improved in both patients, following a similar progression as at the onset: improvement first involved the adduction movements in both eyes, whereas bilateral abduction paresis still persisted for a few weeks, before complete recovery of eye movements. Bilateral damage to the medial longitudinal fasciculus and subsequent lateral extent of damage to the region of the two abducens emerging fibres may explain the clinical findings. In both cases, the cause was probably multiple sclerosis.- - - - - - - - - - ranking = 1.0343889354697keywords = paralysis (Clic here for more details about this article) |
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