Cocaine (from French: cocaïne, from Spanish: coca, ultimately from Quechua: kúka)[14] is a central nervous system (CNS) stimulant. As an extract it is mainly used recreationally and often illegally for its euphoric effects, but it is Schedule II in the U.S. and recognized for its medical value. It is primarily obtained from the leaves of two Coca species native to South America: Erythroxylum coca and E. novogranatense.[15][16] These medicinal herbs naturally contain cocaine and have a history of use among indigenous American peoples. After extraction from the plant, and further processing into cocaine hydrochloride (powdered cocaine), the drug is administered by being either snorted, applied topically to the mouth, or dissolved and injected into a vein. It can also then be turned into free base form (crack cocaine), in which it can be heated until sublimated and then the vapours can be inhaled.[12] Cocaine stimulates the reward pathway in the brain.[16] Mental effects may include an intense feeling of happiness, sexual arousal, loss of contact with reality, or agitation.[12] Physical effects may include a fast heart rate, sweating, and dilated pupils.[12] High doses can result in high blood pressure or high body temperature.[17] Effects begin within seconds to minutes of use and last between five and ninety minutes.[12] As cocaine also has numbing and blood vessel constriction properties, it is occasionally used during surgery on the throat or inside of the nose to control pain, bleeding, and vocal cord spasm.[18]
3d create visual components crack cocaine
Cocaine is a central nervous system stimulant.[43] Its effects can last from 15 minutes to an hour. The duration of cocaine's effects depends on the amount taken and the route of administration.[44] Cocaine can be in the form of fine white powder, bitter to the taste. Crack cocaine is a smokeable form of cocaine made into small "rocks" by processing cocaine with sodium bicarbonate (baking soda) and water.[12][45] Crack cocaine is referred to as "crack" because of the crackling sounds it makes when heated.[12]
Acute exposure to cocaine has many effects on humans, including euphoria, increases in heart rate and blood pressure, and increases in cortisol secretion from the adrenal gland.[65] In humans with acute exposure followed by continuous exposure to cocaine at a constant blood concentration, the acute tolerance to the chronotropic cardiac effects of cocaine begins after about 10 minutes, while acute tolerance to the euphoric effects of cocaine begins after about one hour.[27][66][67][68] With excessive or prolonged use, the drug can cause itching, fast heart rate, and paranoid delusions or sensations of insects crawling on the skin.[69] Intranasal cocaine and crack use are both associated with pharmacological violence. Aggressive behavior may be displayed by both addicts and casual users. Cocaine can induce psychosis characterized by paranoia, impaired reality testing, hallucinations, irritability, and physical aggression. Cocaine intoxication can cause hyperawareness, hypervigilance, and psychomotor agitation and delirium. Consumption of large doses of cocaine can cause violent outbursts, especially by those with preexisting psychosis. Crack-related violence is also systemic, relating to disputes between crack dealers and users.[70] Acute exposure may induce cardiac arrhythmias, including atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation. Acute exposure may also lead to angina, heart attack, and congestive heart failure.[71] Cocaine overdose may cause seizures, abnormally high body temperature and a marked elevation of blood pressure, which can be life-threatening,[69] abnormal heart rhythms,[72] and death.[72] Anxiety, paranoia, and restlessness can also occur, especially during the comedown. With excessive dosage, tremors, convulsions and increased body temperature are observed.[43] Severe cardiac adverse events, particularly sudden cardiac death, become a serious risk at high doses due to cocaine's blocking effect on cardiac sodium channels.[72] Incidental exposure of the eye to sublimated cocaine while smoking crack cocaine can cause serious injury to the cornea and long-term loss of visual acuity.[73]
Crack baby is a term for a child born to a mother who used crack cocaine during her pregnancy. The threat that cocaine use during pregnancy poses to the fetus is now considered exaggerated.[96] Studies show that prenatal cocaine exposure (independent of other effects such as, for example, alcohol, tobacco, or physical environment) has no appreciable effect on childhood growth and development.[97]However, the official opinion of the National Institute on Drug Abuse of the United States warns about health risks while cautioning against stereotyping:
Smoking freebase cocaine has the additional effect of releasing methylecgonidine into the user's system due to the pyrolysis of the substance (a side effect which insufflating or injecting powder cocaine does not create). Some research suggests that smoking freebase cocaine can be even more cardiotoxic than other routes of administration[123] because of methylecgonidine's effects on lung tissue[124] and liver tissue.[125]
Powder cocaine (cocaine hydrochloride) must be heated to a high temperature (about 197 C), and considerable decomposition/burning occurs at these high temperatures. This effectively destroys some of the cocaine and yields a sharp, acrid, and foul-tasting smoke. Cocaine base/crack can be smoked because it vaporizes with little or no decomposition at 98 C (208 F),[127] which is below the boiling point of water.
Crack is a lower purity form of free-base cocaine that is usually produced by neutralization of cocaine hydrochloride with a solution of baking soda (sodium bicarbonate, NaHCO3) and water, producing a very hard/brittle, off-white-to-brown colored, amorphous material that contains sodium carbonate, entrapped water, and other by-products as the main impurities. The origin of the name "crack" comes from the "crackling" sound (and hence the onomatopoeic moniker "crack") that is produced when the cocaine and its impurities (i.e. water, sodium bicarbonate) are heated past the point of vaporization.[128]
TA-CD is an active vaccine[158] developed by the Xenova Group which is used to negate the effects of cocaine, making it suitable for use in treatment of addiction. It is created by combining norcocaine with inactivated cholera toxin.
In many countries, cocaine is a popular recreational drug. In the United States, the development of "crack" cocaine introduced the substance to a generally poorer inner-city market. The use of the powder form has stayed relatively constant, experiencing a new height of use during the late 1990s and early 2000s in the U.S., and has become much more popular in the last few years in the UK.[citation needed][when?]
Before the early 1900s, the primary problem caused by cocaine use was portrayed by newspapers to be addiction, not violence or crime, and the cocaine user was represented as an upper- or middle-class White person. In 1914, The New York Times published an article titled "Negro Cocaine 'Fiends' Are a New Southern Menace", portraying Black cocaine users as dangerous and able to withstand wounds that would normally be fatal.[201] The Anti-Drug Abuse Act of 1986 mandated prison sentences for 500 grams of powdered cocaine and 5 grams of crack cocaine.[202] In the National Survey on Drug Use and Health, Whites reported a higher rate of powdered cocaine use, and Blacks reported a higher rate of crack cocaine use.[203]
The major objective of this study was to examine the persistence of abnormal quantitative EEG (qEEG) measures over a six month time interval in subjects in strictly supervised drug free residential treatment for crack cocaine dependence. Seventeen subjects were assessed with qEEG at five to 10 days, one month and six months following their last use of cocaine. No significant changes were noted over time in abnormal qEEG measures, which included deficits of absolute and relative power in the delta band and increased relative alpha power. The persistence of qEEG abnormality in crack cocaine withdrawal suggests a persistent neurobiologic alteration resulting from chronic cocaine exposure. The specificity of the qEEG findings is discussed, and an interpretation is suggested with reference to the hypothesis of neural sensitization in cocaine dependence.
Work performed in this laboratory and elsewhere indicates profile of quantitative EEG (qEEG) abnormality in crack cocaine dependence (Alper et al. 1990; Roemer et al. 1995; Prichep et al. 1996b). In subjects evaluated within 30 days of their last use of crack cocaine, consistent and statistically robust differences from normal subjects include reduced delta absolute and relative power, and increased alpha relative power. This question of whether this profile of qEEG abnormality persists over longer intervals of abstinence is of interest for several reasons. Sensitization due to repeated psychostimulant exposure, which is suggested to be an etiologic factor in cocaine dependence, persists with a time frame of months to years (Kalivas et al. 1993a; Grace 1995; Johanson and Schuster 1995). Also, in the therapeutic community (TC), a long term drug free residential treatment environment, the minimum time of retention required to produce statistical evidence of benefit with regard to outcome is reportedly on the order of three to six months (DeLeon 1991; Condelli and Hubbard 1994). It is of interest whether the qEEG abnormality, seen at baseline, persists or begins to normalize over a time period apparently associated with clinical change.
With regard to other substance use disorders that are frequently comorbid with crack cocaine dependence, the qEEG findings of this study do not resemble qEEG profiles reported for alcohol dependence in which alpha power is reportedly decreased and theta increased (Alper 1995), or cannabis dependence in which slow EEG power is not reportedly decreased (Struve et al. 1989, 1994). qEEG data on heroin dependence is scant. However, reported histories of dependence on heroin or intravenous drug assumption (IVDA) were exclusion criteria and positively affirming crack cocaine as a drug of choice was an inclusion criteria, which tended to mitigate against a potential confound of opiate dependence. Crack cocaine is a reported risk factor for human immunodeficiency virus (HIV), another confound related to drug abuse (Booth et al. 1993). Abnormal qEEG has been reported in HIV seropositive patients (Riedel et al. 1995), however a reported history of HIV seropositivity, or constitutional signs of HIV was an exclusion criterion in this study. The New York City Department of Health has been conducting a large blind HIV seroprevalance study at Phoenix House since 1993 (Lehner et al. 1995) involving 1482 clients to date, and reports an overall seroprevalance of only 7.6%, probably due to the relatively low prevalence of a history of intravenous drug abuse in the Phoenix House population. In any event, the qEEG findings reported here do not resemble those of early HIV infection in which slow frequency EEG power is reportedly increased (Riedel et al. 1995). 2ff7e9595c
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