INDIAN PSYCHOSOCIAL FOUNDATION
 
   INDIAN PSYCHOSOCIAL FOUNDATION
         
IJPS >
IJPS April 2011
IJPS October 2011
IJPS April 2012
IJPS October 2012
IJPS April 2013
IJPS October 2013
IJPS Apirl 2014
IJPS October 2014
IJPS Apirl 2015
IJPS Apirl 2016
IJPS October 2016
IJPS Apirl 2017
 
 
 
SCHIZOPHRENIA CO-MORBID WITH OCD

SCHIZOPHRENIA CO-MORBID WITH OCD, ADHD: CASE REPORT

 Madhao Raje

Consutant Psychiatrist & Psychotherapist Nagpur, India.

 

Abstract

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, ADHD, OCD

 

 

Introduction

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.

Clinical picture & 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.

Case report

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.  

On clinical 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.

Table 1 Showing Neurotrophic scale assessment.

Scale

Before treatment

After treatment  (9 months)

Adult ADHD

87  significant

13  insignificant

Y-BOCS

39  extreme ocd

14  mild ocd

PANSS

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.

Discussion

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

Psychotic symptoms 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.

Psychotherapeutic 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.

Release of 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 Antipsychotic (AAP).

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 recovery.

Take home message

1.       It is essential to search OCS/OCD while diagnosing Schizophrenia.

2.       ADHD needs to be ruled out while diagnosing Schizophrenia co morbid with     OCD.

3.       Use of Clonidine should be explored as adjunctive medication while treating schizophrenia with co morbid conditions.

 

References

1.       Alexandra Bottas, MD, Psychiatric Times. April 15, 2009, Vol. 26, 4.

2.       Peter F. Bukley, Brian J. Miller, Douglas S. Leher, et al. Schizophrenia Bulletin, 2009, Vol. 35, 2,383-402. 

3.       Paul H Lysaker, & Kriscinda A Whitney, Obsessive –Compulsive symptoms in schizophrenia: prevalence, correlates & treatment, Expert Rev. Neurother, 2009, 9(1):99-107.

4.       David R. Rosenberg, Shauna N. MacMillan, and chapter 113, Imaging & Neurocircuitry of OCD: Neuropsychopharmacology: Fifth Generation of Progress.

5.       Ann M. Graybiel & Scott L. Rauch, Toward a Neurobiology of Obsessive-compulsive Disorder, Neuron, November 2000, vol.28: 343-347.

6.       Elias Tsakanikos, Phil Reed, J Behav. Ther. & Exp. Psychiat. 36(2005), 300-312.

7.       The Neurobiology of ADHD, ADHD.org.nz, PO Box 249, Tauranga, New Zealand.

8.       Ganesan Venkatsubramanian, Naren P. Rao, Rishikesh V. Behere, Neuroanatomical, Neurochemical, & neurodevelopmental basis of OCS in Schizophrenia. Indian J Pschol Med. 2009 Jan-Jun; 31(1):3-10.

9.       http//wiki.medpedia.com/clinical:Schizophrenia_With_Obsessive-compusive Disorder-Medpedia.

10.   Niedermeyer E., Naidu S B, ADHD & frontal-motor cortex disconnection, Clin Electroencephalogr 1997 Jul; 28 (3), 130-6.

11.   Hirao K., Miyata J, Fujiwara H, et al, Theory of Mind & frontal lobe pathology in Schizophrenia: a Voxel based Morphometric study, Schizophr. Res. 2008 Oct, 105 (1-3); 165-74. 

12.   Julia W. Tossell, Deanna K. Greenstein, Anna L. Davidson, et al, Stimulant drug treatment in chidhood onset Schizophrenia with co morbid ADHD,                         Journal of Child and Adolescent Psychopharmacology. Fall 2004, 14(3): 448-454.

13.   Freedman R, Kirch D, Bell J, et al, Clonidine treatment of Schizophrenia. Acta Psychiatr Scand. 1982 Jan; 65 (1):35-45.

14.   Oranje B, Glenthoj BY, Clonidine normalizes sensorimotor gating deficit in patients with Schizophrenia on stable medication,  Schizophr Bull. 2012 Aug 27.