Headache in Cocaine Users: Epidemiology, Clinical Features, and Putative Pathophysiological Mechanisms

Headache is a frequent symptom in cocaine users (CUs). Chronic cocaine use may induce headache in previously unaffected individuals or worsen a preexisting headache. Cocaine-induced headache is usually migraine-like, and less commonly tension type- or cluster-like. The latency between acute cocaine use and headache onset ranges from minutes to several days. Cocaine-induced headache, as currently defined, develops ≤1 hour after cocaine administration and subsides ≤72 hours later. Given that headache often begins 2–12 hours after cocaine use these criteria remain open to debate. Acute cocaine use commonly worsens spontaneous migraine attacks, and rarely improves cluster episodes. Putative pathophysiological headache mechanisms in CUs include massive sympathomimetic stimulation followed by monoamine depletion, increased glutamatergic activity, and trigeminal or sphenopalatine ganglia activation. Being aware about headache in CUs is important so that we can manage this complication properly and treat patients adequately. Understanding more about the underlying mechanisms should also improve our knowledge of headache pathophysiology.