WHAT WE NOW KNOW
most shrinks agree that cannabis smoking-->incr risk of psychosis esp schizophrenia
people with FHx of schizophrenia esp vulnerable to psychotomimetric effects of drug
at highest risk of developing schizo with cannabis use
there are no consistent reports of brain structural abn assoc c use by healthy population
this does NOT prove that potsmoking is safe without family schizo history
Dr. Welch and colleagues
compared structural changes in the thalamus and amygdala-hippocampal complex over time
n=57, ages 16-25yrs, well but with family hx of schizophrenia
duration: 2 years, MRIs before and after
no sig diff btw brains before, no sig diff on scores: Rust Inventory of Schizotypal Cognitions
at end: evaluation of drug, alcohol and tobacco use during time between MRIs
none had psychotic breaks, sounds like
25/57 had smoked pot and had reduction of thalamic volume
significant on left side of thalamus (F = 4.47; P = .04)
highly significant on right (F = 7.66; P = .008)
no loss of thalamic volume in non-pot smokers
results remained significant when controlled for other drug use incl: ecstasy, amphetamines
no significant diff between the groups re volumeric change in amygdala-hippocampal complex
(jives with subject impression: pot-influenced development doesn't impede attraction/aversion)
change due to abnormal brain development?
maybe so: THE THALAMI OF NONUSERS GREW. This effect was significant in the left thalamus, at a volumeric increase of 26.66 mm3 in nonusers and a decrease of 181.39 mm3 in users, and highly significant in the right thalamus, at an increase of 32.84 mm3 and a decrease of 264.48 mm3 in nonusers and users, respectively.
would adults have same thalamic loss?
does this create a lifelong pothead personality?
decrease in the volume of the thalamus assoc w psychosis and schizophrenia
thalamus has high level of cannabinoid receptors
why does the right side shrink more?
how does this affect people later in life?
what is the difference in the sides of the thalamus?
ANATOMY OF THALAMUS
between the cerebral cortex and midbrain
surrounds the third ventricle
sits on top of brain stem
largest structure derived from the embryonic diencephalon
diencephalon also incl: prethalamus, zona limitans intrathalamica, hypothalamus, epithalamus, pretectum, pineal gland
blood supply: posterior communicating artery, paramedian thalamic-subthalamic arteries, inferolateral (thalamogeniculate) arteries, posterior (medial & lateral) choroidal arteries
switchboard, relay station, center for deciding agreeableness/disagreeableness of experience
relays sensation, spatial sense, and motor signals to the cortex
has a nucleus for every sensory system except olfaction
regulates consciousness, sleep, and alertness
close connection to basal ganglia
THALAMUS IS PART OF LIMBIC SYSTEM
limbic: hippocampus, amygdala, anterior thalamic nuclei, septum, limbic cortex & fornix
anterior thalamic nuclei receive afferents from the mammillary bodies and subiculum
project to the cingulate gyrus
involved in learning and memory
thought to play a role in alertness
Korsakoff's syndrome (B1 def more in alcoholics) = damage to mamillary body (part of thalamus)
Fatal familial insomnia = inherited prion dz that shrinks thalamus
thalamotomy (destrx of contralateral side from worst tremor) for Parkinson's
thalamic stimulator for tremor tx approved by FDA in 1997
tranquilizers and opiates depress thalamus, block unpleasant sensation trans to cortex
ABSTRACT OF NEW STUDY
Impact of cannabis use on thalamic volume in people at familial high risk of schizophrenia
Killian A. Welch, MD, MRCPsych, et al.
No longitudinal study has yet examined the association between substance use and brain volume changes in a population at high risk of schizophrenia.
To examine the effects of cannabis on longitudinal thalamus and amygdala-hippocampal complex volumes within a population at high risk of schizophrenia.
Magnetic resonance imaging scans were obtained from individuals at high genetic risk of schizophrenia at the point of entry to the Edinburgh High-Risk Study (EHRS) and approximately 2 years later. Differential thalamic and amygdala-hippocampal complex volume change in high-risk individuals exposed (n = 25) and not exposed (n = 32) to cannabis in the intervening period was investigated using repeated-measures analysis of variance.
Cannabis exposure was associated with bilateral thalamic volume loss. This effect was significant on the left (F = 4.47, P = 0.04) and highly significant on the right (F= 7.66, P= 0.008). These results remained significant when individuals using other illicit drugs were removed from the analysis.
These are the first longitudinal data to demonstrate an association between thalamic volume loss and exposure to cannabis in currently unaffected people at familial high risk of developing schizophrenia. This observation may be important in understanding the link between cannabis exposure and the subsequent development of schizophrenia.