WHY DO BRAINS MATTER FOR UNDERSTANDING
STRESS AND ANXIETY
Anxiety is our body’s natural response to stress or
expected stressors. Occasional anxiety and stress are
common life experiences and are vital for ensuring
that we’re able to avoid potentially life-threating
and dangerous situations. Unfortunately, sustained
anxiety and chronic stress can result in changes in
the brain that contribute to mental illness due to our
brain’s response to stress.
1
3 2. Amygdala quickly assesses the threat
4 3. Communicates with hypothalamus to activate the
2 HPA axis (Hhypothalamic-pituitary-adrenal) axis
4a
4b
5
UNDERSTANDING HOW THE BRAIN
RESPONDS TO STRESS TO RESULT IN
STRESS AND ANXIETY-RELATED MENTAL
ILLNESSES CAN YIELD FASTER DIAGNOSES,
MORE EFFECTIVE TREATMENTS, AND
POTENTIAL PREVENTION STRATEGIES
HOW DOES THE BRAIN RESPOND TO STRESS?
1. Sensory systems and thalamus detect a stressor or
potential threat
4. Hypothalamus mobilizes the immediate fight-or-
flight response
4a. Signals the pituitary to release adrenocortico-
tropic hormone (ACTH) into the bloodstream
AND the release of epinephrine from the adrenal
gland
4b. ACTH stimulates release of cortisol by the adrenal
glands
5. Epinephrine and cortisol target organs throughout
the body to allow for fast response to the threat:
increase sweat production, stimulate lungs to
increase respiration, increase heat
HOW DOES THE BRAIN RESPOND AND
ADAPT TO CHRONIC STRESS?
1. Amygdala The emotion center of the brain
becomes hyperactive and responsive to potential
threats following chronic stress and now
hypervigilant to any potential stressor or threat
2. D
 orsal Anterior Cingulate Cortex (dACC) A region
of the frontal lobe that following chronic stress
amplifies signals from the amygdala about fearful
or threating stimuli; the dACC of individuals with
low anxiety shows less amplification
3. Ventromedial Prefrontal Cortex (vmPFC) Another
region of the frontal lobe that following chronic
stress is less able to reduce signals from the
amygdala about fearful or threating stimuli; the
vmPFC of individuals with low anxiety shows
greater ability to quiet amygdala signals
HOW DO CURRENT TREATMENTS
TARGET BRAIN CHANGES ASSOCIATED
WITH STRESS AND ANXIETY?
Current medications include the use of benzodiaz-
epines, which lessen anxiety by reducing amygdala
hyperactivity; beta-blockers, which can target the
physical symptoms of anxiety, including heart
palpitations; and antidepressants, which have been
shown to increase the production of neurotrophic
factors, including BDNF, and can have a beneficial
impact on promoting neuron health in the cortex
and hippocampus.
BENZODIAZEPINES
BETA-BLOCKERS

4. Hippocampus The seat of memory formation

in the brain, which is also important for helping
memories have defined context for what, when,
and where threat or stress experiences happened,
begins to lose neurons in response to long-term
elevations of stress hormones; hippocampus is
less able to help determine safe versus dangerous
contexts
Amygdala Dorsal Anterior Cingulate Cortex (dACC)
h with fear aquisition h with fear aquisition
i with fear extinction i with fear extinction
1 2
ANTIDEPRESSANTS
Psychotherapy Exposure therapy aims to expose
individuals to their stress triggers in a safe
environment to allow for better identification of
safe versus dangerous contexts. Cognitive therapies
instead aim to focus on allowing individuals to
become aware of their responses to stressors and
gain tools to mitigate the negative responses. Often
psychotherapies are utilized in combination with
medications, and work has begun to suggest that
psychotherapy can aide in boosting the ability of the
vmPFC to quiet the amygdala.

EXPOSURE THERAPY

COGNITIVE THERAPY

PSYCHOTHERAPY
+
MEDICATIONS

3
Ventromedial Prefrontal
Cortex (vmPFC)
i with fear aquisition
4
h with fear extinction Hippocampus
Mixed findings
Primoridial for
contextual information