SCHIZOPHRENIA CO-MORBID WITH OCD
SCHIZOPHRENIA CO-MORBID WITH OCD, ADHD: CASE REPORT
Psychiatrist & Psychotherapist Nagpur, India.
Introduction: 10-50% patients of Schizophrenia reveal
OCD Symptoms (OCS). COD & ADHD is routinely observed. But all 295, OCD, and
ADHD together is not commonly seen. Co morbid conditions usually delays
recovery. But it is interesting to note that ADHD in this case is probably
preventing cognitive deterioration.
Case report: A 30 year old govt-employee presented
with muttering-self, gesturing, auditory hallucination, delusions, lack of
concentration, fidgety, repeatedly washing hands. On the base of Psychometric
scales like PANSS, Y-BOCS, and Adult ADHD & Psychiatric clinical interview
patient was diagnosed with all inclusive co morbidities. He was treated with
Oleanzapine, Fluoxetine, Amitryptilline, & Clonidine successfully.
Discussion: Patient showed dramatic recovery within
one month. His insight is prominently noticed. His sincerity, regularity,
motivation to take over the symptoms is clearly noticed. Such
self-awareness/motivation is not seen among patients of schizophrenia (Poyurovsky M,
et al ).
This picture/ recovery compel to ponder if ADHD & OCD helps
schizo-pathology recover/facilitate remission? Deterioration of functioning of
Orbito-frontal-lobe seen among schizophrenics is inhibited as a result of
pathological over activity of ADHD (Clin Electroencephalogr. 1997 Jul;
28(3):130-6). OCS help gain insight among schizophrenics (J Nerv Ment Dis. 2007 Sep;
195(9):765-8). Thus remission or recovery takes place with minimum dose of above
mentioned medicines because neuropathology of these conditions counteract with
each other. E.g. Motor inactivity in 295 is due to ‘sick frontal lobe’ which
was counter balanced by ‘lazy frontal lobe’ of ADHD neuropathology. So this is
blessings in disguise, ADHD & OCD helping Schizophrenia recover.
Key Words: Schizophrenia,
Co morbidity is not
uncommon, but co morbidity of Schizophrenia to gather with OCD & ADHD is
not commonly reported. This may be because diagnosis of OCD along with
Schizophrenia was not universally accepted. Till today there is no universally
accepted method of diagnosing Schizophrenia & OCD to gather1.
Though, around 10
to 50% of Schizophrenic patients do reveal o c symptoms (OCS). However,
recently a few researchers have used structured clinical interview & Y-BOCS
to diagnose OCD among Schizophrenic patients1. But, this method is
yet to be uniformly implemented. Though, it is reported around 8 to 26 % of
schizophrenic patients do suffer from OCD1.
Common co morbid of
Schizophrenia are substance abuse & depression (40 – 50%)2.
Anxiety symptoms are also commonly encountered. Estimated prevalence of OCD co
morbid with Schizophrenia is around 30%. Some of the researchers proposed that
co morbidity might be distinct ‘phenotype’ of schizophrenia2.
Similarly, ADHD is also common co morbid of OCD. ADHD patients are vulnerable
to have Bipolar disorders or mania co morbid (Di Tommaso MC, 2012). However,
ADHD & Schizophrenia are not common co morbid conditions. Depression,
Phobia, Panic Disorder, Body Dysmorphic disease (BDD), Hypochondrias is, etc.
is common co morbid conditions observed in OCD. Bipolar Disorder co morbid with
OCD is also seldom reported. However, Schizophrenia co morbid with COD &
ADHD to gather is not commonly reported. Though, there is substantial dearth of
published research about existence of co morbidity9.
& response to treatment is unique in this case. It is unique because
usually co morbid conditions deteriorate illness or delays remission2.
But this patient neither deteriorated extensively & nor responded with
delay. So it is reported with proposed hypothecation about clinical,
neuropathological & treatment relevance.
A 30 year old
unmarried Hindu male, govt. employee from middle socioeconomic status,
graduate, with F/h/o psychiatric illness approached along with his friend. He
complained of severely distressing rumination, muttering with self, gesturing,
not mixing with others at office & at home, Insomnia, etc. He used to hear
voices (Auditory hallucination), delusion (people are making mockery of him).
As a result of these symptoms, he used feel dejected, guilty, and sad. He was
well aware of involuntary movement of his lips & gesturing, and he
expressed his inability and desperation to control it. Duration of all these
symptoms was 3 to 4 years. Despite his symptoms he continued his duty regularly
& had insight to seek treatment. His p/h/s/o childhood ADHD. It remained
untreated. His personal history was devoid of substance abuse.
examination he appeared slightly untidy, dirty & tired. His mood was sad
& he looked distressed. He was repeatedly urging me to help him come out of
this distressing situation. Clinical impression was kept Schizophrenia with OCD
with adult ADHD. His adult ADHD & PANSS scale confirmed the diagnosis. See
Table 1 Showing
Neurotrophic scale assessment.
After treatment (9 months)
39 extreme ocd
14 mild ocd
P – 31
N - 26
G – 61
P – 1
N – 16
G – 15
He talked about his
delusions, hallucination & wanted all that to stop. He was given brief
client oriented Psychotherapy, which included Psycho education, reassurance,
& motivation. He reported 95% relief in first follow up, except his ADHD
symptoms. After 4 to 5 months he reported near complete recovery.
He was treated with
Oleanzapine 5 mg, Fluoxetin 20 mg, Clonidine 100umg, & Amitrptyline 50 mg
once a day.
The sincerity and
motivation to overcome symptoms is clearly noticed in this patient. Such self
awareness, motivation is not common in schizophrenia3. This clinical
picture & recovery compels to ponder on ‘beneficial inter-play’ within the
co morbid conditions. Treatment implication of such co morbidity is presently
poorly understood & appreciated2, so discussion of clinical
implications becomes pertinent.
Clinical Implications of co morbidity Slowing of
functioning of frontal lobe in schizophrenia is counteracted by deficit in
response inhibition ability, core deficit of OCD4,10 . Functional
theory of OCD Circuit explains that increased excitatory output from PFC
induces increased caudate N. activity which causes inhibition of Thalamus.
Inhibited Thalamus facilitates loss of control over PFC, which as a result
fires excessively. Thus hyperactivity of ADHD takes place due to loss of cortical
inhibition from Thalamus8.
OCS does not help
improve insight if present with schizophrenia10. Higher the OCS
worsens the general quality of life. OCS causes deficit in neuro cognition in
schizophrenia3. But, ‘lazy frontal lobe’ of ADHD and ‘Sick frontal lobe’
of schizophrenia to gather attenuates the over activity of ‘OCD circuit’ and
thus general quality of life & cognition in this case were not hampered.
Thus it is proposed that early remission/recovery took place with treatment
because neuropathology of these conditions counteracted with each other. E.g.
Motor inactivity in schizophrenia is due to ‘sick frontal lobe’ which was
counter balanced by excessive hyperactivity of OCD Circuit3.
of schizophrenia are reported to cause anxiety disorders like OCD, PTSD, and
Phobia. Many surveys have reported ocs as part of psychosis prodrome. Peak of
depression coincides with peak of psychosis2. So as a consequence,
treatment of schizophrenia may remit ocs2. Hence it is
inferred that clonidine in this case has worked to antagonize psychosis of
schizophrenia, de-accentuate impulse driven hyperactivity of ADHD & down
regulate the abnormal activity seen in OCD circuit5.
Symptom correlates Symptom-overlap is conspicuous in
this case. Delusions of schizophrenia & obsess ional delusions of OCD or
Psychosis prodrome overlap2 is difficult to differentiate. So unless
OCS is treated with SSRI schizophrenia with co morbid don’t recover adequately.
Depression co morbid with OCD or depression caused by OCD or post psychotic
depression of schizophrenia or anti-psychotic induced depression or depression
co morbid with schizophrenia overlap9 and need to be taken care of
by clinician. Co morbidity of two diseases usually causes severe impairment.
However, any unique pattern of impairment hasn’t yet been identified. In the
present case there are three diseases interacting with each other, probably in
a peculiar way (Hypothesis) to alleviate symptoms.
In such cases, it
is observed by many clinicians that Psychotherapeutic intervention always
facilitates recovery3. In this case, depression was co morbid with
OCD. Hence, Psychotherapeutic intervention was sought since beginning. Second
reason was also unrelenting demand from patient; compelled author to begin
psychotherapeutic intervention since very first consultation. It is uncommon to
experience a schizo-psychotic patient demanding to know reason/s behind his
uncontrollable odd behavior like smiling with self, awkward gesturing in public
despite his broad day light consciousness. Hence PEP was offered since first
contact. He was told in brief about ‘dis-inhibitory effect of Thalamus’ on PFC.
Functioning of Cortico-striatal-thalamo-cortical pathways was appraised. He was
informed that by any chance he is not at all responsible for his odd behavior,
but it is organic defect which has cropped up; is making his life miserable. He
was reassured. He realized & comprehended positively.
intervention would involve Psycho-education (PEP), Motivational interview (MI),
client centered Psychotherapy emphasizing ‘theory of acceptance’, CBT, family
therapy (especially systemic family therapy, which illustrates ‘circular’
impact of family interaction), REBT, etc. would be available options to
clinicians. ‘Client centered psychotherapy’ clubbed with theory of acceptance
proved vital in negotiating depression & guilt in the present case.
Psychotherapy worked well because shift learning, poor motivation, generalized
deficit in functioning, response inhibition, which comprises cognitive domain6
part of symptomatology in schizophrenia was remarkably negligible in this
patient, may be as result of ADHD pathology.
Neuropathology correlates Regions of brain
pathology overlap in these co morbid conditions. But paradox in functioning is
interestingly intricate. Cortical reduction of ventrolateral prefrontal lobe
(VLPFC) is seen in schizophrenia11.
Prefrontal-thalamic-cerebellar-prefrontal pathway dysfunction causes symptoms
of schizophrenia. Common areas involved in ADHD are prefrontal cortex (PFC),
Basal Ganglia & cerebellum. Cortico-straital-thalamic circuit dysfunction
& abnormal neurochemistry form the basis of OCD neuropathology. Basal
Ganglia, seat of OCD pathology shows hyper function in OCD patients (OCD Circuit)
while patients of ADHD exhibit (on PET scan) decreased functional activity in
basal ganglia7. Cortical slowing is seen in schizophrenia while more
activity is noticed in motor areas of cortex (Schweitzer) accounting for
fidgeting of ADHD7. Such observations may suggest hypothecation that
ADHD to gather with Schizophrenia is counter balanced by neuro-pathology of OCD
or Schizophrnia pathology gets paradoxical effect by ADHD pathology8.
Similar hypothecation is also proposed by Carlsson about paradoxical
coexistence of OCD & ADHD.
Neurotransmitter initiates Neurotransmission. It depends on frequency of axon
firing. Firing frequency changes as per neurochemical events. It depends on
feed-back & feed-forward neural circuit. This circuit revolves around activity
of pre-synaptic receptors & on release of neurotransmitter in post synaptic
extra-cellular space. Extent of neurotransmission also depends on density of
reuptake sites of receptors, sensitivity of receptors & concentration of
transporters which alter as a result of neuropathology of disease3.
For example: in Adult ADHD, dopamine transporters are elevated in Rh. caudate
nucleus which hastens the removal of extracellular dopamine from nerve
terminals. Less amount of dopamine at nerve terminals induces impulse-triggered
release of dopamine which causes impulsive hyperactive behavior of ADHD. It is
accepted now that striatal dopamine receptors (D2) are hyperactive & PFC
dopamine receptors (D1) are hypoactive while Glutamate transport is altered in
schizophrenia. Hyperactive D2 receptors are responsible for positive symptoms
of Schizophrenia. But decreased metabolic function in basal ganglia & Rh.
PFC is observed in patients of adult ADHD. On the basis of this observation
hypothecation is proposed that High D2 functioning of schizophrenia could have
been neutralized/normalized by decreased metabolic functioning of Basal Ganglia
& Rh. PFC implicated by ADHD. Similarly, low D1 functioning is compensated
by overactive PFC of ADHD to negotiate negative symptoms in this case. Adult
ADHD reveal elevated dopamine neurotransporters in right caudate nucleus, there
by depleting extracellular dopamine to cause impulse triggered release of
dopamine which causes hyperactive behavior3. While in Schizophrenia,
especially HighD2 patients show depleted Dopamine in post-synaptic
cleft/extra-cellular space due to increased transport of dopamine, which causes
negative symptoms. This paradox probably raises Hypothecation to explain
absence of negative symptoms or post psychotic depressive symptoms in this
patient, i.e. Dopamine neuropathology of ADHD might be counteracting on
dopamine neuropathology of Schizophrenia.
Treatment correlates Clonidine was
selected to treat ADHD instead of regular stimulants because administration of
psycho stimulants is controversial in psychotic patients12.
Clonidine was also found to facilitate recovery among patients of schizophrenia13.
Clonidine, α-2 Agonist, normalizes cognitive function in schizophrenia by
‘gating’ sensorimotor deficit14. So clonidine became my first choice
in this case because it was effective for schizophrenia, ADHD, depression &
impulsive behavior of OCD. Amitryptiline was selected to reinforce the effect
of clonidine. Amitryptilline would have been useful for ADHD, Depression &
also for schizophrenia. Similar views about use of TCA in schizophrenia were
also reported by Siris et al (1978) & Prusoff et al (1979) as ‘adjunctive
medication’ in schizophrenia. Hence, Amithryptiline was preferred to SSRI.
Though there are reports mentioning increased efficacy of SSRI when used along
with dopamine receptor agonist (McDougal’s et al, 1994), but in this case task
of treating ADHD was also daunting. So Amitryptiline was preferred against
clomipramine among TCA. Among SSRI, Fluoxetin was preferred to treat OCS
because patient demanded ‘no’ day time sedation due to his goal oriented work
schedule. Olanzepine was a natural & noncontroversial choice as an atypical
Conclusion On the basis of clinical symptoms &
response to treatment, hypothecation is proposed that ADHD when co morbid with
Schizophrenia and OCD not only retards progress of Schizophrenia but augments
Take home message
It is essential
to search OCS/OCD while diagnosing Schizophrenia.
ADHD needs to be
ruled out while diagnosing Schizophrenia co morbid with OCD.
Use of Clonidine should be explored as adjunctive medication
while treating schizophrenia with co morbid conditions.
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