Originally found on https://www.medicalnewstoday.com/articles/305468.php
The researchers – led by Dr. Linda Mah of the Rotman Research Institute at Baycrest Health Sciences in Canada – publish their results in the journal Current Opinion in Psychiatry.
To conduct their research, they reviewed previously published animal and human studies that examined brain areas affected by chronic anxiety, fear, and stress.
In detail, they reviewed recent evidence from studies of stress and fear conditioning in animals, as well as neuroimaging studies of stress and anxiety in both healthy people and clinical populations.
For many of us, fear, anxiety, and stress are a normal, occasional part of life; we get stressed before taking a test or going for a job interview, for example. It is when these instances of anxiety become more frequent that they interfere with daily life.
The team defines chronic stress as “a pathological state that is caused by prolonged activation of the normal acute physiological stress response,” which can then, in turn, cause problems for the immune, metabolic and cardiovascular systems.
Likewise, chronic stress can cause the brain’s hippocampus to atrophy. This brain area is important for long-term memory and spatial navigation.
‘See-saw relationship’ between amygdala and prefrontal cortex
For their review, Dr. Mah and colleagues zeroed in on key structures involved with the neurocircuitry of fear and anxiety, which includes the amygdala, medial prefrontal cortex (PFC) and the hippocampus. These brain areas are impacted during chronic stress.
Results revealed that there were similar patterns of aberrant brain activity in the wake of fear, anxiety and chronic stress. In detail, the amygdala was overactive and the PFC – which contains the “thinking areas” of the brain that regulate emotional responses – was underactive.
Interestingly, over a decade ago, renowned neurologist Dr. Helen Mayberg first identified what the researchers call the “see-saw relationship” between the amygdala and the PFC in a breakthrough study.
Commenting on their findings, Dr. Mah says:
“Pathological anxiety and chronic stress are associated with structural degeneration and impaired functioning of the hippocampus and the PFC, which may account for the increased risk of developing neuropsychiatric disorders, including depression and dementia.”
However, not all hope is lost. Dr. Mah also suggests that damage to the hippocampus and PFC as a result of stress is not entirely irreversible. She notes that both anti-depressant treatment and physical activity have both shown promise in increasing hippocampal neurogenesis.
The researchers conclude their study by writing:
“Whether anti-anxiety interventions can reduce the risk of developing neuropsychiatric illness needs to be established with longitudinal studies.”
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