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Whiplash injuries or the group of whiplash-associated disorder (WAD) occur when there is shifting and movement of energy, during a crash or collision, from acceleration-deceleration mechanism transferred 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.Although motor vehicle collisions are the majority of trauma responsible for WAD, other causes also include contact sports injuries, falls, physical and domestic abuse, and other types of traumas.The clinical picture and presentation are variable. In general, this includes neck pain, decreased range of motion of neck, headaches, arm or arms numbness, and other related symptoms and signs that depend on the extent of the insult. This possibly may include consequences of fractures, joint dislocations, and even traumatic brain injuries/post-concussional syndrome, with its subsequent clinical outcomes.The trauma associated with WAD outcome can result in acute and chronic pain syndromes, functionality limitations and restrictions, psychological and psychosocial ramifications, financial crisis, unemployment, and in cases, prolonged disability. This causes a significant economic burden on country.This review manuscript will review the latest in WAD etiologies, biomechanics, diagnosis, management, and prognosis. We base out review on relevant databases such as PubMed, Ovid-Medline, Embase, Web of Science, NIH website, Google Scholar, and the Cochrane Library. No Institutional Review Board permission was obtained since this manuscript does not directly involve animals or humans.

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This manuscript will review the crucial role of BDNF as a pain mediator and modulator of neuroinflammation and neuropathic pain.BDNF belongs to of the neurotrophin family of growth factors that is encoded by the bdnf gene. Its role as modulator was found to act on neuronal excitability and synaptic plasticity has triggered huge interest in neurobiological pain research. This pointed to renewed interest as a potential target for pharmacological agents in its long cascade of mechanism of actions.There is no clear-cut explanation on how BDNF works. One thing we know is that BDNF mechanism of action depends on whether we are dealing with a normal nerve, after an acute injury, or following chronic state. It is considered a major tertiary mediator in the genesis of central sensitization. It mediates inflammatory and peripheral injury-induced pain and play a role by increasing dorsal horn excitability. Hence disrupting these cycles can potentially curb the genesis of chronic pain. Some suggested mechanisms of action of BDNF in neuropathic pain is via enhanced neuronal sensitivity to painful stimuli and an enhanced co-expression of thermo-TRP channels. Another possible mechanism entails the involvement of microglia in pain. Following a peripheral injury, GABA-BDNF plays an essential role in formation of neuropathic pain. BDNF increases both the excitatory and inhibitory synaptic drives to putative excitatory interneurons while attenuating synaptic transmission to inhibitory GABAergic neurons.In the absence of any injury and in normal states, BDNF-mediated effects contribute to pain. An increase in BDNF and TrkB expression activate MAPK/ERK and PLC-PKC kinase pathways.In the acute stage of nerve injury, the levels of both BDNF and TrkB are decreased in the spinal cord dorsal horn. During the chronic stage of injury, pERK levels are also noted to increase. This may result from increases in both BDNF-TrkB signaling and TNF𝛼-TNFR signaling.BDNF may also potentially modulate spinal neuron responsiveness by potentiation of postsynaptic N-methyl-D-aspartate (NMDA) receptors.BDNF noticeably enhanced the frequency of miniature excitatory postsynaptic currents (EPSCs) recorded in superficial dorsal horn neurons.All these mechanisms and theories may potentially be a dream for clinicians to work on and modulate pain.

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