Licit and Illicit Drug Use in Cluster Headache

Abstract

Cluster headache patients seem to use more licit and illicit substances than the general population. The epidemiologic data supporting this is growing. We included the licit drugs in this review because their use seems to be driven by the same addiction mechanisms leading to illicit drug abuse. Some drugs may be used in an attempt to treat cluster headache, especially cocaine and hallucinogens. Drug exposure may also play a role in CH pathophysiology, as suggested by interesting data on tobacco use and second-hand smoke exposure. A common factor may contribute both to CH and drug use predisposition. Genetic factors may be at play, and the dopaminergic and orexinergic pathways could be targeted for future studies.

Tobacco, Nicotine, and Headache

“…Nicotine readily crosses the blood–brain barrier with uptake by passive diffusion and active transport by the choroid plexus. Within the brain, tritiated S‐nicotine binds to cortical, hippocampal, nigrostriatal, mesolimbic, thalamic, hypothalamic, midbrain, and brain stem receptors, with hypotheses that for certain headaches, nicotine central nervous system (CNS) action is direct, for example, in cluster at the hypothalamus . Nonetheless, in human studies and pain models, the effects of nicotine are often inconsistent and sometimes conflicting .…”

“…More CH patients smoke than migraineurs, smoke more heavily, and use more substances . In a study of possible predictive factors in the evolution of episodic to chronic CH, Torelli et al concluded cigarette‐smoking rates and causality still cannot be established with certainty .…”

“…In a recent paper, Ferrari et al state it is unlikely that there is a causal relationship between CH and smoking, as CH patients rarely improve after quitting smoking . For further discussion of this topic, please reference an excellent recent review of CH and substance issues including tobacco …”

“…Within the brain, tritiated S-nicotine binds to cortical, hippocampal, nigrostriatal, mesolimbic, thalamic, hypothalamic, midbrain, and brain stem receptors, 18 with hypotheses that for certain headaches, nicotine central nervous system (CNS) action is direct, for example, in cluster at the hypothalamus. 19,20 Nonetheless, in human studies and pain models, the effects of nicotine are often inconsistent and sometimes conflicting. 21 These inconsistencies in human outcomes may be due to the rapid washin and washout period of nicotine after smoking.…”

“…More CH patients smoke than migraineurs, smoke more heavily, and use more substances. 20,132 In a study of possible predictive factors in the evolution of episodic to chronic CH, Torelli et al concluded cigarette-smoking rates and causality still cannot be established with certainty. 133 In a recent paper, Ferrari et al state it is unlikely that there is a causal relationship between CH and smoking, as CH patients rarely improve after quitting smoking.…”