ABSTRACT
Chronic pain, pain catastrophizing, and mental health disorders such as anxiety or depression frequently occur together and are challenging to treat. To help understand the relationship between these conditions, we sought to identify distinct phenotypes associated with worse pain and function. In a cohort of people with chronic pain on opioids seeking medical cannabis in New York, we conducted latent class analysis to identify clusters of participants based on pain catastrophizing and mental health symptoms of depression, anxiety, post-traumatic stress disorder (PTSD) and attention deficit/hyperactivity disorder (ADHD). We then compared clusters with respect to sociodemographic and clinical characteristics using descriptive statistics. Among 185 participants, we identified four discrete groups: low pain catastrophizing and low mental health symptoms (49% of participants), low pain catastrophizing and ADHD-predominant mental health symptoms (11%), high pain catastrophizing and anxiety-predominant mental health symptoms (11%), and high pain catastrophizing and high mental health symptoms (30%). The group with high pain catastrophizing and high mental health symptoms had the worst pain intensity and interference, disability, insomnia, and quality of life, compared to the two groups with lower pain catastrophizing, though not all differences were statistically significant. Our findings highlight the importance of identifying and addressing pain catastrophizing in patients with comorbid chronic pain and mental health symptoms.
ABSTRACT
The role of cannabis in the etiology of schizophrenia has been documented as possibly the strongest environmental risk factor. However, the pathomechanism whereby cannabis use increases this risk has not yet been identified. We argue that this pathomechanism may involve direct effects of exogenous cannabinoids on T-type calcium channels in the thalamus. These channels are crucial for amplification of corticothalamic inputs, as well as for the ability of the thalamus to generate neuronal burst firing. Cortically induced thalamic burst firing has been found to be important in trans-thalamic cortico-cortical interactions. Therefore, any potential interference with the burst firing mode in the thalamus could lead to an impairment in these interactions, which in turn causes a relative disconnection between cortical areas. This in turn could result in reduced ability to recognize re-afferent sensory inputs and psychosis. We also argue that the effects of Δ(9)THC are more detrimental compared with the effects of cannabidiol, as the former may increase the excitability of thalamic neurons by its direct effect on T-type calcium channels.