Nerve paralysis

Detectable odour Conjunctivitis Olfactory nerve paralysis... 

Respiratory acidosis Autonomic nerve paralysis Urticaria... 

Delayed-action paralytic neurotoxins that block the release of acetylcholine causing a symmetric, descending flaccid paralysis of motor and autonomic nerves. Paralysis always begins with the cranial nerves. Toxins are obtained from an anaerobic bacteria (Clostridium botulinum). Toxin A is a white powder or crystalline solid that is readily soluble in water. It is stable for up to 7 days as an aqueous solution. All toxins are destroyed by heat and decompose when exposed to air for more than 12 h. 

Facial nerve paralysis - 100 mg twice daily for 14 to 21 days. 

In elapid envenomation, the patient complains of pain and numbness at the site of the bite, paralysis of muscles around the bite, lassitude, and drowsiness. These are followed by clouding of consciousness, dimness of vision, breathing difficulty, and cranial nerve paralysis with ptosis, dysarthria, dysphagia and dribbling of saliva. The patient passes into coma, respiration ceases and convulsions appear. In krait bite, symptoms occur later, and cramp-like abdominal pains are common. 

Acute poisoning is characterized by symptoms similar to those appearing in poisoning by nitrobenzene. Lazarev [16] thought nerve paralysis might occur, as well as loss of reflex and tonic spasm. Skin irritation also takes place. 

One girl in her third year, who had been immunized against tuberculosis at birth, developed an abscess of the associated lymph nodes (which were extirpated) and some weeks later developed intestinal BCG dissemination, which appeared to be cured by tuberculostatic treatment. Despite this, at the age of 22 years she developed a leftsided hemiplegia due to aneurysms and thrombosis of cerebral arteries, and 4 years later an oculomotor nerve paralysis was diagnosed. She died at 26 from recurrent intestinal BCG dissemination, which developed at the end of a pregnancy (a healthy premature child was bom). 

An 80-year-old woman had severe difficulty in swallowing and flaccid paralysis of her cervical muscles starting 4 days after the periocular injection of botulinum toxin 120 MU for blepharospasm (12). She also developed bilateral facial nerve paralysis and slurred speech and could not fully close her eyes. Barium swallow and fluoroscopy showed signs of aspiration. The serum concentration of antiacetylcholine receptor antibodies was 6.9 units (reference range 0-0.7 units). Mestinone and prednisone improved her symptoms. She had been treated with botulinum toxin on 18 occasions over the previous 13 years without any untoward effects. 

Other isolated reports of ophthalmic abnormalities refer to optic neuritis with blurring of vision, cortical blindness with fatal encephalopathy, mononeural abducent nerve paralysis, and complete but reversible bilateral oculomotor nerve paralysis (SED-13,1096) (94-97). 

Fukumoto Y, Shigemitsu T, Kajii N, Omura R, Harada T, Okita K. Abducent nerve paralysis during interferon alpha-2a therapy in a case of chronic active hepatitis C. Intern Med 1994 33(10) 637-. ... 

Bauherz G, Soeur M, Lustman F. Oculomotor nerve paralysis induced by alpha Il-interferon. Acta Neurol Belg 1990 90(2) 111-14. 

There have been several reports of isolated vincristine-induced recurrent laryngeal nerve paralysis (38,43-47). 

Tobias JD, Bozeman PM. Vincristine-induced recurrent laryngeal nerve paralysis in children. Intensive Care Med 1991 17(5) 304-5. 

Delaney P. Vincristine-induced laryngeal nerve paralysis. Nemology 1982 32(ll) 1285-8. 

Whittaker JA, Griffith IP. Recurrent laryngeal nerve paralysis in patients receiving vincristine and vinblastine. BMJ 1977 l(6071) 1251-2. 

Elapidae venom is composed of different components that vary among species. The venom of North American species contains fractions that are primarily neurotoxic. The venom results in a bulbar-type cranial nerve paralysis. In contrast to Crotalinae species, venom from North American elapids lacks most of the enzymes and spreading factors that cause local tissue destruction. Elapids from countries other than the United States can contain venom components different than that of North American coral snakes. 

Lead poisoning in horses is characterized by neurological effects. Affected horses will be either depressed or excited. Colic and diarrhea are also seen. Because of laryngeal nerve paralysis, horses poisoned by lead also present with difficult respirations and a roaring syndrome. Abortions may also occur. 

Horner s syndrome Phrenic nerve paralysis Pericardial effusion/tamponade Tracheal obstruction... 

How lead poisoning happens Lead gets into the body when materials containing lead compounds are ingested with food and drink, or when lead-containing dust in the air is inhaled or absorbed through the skin. As lead intake increases, the body s ability to get rid of it decreases. Over a period of time, the accumulation of lead in the liver, kidneys, bones, and other body tissues becomes critical. Symptoms of abdominal pains, anemia, lethargy, and nerve paralysis of hands and feet develop. 

As with middle ear adenomas, ELSTs occur over a broad age range (average = 40 years) and affect both sexes equally. Unilateral hearing loss, tinnitus, and vertigo are the usual presenting symptoms, occasionally associated with facial nerve paralysis. 

HEALTH SYMPTOMS inhalation (nausea, vomiting, diarrhea, polyneuritis, degeneration of peripheral motor nerves, paralysis of extremities). 

The thiamin (vitamin BO molecule contains a quaternary ammonium functionality and is thus badly absorbed. In healthy patients the necessary amounts of thiamin are absorbed thanks to an active transport mechanism coupled with ATP consumption. However, these mechanisms are rapidly saturable and easily inhibited, especially by chronic alcoholic consumption. As a consequence of the insufficient absorption of thiamin, alcoholism often entails Wernicke s encephalopathy (neurological disorders such as nystagmus, ocular motor nerve paralysis, memory losses, disorientation). The design of lipophilic prodrugs, able to reach the CNS by passive diffusion was then undertaken compounds like (a) and (b) result from lipophilic disulphide derivation of the open ring thiolate anion corresponding to thiamine (Fig. 33.39). 

De Silva. H. J., Sanmugianathan, P. S., and Senanayake. N. (1994). Isolated bilateral recurrent laryngeal nerve paralysis A delayed complication of organophnsphorus poisoning. Hum. Exp. Toxicxd. 13,171-173. 

Phrenic nerve paralysis causing diaphragmatic paralysis... 

II. Toxic dose. The characteristic rotten egg odor of hydrogen sulfide is detectable at concentrations as low as 0.025 ppm. The recommended workplace limit (ACGIH TLV-TWA) is 10 ppm (14 mg/m ) as an 8-hour time-weighted average, with a short-term exposure limit (STEL) of 15 ppm (21 mg/m ). The Federal OSHA permissible exposure limit (PEL) is 20 ppm as a 15-minute ceiling during an 8-hour workday. Marked respiratory tract irritation occurs with levels of 50-100 ppm. Olfactory nerve paralysis occurs with levels of 100-150 ppm. The level considered immediately dangerous to life or health (IDLH) is 100 ppm. Pulmonary edema occurs at levels of 300-500 ppm. Levels of 600-800 ppm are rapidly fatal. 

IV. Diagnosis is based on a history of exposure and rapidly progressive manifestations of airway irritation and cellular asphyxia, with sudden collapse. The victim or coworkers may describe the smell of rotten eggs, but because of olfactory nerve paralysis the absence of this smell does not rule out exposure. Silver coins in the pockets of victims have been blackened (by conversion to silver sulfide). 

Four out of 14 patients with ALL given induetion chemotherapy with weekly injections of vincristine (with prednisone, daunorubicin and asparaginase) and antifungal prophylaxis with itraconazole 400 mg daily, developed severe and early vincristine-induced neurotoxicity (paraesthe-sia and muscle weakness of the hands and feet, paralytic ileus, mild laryngeal nerve paralysis). The degree and early onset of these neurotoxic reactions were unusual, and were all reversible except for mild paraesthe-sia in one patient. The complications were more serious than in a previous... 

Cramps, Paresthesia, heaviness, and pain in the limbs, facial nerve paralysis, spasms, epilepsy, hemiplegia, migraine, neuralgia, arthritis... 

Spence LD, Adams J, Gibbons D et al (1998) Rice body formation in bicipitoradial bursitis ultrasound, CT, and MRI findings. Skeletal Radiol 2730-32 Spinner M (1968) The arcade of Frohse and its relationship to posterior interosseous nerve paralysis. J Bone Joint Surg Br 50 809-812... 

---