External stimuli are received via specialized neurologic structures called sensation receptors. Receptors are intensively located in the skin but are also located in the muscles, periosteum, capsule of internal organs, and vessel walls [7, 8]. Activation of the receptors induces release of algogenic substances like bradykinin, potassium, prostaglandins, hydrogen ions, serotonin, and substance P. These algogenic substances stimulate the sensation receptors aggressively and make them much more sensitive [9–11]. The receptors are sensitive to different forms of physical energy (mechanical, thermal, and chemical). Stimulated sensation receptors transform the external stimulus to “electrochemical energy,” which is brought to the spinal cord dorsal horn via A–delta fibers (fast, surrounded by thin myelin film) and C–afferent fibers (slow, unmyelinated) (transduction [membrane potential], transformation [action potential]) [2, 12]. This message (action potential) activates the spinal cord dorsal horn neurons that reach the central part of the brain, thalamus, and frontal cortex and produces suprasegmental reflexes and cortical responses via afferent fibers (transmission) [2]. Tissue damage activates neurological pathways, and various mechanisms form which control the quantity of transported afferent activation when the stimuli are transported to central areas. Consequently, the stimuli transport is inhibited or facilitated at the spinal cord or supraspinal levels (modulation) [2]. There is simultaneous efficiency of afferent fibers and efferent inhibitor fibers for this purpose [2]. Spinal cord dorsal horn cells are the first level that processes the painful stimulus [2, 4]. The stimulus comes from the peripheral sensation nerve fibers terminating at this level. There are three types of neurons in the spinal cord dorsal horn: projection neurons, excitatory neurons, and inhibitory neurons [4]. Projection neurons transmit the stimulus to the upper centers via the anterolateral afferent system [13]. Excitatory neurons transmit the painful stimulus to the projection neurons and stimulate them [13]. Inhibitory neurons are activated with the signals that come via C-delta and A-delta fibers and transmit the painful stimulus to the projection neurons. When they are activated via large fibers, they inhibit the projection neurons [4]. On the other hand, pain is the patient’s experience, not only a physical stimulus. When the stimulus reaches the cerebral cortex, the patient’s previous experiences and perception of stimulus are the important factors for specification of pain (Perception) [2]. Perception of pain is the last stage of neuronal painful stimulus transport. Painful stimulus reaching thalamus and brain system activate various cortical areas, and then responses appear. These are the reticular system, somatosensory cortex, and limbic system [7, 8]. Reticular system plays a major role in the formation of autonomic and motor responses (sudden movement of the back of hand after touching a hot object). Also, it has a role in affective motivational response too (looking at the hand and estimating the injury after moving back of the hand from the surface of a hot object) [7, 8]. Somatosensory cortex establishes pain severity, localization, and type, and associates it with previous experiences and memory [7, 8]. Limbic system produces emotional and behavioral responses in response to pain (attention, emotional state, and motivation) [7, 8].