Neuritis

Toxicology. The acute oral and dermal toxicity of naphthalene is low with LD q values for rats from 1780—2500 mg/kg orally (41) and greater than 2000 mg/kg dermally. The inhalation of naphthalene vapors may cause headache, nausea, confusion, and profuse perspiration, and if exposure is severe, vomiting, optic neuritis, and hematuria may occur (28). Chronic exposure studies conducted by the NTP ia mice for two years showed that naphthalene caused irritation to the nasal passages, but no other overt toxicity was noted. Rabbits that received 1—2 g/d of naphthalene either orally or hypodermically developed changes ia the lens of the eye after a few days, foUowed by definite opacity of the lens after several days (41). Rare cases of such corneal epithelium damage ia humans have been reported (28). Naphthalene can be irritating to the skin, and hypersensitivity does occur. 

Uses. Aspirin has analgesic, antiinflammatory, and antipyretic activity. It is used for the reHef of less severe types of pain, such as headache, neuritis, acute and chronic rheumatoid arthritis, and toothache. Aspirin can be purchased in a variety of OTC and prescription dosage forms made and formulated by many companies. Tablets, ie, buffered, plain, or enteric-coated, are the most familiar in the United States, but other forms such as powder and effervescent formulations are of considerable importance in other parts of the world. 

A deficiency of niacin also affects the nervous system. Numbness is initially observed and later, paralysis, particularly in the extremities is common. Severe cases are characteri2ed by tremor and a spastic or ataxic gait and are frequentiy associated with peripheral neuritis. Left untreated, severe thought disorders can ensue (1). 

Optic neuritis (a decrease in visual acuity and changes in color perception), which appears to be related to the dose given and die duration of treatment, has occurred in some patients receiving ethambutol. Usually, tiiis adverse reaction disappears when the drug is discontinued. Other adverse reactions are dermatitis, pruritus, anaphylactoid reactions (unusual or exaggerated allergic reactions), joint pain, anorexia, nausea, and vomiting. 

The nurse instructs patients to report any symptoms of infection such as an elevated temperature (even a slight elevation), sore throat, difficulty breathing, weakness, or lethargy. The patient must be aware of possible signs of pancreatitis (nausea, vomiting, abdominal pain, jaundice [yellow discoloration of the skin or eyes]) and peripheral neuritis (tingling, burning, numbness, or pain in the hands or feet). Any indication of pancreatitis or peripheral neuritis must be reported at once. 

Severe acute and chronic allergic and inflammatory processes, keratitis, allergic corneal marginal ulcers, herpes zoster of the eye, iritis, iridocyclitis, chorioretinitis, diffuse posterior uveitis, optic neuritis, sympathetic ophthalmia, anterior segment inflammation... 

Cbnvulsions, steroid-induced catatonia, increased intracranial pressure with papilledema (usually after treatment is discontinued), vertigo, headache, neuritis or paresthesia, steroid psychosis, insomnia... 

Disulfiram produces a variety of adverse effects, which commonly include drowsiness, lethargy, and fatigue (Chick 1999). Other more serious adverse effects, such as optic neuritis, peripheral neuropathy, and hepatotoxicity, are rare. Psychiatric effects of disulfiram are also uncommon. They probably occur only at higher dosages of the drug and may result from the inhibition by disulfiram of a variety of enzymes in addition to ALDH. Included among the enzymes inhibited by disulfiram is dopamine P-hydroxylase, inhibition of which increases dopamine levels, which in turn can exacerbate psychotic symptoms in patients with schizophrenia and occasionally may result in psychotic or depressive symptoms in patients without schizophrenia. 

The water-soluble vitamins comprise the B complex and vitamin C and function as enzyme cofactors. Fofic acid acts as a carrier of one-carbon units. Deficiency of a single vitamin of the B complex is rare, since poor diets are most often associated with multiple deficiency states. Nevertheless, specific syndromes are characteristic of deficiencies of individual vitamins, eg, beriberi (thiamin) cheilosis, glossitis, seborrhea (riboflavin) pellagra (niacin) peripheral neuritis (pyridoxine) megaloblastic anemia, methyhnalonic aciduria, and pernicious anemia (vitamin Bjj) and megaloblastic anemia (folic acid). Vitamin C deficiency leads to scurvy. 

Thiamin deficiency can result in three distinct syndromes a chronic peripheral neuritis, beriberi, which may or may not be associated with heart ilure and edema acute pernicious (fulminating) beriberi (shoshin beriberi), in which heart failure and metabolic abnormalities predominate, without peripheral neuritis and Wernicke s encephalopathy with KorsakofPs psychosis, which is associated especially with alcohol and dmg abuse. The central role of thiamin diphosphate in... 

Brodt HR, Kamps BS et al (1997) Changing incidence of AlDS-defining iUnesses in the era of antiretroviral combination therapy. AIDS 11(14) 1731-1738 Calabrese LH, Proffitt MR et al (1987) Acute infection with the human immunodeficiency virus (HIV) associated with acute brachial neuritis and exanthematous rash. Ann Intern Med 107(6) 849-851... 

In diphtheria, the organism C. diphtheriae eonfmes itself to epithelial surfaces of the nose and throat and produces a powerfiil toxin which affects the elongation factor involved in protein biosynthesis. The heart and peripheral nerves are particularly affected resulhng in myocarditis (inflammation of the myocardium) and neuritis (inflammation of a nerve). Little damage is produeed at the infective site. 

Guy, J., Ellis, E., Hope, G. and Rao, N.A. (1989b). Antioxidant enzymes reduce loss of blood-brain barrier integrity m experimental optic neuritis. Arch. Ophthalmol. 107, 1359-1363. 

Neuritic or senile plaques are extracellular protein deposits of fibrils and amorphous aggregates of P-amyloid protein.11 This formed protein is central to the pathogenesis of AD. The P-amyloid protein is present in a non-toxic, soluble form in human brains. In AD, conformational changes occur that render it insoluble and cause it to deposit into amorphous diffuse plaques associated with dystrophic neuritis.14 Over time, these deposits become compacted into plaques and the P-amyloid protein becomes fibrillar and neurotoxic. Inflammation occurs secondary to clusters of astrocytes and microglia surrounding these plaques. 

Biologic response modifiers (BRMs) are indicated in patients who have failed an adequate trial of DMARD therapy.1 BRMs may be added to DMARD monotherapy (i.e., methotrexate) or replace ineffective DMARD therapy.22 The decision to select a particular agent generally is based on the prescriber s comfort level with monitoring the safety and efficacy of the medications, the frequency and route of administration, the patient s comfort level or manual dexterity to self-administer subcutaneous injections, the cost, and the availability of insurance coverage.23 In general, BRMs should be avoided in patients with serious infections, demyelinating disorders (e.g., multiple sclerosis or optic neuritis) or heart failure.21... 

Diphtheria, tetanus, acellular pertussis Dtap 0.5 mL Intramuscular Systemic neurologic reaction from previous vaccine Brachial neuritis Cried for 3 hours non-stop after previous dose Temperature greater than 40.5°C (105°F)... 

Optic neuritis Usually monocular central visual acuity loss and ocular/periorbital pain caused by demyelination of the optic nerve. 

Chronic Bronchitis Chronic Gastritis Gastroenteritis Chronic Hepatitis Neuritis, Neuralgia Sciatica... 

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