“Brain Drain”: Drug-Induced Loss of Brain Function Dr. Sandra Welch Professor Virginia Commonwealth University Photo courtesy of the NIDA Web site.

Download Report

Transcript “Brain Drain”: Drug-Induced Loss of Brain Function Dr. Sandra Welch Professor Virginia Commonwealth University Photo courtesy of the NIDA Web site.

“Brain Drain”:
Drug-Induced Loss of Brain Function
Dr. Sandra Welch
Professor
Virginia Commonwealth
University
Photo courtesy of the NIDA Web site. From A
Slide Teaching Packet: The Brain and the
Actions of Cocaine, Opiates, and Marijuana.
We Have Generated A Lot of
Evidence Showing That…
Prolonged Drug Use Changes
the Brain and
In Fundamental
and Long-Lasting Ways
AND…
We Have Evidence That
These Changes Can Be Both
Structural and Functional
BRAIN IMAGING
Positron Emission Tomography
Magnetic Resonance Imaging
Illustration used with permission,
courtesy of Lydia V. Kibiuk and
the Society for Neuroscience.
Brain Maturation from
Ages 5 to 20
Copyright ©2004 by the National Academy of Sciences
Gogtay, Giedd, et al. (2004) Proc. Natl. Acad. Sci. USA 101,
Photo courtesy of the NIDA Web site. From A
Slide Teaching Packet: The Brain and the
Actions of Cocaine, Opiates, and Marijuana.
Dopamine Pathways
striatum
frontal
cortex
hippocampus
Functions
•reward (motivation)
nucleus
•pleasure,euphoria
accumbens
•motor function
(fine tuning)
•compulsion
•perserveration
•decision making
substantia
nigra/VTA
Serotonin Pathway
raphe
Functions
•mood
•memory
processing
•sleep
•cognition
For Example…
We Know That Despite
Their Many Differences, Virtually
All Abused Substances Enhance
Dopamine (neurotransmitter) Activity
(particularly related to pleasure,
motor, and cognitive function
• Other pathways also involved!
Accumbens
1100
1000
900
800
700
600
500
400
300
200
100
0
AMPHETAMINE
Much greater
DA
DOPAC
Activity than
any
HVA
Other drug of abuse
-causes neurotoxicity
250
NICOTINE
200
Accumbens
Caudate
150
100
Accumbens
COCAINE
DA
DOPAC
HVA
300
200
100
0
5 hr
250
% of Basal Release
1
2
3
4
Time After Amphetamine
% of Basal Release
400
0
% of Basal Release
% of Basal Release
Effects of Drugs on Dopamine Release
0
1
2
3
4
Time After Cocaine
Accumbens
5 hr
ETHANOL
Dose (g/kg ip)
200
0.25
0.5
1
2.5
150
100
0
0
1
2
3 hr
0
Time After Nicotine
Source: Di Chiara and Imperato
0
1
2
3
Time After Ethanol
4hr
200
% of Basal DA Output
NAc shell
150
100
Empty
50
Box Feeding
200
150
100
15
10
5
0
0
0
60
120
Time (min)
180
ScrScr
BasFemale 1 Present
Sample 1 2 3 4 5 6 7 8
Number
Scr
Scr
Female 2 Present
9 10 11 12 13 14 15 16 17
Mounts
Intromissions
Ejaculations
Source: Di Chiara et al.
Source: Fiorino and Phillips
Copulation Frequency
DA Concentration (% Baseline)
Natural Rewards Elevate Dopamine
Levels
FOOD
SEX
Common Underlying
Neurobiological
Factors Can Be:
Neurochemical (imbalance of
neurotransmitters)
Structural/anatomical
(same regions and pathways)
Genetic (inherited factors that
compromise function)
Drugs of abuse
can cause symptoms that mimic
most forms of mental illness because
they alter the same
neurotransmitters that are altered in
mental illnesses.
Drug
Disorder
Cocaine and Methamphetamine Schizophrenia, paranoia,
anhedonia, compulsive
behavior
Stimulants
LSD, Ecstasy & psychedelics
Alcohol, sedatives, sleepaids
& narcotics
PCP & Ketamine
Anxiety, panic attacks,
mania and sleep disorders
Delusions and hallucinations
Depression and mood
disturbances
Antisocial behavior
Chronic use of some of these drugs
of
abuse may alter the way the brain
functions, making persons
particularly
susceptible to mental illness
People With Comorbid
Mental and Addictive Disorders
Have a Double
DoubleBrain Disease
Mental
Disorder
Comorbid
Disorders
Addictive
Disorder
Outline of talk:
Alcohol - a depressant
Cocaine - a stimulant
MDMA and Club Drugs - stimulants
Marijuana
Inhalants
Opioids
Alcohol Abuse and Alcoholism
Important neurotransmitters in the
reward pathway for alcohol





Dopamine
Opioid
Serotonin
GABAA
Glutamate
well-being, arousal, reward
rewarding and reinforcing
behavioral inhibition
inhibitory
excitatory
Overview:
Statistics on teen drinking
Short- and long-term effects of
alcohol
Statistics on Teen Drinking
Monitoring the Future (MTF) reported
that in 2007, nearly one in five 8th
graders, more than one in three 10th
graders, and nearly one in two 12th
graders had a drink in the
past month.
Teen Statistics (cont.)
From National Survey on Drug Use and
Health (2005):
10.9 million users ages 12-20
7.2 million “binge drinkers”
Short-term Effects
Slower reaction times/reflexes
Heavy sweating
Blurry vision
Nausea and vomiting
Lowered reasoning ability
Short-term Effects (cont.)
Poor motor coordination
Slower heart rate/breathing rate
Increased blood pressure
Anxiety/restlessness
Lower inhibition
Short-term Effects (cont.)
Mental confusion
Memory loss
Coma
Death from respiratory arrest
Long-term Effects
Nervous system
Muscles
Lungs
Liver
Long-term Effects (cont.)
Sexual organs
Brain
Heart
Esophagus/stomach
Drug and Alcohol Intoxication MARKEDLY
Disrupt Brain Function:
Effects of alcohol intoxication on brain metabolism
sober
intoxicated (0.1 mg%)
Studies on Teen Drinking
"I used to worry about my short attention span - but not for
very long."
- Strange de Ji
Studies on Teen Drinking
Early drinking onset is
associated with increased
risk of alcoholism
NIAAA
Comorbidity with alcoholism






Drug abuse (opioids, cocaine, cannabis)
nicotine addiction
antisocial personality disorder
major depression
anxiety disorders
bulimia nervosa
Alcoholism and Nicotine
Addiction
Heavy smokers
> 20 cigarettes / day
 70% of alcoholics
 10% of the general
population
Structure and Functional
Consequences of Intoxication
Structural damage to the brain resulting from chronic alcohol abuse
can be observed in different ways:
•Results of autopsy show that patients with a history of chronic alcohol
abuse have smaller, less massive, and more shrunken brains than
nonalcoholic adults of the same age and gender.
•The findings of brain imaging techniques, such as CT scans
consistently show an association between heavy drinking and physical
brain damage, even in the absence of chronic liver disease or dementia.
•Brain shrinking is especially extensive in the cortex of the frontal
lobe2 - the location of higher cognitive faculties.
•The vulnerability to this frontal lobe shrinkage increases with age.
After 40 some of the changes my be irreversible, but some changes are
not reversible at any age!
•Repeated imaging of a group of alcoholics who continued drinking over
a 5-year period showed progressive brain shrinkage that significantly
exceeded normal age-related shrinkage. Moreover, the rate of
shrinkage correlated with the amount of alcohol consumed.
In Adults, Emotional Self Regulation Is Normally
Implemented By A Neural Circuit Comprising
Various Prefrontal Regions…
Sexual Arousal Condition
& Subcortical
Limbic Structures
Attempted Inhibition Condition
Attempted Inhibition
Condition
Source: Beauregard, M. et al., Journal of Neuroscience 21 RC165, 2001.
Effects of Alcohol Intoxication on Brain Glucose
Metabolism (Marker of Brain Function)
Decreases
prefrontal cortex
cingulate gyrus
Increases
amygdala
Alcohol decreases activity of areas involved with control and
increases activity of areas involved with emotional reactivity
Fetal Alcohol Syndrome
>10% of children exposed in utero to alcohol toxicity
7-14 drinks/wk (particularly > 5/occasion) can cause
moderate fetal damage
FAS: growth deficiency, abnormal facies, mental retardation, attentional
and behavioral problems
FAE: learning disabilities, intellectual impairment, behavioral problems
Your Brain on Drugs: Cocaine
1-2 Min
3-4
5-6
6-7
7-8
8-9
9-10
10-20
20-30
Photo courtesy of Nora Volkow, Ph.D. Mapping cocaine binding
sites in human and baboon brain in vivo. Fowler JS, Volkow ND,
Wolf AP, Dewey SL, Schlyer DJ, Macgregor RIR, Hitzemann R,
Logan J, Bendreim B, Gatley ST. et al. Synapse 1989;4(4):371-377.
Your Brain After Drugs
Normal
Cocaine Abuser (10 days)
Cocaine Abuser (100 days)
Photo courtesy of Nora Volkow, Ph.D. Volkow ND, Hitzemann R, Wang C-I, Fowler IS, Wolf AP, Dewey SL. Long-term frontal brain metabolic changes in cocaine
abusers. Synapse 11:184-190, 1992; Volkow ND, Fowler JS, Wang G-J, Hitzemann R, Logan J, Schlyer D, Dewey 5, Wolf AP. Decreased dopamine D2 receptor
availability is associated with reduced frontal metabolism in cocaine abusers. Synapse 14:169-177, 1993.
Important neurotransmitters in the
reward pathway for stimulants
 Dopamine
well-being, arousal, reward
 Opioid
rewarding and reinforcing



Serotonin
GABAA
Glutamate
behavioral inhibition
inhibitory
excitatory
Drug Use Has Played a Prominent
Role in the HIV/AIDS Epidemic
In Several Ways
Disease Transmission
IV Drug Use
Drug User Disinhibition Leading to
High Risk Sexual Behaviors
Progression of Disease
In Addition to Increasing the Risk of
HIV Transmission Some Psychoactive Drugs
May Also Accelerate HIV Progression
Effects of Cocaine Combined with
HIV Infection In Vivo
105
8
6
4
*
2
HIV RNA copy no.
CD4: CD8 ratio
10
*
104
103
102
0
Control Cocaine
Control Cocaine
Roth, M.D. et al., The Journal of Infectious Diseases, 185, pp. 701-705, 2002.
Acceleration of HIV Degeneration of
Dopamine Cells With Cocaine
Seronegative
HIV
HIV + Drug
Drugs Have
Long-term
Consequences
Photo courtesy of NIDA from research conducted by
Melega WP, Raleigh MJ, Stout DB, Lacan C, Huang SC,
Phelps ME.
Amphetamine and the Hallucinogen DOI
Produce Different Protein Profiles in
Brain
Normal
AMPH
DOI
The Memory of Drugs
Front of Brain
Amygdala
not lit up
Amygdala
activated
Back of Brain
Nature Video
Photo courtesy of Anna Rose Childress, Ph.D.
Cocaine Video
CEWG Advance Report
NIDA Community Epidemiology Workgroup
25th Anniversary Meeting
MDMA & Club Drugs
Seattle
Minneapolis
Boston
New York
Newar k
Philadelphia
Detr oit
Chicago
San Fra ncisc o
Denv er
St. Louis
D.C.
Los Angeles
Phoenix
San Diego
Honolulu
Atlanta
Austin
Ne w Orleans
Miami
• Consequences UP in 13 of 20 cities
• More routine settings: home and school
• More concomitant and sequential abuse
“Ecstasy” may not be MDMA
Methyl
Salicylate,
Caffeine
90%
DXM
MDMA
MDA
These are some of the “Ecstasy” pills tested
by the dancesafe organization
(www.dancesafe.org)
MDMA Users (N=55)
Selected other drugs used - last three months
Ketamine
Methamphetamine
Inhaled cocaine
Inhaled nitrites (poppers)
Viagra
GHB
Anabolic steroids
LSD
Mushrooms
Marijuana
Injected last three months
Enrolled in drug treatment program- ever
%
69
56
55
53
38
24
13
13
7
76
11
15
MDMA Brief Historical Overview
1912
1950s
MDMA was synthesized (Merck)
U.S. army studied as potential agent in
psychological warfare
1970s
MDMA used in psychotherapy –
“penicillin for the soul”
1985
MDMA became illegal in the U.S.; 1988
in the Netherlands
1990s… Still limited knowledge of prevalence of
use, levels of risk and consequences
EFFECTS OF MDMA USE
PHYSIOLOGICAL
Sensatory awareness
Loss of appetite
Nausea
Muscle ache
Tachycardia
Hypothermia
Cardiological
complications
Liver damage
PSYCHOLOGICAL
Euphoria
• Anxiety, depression,
and panic attacks
Depersonalization
Paranoia
Psychotic
experiences
Cognitive
deficiencies, e.g.,
memory loss and
decreased planning
ability
Settings of Use
The settings at which MDMA is being used
Are diversifying according to all presenters
And these include:




Raves and concerts
Clubs and bars
House parties
At home with friends or other private settings
MDMA Administration
Intranasal
 Bumpers
 Inhale “bumps” from the back of the hand
 Other paraphernalia such as spoons, pen
caps
Oral
 Pills and capsules
Anal Insertion
 “Booty bumping”
HIV Risks
24 percent of current MDMA users in NIDA studies are
HIV positive.
Unsafe sex reported but is almost always attributed to
other drugs such as methamphetamine.
Unwanted sexual attention (rape) and sex has been
reported in the context of MDMA use.
Challenges - Prevention
Prevention messages regarding MDMA use
have had little effect among all age groups.
Other drugs such as GHB are seen as more
dangerous, have become stigmatized, and
use has reduced.
While MDMA is not perceived as a safe drug,
it is seen as much safer than other drugs.
Effect of MDMA on cerebral blood flow:
A SPECT and MRI study
Baseline
2 Weeks Post
MDMA
Highest Dose
Lowest Dose
L. Chang Psychiat Res (2000) 98: 15)
Rat Hippocampus (2 wks after 20 mg/kg; 2X daily, 4 days)
• Result:
long-term
loss of
nerve
fibers
5-HT levels in monkey after MDMA (two 5 mg/kg daily for 4 days)
• Result:
-long-term
loss of nerve
fibers in
monkeys
2 weeks
7 years
(caudate nucleus)
(Hatzidimitriou et al., J. Neurosci. 19 [1999] 5092)
-some
recovery
Partial Recovery of Brain
Metabolism and Function in
Methamphetamine Abusers After
Protracted Abstinence
Short Abstinence
% Metabolic Change
Protracted Abstinence
Improved memory correlates
with thalamic recovery
Adapted from Wang, Volkow, et al, (2004) American Journal of Psychiatry 161: 242-8 (scans unpublished)
MOTOR FUNCTION
• Slowed gait
•Impaired balance
• Impairment correlates with
damage to dopamine system
Implication:
Brain changes resulting from
prolonged use of psychostimulants,
such as methamphetamine
may be reflected in compromised
cognitive and motor functioning
Photo courtesy of the NIDA Web site.
From A Slide Teaching Packet: The
Brain and the Actions of Cocaine,
Opiates, and Marijuana.
Important neurotransmitters in the
reward pathway for stimulants
 Dopamine
 Opioid
 Serotonin
 GABAA
 Glutamate
well-being, arousal, reward
rewarding and reinforcing
behavioral inhibition
inhibitory
excitatory
Important neurotransmitters in the
reward pathway for stimulants
 Dopamine
 Opioid
 Serotonin
 GABAA
 Glutamate
well-being, arousal, reward
rewarding and reinforcing
behavioral inhibition
inhibitory
excitatory
Important neurotransmitters in the
reward pathway for stimulants
 Dopamine
 Opioid
 Serotonin
 GABAA
 Glutamate
well-being, arousal, reward
rewarding and reinforcing
behavioral inhibition
inhibitory
excitatory
Dopamine D2 Receptors in Addiction
Cocaine
Meth
Alcohol
Food
DOE/BNL, NIDA, ONDCP
Reward System in Addiction
More
Cocaine
Alcohol
Food
treated
METH
Ability to Experience
Rewards Is Damaged
Less
Their Brains…
Get Rewired
by Drug Use
Is There Recovery?
• Good News: After 2 years some
of the dopamine deficits are
recovering
• Bad News: Functional deficits
persist
• What does this mean???
… Is it
worth
the risk?
Photo courtesy of NIDA.
Don’t Worry
Be Happy!