characterize Schizophrenia as a disorder which is too bizarre or alien
for the average individual to empathize with, and certainly as separate
from other disorders in it's severity of expression and debilitation
of it's victims (Bellack and Hersen 1993, Lehrmann 1955, Modrow 1995).
Similarly, Tourette's Syndrome, and it's associated symptoms, are considered
"bizarre" (Blakeslee, 1996), "strange" (Sacks, 1995),
and "crazy" (Yelaja, 1997). This paper will discuss current
theory which links Tourette's Syndrome and various comorbid conditions
to a common etiology, and will explore the possibility that even Schizophrenia
may fit within this new perspective of many mental disorders.
until recently, was considered to be a dominant-gene disorder with relative
scarcity within the population - about 1 in 20,000 (Comings, 1990).
Recent concordance studies and pedigree analyses (Comings, 1990) have
suggested that Tourette's Syndrome is but one manifestation of a Generalized
Disinhibition Disorder, caused by a semi-dominant, semi-recessive gene
or genes. While this predisposition to be disinhibited may manifest
as Tourette's Syndrome, it may also appear in other motoric guises (motor
hyperactivity, chronic tics), as frontal lobe dysfunction (ADHD, Conduct
Disorder), in learning and memory (LD, dyslexia), as anxiety (phobias,
panic, GAD), or in obsessive-compulsive tendencies (substance abuse,
obesity, OCD) (Pauls, Towbin & Leckman 1986, Cumings & Frankel
1985, Green & Pitman 1986). Currently, TS is thought to be the manifestation
of two of these Gts genes; individuals carrying only one Gts gene "may
either have no symptoms or one or more of the behaviours listed above"
(Comings, 1990). This would explain why the comorbidity of such disorders
as ADHD and OCD with TS are much higher than the comorbidity of TS with
them (Comings, 1990).
There are many
similarities between Schizophrenia and this hypothesized group of "Disinhibition
Disorders". Schizophrenia, like the disinhibition disorders, is
believed to be genetic, and both are postulated to be genetically additive
(Comings, 1990, Bellack & Hersen, 1993). Emil Kraepelin, hailed
as the "Father of Modern Psychiatry" and who first discriminated
dementia praecox from manic depression, noted in his extensive observations
of Schizophrenics that many afflicted had odd mannerisms and/or movement
disorders. It is also interesting that Tardive Dyskinesia, a movement
disorder resembling Tourette's Syndrome, develops after prolonged usage
of anti-psychotic medications such as Haldol (Sandor, 1995). Tardive
Dyskinesia can also occur in the treatment of TS with the same drugs
(Sandor, 1995), and in general it is not unusual for the symptoms of
a different disinhibition disorder to develop during medication of the
current disinhibition disorder (such as tics appearing during the treatment
of ADHD or OCD increasing in the treatment of TS - Greenhill, 1989).
Attentional and distraction problems are also cited as being associated
with Schizophrenia - either as a focal symptom (McGhie & Chapman
in Buss & Buss, 1969) or as associated ones (APA, 1994). Early Behaviourists
suggested that the loose associations in Schizophrenia are actually
a learned response to avoid anxiety (Mednick in Buss & Buss, 1969)
- in effect, a severe attention deficit is self-trained to the extent
that the individual becomes schizophrenic. Fully remitted schizophrenics
describe intense obsessions and intrusive thoughtsthat literally never
stop for 24 hours a day (Modrow, 1995), and research shows that the
symptoms of OCD and schizophrenia do co-occur (Bellack & Hersen,
1993). The presence of OCD and psychotic-like symptoms oftentimes indicate
the presence of a schizotypal personality style (Bellack & Hersen,
1993), which is considered by some to be the precursor to Schizophrenia
(Meehl in Buss & Buss, 1969) and used to be the Simple subtype of
Schizophrenia (Davison & Neale, 1994).
With regards to
physiology, there are many similarities between Schizophrenia and disinhibition
disorders as well. Enlarged ventricles are typical of process schizophrenics
(Frith, 1992) movement disorders (Owens et. al., 1985, in Frith, 1992),
and Obsessive-Compulsive Disorder (Bellack & Hersen, 1993). The
striatum (a component of the basal ganglia) is implicated in Schizophrenia
(Frith, 1995), TS (Comings, 1990), and OCD (Bellack & Hersen, 1993).
Frontal lobe dysfunction in recent years has become an area of research
in Schizophrenia (Bornstein, 1991). The frontal lobes are involved in
judgment, rationality, and critical thinking, and it has been discovered
that in Schizophrenia the left frontal cortex shows much less metabolism
during activity (Frith, 1995). Left frontal underactivity has also been
identified in OCD (Bellack & Hersen, 1993), and TS (Doran, 1996);
frontal "brown-out" is also a hallmark of ADHD (Doran 1996;
Kronenberger & Meyer 1996). Abnormal catecholamine levels are involved
with ADHD, OCD, TS, and Schizophrenia (Comings, 1990, APA, 1994) and
dopamine specifically is discussed in Schizophrenia (Frith, 1992) and
TS (Comings, 1990). In sum, it seems that problems with the connections
and communications between the striatum (which is influenced by dopamine
levels, and is involved in the willing and execution of movement) and
the prefrontal cortex (the "goal-centers") cause the symptoms
of Schizophrenia (Frith, 1992) including the obsessional components
and perseverances also seen in TS.
The prognoses of
Schizophrenia, TS, ADHD, and OCD parallel one another - all can be chronic,
lifelong conditions, or can completely remit. It is only in the past
few years that ADHD in adulthood has reached wide acknowledgment (Kronenberger
& Meyer, 1996), and a portion of the TS population does remit in
their early 20's (Comings, 1990). As the fundamental problem with being
overly disinhibited is a high level of stimulation, environmental stressors
have a significant impact on the course of disinhibition disorders.
Likewise, meta-analyses have shown that disturbed and distressing parental
interactions can trigger and influence the expression of Schizophrenia
(Goldstein & Strachen in Vinogradov, 1995). The negativism and immobility
in catatonic schizophrenia that suddenly erupts into violent outbursts
(Davison & Neale, 1994) is reminiscent of ADHD and Tourettic rage
when stimulation thresholds are reached (Pruitt, 1996).
Despite all of
the overlap between various disinhibition disorders, and between Schizophrenia
and disinhibition disorders, there are still obvious differences. Schizophrenia
is much more severe than TS, ADHD and OCD. Onset of schizophrenia tends
to be much later - early 20's for men to early 30's for women (Jablensky,
1992) versus four for ADHD (Kronenberger & Meyer, 1996), seven for
TS (Comings, 1990), and late adolescence for OCD (Bellack & Hersen,
How then do we
conceptualize the overlap of these various conditions? Just as the various
and diverse forms of Schizophrenia are believed to be bound by the fundamental
and primary feature of loosening of associations (Bleuler, in Arieti,
1955), all of these conditions are different manifestations of the common
process of disinhibition. TS can be conceptualized as a motoric disinhibition,
ADHD as a disinhibition of the focusing of attention, and OCD as a disinhibition
of specific concerns, wishes, and/or cognitions. Schizophrenia, then,
is a disinhibition of thinking in a generalized sense - rather than
experiencing a specific enervation or stimulation in a localized area
of the brain (a motoric centre, or particular ruminations) causing repetition
and attendance to a particular ritual or thought, a more generalized
overstimulation occurs. The result is that ALL cognitions are in a state
of arousal. While in this heightened state, it would take little additional
stimulation for each association to reach threshold for awareness, and
odd associations between unrelated cognitions would be forged due simply
to the fact that both are simultaneously aroused (Hebb, 1949). Thus
the individual's attention would bound from association to association,
no matter how tangentially related; while a normally inhibited individual
can remain coherent and "on-track" because the next logical
associative thought is stimulated to a greater degree than distantly
related associations, this differential is lost in individuals with
imagine walking a dog through a cat-show on a leash. The dog very much
wants to "associate" with ALL of these various felines, however
it will remain to "associate" with it's master, as the leash's
strength is stronger than the allure of the cats. Thus the dog will
continue on a progressive and planned course throughout the cat-show
with its master. What if suddenly the leash is cut (i.e., the differential
strengths of associations is eliminated)? Of course the dog will tear
off hysterically after the first cat it sees, and if another, closer
cat catches it's attention it will abruptly shift course and aim for
the new target, until another grabs it's eye, and another, and another.
Obviously the result is chaos.
(1992) postulated a model of Schizophrenia in which symptoms are the
result of a failure to self-monitor. Positive symptoms (i.e. hallucinations
and delusions) occur when a willed action is carried out by the basal
ganglia, but the latter fails to send a feedback message to the perceptual
center. In other words, an individual will "self-talk" or
initiate a movement but will not be AWARE that (s)he is/did. Hallucinations
are the interpretations of "self-talk" in the absence of self-awareness,
and delusions (such as delusions of control) are the interpretations
of movements without the knowledge that (s)he planned them (Frith, 1992).
Negative symptoms are considered to be even heavier damage to communications
between the cortex, basal ganglia, and the perceptual centers - wills
are no longer able to generate intentions to act at all.
This theory requires
only slight modification to fit the disinhibition model. Positive symptoms
will be addressed first. Assuming that the basal ganglia is designed
to deliver a "normal" number of feedback messages to the perceptual
system, in a state of generalized disinhibition (overstimulation), it
may be that the system either "shorts out", or continues to
work but "misses" some messages. These "missed"
messages are then the ones attributed as hallucinations and delusions.
Frisk (1992) also suggested that positive symptoms could be the result
of stimulus-driven actions (afforded actions) that are not inhibited
by one's goals (communication problems between the prefrontal cortex
and the striatum). This is more or less synonymous with the definition
With regards to
negative symptoms, under a state of extreme stimulation one is less
likely to initiate actions at all - despite a will to involve oneself
in life in various ways, overstimulation deters one from developing
an intention. Recall Hans Eysenck's theory on introversion-extroversion:
introverts do not need to seek sensation (or initiate actions) to the
same degree as do extroverts, as their internal stimulation is already
high (Day, 1992). Individuals with disinhibition disorders (ex. TS)
sometimes will avoid social contact in an attempt to minimize stimulation
(1992) theories of schizophrenia so that they are framed within the
context of disinhibition helps to explain certain facts that were inconsistent
with Frith's original conceptions. First, there is considerable research
that suggests that even the most severely debilitated of schizophrenics
can recover - some undergo complete remission (Modrow, 1995). If there
were actual structural lesions in schizophrenia this would not be possible
(although it is certainly possible that after years of overstimulation
certain irreversible structural damages could occur, thus rendering
the condition permanent). There have also been reports of professionals
being treated after-hours for schizophrenia, and incidents where seemingly
completely debilitated schizophrenics have somehow "suppressed"
their symptoms long enough to operate normally for some time before
returning to their debilitated state (Modrow, 1995). Hyperfocusing in
ADHD (Doran, 1996) and temporary suppression of tics in TS (Comings,
1990) are well-documented and analogous phenomena.
Second, if there
were actual mechanical problems with the relay of messages why do dopamine-blocking
drugs completely eliminate hallucinations and delusions? Frith (1992)
suggested that dopamine-blockers operate indirectly; by tranquilizing
the individual globally, one reduces the number of movements that could
be misattributed to hallucinations and delusions because one reduces
the overall number of movements. With a structural-problem hypothesis,
one would REDUCE hallucinations and delusions, but as long as the individual
made ANY movement hallucinations and delusions would still exist. Within
the disinhibition model, however, this inconsistency is eliminated -
by reducing the amount of stimulation, and hence number of messages,
impinging on the basal ganglia to "normal" levels, the system
is no longer overtaxed, it resumes "normal" activity, and
no messages are "missed" (and misattributed) anymore.
Finally, it is
difficult to explain how stimulants can mimic Schizophrenia if structural
problems are definitive of the disorder (as in Amphetamine Psychosis
- APA, 1994), but it makes perfect sense within a disinhibition model
- in "natural" schizophrenics, overstimulation is caused by
disinhibition. In "amphetamine" schizophrenics the overstimulation
is artificial. Regardless of the locus of the overstimulation, the effects
are the same.
In sum, Frith's
(1992) theory that schizophrenic symptoms are caused by a problem in
self-monitoring seems valid. It is interesting to note that one popular
method of treating individuals with TS is to explicitly teach self-monitoring
strategies (Kronenberger & Meyer, 1996). Frith's reasons for the
self-monitoring problems were questioned, however; the hypothesis that
self-monitoring difficulties are the result of overstimulation due to
disinhibition seems to fit the known facts better than the hypothesis
that there is actual structural damage to the brain (Frith, 1992).
IS to be considered as a disinhibition disorder, it is obviously the
most debilitating and severe of them all. While the predominant feature
of Schizophrenia has been outlined to be the disinhibition of general
thought associations, it seems to have characteristics of many other
disinhibition disorders such as ADHD, TS, and OCD (as described earlier).
The idea that genes could work additively was previously mentioned -
it may be that, just as TS is considered by some to be "ADHD +
tics" (Doran, 1996), Schizophrenia is "ADHD, OCD, TS, etc.
+ thought disinhibitions". Genetic heterogeneity (Bellack &
Hersen, 1993) is the current genetic theory of Schizophrenia - it suggests
that while there is an additive genetic component to Schizophrenia,
there are one or two dominant Schizophrenia genes which are necessary
and sufficient for the disorder (Bellack & Hersen, 1993). Perhaps
there does exist a particular gene that causes the disinhibition of
thought, and these "additive genes" are other disinhibition,
or Gts, genes. It does not seem unreasonable to suspect that many genes
exist whose functions involve a wide range of disinhibitory functions
- disinhibition in general is essential to survival in order to manipulate
the environment, and certain disinhibitions (for example, sexual) have
been postulated to have particular adaptive advantage (Comings, 1990).
Considering that the human cortex has evolved to be inhibitory, the
need for SOMETHING to cause disinhibition is of course essential.
having developed dimensions of disinhibition, the next theoretical step
in such a discussion seems to be to discuss spectrums of disinhibition.
Are all of these different disinhibition disorders, including Schizophrenia,
merely different manifestations of the same amount of overstimulation,
or are some disorders characterized by more disinhibition than others?
One might tentatively postulate a spectrum such as:
-- Introvert -- ADHD -- TS/OCD -- Reactive Sx -- Process Sx
would seem to apply not only to degree of internal disinhibition, but
also to age of onset [Infants as young as 22 months can be categorized
by temperament (Plomin & Rowe 1979 in Day, 1992)], and prognosis.
the evidence supporting the consideration of Schizophrenia as a disinhibition
disorder seems persuasive and plentiful. Current neurophysiological
models of Schizophrenia can be modified to reflect overstimulation of
thought associations as the fundamental cause of both positive and negative
symptoms; in this altered form these models can account for more findings
in the literature than they could without incorporating the idea of
disinhibition. Schizophrenia may fit on a spectrum of disinhibition,
in which it is the accumulation of an assortment of other disinhibition
disorders and, thus, the most severe of all subtypes.
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