Download Drug-Induced Psychosis and Schizophrenia

Drug-Induced Psychosis and Schizophrenia: A Changing Perspective
M. Zahalka
A crisis center sees a lot of people on the worst day of their lives. The particular crisis center I
work for helps people suffering from chronic homelessness, abuse, mental illness, and drug
addiction and detoxification. These are often interlinked, in which case we generally term clients
with “co-occurring disorders” or “dual-diagnoses”. This is a fairly recent way of defining
persons living with mental illness as well as substance abuse, and is a very grey area within the
world of behavioral health. Many clients’ complaints about treatment is that most programs treat
a mental illness or a substance abuse problem, with a great majority of them refusing to treat
cognitive issues before the client maintains sobriety for any length of time. According to the
American Psychiatric Association, there are significant difficulties facing those perceived to
have a mental illness in drug abuse treatment and vice versa-many of the challenges stem from
not knowing which is related to which. It is difficult for clients to fit their very individualized
selves into very generalized treatment programs-often the counselors are geared toward one
direction or another, and can make the clients feel unwelcome, unwanted, or without hope for
recovery as the program continues and the client’s recovery stalls and his or her sense of anomie
increases (APA DSM IV-RT p123) . Often clients at the crisis center are treated vastly different
outside our facility depending on the reasons behind their behavior, with less help and
compassion offered to those with perceived “self-induced” mental health issues (such as druginduced psychosis, organic brain damage from alcoholism, ect…). The similarities between a
person with paranoid schizophrenia and a long-term meth user detoxing are strikingly similiar,
and have been the source of interest to me for some time now. It was my hope initially to reveal
the links between meth and schizophrenia, to show that no matter the path to the behavior, both
should be treated equally, without equating guilt or punitive reaction to the drug user. These
particular issues face a lot of people today, though often they are both stereotyped or ignored
completely due to their extreme behavioral displays and altered lifestyles that are difficult for
many ‘normies’ to handle. A family member with schizophrenia or a friend that divulges her
weight loss is from methamphetamine abuse are not uncommon, however, and so I hope that this
research will help shed light on the very real issues that arise cognitively from both. At the
advent of this endeavor, I knew only what I had observed-some behavioral attributes that were
shared between clients with Schizophrenia and those with methamphetamine dependence.
Some initial questions that initiated this research are very basic ones, seeking causes of the
behaviors on the neural level. I decided to tackle what the roots of paranoid Schizophrenia are,
then study what centers of the brain are effected by methamphetamine use and abuse, and see if
there was any relationship between the two. Reading through MD J. Thomas Noga’s article on
schizophrenia, I found that schizophrenia is a dynamic, mystifying disease. It is not nearly as
concise as I had anticipated; in fact, despite multiple years of study and
experimentation, schizophrenia is still one of the least understood mental illnesses, if
not the least understood. There is no identifiable genome that causes it, yet it is more frequently
diagnosed in individuals whose family members have it, giving it a strong argument for genetic
influence or causation. Additionally, twin studies have shown that there are higher rates of
physical complications during pregnancy and childbirth with one schizophrenic twin-however,
these complications could be resultant of a variety of factors, including a slightly more difficult
intrauterine environment with additional stressors. These stressors, research supposes, could
encourage normally ‘silent’ genes to express themselves in the individuals after birth (Noga,
2002). This still doesn’t quite get to the neural roots I was seeking: so, specifically, what
chemicals, neurons, and areas of the brain are affected by the disease of schizophrenia? Looking
on E-Mental Health, I found that schizophrenia often develops in three main ways: genetic
predisposition, prenatal viruses, and brain damage. Any of these three things affect the
neurotransmitters in the schizophrenic brain, causing a surplus of dopamine while also affecting
the serotonin levels. This is why antipsychotics, which often affect the transmission of dopamine
and serotonin production and reuptake, are often affective in the treatment
of schizophrenia (Sharma & Chitnis 2001).
I was fortunate enough to speak at length with a woman who is the one in the approximated five
individuals with schizophrenia that is in recovery. Jane* is a kind woman, who was married
happily to the love of her youth and employed with GE at a very young age in the 70’s. She
worked full time, attended college, and was, as she put it, “blissfully happy.” She turned 25 and
shortly after, her husband, who had been a veteran of the Vietnam War, committed suicide. It
was completely unprecedented and she still cannot recall any warning signs whatsoever. She said
she continued to work in a sort of shocked state for about three years, and then began the long,
painful experience that would be her psychotic break for the next 25 years. She would walk
outside at work holding what she believed was Jesus’ hand, while believing she was floating
three feet above the ground. She would often think she was a ‘biker chick’, dying her hair bright
red and purposefully starting fights with passersby. She drank heavily, became dependent on a
variety of illicit and legal drugs, and was often detained against her will by the courts. Jane lost
her job, her relationships, her health, and her sanity in one fell swoop, and only now is on
antipsychotics that work for her. Jane is somewhat of an anomaly: she is highly intelligent, high
functioning, and in recovery. She is employed full time, able to drive, able to manage her own
medications, and, to illustrate just how intelligent she is, relaxes on her porch swing with one of
her many physics text books. “The sense…” she says of the books, “The absolute sense they
make to me calms my brain down, brings me to a level of manageability that my meds
sometimes can’t do.” Interestingly, Jane states that when she overdosed or used a particular
substance (primarily methamphetamines) frequently, her symptoms would be the same as those
of her psychosis. “I’ve been detained for my breaks and I’ve been locked in detox for my
addictions: I’m the same in both instances. I would hear those voices all day, all the time, I’d tear
my surround sound out of my walls 20, 30 times a month because I thought the neighbors were
listening to me and talking to me through them. My brain does something in reaction to both
drugs and psychosis-it’s like an information overload.”
Speaking with Jane allowed me to delve a little deeper into not only the neurology of psychosis
(both drug-induced and paranoid type schizophrenia), but to the way people are treated when in
the midst of it. I posited a question to both myself and a few random people of my acquaintance:
would you hold someone who chronically abuses methamphetamines responsible for an act of
violence in a psychotic state? The general supposition is ‘yes’. Then I ask, would you hold a
person with schizophrenia responsible for an act of violence when they are in a psychotic state?
The answer is more muddled. Immediately, our minds seek out a person to blame-a counselor
who didn’t see the warning signs, a doctor who prescribed ineffective medications, a hospital
that released the patient too soon. The evidence I am unearthing, however, indicates that this
grey area is much foggier than I could have imagined: they are both the result of organic brain
damage. Jane’s story also illustrated another key point: she became psychotic and received the
diagnoses of both Schizoaffective Disorder and Schizophrenia (Paranoid Type) from two
different psychiatrists. The difference is in the interpretation: generally speaking, the DSM IV-
RT hints that Schizoaffective Disorder is more ‘undefined’-it has more variables to it and is
slightly more unpredictable (APA DSM IV-RT, p539). Jane supposes that particular diagnosis
was given due to her ability to function at such a high level.
In further research, I went to scholarly articles. The sheer amount of research done
on schizophrenia and drug addiction is exponential. I decided to narrow it down by cutting out
the behavioral and psychosocial aspects for the moment, and focus on the biological and
neurological components of drug abuse, dependence, and psychosis in the mentally ill. Reading
research published in Acta Neuropsychiatrica, I learned that schizophrenia is not only classified
in stages up to chronic (which I am focusing on in this paper), but that it is considered a
‘progressive disease’ in that it persists and the frequency and intensity of psychotic episodes, if
left untreated, will increase. Specifically, in post-mortem observations of schizophrenic brains,
the areas that showed significant variance to those of normally functioning brains were the
myelin sheath (the fatty insulation around the axon of a neuron that speeds signals along in the
neurological process), the oligodendroglia (cells that wrap, sheet-like, to form the myelin
sheath), and interstitial neurons (these are cells that exist in the cortical sub-plate, which serves
as a transition point for the development of the cerebral cortex. They somehow outlive the
scheduled cell-death in schizophrenic patients, and create abnormalities in the cerebral cortex’s
connections) (Ota, Obu, Sato, Mizukami, & Asada, 2009). Along with this very specific
information, there are general scholarly studies that state the regions affected
by schizophrenia are the primarily the frontal and temporal lobes, where our reasoning, planning,
memory, language and speech (among many other functions) are processed. Hypofrontality is a
term used to described decreased (or ‘lower than average’) blood flow in the frontal lobe,
something that paranoid schizophrenics show on fMRIs and PET scans. The behaviors that are
produced as a result of these different brain functions (for paranoid schizophrenics) are auditory
and visual hallucinations, hyper motor activity, decreased cognitive ability and awareness,
memory disruption, and language disruption. Paranoia results from an increase in information
processing that becomes disconnected from reality, for example, the belief that various authority
figures (FBI, CIA) are seeking out the individual, or intense religious conviction that results in
associating thoughts with a voice commanding certain actions (Dore, & Sweetin, 2006).
When moving into methamphetamine abuse, dependence, and psychosis, I wanted first to search
for the areas of the brain that are affected by methamphetamine. Methamphetamine works on the
dopaminergic system-it helps to release large amounts of dopamine while simultaneously
blocking its reuptake, causing the intense ‘rush’ or euphoria that many other drugs cause. It acts
similarly on serotonin. Methamphetamine affects the brain’s processes of reward, motivation,
the experience of pleasure, and motor function. In chronic users, brain scans have revealed
effects on the dopamine system-including reduced motor skills and impaired speech and
language learning or development (Volkow, 2001). The brains of chronic users also show
changes in the frontal lobe-both functional and structural. The frontal lobe, of course, controls
emotion, cognition, and memory. Even at this point, the similarities mount. Further questions
popped into my mind: could the increased activity in the dopamine neurotransmitters lead to a
breakdown in the myelin sheath around specific axons? Could the hyperactivity of these
chemicals and disruption of their everyday functions lead to, eventually, the same psychosis as
paranoid schizophrenia?
In a study published in Psychopharmacology in 2009, researchers state that drug use in
persons with schizophrenia is approximately four times that of the general population, and state
that “…it is suggested that drug abuse vulnerability and schizophreniashare a common substrate
at the neurotransmitter or neurocircuit level.” They go on to illustrate that, through observation
of locomotor hyperactivity (the animal equivalent of psychosis), they are able to deduce the
effects of serotonin depletion through routine injections of varying amounts of
methamphetamine. One of the conclusions drawn was that the disruption of serotonin levels in
the hippocampus of the brain may be one of the key factors in schizophrenia’s neurobiology
(Adams, Ayton, & van den Buuse, 2009). Methamphetamine affects these neurotransmitters-as
do many other drugs. The key difference to the varying effects or likelihood of drug-induced
psychosis in relation to drugs is the quality, quantity, frequency, method of use, and biological
makeup of the individual abusing the substance. Methamphetamine is more likely to be abused
more frequently and in higher amounts. It’s availability through everyday items that contain
ephedrine (cough syrup, allergy medication) and its ability to be broken down easily (through
household bleach, for instance) and manufactured at home (a convection oven, pyrex dish, and
freezer are all that is necessary for crystal meth production) make it widely available, cheap, and
toxic. Meth is rarely cut with another drug-its widespread availability actually makes it the prime
candidate to cut other substances with.
In addition to this, individuals that abuse methamphetamine and experience a drug-induced
psychotic episode are more likely to experience another psychotic episode, without using.
Because methamphetamines affect the brain’s dopaminergic system, meth abuse affects the
brain’s response to stress. In chronic users (whether in recovery or actively using), mild stress
sets off increased adrenal (fight or flight feelings) activity, where intense stress triggers psychotic
episodes: the brain’s response system is altered because of the damage done to the natural,
biochemical processes within it (Yui, Goto, Ikemoto, Ishiguro, & Angrist, 1999). Eventually, the
receptors become so damaged and altered that brain function and structure in methamphetamine
dependent individuals shows visible organic destruction. Disorganization of thoughts, altered
realities, disruption of memory, false memories, language degeneration, altered motor activity,
and hallucinations are all commonplace during psychosis-a state, if chronically reached, can
become permanent. This is loosely referred to by society as ‘perma-fried’, indicating a person is
beyond reparation, beyond their ability to ever have normally functioning brain activity once
more.
Through observation, I have witnessed paranoid schizophrenia as well as drug-induced psychosis
(from methamphetamine and polysubstance abusers). The neurochemical and neurobiological
ramifications of these diseases (schizophrenia and addiction) are evidenced in the behavior of
their hosts. Erratic speech, fear, memory loss, hyper mobility, an inability to remain functional
and in constant need of affirmation as to what is real or imagined are symptoms that would fit
either. The difference is in that the addict has an opportunity to stop their psychosis before it
becomes a diagnosis. The addict is often labeled and pushed out of sight, as are the chronically
mentally ill. After researching the evidence of their strikingly similar effects on the brain, I am
convinced that addiction lies less in the moral choices of the individual and more in the realm of
their biochemistry, just as those suffering from schizophrenia are not to be blamed for their
cognitive function.
I have learned not only that schizophrenia is a chemically and functionally degenerative disease,
but also that substance addiction acts very much in the opposite way as an antibiotic; it slowly
eats away at a healthy organism until it is unable to function in the way it was meant to, and
creates within it a disease that must be treated, or will result in death. These two families:
degenerative mental illness and addiction are attacks on brain function, and only through
medicine, treatment, and understanding can we hope to help those afflicted manage them.
References
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Third
Edition, Revised. Washington, D.C.: American Psychiatric Association, 1987.
Noga, T. (2002). Schizophrenia as a brain disease: what have we learned from neuroimaging
studies of twins?. MedGenMed Psychiatry and Mental Health , 3(1).
Sharma, T, & Chitnis, X. (2001, November/December). Brain imaging in schizophrenia. EHealth Images and Applications, 5(6), Retrieved
from http://www.ementalhealth.com/schizophrenia.htm
Ota, Miho, Obu, Satoko, Sato, Noriko, Mizukami, Katsuyoshi, & Asada, Takashi. (2009).
Progressive brain changes inschizophrenia: a 1-year follow-up study of diffusion tensor
imaging. Acta Neuropsychiatrica, 21(6), 301-317.
Dore, G., & Sweetin, M. (2006). Drug-induced psychosis associated with crystalline
methamphetamine. Australasian Psychiatry, 14(1), 86-89.
Adams, W, Ayton, S, & van den Buuse, M. (2009). Serotonergic lesions of the dorsal
hippocampus differentially modulate locomotor hyperactivity induce by drugs of abuse in
rats: implications for schizophrenia. Psychopharmacology, 10(206), 665-676.
Yui, K, Goto, K, Ikemoto, S, Ishiguro, T, & Angrist, B. (1999). Neurobiological basis of relapse
prediction in stimulant induced psychosis and schizophrenia: the role of sensitization.
Molecular Psychiatry, 25(4), 512-523.
Volkow, N. (2001). Researchers document brain damage, reduction in motor and cognitive
function from methamphetamine abuse. Brookhaven National Laboratories, 1(16),
Retrieved from http://www.bnl.gov/bnlweb/pubaf/pr/2001/bnlpr030101.htm