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 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A 30-year-old man with brainstem cavernoma experienced hemorrhage and was operated in 2008. Six months after the operation, the patient presented with new complaints of left arm tremor namely Holmes' tremor. Neurological examination also revealed left-sided internuclear ophthalmoplegia, left-sided mild paresis, and increased deep tendon reflexes of the left upper extremity, truncal ataxia, and dysarthria. Brain magnetic resonance imaging showed a postoperative cavity and gliosis at the level of the superior and inferior colliculus in the right tegmentum and right red nucleus with extension to the substantia nigra. Fahn-Tolosa-Marin tremor rating scale (TRS) for his left upper extremity (Part A, score 6) was 11 for the proximal and the distal arm. After the failure of medical treatment, the patient underwent right globus pallidum internus and ventral intermediate thalamic nucleus deep brain stimulation. There were no side effects related to the stimulation. Final TRS months after operation was 3 for the proximal and 4 for the distal arm.
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PMID:Unilateral thalamic Vim and GPi stimulation for the treatment of Holmes' tremor caused by midbrain cavernoma: case report and review of the literature. 2331 30

We recently encountered experienced a rare case of transient pupil-sparing oculomotor nerve palsy(PSONP)caused by an aneurysm at the junction of the internal carotid-and posterior communicating arteries(IC/PC AN)in an 87-year-old, non-diabetic woman. She initially presented with diplopia 4 years previously, and was diagnosed, based on incomplete right oculomotor paresis without pupil involvement(PSONP), as external ophthalmoplegia. MR-angiography revealed a long protrusion of the IC/PC AN with posterior-inferior projection, for which she chose to receive conservative management. Thirty nine months later, she presented with another transient PSONP. CT angiography(CTA)showed that the aneurysm was enlarged in the posterior-inferior direction. Two days after this last CTA imaging, the aneurysm ruptured with upward enlargement of the bleb. Despite complete external ophthalmoplegia and ptosis, her pupil involvement was still minimal and transient. By reviewing reported cases and our own case, we found that a narrow and long aneurysm body and posterior-inferior projection are characteristic for the IC/PC AN that causes PSONP, implying a possible mechanism for PSONP by upward compression of the oculomotor nerve. Though rare in its incidence, IC/PC AN could present with PSONP prior to their rupture. Therefore, immediate imaging evaluation in patients presenting with PSONP is essential to prevent devastating rupture events.
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PMID:[Rupture of an internal carotid-posterior communicating artery aneurysm formerly presented with transient pupil-sparing oculomotor nerve palsy in an extremely elderly patient]. 2373 62

The gathering of visual information is a complex process that relies on concerted movements of the eyes, and cranial nerves II-VIII are at least partially involved in the visual system. The cranial nerves do not function in isolation, however, and there are multiple higher-order cortical centers that have input into the cranial nerves to coordinate eye movement. Among the functions of the cortical reflex pathways are (a) controlling vertical and horizontal gaze in response to vestibular input to keep the eyes focused on an object as the head moves through space, and (b) controlling rapid, coordinated eye movement to a new visual target (saccades). There are also reflex pathways connecting the cranial nerves involved in vision that produce consensual blinking of the eyes in response to corneal stimulation of one eye and consensual pupillary constriction in response to light input on one pupil. A variety of intracranial pathologic conditions, including benign and malignant neoplasms, infection, trauma, autoimmune diseases, vascular anomalies, degenerative diseases, and inherited-congenital disorders, can disrupt the cranial nerves and visual reflex pathways. This disruption can manifest in myriad ways-for example, as extraocular muscle paresis, afferent pupillary defect, oculosympathetic paresis (Horner syndrome), internuclear ophthalmoplegia, dorsal midbrain (Parinaud) syndrome, or loss of the corneal reflex. Knowledge of the function and anatomy of the cranial nerves and visual reflex pathways, coupled with selection of the proper magnetic resonance pulse sequence, will allow the radiologist to order appropriate imaging of the involved cranial nerve or visual reflex pathway based on the patient's symptoms and thereby play an essential role in establishing the diagnosis and planning appropriate therapy.
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PMID:Intracranial causes of ophthalmoplegia: the visual reflex pathways. 2402 40

We report a recent case of common adder (Vipera berus) envenoming causing paralytic signs and symptoms. A 12-year-old girl was bitten by the nominate subspecies of the common adder (V. berus berus) in eastern Hungary on May 2, 2012, 22 km away from where the first neurotoxic V. berus berus envenoming was reported in 2008. The patient developed unambiguous cranial nerve disturbances, manifested in bilateral impairment characterized by oculomotor paralysis with partial ptosis, gaze paresis, and diplopia. Drowsiness and photophobia were her additional symptoms; both occurred only during the first day of envenoming. Until now among viper envenomings in Europe, photophobia has only been documented by victims of Vipera aspis. Supportive and symptomatic treatments were administered during 3 days of hospitalization. Although case reports of V. berus berus envenomings are often published, clinical experience with neurotoxicity by this subspecies still remains rare. Population-based and geographic variation of venom composition in V. berus berus seems to include neurotoxic envenomings in certain populations. This second authenticated case provides new clinical evidence for the existence of a possible neurotoxic V. berus berus population in a restricted geographical area in eastern Hungary.
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PMID:Further clinical evidence for the existence of neurotoxicity in a population of the European adder (Vipera berus berus) in eastern Hungary: second authenticated case. 2407 91

Acute and chronic peripheral and/or central disorders of the voluntary motor system can produce profound paresis or paralysis, at times with ophthalmoplegia, while preserving consciousness and language function. Although at times appearing to be unconscious, these patients are awake and alert but unable to communicate, manipulate their environment, or participate in medical decision-making. Clinicians caring for these patients are ethically tasked with recognizing this clinical reality, enacting measures to facilitate communication, and abiding by ethical and legal principles that support autonomous patient-centered decision-making. This chapter reviews the various disorders that may cause this state while using three exemplary disorders - locked-in syndrome, caused by an anterior pontine lesion; high cervical spinal cord lesion; and amyotrophic lateral sclerosis - to discuss the management of these patients.
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PMID:Ethical issues in states of impaired communication with intact consciousness and language. 2418 81

Pituitary apoplexy is a clinical syndrome of sudden headache and visual decline associated with acute hemorrhagic or ischemic change of an intrasellar mass, and comprises only a subset of hemorrhagic pituitary lesions. The most common presenting symptoms include headache, nausea, diminished visual acuity or visual field, ophthalmoplegia/paresis, and impaired mental status. Multiple risk factors have been reported, although the majority of cases have no identifiable precipitants. MRI is the most sensitive diagnostic modality, with specific imaging findings dependent on the timing post-hemorrhage. Early clinical suspicion is imperative to allow for corticosteroid replacement and hemodynamic stabilization when indicated. Transsphenoidal surgical decompression improves outcome in a majority of cases, although conservative management may be appropriate in select scenarios.
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PMID:Pituitary apoplexy. 2506 8

A twelve-year-old African-American female presented with two week history of progressively worsening headache and fatigue, and vision difficulties for the past week. The physical examination was normal. The neurological evaluation was normal, except for cranial nerves (CN) testing, which showed bilateral restriction of adduction (CN III) and up gaze (CN IV) motions, vertical nystagmus, and left side facial paresis of central origin (CN VII). The bilateral exotropia and ophthalmoplegia are characteristics of WEBINO (Wall-Eyed Bilateral Intranuclear Ophthalmoplegia) syndrome, associated to a brain stem structural lesion. The following causes were evaluated and ruled out: tumor, infection, ischemic stroke, non-infectious inflammation. Pediatric Acquired Demyelinating Syndromes were then considered. Neuromyelitis Optica was ruled out in the absence of neuritis and normal spinal cord MRI. The differential diagnosis between Clinically Isolated Syndrome and Acute Demyelinating Encephalomyelitis, causing an isolated brain stem syndrome, is discussed.
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PMID:A 12-year-old African American girl with subacute bilateral ophthalmoplegia. 2514 58

The uncommon aggressive pituitary tumors are named carcinomas when metastases are detected, either in the central nervous system and/or systemically. Some cases are associated with hormonal overproduction, but most are diagnosed because of local symptoms. These neoplasias are generally refractory to current treatments. A 51 year-old woman presented sudden onset of headache, left arm paresis and left facial hypoesthesia. Computed tomography scan and magnetic resonance imaging revealed a pituitary tumor invading the left sphenoidal and cavernous sinuses. Laboratory data excluded hormonal hypersecretion. The patient underwent transsphenoidal surgery and histological findings showed a neoplasia with Ki-67 estimated at 75%. Medical imaging excluded both a primary occult tumor and central nervous system or systemic dissemination. Three weeks postoperatively, neurological condition worsened, with new onset of ataxia, bilateral ptosis, ophthalmoplegia and an increase in the size of the lesion, leading to surgical intervention by craniotomy, followed by only a few sessions of radiotherapy, because of severe disease progression. Patient died nearly 2 months after the initial manifestations. This case illustrates the aggressiveness of some pituitary lesions, the limited efficacy of current treatment modalities such as surgery or radiotherapy and the pitfalls of the current pituitary tumors classification. To our knowledge, this case corresponds to one of the most aggressive pituitary neoplasms reported so far, with a very high Ki-67 index (75%) and short survival (2 months). Ki-67 index could be of prognostic value in pituitary tumors. Pituitary tumors World Health Organization (WHO) classification could be revisited.
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PMID:Aggressive pituitary lesion with a remarkably high Ki-67. 2521 50

Mutations in the dynamin-2 (DNM2) gene can cause autosomal dominant or sporadic centronuclear myopathy (CNM). We aimed to analyze the clinical, pathological and genetic characteristic of patients with DNM2-related CNM in China. We studied seven patients, all of whom underwent clinical examination, muscle biopsy, electromyography, and genetic tests. DNM2 gene analysis revealed two sporadic patients harboring the p.E368K mutation, two patients from one family carrying p.R369Q, one with p.R369W, one with p.R523G and one with compound heterozygous mutations of p.R522H and p.R718Q. In DNM2-related CNM, ptosis, ophthalmoplegia/paresis, and facial weakness are the frequently observed manifestations. However, among these seven patients, only one had bilateral ptosis; one, external ophthalmoplegia and one, facial weakness. Muscle biopsy showed that the percentage of muscle fibers with centrally located nuclei ranged from 67 to 93 %, all with radial sarcoplasmic strands. To date, five different CNM-related DNM2 mutations have been observed in China. Here, a patient with compound heterozygous DNM2 mutations was reported for the first time. Facial weakness, ptosis and ophthalmoplegia did not appear to be common in Chinese patients. This study on Chinese patients broadens the spectrum of DNM2-related CNM.
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PMID:Clinical, pathological, and genetic features of dynamin-2-related centronuclear myopathy in China. 2550 59


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