Cannabis and Brain Damage: EEG Evidence

Repost from the old site.
The original post in its native form was far too long, so I have decided to break it up into seven different posts, in addition to this post. The separate sections are listed below.
The original post, what is left of it, is here.
For an examination of the evidence of whether or not cannabis causes actual structural damage to brain cells, axons or dendrites, see here.
For an analysis of neuropsychological batteries of cannabis users to determine whether or not they suffer brain damage, see here.
For an analysis of studies looking at cerebral blood flow in cannabis users, see here.
For an admittedly impressionistic analysis of whether or not cannabis causes schizotypal symptoms in users, see here.
For a summary comparing the effects of cannabis on the brain compared to other drugs, see here.
For a summary of the findings of cannabis and brain damage, see here.
Struve et al conducted a study of the EEG’s of chronic heavy users and concluded that very long-term use was associated with changes in the EEG which he classified as “hyperfrontality of alpha waves”. Users who had used pot for 15-30 years had increases in the absolute power, relative power and coherence of their theta waves.
A new study by Struve shows that this effect lasts for 28 days after last use. One suggestion is that this change may be due to organic damage, since they also found slower reaction time. They also found neuropsychiatric deficits that persisted after one month abstinence.
Another study found decreases in alpha-2 and beta-2 waves on EEG, heart rate and even thyroid function. This study found these persisting after a month of abstinence. This indicates under-arousal of these bodily functions. The reduced heart rate, even though persistent, would seem to be a good thing. A more typical finding is increased alpha-2 waves in cannabis users. Alpha waves are associated with relaxation.
Solowij found abnormal event-related potentials in the area of the ability to focus on a task and screen out extraneous information. This effect began after five years of marijuana use, regardless of frequency, oddly enough, and increased with years of use. Alternatively, it also began after 50 uses over more than five years.
The problem appeared to be related to a de-coupling of a G-protein from the cannabinoid receptors in the brain, resulting in difficulty in screening out external stimuli. Solowij suggested that cannabis damages the cannabinoid receptors in the brain, causing those receptors to work less well.
Some call this the “cocktail party effect” – the ability, say, at a party, to talk to one person and screen out the conversations of twenty or so others around you. Rick Doblin’s MAPS criticized Solowij’s finding as useful only for

states of consciousness that are efficient for hive-insects who want or need to function within a Newtonian-Cartesian consumer capitalist society. Obviously, people deliberately smoke marijuana to achieve states of consciousness that fall outside of this paradigm.

Nevertheless, Solowij is finding a clear deficit in users, and Solowij’s study is one of the the most damning so far for marijuana users. Solowij also found some deficits in evoked potentials in the area of information processing, but these seemed to be temporary. As noted above, Solowij always finds serious problems with cannabis users in her studies.
However, a study by Patrick, et al found no differences in ERP’s after age and other factors were controlled for. Patrick was looking at visual, auditory and somato-sensory ERP’s.
The Missoula Chronic Clinical Cannabis Use Study said that Solowij’s results were on the P300 latency test, and that Patrick tested the P300 latency and found no problems, but Patrick had only four patients, although they had used for 11-27 years.
The Missoula study also said that the values for P300 in their subjects were normal. These two studies suggest that others have been unable to replicate Solowij’s work, but I do not know if either Patrick or the Missoula Group were trying to specifically replicate Solowij. So at the moment the EEG studies somewhat contradict the neuropsychiatric battery studies in that they may be finding some damage, whereas the batteries did not.
Another study found that cannabis users who had smoked an average of 1½ joints/day for an average of 7 years had altered auditory evoked-related potentials on EEG had lower EEG power and lower signal-to-noise ratios at 20Hz. This was interpreted as a deficit in neural synchronization and sensory processing.
Cannabis users also had elevated scores on a schizotypal personality disorder questionnaire that increased with years of cannabis use. The study attempted to link cannabis use to schizophrenia because schizophrenics show similar response on this ERP test.
However, in schizophrenia the effect shows up at 40hZ (gamma range), not at 20hZ (beta range). We cover the relationship between cannabis and schizophrenia here on this blog.

Cannabis and Brain Damage: Summary

The original post in its native form was far too long, so I have decided to break it up into seven different posts, in addition to this post. The separate sections are listed below.
The original post, what is left of it, is here.
For an examination of the evidence of whether or not cannabis causes actual structural damage to brain cells, axons or dendrites, see here.
For an analysis of neuropsychological batteries of cannabis users to determine whether or not they suffer brain damage, see here.
For an analysis of EEG testing of cannabis users to discover evidence of brain damage, see here.
For an analysis of studies looking at cerebral blood flow in cannabis users, see here.
For an admittedly impressionistic analysis of whether or not cannabis causes schizotypal symptoms in users, see here.
For a summary comparing the effects of cannabis on the brain compared to other drugs, see here.
Original monkey and later rat studies indicating structural brain damage have generally not panned out when conducted in humans, but a recent study from 2008 found damage to the hippocampus and amygdala. The hippocampus findings are contradicted by three earlier studies finding no damage, and the finding on the amygdala was contradicted by an earlier study.
Another study found damage to the corpus callosum in early adolescent users. And another found damaged axons and brain cells in the prefrontal cortex. These findings have not yet been replicated. Yet another study found damage to two areas but improvements in four other areas of the brain. The consequences of this are not known.
At the moment, whether or not cannabis causes structural damage or even improvements to the limbic system, corpus callosum, prefrontal cortex or other areas of the brain is somewhat up in the air.
Neuropsychological studies of long-term users have been somewhat contradictory, but in general have not found significant brain damage, although they did find a “very small effect” on learning and memory. Apparently they did not think it was significant enough to be called brain damage.
New studies show that chronic long-term users perform worse than controls in memory, learning and recall, and the effect worsens as use progresses. These effects last up to one week after the last use. Therefore, daily marijuana users are always going to be somewhat impaired in these areas.
Some EEG studies found some interesting changes in theta waves in users who had used heavily and daily for 15-30 years. The significance of these findings is not yet known; one suggestion that is that the increased theta may be indicative of organic damage. But here again we do not have any clinical correlates of the organic theta change either.
Even this study did not find permanent effects from sporadic or occasional use of marijuana.
Another found problems with screening out external stimuli after five years of use, but it is possible that two attempts to replicate that study may have failed.
A SPECT studies out of Britain showed low CBF in three heavy cannabis users. Another found that low CBF did not clear up in adolescent users even after one month. However, they have been contradicted by two other studies, one showing that the CBF deficits clear up after three months, and another showing increases in CBF as opposed to decreases.
A new study using DTI found damage to the left side of the arcuate fasiculus in adolescent heavy cannabis users. This is one of the most disturbing findings to date, and adds weight to evidence that cannabis should not be used by adolescents, since the arcuate fasiculus is still developing in early adolescence. Nevertheless, no clinical significance has yet been attached to this finding.
But another DTI study looking at the entire brain found no evidence of generalized damage, and if anything, found that teenage cannabis users have less brain atrophy and more brain cells than non-users. We would expect a clinical correlate of this to be more intelligent teenage potheads, but no one is suggesting that.
Unless clinical correlates can be discovered, all findings of damage or enhancement of the brain via marijuana should be viewed with a critical eye.
So the evidence on permanent brain damage from long-term heavy marijuana use is rather contradictory and is still somewhat up in the air.
It looks like cannabis can be used for up to five years, or possibly up to 15 years, even on a daily basis, without any permanent harm to the brain. Beyond that, there may effects, but they appear to be more subtle than profound.