Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most common causes of internuclear ophthalmoplegia (INO) are multiple sclerosis and vascular disease of the brain stem. Rarer causes are tumor, Arnold-Chiari malformation, and syphilis. Myasthenia gravis has, on occasion, presented with ocular abnormalities indistinguishable from INO. A case is described of bilateral INO of brief duration following head trauma. There were no other brain-stem abnormalities. This brings to 11 the number of reported patients in whom head trauma precipitated this abnormality.
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PMID:Internuclear ophthalmoplegia following head injury. Case report. 47 39

A 70-year-old man with known vascular disease, who had bilateral internuclear ophthalmoplegia, and an 18-month-old girl with a long-term variable esotropia culminating in a postinfectious oculopharyngeal neuropathy both responded with a positive edrophonium chloride (Tensilon) test, strongly suggesting the diagnosis of myasthenia gravis. Both subsequently received maintenance doses of neostigmine methylsulfate (Prostigmin).
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PMID:Ocular myasthenia gravis mimicking pseudointernuclear ophthalmoplegia and variable esotropia. 48 61

Saccades (horizontal and vertical) and dissociated nystagmus were quantitatively assessed in four patients with internuclear ophthalmoplegia. Two patients had bilateral medial longitudinal fasciculus (MLF) lesions associated with multiple sclerosis and two had unilateral lesions associated with brain stem vascular disease. Adducting saccades made on the side of an MLF lesion were slowed in each patient (P less than .01). At the same time, abducting saccades in the contralateral eye had normal velocity, but consistently overshot the target. After the overshoot, the eye returned to the target with an exponentially decaying course. With large angular deviations (usually more than 15 degrees), the abducting eye developed nystagmus characterized by slow components that moved toward the midposition with an initially high velocity followed by a segment of slower velocity. The adducting eye had either no nystagmus or a low-amplitude nystagmus characterized by a rounded junction between the fast and slow component. The saccade abnormalities and waveform of the dissociated nystagmus can be explained by a pulse-step mismatch at the agonist motoneurons.
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PMID:Internuclear ophthalmoplegia. I. Saccades and dissociated nystagmus. 66 4

Successful identification of the cranial nerve and ocular muscle responsible for a subjective complaint of diplopia requires an evaluation of the type and character of the double vision and not infrequently the use of a red glass or Maddox rod, especially in incomplete and subtle cases. An isolated third nerve lesion is most commonly seen with a supraclinoid aneurysm (pupil dilated and fixed), vascular disease (pupil spared), and trauma. Mild frontal head trauma and vascular disease are the most common etiologies associated with an isolated fourth nerve paresis. Tumor, vascular disease and trauma should be prime considerations when a patient presents with an isolated sixth nerve paresis. A child's diagnostic possibilities will differ from the adult: third nerve (congenital), fourth nerve (congenital), and sixth nerve (brainstem glioma, postviral or inflammatory). Finally, myasthenia gravis can readily mask or mimic an isolated or mixed cranial nerve palsy. A Tensilon test is always indicated in unexplained diplopia with ophthalmoplegia and normal pupils.
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PMID:Paresis of cranial nerves III, IV, and VI: clinical manifestation and differential diagnosis. 248 13

In 1949, amphetamine sulfate was replaced by propylhexedrine in the nasal decongestant agent Benzedrex because of psychosis, sudden death, and widespread abuse. Propylhexedrine is not without risks, and reported cases of psychosis, myocardial infarction, pulmonary vascular disease and pulmonary hypertension, and sudden death are well documented in the medical literature. We are reporting 2 cases of definite brainstem dysfunction and 5 cases of transient diplopia secondary to IV abuse of Benzedrex. This widely abused drug is prepared by heating Benzedrex and hydrochloric acid, and the resulting crystals are dissolved in water for injection. This agent is called "stove-top speed". All 7 patients had transient diplopia, within seconds after injection. One patient had evidence of a right-internuclear ophthalmoplegia, and another had a depressed right gag reflex and paralysis of the right half of the tongue. The deficits in these two patients, persisted for many months. In young adults with history of drug abuse, the IV use of Benzedrex should be considered in the differential diagnosis of transient or permanent focal brainstem deficits.
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PMID:Intravenous abuse of propylhexedrine (Benzedrex) and the risk of brainstem dysfunction in young adults. 287 25

Although thyrotoxicosis and orbital complications of acute ethmoid or frontal sinusitis are among the most common causes of unilateral exophthalmos, inflammatory pseudotumor is frequently accompanied by progressive acute unilateral proptosis. Because the associated chemosis, scleral erythema, and ophthalmoplegia constitute a spectrum of clinical findings present in numerous inflammatory orbital disorders and systemic diseases, the diagnosis of inflammatory pseudotumor is one of exclusion, often requiring orbital biopsy. Four patients without evidence of sinusitis, endocrinopathy, collagen vascular disease, or Wegener's granulomatosis are described. The diagnosis of orbital pseudotumor was disclosed by computed axial tomography, thus avoiding orbitotomy. The finding of scleral and choroidal thickening with enhancement following intravenous contrast injection represents a select group of patients with orbital pseudotumor and differentiates them from patients with endocrine exophthalmopathy or neoplasms. This noninvasive technique is extremely valuable because early diagnosis is critical for successful treatment. All four patients responded dramatically to high-dose corticosteroid therapy. In the absence of significant clinical response, however, Wegener's granulomatosis, lymphoma, and rhabdomyosarcoma, especially in younger patients, must be carefully excluded. Orbital exploration or decompression or both are used when proptosis, headache, or orbital pain does not resolve promptly, visual acuity deteriorates, or the diagnosis remains unknown.
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PMID:Computerized axial tomography in inflammatory pseudotumor of the orbit. 682 19

The authors report unusual presentations of members of an Irish family with familial AD due to an E280G mutation in exon 8 of presenilin-1. One had spastic paraparesis and white matter abnormalities on cranial MRI. A sibling had an internuclear ophthalmoplegia, spastic-ataxic quadriparesis, and "cotton-wool plaques" with amyloid angiopathy on brain biopsy. Another affected sibling also had MRI white matter abnormalities. The MRI findings may reflect an ischemic leukoencephalopathy due to amyloid angiopathy affecting meningocortical vessels.
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PMID:Presenilin-1 mutation (E280G), spastic paraparesis, and cranial MRI white-matter abnormalities. 1237 Apr 77

The objective of this study is to better define the pathological characteristics of pathologically proven progressive supranuclear palsy (PSP) presenting with the corticobasal syndrome (CBS). PSP is characterized by early falls, vertical supranuclear ophthalmoplegia, and axial rigidity, whereas asymmetric limb features, including rigidity, bradykinesia, apraxia, alien limb phenomena, and cortical sensory loss are characteristic of CBS. We investigated clinicopathological characteristics of 5 cases of PSP that presented with CBS (CBS-PSP). Comprehensive pathological analysis was undertaken to determine the presence of concomitant pathological processes as well as quantitative tau burden in cortical regions of CBS-PSP, compared with 8 typical PSP cases (Typ-PSP). The clinical features in the CBS-PSP cases included asymmetrical features, apraxia, alien limb phenomena, and progressive aphasia. All cases had Parkinsonism, and vertical supranuclear ophthalmoplegia was noted in all but 1 case of CBS-PSP. Secondary neuropathological diagnoses included argyrophilic grain disease (AGD) in 1 of the 8 cases of Typ-PSP, whereas Alzheimer's disease (AD), Lewy body disease, AGD, and vascular disease was found in 3 cases of CBS-PSP. Image analysis of cortical tau burden performed in 8 Typ-PSP and 3 CBS-PSP cases revealed a significant increased tau burden in mid-frontal and inferior-parietal cortices in the CBS-PSP cases. This study demonstrates that when PSP presents as CBS, it is most likely due to either a concurrent cortical pathology from a secondary process such as AD or from the primary pathology of PSP extending into cortical areas that are primarily and commonly affected in CBD.
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PMID:Increased tau burden in the cortices of progressive supranuclear palsy presenting with corticobasal syndrome. 1583 57

Benign angiopathy of central nervous system (BACNS) is rare in children. We report a seven-year-old boy presenting with sudden severe headache and progressive external ophthalmoplegia. Magnetic resonance angiography (MRA) showed diffuse segmental narrowing of major cerebral arteries. Following a course of glucocorticoid, there was complete resolution of vascular lesions and follow-up MRA did not show any evidence of new lesions.
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PMID:Benign angiopathy of central nervous system. 1963 64

Diplopia is a frequent neuro-ophthalmologic symptom with diverse etiologies. This article describes elementary diagnostic tests and frequent causes of diplopia. Monocular diplopia persists when the other eye is closed and usually disappears when the patient looks through a pinhole. It is usually caused by errors in the optical media of the eye and has to be differentiated from spectacle-induced side effect and non-organic disorders. A sign of non-organic etiology is absence of change in image position when the head is tilted. Binocular diplopia disappears regardless of which eye is closed. Binocular diplopia occurs when the images of both eyes cannot be fused. The most frequent direct cause of diplopia is acquired strabismus. Knowledge of several specific types of strabismus enables efficient patient management. Congenital and decompensating strabismus like accommodative esotropia, pathophoria, strabismus surso- and deorsoadductorius, retraction syndrome, Brown's syndrome and esotropia in high myopia only need ophthalmologic treatment. Orbital injury, orbital tumor, ocular myositis, Graves orbitopathy and vascular disease usually require multidisciplinary management. Neurogenic paresis, superior oblique myokymia, ocular neuromyotonia, myasthenia, chronic progressive external ophthalmoplegia (CPEO), internuclear ophthalmoplegia (INO) and skew deviation require specific neurologic examination. Treatment of diplopia includes treatment of the fundamental disorder, monocular occlusion, prisms and strabismus surgery.
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PMID:How to deal with diplopia. 2298 79


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