In a striking 2010 statistics published in 2015, the U.S. Department of Transportation, National Highway Traffic Safety Administration reports there were “32,999 people killed, 3.9 million were injured, and 24 million vehicles were damaged in motor vehicle crashes in the United States”. The economic burden amounted to “$242 billion. This represented the equivalent of nearly $784 for each of the 308.7 million people living in the United States, and 1.6 percent of the $14.96 trillion real U.S. Gross Domestic Product for 2010. These figures include both police‐reported and unreported crashes”.
Whiplash-associated disorder (WAD) occurs when there is shifting and movement of energy, during a crash or collision, from acceleration-deceleration mechanism transferred mainly to the neck region. WAD is characterized by excessive extension-flexion movements, and/or excessive side bending of the head and neck, beyond the normal and regular range of motion.
Motor vehicle collisions account for the majority of trauma related to WAD, but there are other causes such as contact sports injuries, falls, physical and domestic abuse, and other types of traumas.
Clinically, encountering cases of chronic neck pain stemming from untreated, poorly treated, or mis-managed whiplash injuries after motor vehicle collisions has become a more common and challenging encounter. The necessity to address acute whiplash injury pain-related symptoms very aggressively, early on, and in a systematic and interdisciplinary matter is essential to avoid unnecessary and avoidable long-term sequelae.
The latest neurobiological theories, interplay, and interaction point to a triad of neuron-glia-immune cells in the genesis of chronic pain that potentially can also apply for chronic whiplash pain. Chronicity of whiplash injuries is associated with functionality limitations and restrictions, psychological and psychosocial ramifications, financial crisis, unemployment, and in cases, prolonged disability. This causes a significant economic burden on the country.
Once whiplash injury occurs, the pain journey and cascade are initiated through peripheral and central nervous system pathways. Afferent neurons sense nociceptive stimuli from the corresponding cervical spinal cord divisions. Central nervous system (CNS) interneurons signal messages transported via primary somatosensory cortex of the cerebral hemisphere to efferent neurons from CNS to effector organs, such as muscles. Resident and migrating immune cells release mediators that modulate glial cells that surround peripheral nervous system (PNS) and CNS. Glial and immune cells respond to injury and modulate the function of dorsal root ganglion (DRG), trigeminal ganglion, and limbic system to change pain perception. All these received data contribute to the pain cognition and perception of the individual’s pain. At each level and step, neurotransmitters promote signals and inputs, and neuromodulators modulate pain and its perception. Theoretically, therapeutic potential can affect each step of this cascade.
The current pharmacological management of chronic pain is mostly limited to symptomatic treatment rather than disease-modifying. The current treatment is limited in efficacy and has many adverse effects. This area of molecular neurobiology pain research is ever- changing and improving. The traditional thinking that only a few areas, or structures, or elements in the brain are responsible for, or are involved in pain, pain initiation, simple transition from acute to chronic pain, and pain memory is expiring. It is becoming evident that brain has multiple peripheral and central areas involved in pain pathology and hencethe cascade of events that leads to the genesis of chronic pain is multifactorial.