1. IN THE NAME OF GOD Seyed Alireza Haji seyed javadi MD Psychiatrist Assistant Professor and Head Department of Psychiatry school of Medicine Qazvin University of Medical Science Qazvin,Iran Email: dr_ali52@yahoo.comdr_ali52@yahoo.com Telfax: + 98 281 2555054

2. Amphetamine-Induced Mental Disorders

3. Amphetamine-Induced Psychotic Disorder and Intoxication Delirium Acute amphetamine-induced psychosis or intoxication delirium is seen after high doses of amphetamine. Acute psychosis following amphetamine ingestion is not uncommon. In a recent review of presenting symptoms of METH users in an emergency room setting, agitation and tactile hallucinations were among the most common presenting complaints, second to trauma.

4. Amphetamine-Induced Psychotic Disorder and Intoxication Delirium In addition to acute psychosis and/or delirium, some amphetamine users develop a chronic psychotic syndrome that persists for months to years. Studies in Japan suggest that individuals who experience a METH-related psychosis that resolves over time are at increased risk to re-experience psychotic symptoms if re-exposed to amphetamine or if stressed.

5. Amphetamine-Induced Mood Disorder DSM-IV-TR specifies that the onset amphetamine-induced mood disorders can occur during either phase of drug use. As might be anticipated by the pharmacological actions of amphetamines, mood symptoms during acute intoxication are generally manic or hypomanic withdrawal can be associated with a protracted anhedonic state.

6. Amphetamine-Induced Mood Disorder The mood-elevating effects of amphetamines are generally time limited, dissipating as drug is metabolized and excreted. depressive symptoms associated with amphetamine withdrawal typically resolve over weeks, they can persist for months.

7. As with all substance use it is often difficult to determine whether mood symptoms predate or are a consequence of amphetamine use

8. Amphetamine-Induced Anxiety Disorder The acute effects of amphetamines can lead to anxiety, agitation, and panic attacks, likely a result of the catecholamine-enhancing activities of these drugs. Similarly, upon drug cessation, mental discomfort and drug craving can be associated with anxiety. After high doses of amphetamine, some individuals develop time-limited stereotyped behaviors or rituals (picking at clothing, arranging and rearranging items purposelessly) that share some features with the type of compulsions seen in obsessive-compulsive disorder.

9. Amphetamine-Induced Anxiety Disorder If symptoms of an anxiety disorder persist far beyond the period of expected pharmacological action of amphetamines, the possibility that a pre-existing syndrome existed should be entertained and, if suspicions are confirmed, treated as such.

10. Amphetamine-Induced Sexual Dysfunction Amphetamines are sometimes used in a sexual context because of the general notion that they improve sexual function and enjoyment. However, chronic abuse of amphetamine can lead to diminished sexual abilities, loss of libido, and impotence

11. Amphetamine-Induced Sleep Disorder psychostimulants inhibit sleep. lead to disruptions of normal sleep–wake cycles After drug cessation, particularly after continued, heavy use, amphetamine users develop hypersomnolence that can persist for weeks (i.e., “crashes”).

12. Amphetamine-Induced Sleep Disorder Because amphetamines have the potential to damage brain monoaminergic neurons, which are known to play an important role in sleep modulation (“Amphetamine- Induced Neurotoxicity”), abuse of amphetamine-type stimulants may lead to protracted negative effects on sleep.

13. Amphetamine-Related Disorder Not Otherwise Specified neuropsychiatric disorder that does not fall into one of the previously discussed categories It is increasingly clear that chronic METH abusers develop impairments in neurocognitive function.

14. Amphetamine-Related Disorder Not Otherwise Specified In particular, METH users demonstrate cognitive deficits that persist with enduring abstinence in tasks of  verbal memory  perceptual sleep  information processing  executive function

15. Acute Amphetamine Toxicity cardiovascular and central nervous system At high doses, or in vulnerable individuals, amphetamines can lead to prominent and serious toxic cardiovascular and central nervous system (CNS) effects.

16. Acute Amphetamine Toxicity cardiovascular Common cardiovascular symptoms seen in amphetamine toxicity include chest pain, palpitations, and dyspnea. Less common are amphetamine-induced arrhythmias and myocardial infarction. Significant hypotension with bradycardia and metabolic acidosis has been reported after overdoses of amphetamine. Amphetamines can also lead to acute and chronic cardiomyopathy. The cardiomyopathic effects of amphetamines may be multifactorial, resulting from direct toxic effects of amphetamine and indirect effects of amphetamine-induced hypertension and ischemia. Necrotizing angiitis involving multiple organ systems and CNS vasculature have been reported in amphetamine users.

17. Acute Amphetamine Toxicity central nervous system Symptoms of CNS toxicity seen following amphetamine include agitation, anxiety, hallucinations, delirium, psychosis, seizures, hyperthermia, and death. Amphetamines can lead to cerebrovascular accidents due to hemorrhage, vasospasm, or cerebral vasculitis.

18. Acute Amphetamine Toxicity psychiatric symptoms A wide variety of psychiatric symptoms can be seen following amphetamine use, including : anxiety, panic, agitation, confusion, delusions, paranoia, or frank psychosis. high-risk behaviors associated with METH use experienced a violent mechanism of injury were more likely to have attempted suicide.

19. Taken together the physiologic and psychoactive effects of acute METH intoxication have potential to be an extremely dangerous combination

20. Amphetamine-Induced Neurotoxicity The first indication that amphetamine and its analogs have the potential to damage brain monoaminergic neurons was reported in 1963, when it was noted that p-chloroamphetamine (PCA) led to protracted deficits in brain serotonin neuronal markers. damage brain serotonin neurons, brain dopamine neurons, or both. In the case of METH, more than 25 years ago, deficits in axonal markers of DA and/or serotonin.

21. Neurochemical and morphological studies indicate that the reductions in presynaptic DA and serotonin axonal markers are related to destruction of DA and serotonin axons and axon terminals typically with sparing of nerve cell bodies.

22. Amphetamine-Induced Neurotoxicity It is not clear whether the neurotoxic effects of METH cause functional consequences & neuropsychiatric problems that have been described in METH users (psychosis, mood disorders, cognitive deficits) are related to DA or serotonin neurotoxicity.

23. If it is determined that the neurotoxic effects of amphetamines lead to psychiatric problems, future editions of the DSM-IV-TR may need to accommodate additional amphetamine-related diagnoses.

24. ALIREZA HAJ SEYED JAVADI MD. PSYCHIATRIST