Levodopa is widely used, but rarely is the topic of tolerance raised. Escalating requirement and ‘on/off' fluctuations are often ascribed to disease progression, rather than admitted to be iatrogenic. The risk should be discussed before introduction, since ‘weaning off' levodopa is difficult and usually unsuccessful. Dependence onthe mood elevation and relief of anxiety might add to the difficulty. Tolerance develops rapidly, especially after infusion or oral sustained release formulation. It is, in part, pharmacokinetic, being associated with the accumulation of the long t½ metabolite, 3-O-methyldopa. Therefore, effective use of catechol-O-methyl transferase inhibition should reduce tolerance.

Injecting insulin for a suicidal purpose is uncommon. Few series had reported insulin poisoning (IP). Our study aimed to describe IP in a series of cases. Our study was retrospectively conducted over four years between 2012 and 2015. It included all patients admitted for IP in a suicidal attempt and who's presented clinical signs of hypoglycemia (sweats, neurologic and digestive signs).
Forty-three patients aged of 31± 13 years were collected. Their sex-ratio was of 0.72. Only 32% of patients were diabetics. Rapid acting insulin (RI) was found in 30%, long acting insulin (LI) in 58% and mixed intoxication in 3 cases. Route of administration was subcutaneous in all cases with a median injected dose was 120 UI [50; 302]. The median delay of signs onset was 105 minutes [15; 120] for RI and 3 hours [1; 6] for LI with a median consultation delay of 4 hours [1; 48]. Dizziness (53.5%), sweats (42%), palpitations (23%), coma (21%), paresthesia (18%), nausea (14%), seizures (11%) were the most common signs. In patients who didn't receive carbohydrates before admission, the median blood glucose level was 0.33 g/L [0.12; 0.5]. The median required dose of injected carbohydrate was 175 g [90; 200] in addition to oral intake. Outcome was favorable in 93% with hospital discharge in 24 hours [24; 72]. Outcomes were fatal in two cases and one patient remained in chronic coma because of late care. Insulin intoxication may have had good prognosis if patients received early and adequate medical care.

Rationale: There is a lack of knowledge about the therapeutic monitoring in the field of psychopharmacology in Algerian patients with depressive disorders.
Objectives: The aim of this work was to apply a therapeutic monitoring of Amitriptyline for Algerian patients with depressive disorders to follow the steady state plasma concentrations of Amitriptyline and its metabolite Nortriptyline, appreciate the influence of the association with neuroleptics and compare CYP2D6 activity among Algerian patients compared to those reported in the literature.
Materials and methods: A prospective study was conducted in 36 Amitriptyline- treated Algerian patients suffering from depressive disorders. Blood samples are collected 12 to 14 hours after taking the medication in case of a single daily dose, and 4 to 6 hours if divided dose. The determination of Amitriptyline and Nortriptyline concentrations is ensured by using the Chromsystems® chromatographic system.
Results: More than two thirds of the patients are outside of the therapeutic range. The study of the interaction of the Amitriptyline with neuroleptics shows that the latter inhibit CYP2D6 system involved in the hydroxylation of the Amitriptyline. Also, our study reveals a low activity of CYP2D6 system in Algerian patients, something to confirm with specific tests (e.g., debrisoquine test).
Conclusion: The therapeutic monitoring of Amitriptyline allows psychiatrists to optimize the dose and avoid concentration changes due to individual differences and drug interactions (case of associations to neuroleptics).

Methamphetamine administration results in various behavioral, physical, and neurological effects in both humans and animal species. The outcome and consequences of methamphetamine (METH) administration on neuronal damage depends on the dosage and duration of METH as well as additional exogenous and endogenous factors. Prolonged METH administration or high doses of METH result in long term neuronal deficits, mainly in dopamine systems. Several factors contribute to these long term effects of METH on neuronal pathways. This review covers the mechanisms involved in METH neurotoxicity, focusing on hyperthermia, oxidative stress, excitotoxicity, and emerging mechanisms. These effects are discussed in reference to dopamine and, to a lesser extent, serotonin systems chiefly in preclinical models of neurotoxicity. This review begins with a brief summary of the mechanisms of action of METH, the clinical findings in long term METH abusers, and the neuronal markers of METH toxicity. The main sections focus on factors contributing to METH induced neuronal damage including: hyperthermia, oxidative stress, excitotoxicity, and recently identified mechanisms of microglia activation, blood brain barrier dysfunction, and apoptotic pathways.