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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report the cases of two patients who had sudden unilateral alternating and regressive attacks of the cranial nerves. The first patient, a 63 year old diabetic woman, suffered regressive paralysis of the right third nerve, followed two months later by paresthesia of the same side of the face, accompanied by difficulty in swallowing and dysarthria. Six months later, she developed a right facial paralysis while pharyngeal and lingual involvement entirely disappeared. Right carotid angiography revealed stenosis of the middle meningeal artery. Nine months later she developed left-sided ophthalmoplegia followed by a homolateral facial paralysis. The second patient, a 24 year old woman, developed homolateral regressive attacks of the II, V, VII and VIIb, and VIII nerves during recovery from herpes zoster of the right geniculate ganglion. Doppler studies showed inversion of the flow in the right ophthalmic artery. The pathogenesis of these multiple paralyses of the cranial nerves is discussed, a possible cause being ischaemic attacks of the vascular territories of the cranial nerves.
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PMID:[2 cases of vascular syndrome of the cranial nerves of ischemic origin]. 266 Jun 50

66-year-old female patient presents palpebral bilateral ptosis and external ophthalmoplegia with a progressive evolution. The clinical aspects are completed with the affectation of the sensitive and motor trigemen, with the masseter atrophy and bilateral trophic keratitis. The affectation of the facial and acoustic nerves was associated with bilateral perception surditate. The hereditary transmission was dominant, with incomplete penetration. The neurogenic pathogeny was sustained on the basis of the association of neurological multilesions with III, IV, V, VI, VII, VIII nerves, with progressive extension.
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PMID:[Progressive nuclear external ophthalmoplegia]. 828 17

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

False localizing signs (FLS) and other misleading neurological signs have long been an intractable aspect of neurocritical care. Because they suggest an incorrect location or etiology of the pathological lesion, they have often led to misdiagnosis and mismanagement of the patient. Here, we reviewed the existing literature to provide an updated, comprehensive descriptive review of these difficult to diagnose signs in neurocritical care. For each sign presented, we discuss the non-false localizing presentation of symptoms, the common FLS or misleading presentation, etiology/pathogenesis of the sign, and diagnosis, as well as any other clinically relevant considerations. Within cranial neuropathies, we cover cranial nerves III, IV, V, VI, VII, VIII, as well as multiple cranial nerve involvement of IX, X, and XII. FLS ophthalmologic symptoms indicate diagnostically challenging neurological deficits, and here we discuss downbeat nystagmus, ping-pong-gaze, one-and-a-half syndrome, and wall-eyed bilateral nuclear ophthalmoplegia (WEBINO). Cranial herniation syndromes are integral to any discussion of FLS and here we cover Kernohan's notch phenomenon, pseudo-Dandy Walker malformation, and uncal herniation. FLS in the spinal cord have also been relatively well documented, but in addition to compressive lesions, we also discuss newer findings in radiculopathy and disc herniation. Finally, pulmonary syndromes may sometimes be overlooked in discussions of neurological signs but are critically important to recognize and manage in neurocritical care, and here we discuss Cheyne-Stokes respiration, cluster breathing, central neurogenic hyperventilation, ataxic breathing, Ondine's curse, and hypercapnia. Though some of these signs may be rare, the framework for diagnosing and treating them must continue to evolve with our growing understanding of their etiology and varied presentations.
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PMID:Chameleons, red herrings, and false localizing signs in neurocritical care. 3292 23