Summary:
Evidence of cerebral atrophy was demonstrated by air encephalography in ten patients with histories of consistent cannabis smoking over a period of 3-11 years. The average age of the patients was 22 years; all were males. Amphetamines and lysergide (LSD) had also been taken, but in much smaller amounts. Measurements of the lateral and third ventricles were significantly different from those in thirteen controls of a similar age-group.
Introduction:
Personality changes and mental illness have been reported in chronic cannabis smokers of previously normal personality. Addicts often have impairment of recent memory, vegetative symptoms, and a tendency to reversed sleep rhythm suggesting organic brain damage. If organic brain damage were confirmed, this would clearly lead to a different approach to the problem of increasing drug abuse.
This study was prompted by the finding of cerebral atrophy on air encephalography in four young patients referred to one of the researchers (A. M. G. C.) for neurological investigation of headache, memory loss, or behaviour change. A common factor in all four histories was prolonged heavy cannabis smoking. Amphetamines and lysergide (LSD) had also been taken, but in very much smaller amounts. Since no recognised cause of the cerebral atrophy was apparent, neurological and radiological investigation of other cannabis smokers seemed indicated.
Patients:
The first four cases were unselected routine admissions for investigation of neurological symptoms. The next five were under treatment by one of the researchers (M. E.) for drug abuse, and were referred for detailed investigations of cerebral function, including air encephalography. They were selected because of known long-standing-cannabis smoking; two had been attending a drug-addiction centre for some time and the other three were the next cases which presented to psychiatric outpatients with histories of long standing cannabis smoking. The tenth patient was admitted as an emergency with a drug overdose and had a 6-year history of drug abuse with heavy cannabis intake. All these cases were given a full clinical examination and were investigated by air encephalography.
It was fully explained to the patients that the test was to assess possible brain damage with a view to ultimate prognosis, and the patients willingly consented to this investigation, which was done under local anesthesia and sedation.
Discussion:
Significant cerebral atrophy is rare in young people. It may happen after head injury but can be attributed to this only when there has been post-traumatic amnesia of several hours or evidence of focal neurological damage at the time of the injury. None of the patients who had had minor head injuries (cases 1, 3, and 4) would have satisfied these criteria, and it is not considered that their head injuries played a part in the enlargement of the ventricular system. Other causes for cerebral atrophy include head injury at birth, especially in prolonged labour or in conditions causing anoxia; and some cases may also be due to hypoplasia rather than atrophy, and differentiation may not be possible. Severe infections in childhood when encephalitis has supervened, congenital syphilis, and toxoplasmosis may cause atrophy, as may congenital or acquired vascular lesions. Other causes include hereditary disease such as Huntington’s chorea. Diffuse demyelinating conditions can produce quite rapid cerebral atrophy in the second and third decade. It must be stressed that cerebral atrophy indicates irreversible brain damage.
No such causes for cerebral atrophy were found in this series of ten drug addicts.
The brains of monkeys given isotope-labelled cannabinoids intravenously showed concentration of the drug in the frontal lobes and cortex, geniculate bodies, cerebellum, caudate nuclei, and putamen – all structures near the third and lateral ventricles. After 24 hours the drug had spread uniformly throughout the brain. The fat solubility of the cannabinoids make it likely that they would accumulate in nervous tissue, with its high fat content.
There is a very interesting parallel between the picture shown by encephalitis lethargica and that of chronic abuse of cannabis and LSD This was evidenced in some the cases by a reversal of sleep rhythms, hallucinations, and mental changes.
Source: A. M G. CAMPBELL, Department of Neurology, Bristol Royal United Hospitals; M. EVANS, Department of Psychiatry, Whitchurch Hospital, Cardiff J. L. G. THOMSON, Department of Radiology, Frenchay Hospital, Bristol; M J. WILLIAMS, Department of Medicine, Bristol Royal Infirmary. Lancet, December 4, 1971