SYMPOSIA

Abstracts of the Invited Speakers
• Pain symptoms occur in 1/5 – 1/3 of patients with depression. These ratios are approximately 4 times higher than the ratios of those
with no depression. The ratios in the literature about pain symptoms in patients with depression are approximately 65% on average (3).
• Chronic pain is a significant individual risk factor for suicide and self-injury.
• Chronic pain results in increases in treatment costs and a poorer outcome.
• The presence of pain as a residual symptom is the strongest predictor of recurrence.
It should be kept in mind that chronic pain, which is considered as being ‘functional’ in terms of the mechanisms involved in having pain
during depression, is medically unexpected, self-generated and associated with vulnerability to pain. Therefore, central factors should
play a leading role in experiencing it (4). Living with pain causes negative emotions, but beyond that, continuous pain is a physical
symptom of depression. A neurobiological explanation of experiencing these two situations concurrently is not all that difficult when the
broadness and diversity of the mechanisms involved in experiencing depression are taken into consideration (5).
The mechanisms involved in this co-occurrence may be summarized as follows:
• The connection between the emotional and somatic (e.g. pain) symptoms of depression is probably set up through the HPA axis. This
system plays an important function in vulnerability to stress.
• The changes that emerge in the transfer of NA and 5HT in the CNS are of critical significance in terms of both depression and chronic
pain pathophysiology (6). Monoamines regulate both mood symptoms and sensations of pain.
• Pain stimuli are carried from the periphery to the CNS by primary afferent fibers and are regulated by stimulating glutamate and
suppressor GABA.
• The sub-cortical areas involved are the hypothalamus, periaqueductal gray matter, raphe dorsalis and locus coeruleus. These areas are
also regulated by 5HT and NA.
• Cortical processing of a pain sensation is carried out in the relevant areas of the cortex.
In conclusion, it is obvious that common pathophysiological processes underlie the co-occurrence of depression and somatic pain
symptoms seen in this picture and it is important to take such pain symptoms into consideration in a comprehensive treatment approach.
Key words: Pain, depression, clinical characteristics
References:
1. Peveler R, Katona C, Wessley S, Dowrick C: Painfull symptoms in depression: under-recognized and under treatment. British J Psychiatry 2006;188:202-203.
2. Von Knorring L, Ekselius L: Idiopatic pain and depression. Quality of Life Research 1994;3:557-568.
3. Bair MJ, Robinson RL, Katon W, Kroenke K: Depression and pain comorbidity. A literatüre rewiev. Arch Gen Psychiatry 2003;163:2433-2445.
4. Mohr P, Bitter I, Svestka J, Seifritz E, Karamustafalıoğlu O, Koponen H, Sartorius N: Management of depression in the presence of pain symptoms. Psychiatria
Danubina 2010;22:4-13.
5. Nemeroff CB, Vale WW: The neurobiology of depression: inroads to treatment and new drug discovery. J Clin Psychiatry 2005;66 (suppl. 7):5-13.
6. Wise TN, Fishbain DA, Holder-Perkins V: Painfull physical symptoms in depression: a clinical challenge. Pain Med 2007;8 (suppl. 2):75-82.
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S81-2
[PS-16]
Symposium Title: Marijuana; from mellow to madness
Effect of cannabis use on cognitive functions
Cüneyt Evren
Bakirköy Training and Research Hospital for Psychiatry, Neurology, and Neurosurgery AMATEM, İstanbul, Turkey
E-mail: cuneytevren@yahoo.com
If we look at the data of recent years, probation admissions to AMATEM Istanbul, which are mostly related to cannabis use, have increased
significantly; the number of first admissions/number of control admissions for 2008, 2009 and 2010 are 2318/24261, 3759/31862 and
5639/30959, respectively. As for other psychoactive substances, the negative effects of cannabis use on cognitive functions are well
known. Some cannabis-related cognitive function deficits improve after cessation of cannabis use, but growing evidence also suggests
that other deficits persist after cannabis is discontinued and may hinder an individual’s ability to make the best use of behavioral
therapies, putting him or her at greater risk for relapse of cannabis use (1).
Cannabis seems to continue to exert impairing effects in executive functions even after 3 weeks of abstinence and beyond. Although
basic attentional and working memory abilities are largely restored, most enduring and detectable deficits are seen in decision-making,
S82 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org