September 13, 2023
THC interacts with the body’s endocannabinoid system, a complex network of receptors and neurotransmitters involved in regulating various physiological processes, including pain sensation, mood, appetite, and sleep. The two primary cannabinoid receptors, CB1 and CB2, are found throughout the central and peripheral nervous systems. THC’s interaction with these receptors plays a crucial role in modulating neurological functions and potentially addressing disorders affecting the nervous system.
Chronic pain is a prevalent symptom in many neurological disorders. THC has demonstrated analgesic properties, offering potential relief for patients experiencing neuropathic pain, migraines, and multiple sclerosis-related pain. By binding to CB1 receptors, THC can modulate pain perception and provide much-needed relief for individuals struggling with persistent pain.
THC has also shown promise as a neuroprotective agent. Research suggests that it may help protect brain cells from damage caused by oxidative stress, inflammation, and excitotoxicity. This neuroprotective effect of THC could have implications for neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). While further studies are needed to fully understand the mechanisms involved, these initial findings offer hope for potential therapeutic interventions.
Epilepsy, a neurological disorder characterized by recurrent seizures, has garnered significant attention in relation to THC. The U.S. Food and Drug Administration (FDA) has approved a specific medication, Epidiolex, which contains purified CBD (cannabidiol), another compound found in cannabis, for the treatment of certain types of epilepsy. While THC’s role in epilepsy management is still being explored, some studies have indicated its anticonvulsant properties, potentially making it a valuable addition to the treatment options available.
THC’s impact on cognitive function remains a topic of ongoing investigation. While the recreational use of cannabis has been associated with short-term memory impairment and cognitive deficits, studies examining the long-term effects of THC on cognitive function in medical contexts have yielded mixed results. More research is necessary to determine the potential benefits and risks of THC on cognitive performance in patients with neurological disorders.
The long- term effect of cannabis on cognition, still, is less well established. Recent meta- analyses report residual goods of cannabis use on neurocognition, harmonious with previous exploration. A meta- analysis in 2020 concentrated on grown-up near- diurnal cannabis use for> 2 times and set up global neurocognition among druggies (n = 849) to be about one- quarter of an SD worse than that of burnouts (n = 764). Four of the 7 disciplines delved (decision- timber, verbal literacy, retention, superintendent function) showed significant effect sizes ranging from Hedges g = −0.52 to−0.18. A meta- analysis of cannabis druggies< 26 times of age (n = 2152) and burnouts (n = 6575) also showed a one- quarter of an SD difference in global neurocognitive performance but with further specific disciplines affected, albeit with lower effect size compared with that set up. Both demanded support for worse neurocognition in early nonage in that neither set up that age at onset of cannabis use told the association between exposure and cognitive performance.
In discrepancy to these meta- analyses, large longitudinal studies give stronger unproductive consequences by examining change over time. In the CARDIA study (Coronary roadway threat Development in youthful Grown-ups), 3385 actors 18 to 30 times of age were followed up longitudinally. Marijuana use was assessed periodically in the 25- time follow- up. In addition, cognitive assessment was completed 25 times after commencement. In this study, accretive times of exposure to marijuana was associated with worse verbal memory (0.13 lower SD in the verbal memory test for each fresh 5 times of exposure to marijuana). Longitudinal-twin studies use a exploration design that also controls for participated friction from inheritable and environmental factors.
Two large longitudinal binary studies (n = 3066) with neurocognitive measures collected ahead (at 9 – 12 times of age) and after (17 – 20 times of age) cannabis exposure reported that declines in vocabulary and general knowledge were associated with being a cannabis stoner but not with quantum of cannabis consumed. halves discordant for cannabis use showed no differences in IQ declines.
Therefore, differences were likely caused by participated threat factors. Using a analogous design, reported that lower IQ anteceded cannabis use with no substantiation of factual Command declines among 1989 halves assessed at 5, 12, and 18 times of age. Estimated other aspects of neurocognition among 856 individual halves and reported only 1 within- family effect of 70 tested. Specifically, frequency of cannabis use at 17 times of age was associated with poorer superintendent performing at 23 times of age, but administrative functioning problems preexisting cannabis use couldn’t be ruled out.
MRI ways demonstrate discrimination associations of cannabis use with brain structure and function. There have been a variety of variances in cannabis use’s effects on brain anatomy. In a longitudinal study including 1598 MRIs done in adolescents at birth and the 5- time follow- up, a cure-dependent association was observed between cannabis use and PFC thinning.
On the other hand, although a meta- analysis set up that regular cannabis consumption was associated with lower hippocampal( standardized mean difference,0.14( 95 CI,0.02 –0.27)), medium orbitofrontal cortex( formalized mean difference,0.30( 95 CI,0.15 –0.45)), and side orbitofrontal cortex( formalized mean difference,0.19( 95 CI,0.07 –0.32)) volumes relative to disuse, brain volumes weren’t associated with cannabis use duration and lozenge. Other large studies have reported null goods. In 2 large binary samples from the United States( n = 474) and Australia( n = 622), cannabis use was unconnected to volumes of the thalamus, caudate nexus, putamen, pallidum, hippocampus, amygdala, and nexus accumbens. A multisite study of cortical face measures( n = 262) reported no difference in cortical consistence, face area, and gyrification indicator in cannabis druggies versus burnouts, in cannabis dependence versus non dependence versus burnouts, and in early adolescent versus late adolescent onset of cannabis use versus disuse. therefore, brain structural abnormalities affiliated to cannabis use are inconsistent.
Functional MRI studies report further robust goods, particularly after prolonged cannabis use.
A meta- analysis of task- grounded functional MRI studies in current grown-up and adolescent druggies set up abnormalities in activation in both age groups. Relative to non-using control subjects, adult cannabis druggies had lesser brain activation in the superior( seed- grounded d mapping( SDM- Z),1.561; P<0.002) and posterior( SDM- Z,1.479; P<0.003) transverse temporal and inferior anterior gyri( SDM- Z,1.568; P<0.002) and lower activation in the striatum( SDM- Z,−1.843; P<0.001), insula( SDM- Z,−1.637; P<0.001), and middle anterior gyrus across different tasks. Adolescent cannabis druggies also had lesser activation in the inferior parietal gyrus( SDM- Z,1.06; P<0.001) and putamen( SDM- Z,1.008; P<0.001) compared with burnouts across colorful tasks, suggesting compensatory neuroadaptive mechanisms. These functional abnormalities persist despite conclusion of cannabis use and beyond the period when THC metabolites are sensible. A meta- analysis of the same adolescent studies set up that> 25- day continent adolescent cannabis druggies displayed lesser activation in the right inferior anterior gyrus in addition to other areas applicable for administrative functioning and tone-nonsupervisory mechanisms.
Several recent studies examined cannabis goods in populations with premorbid clinical threat factors and those using medical marijuana. A meta- analysis concentrated only on cannabis druggies with psychosis< 25 times of age (n = 529) and no using control subjects with psychosis(n = 901). In this study, there were significant differences in 3 of 11 disciplines assessed (premorbid Command, Hedges g = 0.40(standardized effect size); current Command, Hedges g = −0.17; working memory, Hedges g = −0.76). Among a sample of 215 adult cases with habitual pain handed daily herbal cannabis containing12.5 THC for 1 time, no significant neurocognitive differences were set up compared with 216 control subjects. This is in line with a study of cases with multiple sclerosis in response to oral dronabinol that set up no significant differences in MRI- deduced measures, including periodic chance of brain volume change and circumstance of new lesions, after 12 months of use. These clinical trials suggest no significant adverse effect of THC on neurocognitive symptoms in specific clinical populations.
The potential therapeutic effects of THC in neurological disorders offer new avenues for research and treatment. From pain management and neuroprotection to epilepsy and cognitive function, THC’s interaction with the endocannabinoid system presents a captivating field of exploration. While further studies are needed to establish optimal dosages, delivery methods, and long-term effects, THC holds promise as a valuable addition to the arsenal of treatments available for patients living with neurological disorders.