in Peru and Bolivia, in the mid19th century. In the early 1900s,

it became the main stimulant

drug used in most of the tonics/

elixirs that were developed to

treat a wide variety of illnesses.

Today, cocaine is a Schedule II

drug, meaning that it has high

potential for abuse, but can be

administered by a doctor for

legitimate medical uses, such as

local anesthesia for some eye,

ear, and throat surgeries. 

There are basically two 

chemical forms of cocaine: 

the hydrochloride salt and the

“freebase.” The hydrochloride

salt, or powdered form of

cocaine, dissolves in water and,

when abused, can be taken

intravenously 

(by vein) or

intranasally (in 

the nose). Freebase refers to a

compound that 

has not been 

neutralized by an

acid to make the

hydrochloride 

salt. The freebase

form of cocaine is

smokable.

from the director

Cocaine abuse and addiction 

continues to be a problem that plagues

our nation. For instance, from 

1965 to 1967, only 0.1 percent of

youths had ever used cocaine, but rates

rose throughout the 1970s and 1980s,

reaching 2.2 percent in 1987. After 

a brief decline, lifetime prevalence 

rates peaked at 2.7 percent in 2002.

However, we now know more 

about where and how cocaine acts in 

the brain, including how the drug 

produces its pleasurable effects and

why it is so addictive. Through the 

use of sophisticated technology, 

scientists can actually see the dynamic

changes that occur in the brain as an

individual takes the drug. They can

observe the different brain changes

that occur as a person experiences 

the “rush,” the “high,” and, finally, 

the craving of cocaine. They can also

identify parts of the brain that become

active when a cocaine addict sees or

hears environmental stimuli that 

trigger the craving for cocaine. Because

these types of studies pinpoint specific

brain regions, they are critical to 

identifying targets for developing 

medications to treat cocaine addiction. 

One of NIDA’s most important goals

is to translate what scientists learn

from research, in order to help the 

public better understand drug abuse

and addiction, and to develop more

effective strategies for their prevention

and treatment. We hope that this 

compilation of scientific information

on cocaine will help to inform readers

about the harmful effects of cocaine

abuse, and that it will assist in 

prevention and treatment efforts.

Nora D.Volkow, M.D.

Director

National Institute on Drug Abuse

U . S . Department of Health and Human Services • National Institutes of Health

What is cocaine?

C

ocaine is a powerfully

addictive stimulant that

directly affects the brain.

Cocaine was labeled the drug

of the 1980s and ‘90s, because 

of its extensive popularity and

use during this period. However,

cocaine is not a new drug. In

fact, it is one of the oldest

known drugs. The pure chemical,

cocaine hydrochloride, has been

an abused substance for more

than 100 years, and coca leaves,

the source of cocaine, have been

ingested for thousands of years.

Pure cocaine was first extracted

from the leaf of the Erythroxylon

coca bush, which grows primarily

ResearchReport

NATIONAL INSTITUTE ON DRUG ABUSE

SERIES

COCAINE

Abuse and Addiction
Cocaine is generally sold 

on the street as a fine, white, 

crystalline powder, known as

“coke,” “C,” “snow,” “flake,” or

“blow.” Street dealers generally

dilute it with such inert substances as cornstarch, talcum

powder, and/or sugar, or with

such active drugs as procaine 

(a chemically related local 

anesthetic) or with such other

stimulants as amphetamines. 

What is crack?

C

rack is the street name

given to a freebase form 

of cocaine that has been

processed from the powdered

cocaine hydrochloride form to a

smokable substance. The term

“crack” refers to the crackling

sound heard when the mixture 

is smoked. Crack cocaine is

processed with ammonia or 

sodium bicarbonate (baking

soda) and water, and heated to

remove the hydrochloride. 

Because crack is smoked, the

user experiences a high in less

than 10 seconds. This rather

immediate and euphoric effect 

is one of the reasons that crack

became enormously popular in

the mid 1980s. Another reason 

is that crack is inexpensive both

to produce and to buy. Crack

cocaine remains a serious problem in the United States. The

National Survey on Drug Use

and Health (NSDUH) estimated

the number of current crack users

to be about 567,000 in 2002.

What is the scope

of cocaine use in

the United States?

I

n 2002, an estimated 1.5 

million Americans could be

classified as dependent on 

or abusing cocaine in the past 

12 months, according to the

NSDUH. The same survey estimates that there are 2.0 million

current (past-month) users.

Cocaine initiation steadily

increased during the 1990s,

reaching 1.2 million in 2001.

Adults 18 to 25 years old have

a higher rate of current cocaine

use than those in any other age

group. Overall, men have a higher

rate of current cocaine use than

do women. Also, according to

the 2002 NSDUH, estimated rates

of current cocaine users were 

2.0 percent for American Indians

or Alaskan Natives, 1.6 percent

for African-Americans, 0.8 percent

for both Whites and Hispanics,

0.6 percent for Native Hawaiian

or other Pacific Islanders, and 

0.2 percent for Asians. 

The 2003 Monitoring the

Future Survey, which annually

surveys teen attitudes and recent

drug use, reports that crack

cocaine use decreased among

10th-graders in 30-day, annual,

and lifetime use prevalence 

periods. This was the only 

statistically significant change

affecting cocaine in any form.

Past-year use of crack declined

from 2.3 percent in 2002 to 

1.6 percent in 2003. Last year, the

rate increased from 1.8 percent

to 2.3 percent, and this year’s

decline brings it to approximately

its 2001 level. 

Data from the Drug Abuse

Warning Network (DAWN)

showed that cocaine-related

emergency department visits

increased 33 percent between

1995 and 2002, rising from 

58 to 78 mentions per 100,000

population.

How is 

cocaine used?

T

he principal routes of

cocaine administration are

oral, intranasal, intravenous,

and inhalation. The slang terms

for these routes are, respectively,

“chewing,” “snorting,” “mainlining”

2NIDA RESEARCH REPORT SERIES

Trends in 30-day prevalence of cocaine abuse among

eighth, tenth, and twelfth graders, 1991-1998

Source: Monitoring the Future Study, University of Michigan Number of students (Thousands)

12th grade

3.0

2.5

2.0

1.5

1.0

0.5

0.0 91 92 93 94 95 96 97 98

10th grade

8th grade
or “injecting,” and “smoking”

(including freebase and crack

cocaine). Snorting is the process

of inhaling cocaine powder

through the nostrils, where it is

absorbed into the bloodstream

through the nasal tissues. Injecting

releases the drug directly into the

bloodstream, and heightens the

intensity of its effects. Smoking

involves the inhalation of cocaine

vapor or smoke into the lungs,

where absorption into the 

bloodstream is as rapid as by

injection. The drug also can be

rubbed onto mucous tissues.

Some users combine cocaine

powder or crack with heroin in 

a “speedball.”

Cocaine use ranges from 

occasional use to repeated or

compulsive use, with a variety of

patterns between these extremes.

Other than medical uses, there is

no safe way to use cocaine. Any

route of administration can lead

to absorption of toxic amounts 

of cocaine, leading to acute 

cardiovascular or cerebrovascular

emergencies that could result 

in sudden death. Repeated

cocaine use by any route of

administration can produce

addiction and other adverse

health consequences.

How does cocaine

produce its effects?

Agreat amount of research

has been devoted to

understanding the way

cocaine produces its pleasurable

effects, and the reasons it is so

addictive. One mechanism is

through its effects on structures

deep in the brain. Scientists have

discovered regions within the

brain that are stimulated by

rewards. One neural system that

appears to be most affected by

cocaine originates in a region

located deep within the brain

called the ventral tegmental area

(VTA). Nerve cells originating in

the VTA extend to the region of

the brain known as the nucleus

accumbens, one of the brain’s

key areas involved in reward. 

In studies using animals, for

example, all types of rewarding

stimuli, such as food, water, sex,

and many drugs of abuse, cause

increased activity in the nucleus

accumbens.

Researchers have discovered

that, when a rewarding event is

NIDA RESEARCH REPORT SERIES3

Dopamine 

transporter 

functioning

normally

Dopamine 

transporter 

blocked by 

cocaine

Cocaine

Dopamine receptors

Receiving Neuron

Transmitting

Neuron

Dopamine packaged in vesicles

Cocaine in the brain — In the normal communication process, dopamine is released by a neuron into the synapse,

where it can bind with dopamine receptors on neighboring neurons. Normally, dopamine is then recycled back into the

transmitting neuron by a specialized protein called the dopamine transporter. If cocaine is present, it attaches to the

dopamine transporter and blocks the normal recycling process, resulting in a buildup of dopamine in the synapse, which 

contributes to the pleasurable effects of cocaine.
occurring, it is accompanied by 

a large increase in the amounts

of dopamine released in the

nucleus accumbens by neurons

originating in the VTA. In the

normal communication process,

dopamine is released by a 

neuron into the synapse (the

small gap between two neurons),

where it binds with specialized

proteins (called dopamine 

receptors) on the neighboring

neuron, thereby sending a signal

to that neuron. Drugs of abuse

are able to interfere with this

normal communication process.

For example, scientists have 

discovered that cocaine blocks

the removal of dopamine from

the synapse, resulting in an 

accumulation of dopamine. 

This buildup of dopamine 

causes continuous stimulation 

of receiving neurons, which is

associated with the euphoria

commonly reported by cocaine

abusers. 

As cocaine abuse continues,

tolerance often develops. This

means that higher doses and

more frequent use of cocaine 

are required for the brain to register the same level of pleasure

experienced during initial use.

Recent studies have shown that,

during periods of abstinence

from cocaine use, the memory 

of the euphoria associated with

cocaine use, or mere exposure 

to cues associated with drug use,

can trigger tremendous craving

and relapse to drug use, even

after long periods of abstinence.

What are the

short-term effects

of cocaine use?

C

ocaine’s effects appear

almost immediately after a

single dose, and disappear

within a few minutes or hours.

Taken in small amounts (up to

100 mg), cocaine usually makes

the user feel euphoric, energetic,

talkative, and mentally alert,

especially to the sensations of

sight, sound, and touch. It can

also temporarily decrease the

need for food and sleep. Some

users find that the drug helps

them perform simple physical

and intellectual tasks more

quickly, while others experience

the opposite effect.

The duration of cocaine’s

immediate euphoric effects

depends upon the route of

administration. The faster the

absorption, the more intense 

the high. Also, the faster the

absorption, the shorter the 

duration of action. The high 

from snorting is relatively slow 

in onset, and may last 15 to 

30 minutes, while that from

smoking may last 5 to 10 minutes.

The short-term physiological

effects of cocaine include constricted blood vessels; dilated

pupils; and increased temperature, heart rate, and blood pressure. Large amounts (several

hundred milligrams or more)

intensify the user’s high, but may

also lead to bizarre, erratic, and

violent behavior. These users

may experience tremors, vertigo,

muscle twitches, paranoia, or,

with repeated doses, a toxic

reaction closely resembling

amphetamine poisoning. Some

users of cocaine report feelings

of restlessness, irritability, and

anxiety. In rare instances, sudden

death can occur on the first 

use of cocaine or unexpectedly

thereafter. Cocaine-related deaths

are often a result of cardiac

arrest or seizures followed by

respiratory arrest.

What are the 

long-term effects

of cocaine use?

C

ocaine is a powerfully

addictive drug. Thus, an

individual may have difficulty predicting or controlling 

the extent to which he or she

will continue to want or use the

drug. Cocaine’s stimulant and

addictive effects are thought to

be primarily a result of its ability

to inhibit the reabsorption of

dopamine by nerve cells. Dopamine is released as part of the

brain’s reward system, and is

either directly or indirectly involved in the addictive properties

of every major drug of abuse.

An appreciable tolerance to

cocaine’s high may develop, with

many addicts reporting that they

4NIDA RESEARCH REPORT SERIES

Short-term effects 

of cocaine

Increased energy

Decreased appetite

Mental alertness

Increased heart rate and blood

pressure

Constricted blood vessels

Increased temperature

Dilated pupils
seek but fail to achieve as much

pleasure as they did from their

first experience. Some users will

frequently increase their doses 

to intensify and prolong the

euphoric effects. While tolerance

to the high can occur, users can

also become more sensitive (sensitization) to cocaine’s anesthetic

and convulsant effects, without

increasing the dose taken. This

increased sensitivity may explain

some deaths occurring after

apparently low doses of cocaine.

Use of cocaine in a binge, 

during which the drug is taken

repeatedly and at increasingly

high doses, leads to a state of

increasing irritability, restlessness,

and paranoia. This may result in

a full-blown paranoid psychosis,

in which the individual loses

touch with reality and experiences

auditory hallucinations.

What are 

the medical 

complications 

of cocaine abuse?

T

here can be severe medical

complications associated

with cocaine use. Some of

the most frequent complications

are cardiovascular effects, including disturbances in heart rhythm

and heart attacks; respiratory

effects such as chest pain and

respiratory failure; neurological

effects, including strokes, seizures,

and headaches; and gastrointestinal complications, including

abdominal pain and nausea.

Cocaine use has been linked

to many types of heart disease.

Cocaine has been found to trigger chaotic heart rhythms, called

ventricular fibrillation; accelerate

heartbeat and breathing; and

increase blood pressure and body

temperature. Physical symptoms

may include chest pain, nausea,

blurred vision, fever, muscle

spasms, convulsions, coma, 

and death.

Different routes of cocaine

administration can produce different adverse effects. Regularly

snorting cocaine, for example,

can lead to loss of sense of

smell, nosebleeds, problems 

with swallowing, hoarseness, 

and an overall irritation of the

nasal septum, which can lead 

to a chronically inflamed, runny

nose. Ingested cocaine can cause

severe bowel gangrene, due 

to reduced blood flow. And, 

persons who inject cocaine have

puncture marks and “tracks,”

most commonly in their forearms. Intravenous cocaine users

may also experience an allergic

reaction, either to the drug, or to

some additive in street cocaine,

which can result, in severe cases,

in death. Because cocaine has 

a tendency to decrease food

intake, many chronic cocaine

users lose their appetites and 

can experience significant weight

loss and malnourishment.

Research has revealed a 

potentially dangerous interaction

between cocaine and alcohol.

Taken in combination, the two

drugs are converted by the body

to cocaethylene. Cocaethylene

has a longer duration of action in

the brain and is more toxic than

either drug alone. While more

research needs to be done, it is

noteworthy that the mixture of

cocaine and alcohol is the most

common two-drug combination

that results in drug-related death.

Are cocaine

abusers at risk

for contracting

HIV/AIDS and 

hepatitis B and C?

Yes. Cocaine abusers, especially those who inject, are

at increased risk for contracting such infectious diseases

as human immunodeficiency

virus (HIV/AIDS) and viral 

hepatitis. In fact, use and abuse

of illicit drugs, including crack

cocaine, are major risk factors for

new cases of HIV. Drug abuserelated spread of HIV can result

NIDA RESEARCH REPORT SERIES5

Long-term effects 

of cocaine

Addiction

Irritability and mood disturbances

Restlessness

Paranoia

Auditory hallucinations

Medical consequences of cocaine abuse

Cardiovascular effects

– disturbances in heart rhythm

– heart attacks

Respiratory effects

– chest pain

– respiratory failure

Neurological effects

– strokes

– seizures and headaches

Gastrointestinal complications

– abdominal pain

– nausea
from direct transmission of the

virus through the sharing of 

contaminated needles and paraphernalia between injecting drug

users. It can also result from 

indirect transmission, such as an

HIV-infected mother transmitting

the virus perinatally to her child.

This is particularly alarming

given that 30 percent of all new

AIDS cases are among women.

Research has also shown that

drug use can interfere with judgement about risk-taking behavior,

and can potentially lead to

reduced precautions regarding

sexual behaviors, the sharing of

needles and injection paraphernalia, and the trading of sex for

drugs, by both men and women.

Additionally, hepatitis C (HCV)

has spread rapidly among injection drug users; Centers for

Disease Control and Prevention

(CDC) estimates indicate infection rates of 50 to 80 percent in

this population. While currently

available treatment is not effective

for everyone and can have 

significant side effects, medical

followup is essential for all those

who are infected. At present,

there is no vaccine for the hepatitis C virus. The virus is highly

transmissible via injection, and

HCV testing is recommended 

for any individual who has ever

injected drugs.

What are the 

effects of maternal

cocaine use?

T

he full extent of the effects

of prenatal drug exposure

on a child is not completely

known, but many scientific 

studies have documented that

babies born to mothers who

abuse cocaine during pregnancy

are often prematurely delivered,

have low birth weights and

smaller head circumferences, 

and are often shorter in length.

Estimating the full extent of

the consequences of maternal

drug abuse is difficult, and determining the specific hazard of a

particular drug to the unborn

child is problematic for many

reasons. Multiple factors—such

as the amount and number of all

drugs abused; extent of prenatal

care; possible neglect or abuse of

the child; exposure to violence in

the environment; socioeconomic

conditions; maternal nutrition;

other health conditions; and

exposure to sexually-transmitted

diseases—can contribute to the

difficulty in determining direct

impact of prenatal cocaine use

on maternal, fetal, and child 

outcomes.

Many recall that “crack babies,”

or babies born to mothers who

used crack cocaine while pregnant, were at one time written

off by many as a lost generation.

They were predicted to suffer

from severe, irreversible damage,

including reduced intelligence

and social skills. It was later

found that this was a gross 

exaggeration. However, the 

fact that most of these children

appear normal should not be

overinterpreted as indicating that

there is no cause for concern.

Using sophisticated technologies,

scientists are now finding that

exposure to cocaine during fetal

development may lead to subtle,

yet significant, later deficits in

some children, including deficits

in some aspects of cognitive 

performance, informationprocessing, and attention to

tasks—abilities that are important

for success in school.

What treatments

are effective for

cocaine abusers?

T

here was an enormous

increase in the number of

people seeking treatment 

for cocaine addiction during the

1980s and 1990s. Treatment

providers in most areas of the

country, except in the West and

Southwest, report that cocaine is

the most commonly cited drug 

of abuse among their clients. The

majority of individuals seeking

treatment smoke crack, and are

likely to be polydrug users, or

users of more than one substance. The widespread abuse of

cocaine has stimulated extensive

efforts to develop treatment 

programs for this type of drug

abuse. Cocaine abuse and 

addiction is a complex problem

involving biological changes in

the brain as well as a myriad of

social, familial, and environmental

factors. Therefore, treatment of

cocaine addiction is complex,

and must address a variety of

problems. Like any good treatment plan, cocaine treatment

strategies need to assess the 

psychobiological, social, and

pharmacological aspects of the

patient’s drug abuse.

Pharmacological Approaches

There are no medications currently available to treat cocaine

addiction specifically. Consequently, NIDA is aggressively

pursuing the identification and

testing of new cocaine treatment

medications. Several newly

emerging compounds are being

6NIDA RESEARCH REPORT SERIES
investigated to assess their safety

and efficacy in treating cocaine

addiction. Topiramate and

modafanil, two marketed medications, have shown promising

signals as potential cocaine 

treatment agents. Additionally,

baclofen, a GABA-B agonist,

showed promise in a subgroup

of cocaine addicts with heavy

use patterns. Because of mood

changes experienced during

the early stages of cocaine

abstinence, antidepressant

drugs have been shown to

be of some benefit. In addition to the problems of treating

addiction, cocaine overdose

results in many deaths every

year, and medical treatments are

being developed to deal with the

acute emergencies resulting from

excessive cocaine abuse.

Behavioral Interventions

Many behavioral treatments

have been found to be effective

for cocaine addiction, including

both residential and outpatient

approaches. Indeed, behavioral

therapies are often the only

available, effective treatment

approaches to many drug problems, including cocaine addiction, for which there is, as yet,

no viable medication. However,

integration of both types of treatments may ultimately prove to

be the most effective approach

for treating addiction. Disulfiram

(a medication that has been used

to treat alcoholism), in combination with behavioral treatment,

has been shown, in clinical studies, to be effective in reducing

cocaine abuse. It is important

that patients receive services that

match all of their treatment needs.

For example, if a patient is unemployed, it may be helpful to

provide vocational rehabilitation

or career counseling. Similarly, 

if a patient has marital problems,

it may be important to offer 

couples counseling. A behavioral

therapy component that is 

showing positive results in many

cocaine-addicted populations 

is contingency management.

Contingency management may

be particularly useful for helping

patients achieve initial abstinence

from cocaine. Some contingency

management programs use a

voucher-based system to give

positive rewards for staying in

treatment and remaining cocaine

free. Based on drug-free urine

tests, the patients earn points,

which can be exchanged for

items that encourage healthy 

living, such as joining a gym, 

or going to a movie and dinner.

Cognitive-behavioral therapy,

or “Relapse Prevention,” is

another approach. Cognitivebehavioral treatment, for example,

is a focused approach to helping

NIDA RESEARCH REPORT SERIES7
cocaine-addicted individuals

abstain—and remain abstinent—

from cocaine and other 

substances. The underlying

assumption is that learning

processes play an important 

role in the development and

continuation of cocaine abuse

and dependence. The same

learning processes can be

employed to help individuals

reduce drug use and successfully cope with relapse. This

approach attempts to help

patients recognize, avoid, and

cope; i.e., recognize the situations in which they are most

likely to use cocaine, avoid these

situations when appropriate, and

cope more effectively with a

range of problems and problematic behaviors associated with

drug abuse. This therapy is also

noteworthy because of its compatibility with a range of other

treatments patients may receive,

such as pharmacotherapy.

Therapeutic communities

(TCs), or residential programs

with planned lengths of stay of 

6 to 12 months, offer another

alternative to those in need of

treatment for cocaine addiction.

TCs focus on resocialization of

the individual to society, and 

can include on-site vocational

rehabilitation and other supportive services. Of course, there is 

variation in the types of therapeutic processes offered in TCs.

Where can I get

further scientific

information about

cocaine abuse and

addiction?

T

o learn more about cocaine

and other drugs of abuse,

contact the National

Clearinghouse for Alcohol and

Drug Information (NCADI) at 

1-800-729-6686. Information 

specialists are available to 

assist you in locating needed

information and resources.

Fact sheets and other information on the health effects of

cocaine or other drugs of abuse

and other drug abuse topics are

available on the NIDA Web site

(www.drugabuse.gov), and can

be ordered free of charge in

English and Spanish from NCADI

at www.health.org.

8NIDA RESEARCH REPORT SERIES

References

Gold, Mark S. Cocaine (and Crack): Clinical Aspects

(181–198), Substance Abuse: A Comprehensive

Textbook, Third Edition, Lowinson, ed. Baltimore,

MD: Williams & Wilkins, 1997.

Harvey, John A. and Kosofsky, Barry, eds. Cocaine:

Effects on the Developing Brain. Annals of the New

York Academy of Sciences, Volume 846, 1998.

National Institute on Drug Abuse. Epidemiologic Trends

in Drug Abuse: Advance Report, Community

Epidemiology Work Group. NIH Pub. No. 03-5363A.

Washington, DC: Supt. of Docs., U.S. Govt. Print.

Off., June 2003.

National Institute on Drug Abuse. NIDA InfoFacts, Crack

and Cocaine, 1998.

National Institute on Drug Abuse. National Survey

Results on Drug Use From the Monitoring the Future

Survey, 2003.

Office of National Drug Control Policy. The National Drug

Control Strategy, 1998: A Ten Year Plan.

Shoptaw, S. et al. Randomized placebo-controlled 

trial of baclofen for cocaine dependence: 

preliminary effects for individuals with chronic 

patterns of cocaine use. J. Clin. Psychiatry,

64(12):1440–1448, 2003.

Snyder, Solomon H. Drugs and the Brain (122–130).

New York: Scientific American Library, 1996.

Substance Abuse and Mental Health Services

Administration. National Survey on Drug Use and

Health. SAMHSA, 2002.

NIH Publication Number 99-4342

Printed May 1999, Revised November 2004.

Feel free to reprint this publication.

Glossary

Addiction: A chronic, relapsing disease characterized

by compulsive drug-seeking and use and by neurochemical and molecular changes in the brain.

Anesthetic: An agent that causes insensitivity to pain.

Antidepressants: A group of drugs used in treating

depressive disorders.

Cocaethylene: Potent stimulant created when

cocaine and alcohol are used together.

Coca: The plant, Erythroxylon, from which cocaine is

derived. Also refers to the leaves of this plant.

Crack: “Slang” term for a smokable form of cocaine.

Craving: A powerful, often uncontrollable desire for

drugs.

Dopamine: A neurotransmitter present in regions of

the brain that regulate movement, emotion, motivation,

and the feeling of pleasure.

Neuron: A nerve cell in the brain.

Physical dependence: An adaptive physiological

state that occurs with regular drug use and results in 

a withdrawal syndrome when drug use is stopped; 

usually occurs with tolerance.

Polydrug user: An individual who uses more than

one drug.

Rush: A surge of pleasure that rapidly follows 

administration of some drugs.

Tolerance: A condition in which higher doses of a

drug are required to produce the same effect as during

initial use; often is associated with physical dependence.

Vertigo: The sensation of dizziness.

Withdrawal: A variety of symptoms that occur after

use of an addictive drug is reduced or stopped.