Carotid artery dissection dissection is thought to be more commonly caused by severe violent trauma to the head and/or neck. An estimated 0.67% of patients admitted to the hospital after major motor vehicle accidents were found to have blunt carotid injury, including intimal dissections, pseudoaneurysms, thromboses, or fistulas. Of these, 76% had intimal dissections, pseudoaneurysms, or a combination of the two. The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant hyperextension and rotation of the neck, which stretches the internal carotid artery over the upper cervical vertebrae, producing an intimal tear. After such an injury, the patient
Carotid body acid-base transporters (e.g. Na-H) which raise intracellular pH, and activates transporters (e.g. Cl-HCO) which decrease it. Changes in proton concentration caused by acidosis (or the opposite from alkalosis) inside the cell stimulates the same pathways involved in P sensing. Another mechanism is through oxygen sensitive potassium channels. A drop in dissolved oxygen lead to closing of these channels which results in depolarization. This leads to release of the neurotransmitter dopamine in the glossopharyngeal and vagus afferente to the vasomotor area. The type I (glomus) cells in the carotid (and aortic bodies) are derived from neuroectoderm and are thus electrically excitable.