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a patient’s allergic reaction

Pathophysiology. Vestibular seizures, by definition, involve abnormal electrical activity (seizure) affecting those parts of the cerebral cortex believed to mediate vestibular sensation (superoposterior temporal cortex and temporoparietal junction). The rarity of this phenomenon is due to the fact that seizure activity rarely remains restricted exclusively to the small area of vestibular cortex. Seizure activity will more commonly spread, and when it does, other sensory, motor, and cognitive symptoms will ensue, and the salience of these other symptoms tends to overshadow the vestibular symptoms.

Classification Schemes by Pathophysiology

Pathophysiology classification schemes include biochemical, metabolic, neurophysiologic, and/or genetic dynamic processes set in motion by the injury. One widely used physiopathologic scheme in TBI was introduced by Adams et al., who differentiated between primary injury, or unavoidable, immediate-impact parenchymal damage, and secondary injury, or potentially avoidable damage.However, the importance given to secondary insults has gained recognition, and since the 1990s, understanding and prevention of delayed damage have received priority. Secondary lesions are defined as those set in motion by the impact but not pathologically or clinically manifested until minutes, hours, or days after the injury. In addition to secondary ischemic injury, probably the most relevant factor influencing a worse outcome, secondary damage can be caused by neurotransmitter dysfunction, cellular and extracellular edema, blood–brain barrier (BBB) disruption, mitochondrial damage, genetic alterations such as apoptotic induction