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Nerve palsy

DIES-associated neuropathy has a variety of chnical presentations, including painful symmetric or asymmetric sensorimotor neuropathy, distal sensory neuropathy, mononeuritis multiplex, and demyelinating polyneuropathy (Gherardi et al. 1998). Cranial neuropathy without evidence of a more generahzed neuropathy may occur, typically as a facial nerve palsy in association with parotidomegaly (Itescu et al. 1990 Brew 2003). The neuropathy develops subacutely over days to weeks. In some cases, muscle weakness may be a result of an inflammatory myositis (Kazi et al. 1996). [Pg.61]

Humphrey JH, McClelland M. 1944. Cranial-nerve palsies with herpes following general anaesthesia. Br MedJ 1 315-318. [Pg.271]

Cameron C, Lodes MW and Gershan WM. 2007. Facial nerve palsy associated with serum vitamin A level in an infant with cystic fibrosis. J Cyst Fibros 6 241-243. [Pg.212]

For persistent VI nerve palsy of 1 month or longer duration 1.25 to 2.5 units in the medial rectus muscle. [Pg.1341]

Paresthesias, weakness and paralysis of lower extremity, hypotension, high or total spinal block, urinary retention or incontinence, fecal incontinence, headache, back pain, septic meningitis, meningismus, arachnoiditis, shivering cranial nerve palsies due to traction on nerves from loss of CSF, and loss of perineal sensation and sexual function Rare... [Pg.1193]

The main dose-limiting toxicity is neurotoxicity, usually expressed as a peripheral sensory neuropathy, although autonomic nervous system dysfunction with orthostatic hypotension, urinary retention, paralytic ileus, or constipation, cranial nerve palsies, ataxia, seizures, and coma have been observed. While myelosuppression occurs, it is generally milder and much less significant than with vinblastine. The other potential adverse effect that can develop is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). [Pg.1177]

Biochemical changes such as increased aminolaevulinate excretion and inhibition of amino-laevulinate dehydrase may be detected in urine and blood, respectively, at blood lead levels of 0.4 to 0.6 mg mL-1. Anemia is a late feature, however. Neurotoxicity may be detectable at blood lead levels of 0.8 to 1.0 mg mL-1. At blood lead levels greater than 1.2 mg mL-1, encephalopathy occurs. Peripheral nerve palsies are rare, and the foot and wrist drop, which were once characteristic of occupational lead poisoning, only occur after excessive exposure and are now rarely seen. Similarly, seizures and impaired consciousness may result from involvement of the CNS. Bone changes are usually seen in children and are detected as bands at the growing ends of the bones and a change in bone shape. [Pg.392]

Postlumbar puncture syndrome with abducent nerve palsy followed the use of intrathecal prednisolone for the treatment of low back pain and sciatica (451). [Pg.50]

Volpin G, Said R, Simri W, Grimberg B, Daniel M. [Nerve palsies in a soldier with penetrating injuries following prolonged use of limb tourniquets]. Harefuah 1999 136 352-5, 419. [Pg.177]

Paralytic strabismus (III, IV, VI nerve palsy, internuclear opthalmoplegia, skew deviation)... [Pg.215]

Hemifacial spasm/postfacial nerve palsy synkinesis... [Pg.215]

Amphotericin B has been used intrathecally in patients with coccidioidal or cryptococcal meningitis. The side effects associated with this route of administration are headache, paraesthesia, nerve palsy, and visual impairment. To treat coccidioidal arthritis, amphotericin B may be injected intraarticularly (Figure 45.2). [Pg.438]

Mokri B, Silbert PL, Schievink WI et al (1996) Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery. Neurology 46 356-359 Molina CA, Montaner J, Abilleira S et al (2001) Timing of Spontaneous Recanalization and Risk of Hemorrhagic Transformation in Acute Cardioembolic Stroke. Stroke 32 1079-1084 Molina CA, Alvarez-Sabin J, Montaner J et al (2002) Thrombolysis-related hemorrhagic infarction a marker of early reperfusion, reduced infarct size, and improved outcome in patients with proximal middle cerebral artery occlusion. Stroke 33 1551-1556... [Pg.16]

Three cases of radial nerve palsy were reported in demented elderly patients confined to wheelchairs who were treated with haloperidol. The combination of extrapyra-midal and sedative adverse effects, added to wheelchair confinement, may have resulted in pressure on the upper arm with subsequent neuropathy (18). [Pg.296]

Sloane PD, McLeod MM. Radial nerve palsy in nursing home patients association with immobility and haloperidol. J Am Geriatr Soc 1987 35(5) 465-6. [Pg.299]

An unusual case of bilateral sixth nerve palsy associated with ecstasy has been reported (48). [Pg.594]

A 17-year-old man developed horizontal diplopia in all directions of gaze while using ecstasy tablets every 5-7 days for 2 months. A diagnosis of bilateral sixth nerve palsy was confirmed. Ocular motility returned to... [Pg.594]

Schroeder B, Brieden S. Bilateral sixth nerve palsy associated with MDMA ( ecstasy ) abuse. Am J Ophthalmol 2000 129(3) 408-9. [Pg.612]

The presence of cranial neuropathy may result in a misdiagnosis of brainstem stroke. Cranial nerve palsies may result from local pressure from the false internal carotid artery lumen, thromboembolism or hemodynamic compromise to the blood supply of the nerve. Cranial nerve III receives its blood supply from the ophthalmic artery, branches of the internal carotid or the posterior cerebral artery and, consequently, may rarely become ischemic after carotid dissection. [Pg.67]


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