Myasthenic syndrome of snake envenomation: a clinical and neurophysiological study. (1/231)

In this prospective study, 65 consecutive patients with neurological manifestations after snake envenomation, were examined in order to describe the natural history of the reversible nature of muscle weakness. Snake envenoming led to a completely reversible muscle paralysis involving the external ocular muscles with sparing of the pupils, muscles of mastication, facial muscles, palatal muscles, neck and proximal limb muscles. The deep tendon reflexes were preserved with no sensory abnormalities. The muscular weakness usually set in within an hour of envenomation and lasted up to 10 days, with fatigability lasting for 12 days. Respiratory muscle paralysis led to ventilatory failure needing ventilation in severely envenomed patients. Motor and sensory nerve conduction were normal with normal resting compound motor action potentials on electromyography. Repetitive nerve stimulation gave rise to a decremental response during high frequency stimulation. The edrophonium test gave negative results. These manifestations are due to abnormalities of neuromuscular transmission and are not typical of myasthenia gravis. As the exact pathophysiology of venom-related neurotoxicity is not known, it is suggested that the neurological manifestations of snake envenoming be designated a myasthenic syndrome. Further studies to isolate the neurotoxin and its mechanism and exact site of blocking at the neuromuscular junction would pave the way for the development of a novel long-acting neuromuscular blocking agent.  (+info)

Diplopia in a swimmer due to badly fitting goggles. (2/231)

An unusual effect of badly fitting swimming goggles is described. The goggles pressed on the trochlea of the left eye, interfering with the action of the superior oblique muscle. Diplopia resulted, which took several weeks to resolve.  (+info)

Spatial characteristics of cerebral polyopia: a case study. (3/231)

A 41-year-old woman showed bilateral monocular polyopia and an incomplete, right-sided homonymous hemianopia following bilateral cerebral strokes confirmed by neuroimaging. She was tested with briefly-presented visual stimuli to determine whether her polyopic images varied with visual field position of stimuli which evoked them. Stimuli close to her scotoma elicited polyopic images at shorter latency and higher probability than did stimuli more distant from it. RS could maintain stable fixation on small stimuli, suggesting that eye movements were not responsible for her polyopia. We discuss the possibility that cerebral polyopia is due to recoding of visual receptive fields in primary visual cortex and that bilateral occipital lesions are a causative factor in the genesis of the disorder.  (+info)

Prolonged diplopia following a mandibular block injection. (4/231)

A case is presented in which a 14-yr-old girl developed diplopia after injection of the local anesthetic Xylotox E 80 A (2% lidocaine with 1:80,000 epinephrine). Since the complication had a relatively slow onset and lasted for 24 hr, the commonly suggested explanations based on vascular, lymphatic, and neural route theories do not adequately fit the observations. No treatment, other than reassurance, was necessary, and the patient recovered fully.  (+info)

Recurrent proptotic diplopia due to congestive expansion of cavernous haemangioma with relapsing right-sided cardiac failure. (5/231)

A 75-year-old man with a recent history of pulmonary embolism, presented with collapse followed by a gran mal seizure and right-sided non-pulsatile proptosis. On recovery, he had diplopia on lateral and upward gaze and signs of congestive cardiac failure. Further pulmonary embolism was proven by lung scintigraphy. Computed tomography of his orbits confirmed a contrast-enhancing space-occupying lesion of the medial wall of the right orbit, with no intracranial abnormality. The patient was investigated for metastatic tumour as a possible cause of the space-occupying lesion and the unprovoked thromboembolic event, but no evidence of malignancy was found. The orbital lesion was not biopsied because of the risk of bleeding from anticoagulation. Three weeks later, the patient represented with recurrent cardiac failure, proptosis, and diplopia. A transorbital ultrasound confirmed an encapsulated, well-defined vascular lesion, with typical appearances and Doppler flow characteristics of a cavernous haemangioma. Diuretic therapy abolished the proptosis and diplopia in tandem with relief of the cardiac failure. This is the first description of recurrent proptosis with diplopia due to recurrent congestive expansion of an orbital cavernous haemangioma.  (+info)

Auditory saccade impairment after central thalamus lesions. (6/231)

Visual and auditory saccades were studied in three patients with an isolated lesion located in the central thalamus. Visual saccades proved to be normal, whereas for auditory stimuli, the amplitude of the first saccade was asymmetric: saccades ipsilateral to the lesion were significantly smaller than those directed to the contralateral side. The patients were able to make a corrective saccade and hence to improve gain and to decrease gain asymmetry. It is suggested that patients were able to localise auditory targets correctly, but did not correctly take into account eye position during the saccade, probably as a consequence of an inaccurate efference copy (corollary discharge) signal. The findings are in keeping with the hypothesis that the central thalamus deals with saccades that are based on extraretinal signals.  (+info)

Can myasthenia gravis be diagnosed with the 'ice pack test'? A cautionary note. (7/231)

The ice pack test may be helpful in establishing that ptosis is due to ocular myasthenia gravis, since cold improves neuromuscular transmission. However, the role of the test in determining whether diplopia is of myasthenic origin has yet to be established.  (+info)

Graves' ophthalmopathy: eye muscle involvement in patients with diplopia. (8/231)

BACKGROUND: Diplopia identifies patients with eye muscle involvement in Graves' ophthalmopathy (GO). OBJECTIVE: To identify clinical parameters that could eliminate the need for magnetic resonance imaging (MRI) to assess the activity of inflammation in the eye muscles of GO patients with diplopia. METHODS: In 43 patients with GO with recently developed diplopia, orbital ultrasound and MRI were performed. Muscle diameters and MRI T2 relaxation times were measured, and the amount of orbital connective tissue was calculated from MRI scans and compared with ultrasound readings, diplopia grades, degree of protrusion, ocular pressure, tear production, antibody levels and hormonal parameters of thyroid function. RESULTS: No correlation was found between diameters of 233 extraocular muscles measured by MRI and by ultrasound. For each of the four muscles, there was a diameter above which ultrasound was always unreliable. MRI data were used in further analysis. Of the muscles examined, the inferior rectuses were the most frequently enlarged - at least one, in 93% of cases. Medial, lateral and superior rectuses were enlarged in 59%, 37% and 34% of the orbits respectively. The pattern of muscle involvement of the two orbits tended to be symmetric (r=0.49, P=0.003), particularly for the medial rectuses (r=0.90, P=0.000). Proptosis correlated with the sum of the muscle diameters for a given eye (right eye: r=0.54, P=0.003; left eye: r=0.57, P=0.001), but it failed to correlate with the amount of orbital connective tissue. In 53% of the patients, normal T2 relaxation times were found in all eight muscles. There was only a weak correlation between muscle thickness and T2 relaxation time (r=0.49, P=0.003), indicating that muscle enlargement alone is not a sign of disease activity. The severity of diplopia was independent of T2 relaxation time. The amount of orbital connective tissue showed a negative correlation with the greatest T2 relaxation time for a given eye (r= -0.52, P=0.004); this suggests that disease types exist that have predominant muscle involvement and predominant connective tissue expansion. No correlation between connective tissue expansion and proptosis, diplopia grade, muscle thickness or disease duration was found - that is, connective tissue expansion is not a major factor in diplopia. Both muscle and connective tissue findings were independent of thyroid function. CONCLUSION: Ultrasound and MRI eye muscle diameter readings do not correlate, because of the inherent inaccuracy of orbital ultrasound. Muscle enlargement alone does not mean oedematous swelling and active disease. Neither ultrasound, nor any combination of 11 clinical and laboratory parameters provided the degree of information on muscles and connective tissue that was obtainable by MRI. In unclear cases of recently developed diplopia, before orbital decompression surgery, in the case of treatment failure or if, for any other reason, imaging is needed in GO, MRI is the method of choice.  (+info)