Kawsar Alami - Department of Physiology, Fac- ulty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
Fatemeh Jalali - Department of Physiology, Fac- ulty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
Hossein Azizi - Department of Physiology, Fac- ulty of Medical Sciences, Tarbiat Modares University, Tehran, Iran

Nowadays pain is the most commonly reported symptom in clinical practice. It is defined as “a complex emotional and sensorial experience that is associated with potential or actual damage” [۱, ۲]. Pain pathways represent a complex sensory system, with emotional, cognitive, and behavioral elements having evolved to detect and integrate a protective response to noxious stimuli [۳, ۴]. The protective nature of pain is true for acute pain, which is provoked by a specific disease or injury. However, chronic pain is not protective and is considered a disease state [۵]. Pain sensitivity is one of the factors that determine the perceived severity, course, prognosis, and also treatment efficacy of clinical pain. It can be defined as increased or decreased pain responsiveness to noxious or non-noxious stimuli [۶, ۷]. Reduced sensitivity to pain is associated with the risk of delayed diagnosis or undermined treatment efficacy of conditions associated with acute pain. On the contrary, hypersensitivity is unpleasant and increases health care costs, risk of anxiety, and susceptibility to chronic pain conditions [۸, ۹]. Pain sensitivity widely varies among different individuals. There are several reports that factors, including genetic and environmental factors, affect an individual pain perception and sensitivity [۸]. One of the environmental factors affecting pain perception that has not yet received much attention is the history of drug abuse [۱۰].

Pain, drug exposure, Early life