Neurological adverse reactions

Other rare neurological adverse reactions include development of autonomic... 

The adverse effects iaclude digestive disturbances, neurological symptoms, and manifestations of allergic responses. As many as half of the patients taking it are iacapacitated by some of these adverse reactions for several hours. Whether these symptoms are caused by hypersensitivity to the dmg, the parasite, or by a manifestation of the disease is not known. Overall, effects are dose-related and transient. 

Immediately report the occurrence of the following adverse reactions severe vomiting, dehydration, changes in neurologic functioning, or yellowing of the skin or eyes. 

Ora/-Adverse reactions requiring discontinuation include Pulmonary infiltrates or fibrosis paroxysmal ventricular tachycardia CHF elevation of liver enzymes visual disturbances solar dermatitis blue discoloration of skin hyperthyroidism hypothyroidism. Adverse reactions occurring in at least 3% of patients include CFIF Gl complaints (nausea, vomiting, constipation, anorexia) dermatologic reactions (photosensitivity, solar dermatitis) neurologic problems (malaise, fatigue, tremor/abnormal involuntary movements, lack of coordination, abnormal gait/ataxia, dizziness, paresthesias) abnormal liver function tests. 

Adverse reactions occurring in at least 3% of patients include the following abdominal pain, diarrhea, dizziness, headache, insomnia, jaundice/scleral icterus, myalgia, nausea, peripheral neurologic symptoms, rash, vomiting. 

Neurologic symptoms Motor weakness has been reported rarely. Most of these cases occurred in the setting of lactic acidosis. The evolution of motor weakness may mimic the clinical presentation of Guillain-Barre syndrome (including respiratory failure). Symptoms may continue or worsen following discontinuation of therapy. Stavudine therapy has been associated with peripheral neuropathy, which can be severe and is dose-related. Peripheral neuropathy has occurred more frequently in patients with advanced HIV disease, a history of neuropathy, or concurrent neurotoxic drug therapy, including didanosine (see Adverse Reactions). 

Adverse reactions include nausea, vomiting, fatigue, diarrhoea and abdominal pain, rashes including photosensitivity, urticaria, pruritus, increase in blood urea and creatinine, reversible rise in bilirubin and liverrelated enzymes. Neurological adverse effects are headache, dizziness, confusional state, hallucinations, sorrmolence and convulsions. 

Solanine hydrochloride has been used as a commercial pesticide. It has sedative and anticonvulsant properties, and has sometimes been used for the treatment of asthma, as well as for cough and common cold. However, gastrointestinal and neurological disorders result from solanine poisoning. Symptoms include nausea, diarrhoea, vomiting, stomach cramps, burning of the throat, headaches and dizziness. Other adverse reactions, in more severe cases, include hallucinations, loss of sensation, paralysis, fever, jaundice, dilated pupils and hypothermia. Solanine overdose can be fatal. 

Weber, R.W. 2008b. Neurological reactions to foods and foods additives. In Food Allergy. Adverse Reactions to Foods and Food Additives, 4th ed., D.D. Metcalfe, H.A. Sampson, and R.A. Simon, Eds., pp. 531-542. Blackwell Publishing, Malden, MA/Oxford, U.K. 

This chapter will describe some of the most common, reversible, drug-induced neurological reactions acute dystonia acute akathisia parkinsonism and a broad, ill-defined category called dysphoria. All of them tend to begin early in treatment but can start later on as well. Chapters 4 and 5 will review the sometimes delayed and often persistent adverse reactions, including irreversible forms of akathisia and dystonia. 

Swartz and Jones (1994) reviewed the literature and presented three cases concerning severe and often persistent adverse reactions to the abrupt withdrawal of lithium in patients suffering from elevated serum levels during routine treatment. One of the patients became severely demented. In their review of 50 cases obtained from the Lithium Information Center of the University of Wisconsin, they found that many patients became demented or otherwise deteriorated severely when abruptly withdrawn from lithium. Patients subjected to kidney dialysis for lithium toxicity often deteriorated mentally with a rapid drop in lithium levels. Neurologic sequelae persisted in 30% of the 50 patients. The authors found substantial neurotoxic risks in rapidly withdrawing patients from high lithium levels. 

If rapid withdrawal from high lithium levels can produce mania and disable neurologic reactions, then it is probable that rapid withdrawal from lower levels may produce more subtle adverse reactions. 

Isoniazid can cause neuropsychiatric syndromes, including euphoria, transient impairment of memory, separation of ideas and reality, loss of self-control, psychoses (421), and obsessive-compulsive neurosis (422). Isoniazid should be used with caution in patients with pre-existing psychoses, as it can cause relapse of paranoid schizophrenia (423). Patients on chronic dialysis appear to be vulnerable to neurological adverse drug reactions, because of abnormal metabolism of uremic toxins. It is therefore recommended that a... 

It has long been known that intramuscular procaine penicillin can cause some peculiar psychological adverse reactions, and that other penicillin derivatives, such as amoxicillin, can cause psychiatric reactions, such as hallucinations (SEDA-21, 259). In a report from the Netherlands, neuropsychiatric symptoms occurred in six patients who received cefepime for febrile neutropenia (33). The patients, two men and four women, aged 32-75 years, received 6 g/day (n = 5) or 3 g/day (n = 1). The symptoms started 1-5 days after the first dose and varied from nightmares, anxiety, agitation, and visual and auditory hallucinations to coma and seizures. After withdrawal of cefepime, they recovered within 1-5 days. The causality between their neuropsychiatric symptoms and cefepime was considered as probable (WHO criteria) because of the temporal relation, lack of other causal neurological explanations, and positive rechaUenge in five patients. 

In France, dapsone is available in combination with ferrous oxalate as Disulone (Aventis), and in 1983-98, 249 adverse reactions were reported to French pharma-covigilance centers, mainly blood dyscrasias (often neutropenia and agranulocytosis, rarely hemolysis and anemia) (11). Five patients died three of them had septicemia secondary to agranulocytosis. There were 29 cases of dapsone syndrome, 39 skin reactions, 27 cases of hver damage, and 27 cases of neurological and psychiatric adverse effects. Patients taking dapsone need to be under close medical supervision for early recognition of adverse reactions. 

Supposed neurological adverse effects of diphtheria immunization have been reported, but a causal connection was unclear (11). Of five cases of neurological complications after diphtheria or diphtheria-tetanus immunizations two were classified as vaccine-induced pohomyehtis the other three could be traced back to a hjrperergic reaction to diphtheria toxoids in the cerebral vessels (12). 

By 1988 it was possible to summarize the adverse effects reported after the distribution of over 1.8 million doses of plasma-derived hepatitis B vaccine (Table 1) (2). From 1982 onwards, the Centers for Disease Control, the Food and Drug Administration, and the manufacturers, Merck Sharp Dohme, had supported a special surveillance system to monitor spontaneous reports of reactions to plasma-derived hepatitis vaccine. During the first 3 years, about 850 000 persons were immunized. In all, 41 reports were received for one of the following neurological adverse events convulsion (n = 5), Bell s palsy (n — 10), Guillain-Barre syndrome (n = 9), lumbar radiculopathy (n — 5), brachial plexus neuropathy (n = 3), optic neuritis (n — 5), and transverse myelitis (n = 4). Half of these events occurred after the first vaccine dose. However, no conclusive causal association could be made between any neurological adverse event and the vaccine (3). 

Postmarketing surveillance data of adverse events after Japanese encephalitis immunization in Japan and the USA have been compared (7). The rates of total reported adverse events were 2.8 per 100 000 doses in Japan and 15.0 per 100 000 doses in the USA. In Japan, 17 neurological disorders were reported from April 1996 to October 1998 (0.2 per 100 000 doses), whereas in the USA there were no serious neurological adverse events temporally associated with Japanese encephalitis vaccine from January 1993 to June 1999. Rates for systemic hypersensitivity reactions were 0.8 and 6.3 per 100 000 doses in Japan and the USA respectively. 

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