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Published Online: 1 May 2011

Response to De Nadai Letter

To the Editor: We appreciate the opportunity to respond and comment on this fascinating case, in which the presentation of obsessive-compulsive symptoms immediately followed the incidence and treatment of a pineal gland germinoma in an adolescent young man. In our case, the patient began to exhibit psychotic symptoms (e.g., olfactory and auditory hallucinations, belief in mind reading) and obsessive-compulsive symptoms (e.g., making idiosyncratic hand gestures, exhibiting a preoccupation with checking the time, and insisting that the bed covers be folded a certain way) during the development of a pineal tumor, but the precise etiology was obfuscated by a variety of factors, including a basal ganglia stroke. While the psychotic symptoms remitted after successful treatment of the tumor with chemotherapy, the obsessive-compulsive symptoms persisted. This is consistent with the case report of “Jonathan,” reported by Mr. De Nadai and colleagues, for whom the onset of obsessive-compulsive symptoms began abruptly after the successful treatment of a pineal germinoma. In contrast to our case, however, Jonathan had no known basal ganglia involvement. These findings further implicate pineal body dysfunction in the pathophysiology of obsessive-compulsive disorder (OCD).
As noted in our report, through the production of melatonin and subsequent modulation of sex hormones, the pineal gland is a key structure involved in sexual development and regulation of the onset of puberty (1). It is notable that both cases involve adolescent young men. Although it is not clear whether pineal involvement in OCD and psychosis has the same pathophysiologic significance, disruption of the pineal body during this developmental stage may lead to common behavioral manifestations in the two cases described. The average age at onset for both OCD and psychotic illness is earlier for men, and the emergence of symptoms in both disorders often closely follows the transition to puberty. Furthermore, both disorders are marked by significant disruption in circadian rhythm and sleep (2), suggesting abnormalities in melatonin regulation. Finally, in addition to the synergistic effects with serotonin noted by De Nadai et al., there is also evidence that melatonin may have antioxidant and neuroprotective effects (3). Disruption of the pineal body may thus have lasting effects in the developing brain, and understanding these relationships may shed light on how hormonal changes are related to the onset of idiopathic psychosis or OCD.
Continued work aimed at determining how a pineal tumor may be etiologically related to both psychotic and obsessive-compulsive symptoms may increase our understanding of factors underlying the complex relationship between these two disorders. Indeed, pineal abnormalities and melatonin continue to be routinely implicated in psychotic illness as well (4). As both OCD and attenuated psychotic symptoms are highly comorbid in the schizophrenia prodrome (5), longitudinal studies of youths at high risk for both disorders are necessary to further develop our understanding of possible common etiologic mechanisms.

Footnote

Accepted for publication in March 2011.

References

1.
Canallo A: Melatonin and human puberty: current perspectives. J Pin Res 1993; 15:115–121
2.
Szelenberger W, Soldatos C: Sleep disorders in psychiatric practice. World Psychiatry 2005; 4:186–190
3.
Srinivasan V, Pandi-Perumal SR, Maestroni GJM, Esquifino AI, Hardeland R, Cardinali DP: Role of melatonin in neurodegenerative diseases. Neurotox Res 2005; 7:293–318
4.
Pacchierotti C, Iapichino S, Bossini L, Pieraccini F, Castrogiovanni P: Melatonin in psychiatric disorders: a review on the melatonin involvement in psychiatry. Front Neuroendocrinol 2001; 22:18–32
5.
Niendam T, Berzak J, Cannon T, Bearden C: Obsessive compulsive symptoms in the psychosis prodrome: correlates of clinical and functional outcome. Schizophr Res 2007; 108:170–175

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Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 550 - 551
PubMed: 21536703

History

Accepted: March 2011
Published online: 1 May 2011
Published in print: May 2011

Authors

Affiliations

Vijay A. Mittal, Ph.D.
Tyrone D. Cannon, Ph.D.
Carrie E. Bearden, Ph.D.

Funding Information

The authors' disclosures accompany the original article.

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