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Cranial palsy

Pcom aneurysms are associated with third nerve cranial palsy with or without subarachnoid hemorrhage (Birchall et al. 1999 Perneczky and Czech 1984). From a surgical point of view the approach to these aneurysms is not too difficult. However, many of them have a small neck and are good candidates for endovascular therapy. In case of aneurysms smaller than 4mm we always use a microballoon in order to be prepared for eventual rupture occurring more often in this location than somewhere else (our experience We don t have any scientific data about... [Pg.230]

The recent case of a parturient who developed a massive spinal block with hemi-cranial palsy after a test dose of 2.5 ml of 2% chloroprocaine, administered with the patient in the sitting position, demonstrates the dangers of giving a test dose of a hypo-baric solution with the patient in this position (21 ). One always has to bear in mind the possibility of infection after epidural and spinal anaesthesia. The recommendation has been made to place a bacterial filter between the syringe and the catheter. Five out of 101 syringes were contaminated by skin commensals, but all the catheter tips remained sterile when a bacterial filter was used. [Pg.110]

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]

Peripheral neuropathy primary dose-limiting toxicity motor sensory, autonomic, and cranial nerves may all be affected (paresthesias, ileus, urinary retention, facial palsies) may be irreversible mild emetogen SIADH vesicant extravasation injury... [Pg.1409]

Diabetes mellitus is the most common cause of peripheral neuropathy in the United States. Approximately half of all diabetics demonstrate evidences of neuropathy. The usual clinical pattern is that of a slowly progressive, mixed sensorimotor and autonomic polyneuropathy. More acute, asymmetrical motor neuropathies are also seen, usually affecting the lumbosacral plexus, particularly in older persons with type 2 (non-insulin-dependent) diabetes mellitus. Patients with diabetes mellitus are also prone to develop isolated palsies of cranial nerve III or VII, and there is a high incidence of asymptomatic focal demyelin-ation in the distal median nerve. [Pg.624]

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]

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]

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]

Botulism-like Acute paralytic conditions consistent with botulism such as cranial nerve palsy, ptosis, decreased gag reflex Acute descending motor paralysis Acute symptoms consistent with botulism such as diplopia, dysphagia Botulism... [Pg.427]

A review of certain chemicals is essential. Ethylene glycol is an antifreeze used for gasoline engines and may produce somnolence, imreactive pupils, disc swelling, and kidney failure. Systemic lead poisoning produces headaches, coma, cranial nerve palsies, and papilledema. Wood alcohol, or methanol, may produce severe toxic neuropathy and disc edema. Drugs known to produce toxic optic neuropathy include amiodarone (an antiar-rhythmic), quinine, aminoquinolines, ibuprofen, ethambutol, isoniazid, and chloramphenicol. [Pg.371]

Evaporative loss can also occnr from abnormal ocular surfece exposure, due to incomplete blink, nocturnal lagophthalmos, exophthalmos, proptosis, cranial nerve VII palsy, lid retraction, or other eyelid position and apposition disorders. Contact lenses may also contribute to an increased tear evaporation rate. [Pg.425]


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See also in sourсe #XX -- [ Pg.216 , Pg.217 , Pg.218 ]




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