![]() We extend this idea further to include kindling and sensitization induced hyper-inhibitory and disinhibitory processes interacting with excitatory neurons which produce their own effects in fear circuits and symptoms associated with anxiety and trauma, such as numbness, aloofness, and lack of detail and loss of context in the memories of traumatic and anxious incidents. We use the metaphor and mechanisms of kindling induced-seizure development as a basis for a progression of hyperexcitability in excitatory fear circuits to move from adaptive fear to pathological anxiety and trauma disorders. Unraveling the mechanisms of the perceptual fear response may lead to a greater understanding of pathological anxiety because dysfunction or overactivation of the perception of fear leads to anxious thought and maladaptive behavior. This hypervigilance is super-responsiveness to events which may be threatening ( Frijda, 1986). This not only includes fear-related autonomic and behavioral responses activated during pathological anxiety, but the perceptual fear response of greater vigilance. More than 20 years ago we presented a view that pathological anxiety developed through a process of neural sensitization or kindling-like processes that initiate changes in the brain’s adaptive fear circuits leading to enhanced perception and response to subsequent threat and danger ( Rosen and Schulkin, 1998). ![]() ![]() ![]() In this paper we explore and update the idea that pathological anxiety develops from hyperexcitability of neural circuits for adaptive fear. ![]()
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