Neurological patients effects

A. Ethambutol is associated with retrobulbar neuritis, resulting in loss of central vision and impaired red-green discrimination. Ethionamide (B) is an analogue of isonicotinic acid and is associated with GI intolerance and peripheral neuropathy, but not the optic neuritis or color vision discrimination problems. Aminosalicylic acid (C) can cause GI irritation and bleeding problems, so caution is required in peptic ulcer patients. It has no neurological side effects. Rifampin (D) is associated with red-orange discoloration of saliva, tears, and urine but not the color vision problems. Isoniazid (E) is associated with peripheral neuritis in chronic alcoholics and malnourished individuals and requires pyridoxine supplements. It is not associated with optic neuritis. 

The most common side-effects in patients receiving mexilitine are gastrointestinal complaints, especially nausea (Jarvis and Coukell, 1998). Neurological side-effects such as tremor, headache, dizziness, and sleep disorders are rare. Although serious cardiac arrhythmias were not reported in neuropathic pain patients, transient tachicardia and palpitations occurred. 

Adult tapeworm infections in humans are usually treated with praziquantel (Table 12.4), but with adult Taenia solium there may be neurological side effects if patients are also infected with cysts, so niclosamide, that has no effect on the cysts, is the preferred treatment (Garcia et a/., 2003). 

Adverse effects can result from increased plasma concentrations of haloperidol during itraconazole treatment. This has been observed in 13 schizophrenic patients treated with haloperidol 12 or 24 mg/day who took itraconazole 200 mg/day for 7 days (51). Plasma concentrations of haloperidol were significantly increased and neurological adverse effects were more common. Itraconazole is a potent inhibitor of CYP3A4. 

In a 6-week open study of risperidone (mean dosage 4.7 mg/day) in combination with mood-stabilizing treatments (usually lithium, carbamazepine, or valproate) for the treatment of schizoaffective disorder in 102 patients, 95 of whom completed the trial, at week 4 most patients had improved symptom severity and 9.3% were completely symptom-free (35). There were no statistically significant differences between baseline and week 4 in the severity of extrapyramidal symptoms, as measured by the UKU Side-Effect Rating Scale subscale for neurological adverse effects other adverse effects included depressive symptoms (n = 13), exacerbation of mania ( n = 5), drowsiness (n = 3), and impotence (n = 2). 

Meibach RC, Mazurek MF, Rosebush P. Neurologic side effects in neuroleptic-naive patients treated with haloperidol or risperidone. Neurology 2000 55(7) 1069. 

This case shows that, regardless of the formulation of amphotericin, severe neurological adverse effects can occur, in particular in patients who receive large dosages of amphotericin after cranial irradiation. A clinical syndrome of akinetic mutism, incontinence, and parkinsonism has been described in patients who received large doses of amphotericin deoxycholate in association with central nervous system irradiation or infection (67). 

Neurological adverse effects of ciclosporin have been reported in up to 39% of all transplant patients. Most are mild. The most frequent is a fine tremor, the mechanism of which is not known. From many case reports or studies in transplant patients, the pattern of ciclosporin neurotoxicity ranges from common and mild to moderate symptoms, such as headaches, tremors, paresthesia, restlessness, mood changes, sleep disturbances, confusion, agitation, and visual hallucinations, to rare but severe or hfe-threatening disorders, including acute psychotic episodes, cerebellar disorders, cortical blindness (permanent in one report), spasticity or paralysis of the limbs, catatonia, speech disorders or mutism, chorea, seizures, leukoencephalopathy, and coma (SED-13,1124) (SEDA-16, 516) (SEDA-17, 520) (SEDA-20, 343) (SEDA-21, 383) (17-19). 

Neurological adverse effects are more likely to occur in elderly patients with impaired hepatic or renal function. 

Oxamniquine can cause neurological adverse effects (3). At high doses, somnolence was reported in 25% of cases. Somnolence is reportedly more common if the drug is given just before a meal. In a comparison of oxamniquine with praziquantel, there were adverse effects in 45% of patients treated with oxamniquine and 71% of patients given praziquantel somnolence occurred less often (11% of cases) with praziquantel (SEDA-12, 709) (4). 

Patients receiving cranial irradiation and patients with malignant gliomas may be at particular risk of severe skin reactions to phenytoin (SEDA-18, 68) (SEDA-20, 58). Neurological adverse effects can be enhanced in patients with a recent history of severe traumatic brain injury. 

In a randomized study in 390 patients suramin has been given in a fixed low dose (3.192 g/m ), intermediate dose (5.320 g/m ), or high dose (7.661 g/m ) to determine whether its efficacy and toxicity in the treatment of patients with hormone-refractory prostate cancer is dose-dependent (8). There was no clear dose-response relation for survival or progression-free survival, but toxicity increased especially with the higher dose. There were neurological adverse effects in 40% of the patients and cardiac adverse effects in 15%. This raises questions about the usefulness of suramin, particularly in high doses, in advanced prostate cancer. However, in another... 

The milder axonal polyneuropathy is the most common neurological adverse effect of suramin and causes distal paresthesia, reduced pain and vibration sensation in the feet, weak toe extensors, and absent ankle jerks this neuropathy is largely reversible. Milder neuropathies occurred in 50-70% of patients with plasma concentrations below 300 pg/ml, and severe motor neuropathy was rare in this category of patients. 

When neurological symptoms occur in patients taking tacrolimus they are very similar to those seen in patients taking ciclosporin, with more frequent insomnia, tremor, and headaches, but a similar rate of severe neurological adverse effects, such as acute psychosis, peripheral neuropathy, seizures, encephalopathy, coma, and paralysis. Persistent speech disorders (dysarthria, apraxia, expressive aphasia, akinetic mutism), and visual blurring can also occur (SEDA-21, 391) (SEDA-22, 420) (24). 

Reports of neurological adverse effects after tetanus immunization have appeared (8). The most common reported complication is a polyneuropathy. In the majority of cases the onset occurred within 14 days of the last injection, and ranged in severity from a single nerve palsy to profound sensorimotor involvement of the nervous system, including cord and cortex. Recovery was usually complete (eight of 10 patients with onset at less than 14 days after injection) but three patients with onset at more than 14 days from injection had only partial recovery. 

Among the adverse effects of topiramate are reduced appetite and weight loss, and this has been put to use in the treatment of binge eating in an open study in 13 patients (6). Nine patients had a moderate or better response, two had moderate or marked responses that subsequently diminished, and two had a mild response or none. Neurological adverse effects were the most common. Three patients discontinued topiramate because of adverse effects, and two resumed at a later date without significant recurrence. 

The most important risk factors for acyclovir nephrotoxicity are intravascular volume contraction, preexisting kidney desease, and the use of a high-dose, rapid bolus intravenous infusion [7] Nephrotoxicity with oral acyclovir has been reported only rarely [23] The main non-renal toxicities of acyclovir are gastrointestinal and neurologic side effects, which primarily occur in patients on high-dose intravenous acyclovir. As acyclovir is primarily cleared by the kidney, lower intravenous doses and even oral administration can lead to neurotoxicity in patients with decreased kidney function from either CKD or AKI [15,17, 24, 25]. 

Acetazol- amide 125 mg t.i.d. 500 mg t.i.d. 90% 100% 50% Avoid May potentiate acidosis ineffective as diuretic in ESRD may cause neurologic side effects in dialysis patients No data No data Avoid... 

Patients developed grade 2 1 neurological toxic effect... 

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