THE BRAIN FROM TOP TO BOTTOM

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Depression and Manic Depression

Anxiety Disorders

Alzheimer’s-type Dementia

Brain Imaging

Some people who suffer from anxiety disorders cannot recall any traumatic event that might explain their condition. This lack of recall might be due to a stress-induced dysfunctionof the hippocampus.

The massive activation of receptors for the glucocorticoids secreted by the adrenal glands may cause a reduction in the volume of the hippocampus. This may be one explanation for the learning deficits observed in rats that are subjected to stress, or the weak explicit memories of humans who are very anxious.

But what makes the relationship between stress and memory even more complex is the well known phenomenon of “flashbulb memory”, in which memory is enhanced by a moderate, short-term stress, because of the way that epinephrine facilitates the functioning of the hippocampus.

Lastly, stress hormones do not seem to have any deleterious effects on the amygdala and might even improve its functioning, thereby augmenting unconscious emotional memories at the expense of conscious explicit ones. This would be a logical explanation of the mechanism whereby stress prepares us to react promptly to dangers without thinking about them too much first.

BRAIN ABNORMALITIES ASSOCIATED WITH ANXIETY DISORDERS

People with various anxiety disorders display abnormalities in the size or neural activity of various structures in their brains.

For instance, brain-imaging studies of combat veterans with post-traumatic stress disorder show that when they listen to recordings that bring back their worst memories, their amygdalae become more active than other people's.

The amygdala also appears to be involves in triggering panic attacks, through its central nucleus. This structure maintains connections with several other brain structures, particularly in the brainstem, that control autonomic functions such as respiration and heart rate.

Source: Irwin et al., 2001

Activation of the amygdalae by a negative stimulus

The amygdala is thus ideally positioned to set off the various symptoms of a panic attack. And animal studies have in fact shown that stimulating the central nucleus of the amygdala either electrically or with drugs does in fact produce the behaviours associated with panic.

Cross-section of the pons (rostral to the motor nuclei of the trigeminal)

The locus coeruleus is one of the brainstem nuclei that maintains close communications with the amygdala. This small nucleus contains almost half of all the brain neurons that use norepinephrine as a neurotransmitter. The locus coeruleus also projects its axons to those parts of the brain that may be associated with panic disorders (the amygdala, hippocampus, septum, cortex, brainstem, reticular formation, etc).

Stimulating an animal's locus coeruleus, like stimulating its amygdala, produces anxiety behaviours. As therefore follows logically, substances with tranquilizing effects, such as benzodiazepines, alcohol, and opiates, make the locus coeruleus less active.

Other studies indicate that the central grey nuclei, subcortical areas of the brain that are involved in the involuntary component of body movements, are abnormally active in people with obsessive-compulsive disorder.

The cortex plays its own significant part in anxiety disorders. The ventromedial region of the prefrontal cortex, which is recognized for its role as a modulator of the emotions and for its involvement in depression, also seems to play a primary role in the process of extinction that is the basis for many effective therapies for anxiety disorders.