As the biological seat of mental life, the brain is center stage in the investigation of what causes and characterizes mental disorders.
The roots of the various conditions defined by the medical field of psychiatry—such as major depression, schizophrenia, or generalized anxiety disorder—are still not well understood. Further, individuals who share a psychiatric diagnosis do not necessarily have identical conditions—they may have some symptoms in common but not others. It would be too simple to describe a uniform “depressed brain” or “schizophrenic brain.”
But clinical neuroscientists have been able to uncover ways in which the brains of individuals diagnosed with such conditions tend to differ from the norm, on average. As examples of neuroscientific findings linked to some of these diagnoses show, particular aspects of brain structure and (dys)function appear to be especially relevant to certain forms of mental illness.
Are psychiatric disorders brain diseases?
Psychiatric disorders are disorders of the brain in the sense that the dysfunctional thoughts and behaviors they involve are enabled by the brain—as all thoughts and behaviors are. And neuroscientists examining the structure and function of particular parts of the brain have found various differences, on average, between people who have psychiatric diagnoses and those who do not.
However, the fact that particular brain abnormalities are associated with these disorders does not necessarily mean that they cause the development of the disorders. In the case of conditions such as stroke or Huntington’s disease—which are largely treated by neurologists and other professionals outside of psychiatry—the biological progression of the condition is relatively well understood. Given a current lack of understanding of the biological roots of psychiatric disorders, the absence of clear biomarkers for diagnosis, and other reasons, some question the idea that they should be called brain diseases.
Importantly, the factors underlying mental health disorders extend beyond innate differences between the brains of people with and without disorders. These may include external sources of stress as well as additional biological causes such as the composition of the microbiome in the digestive system.
What are some ways the brain differs in people with depression?
Studies of individuals with major depressive disorder have identified lower gray matter volume in a number of brain areas relative to those without depression. These include parts of the prefrontal cortex (important for decision-making and cognitive control), the hippocampus, the anterior cingulate cortex, and others. There is also evidence of a higher degree of folding in the cortex in certain areas and lower white matter integrity in others.
People with depression have also shown functional brain differences in studies, such as reduced activation in a brain area called the striatum when anticipating or receiving a reward. Other research has reported atypical connectivity between some brain structures and levels of activity in brain networks called the fronto-limbic network and the default mode network (active when the brain is disengaged from activities or stimulation).
Widely used antidepressant medications boost the presence of the neurotransmitter serotonin in the brain, and the role of such chemicals in depression has long been of interest. But depression is not believed to be caused simply by low levels of serotonin. Medications targeted to the neurotransmitters norepinephrine and dopamine may also help alleviate depression, and reduced levels of the neurotransmitter GABA have been reported in patients with depression.
Other research on the biology of depression focuses on the potential roles of inflammation and makeup of the microbiome in the digestive system in the development of the condition.
What are some ways the brain differs in people with anxiety disorders?
The amygdala, which is centrally involved in the brain’s response to threats, is thought to play an important role in anxiety. So are other major components of the limbic system, the hippocampus (critical for memory and fear learning) and the hypothalamus (which controls the release of hormones).
Increased activation of the amygdala, and an area that receives input from the amygdala (the insular cortex), has been found in a number of anxiety disorders. And in post-traumatic stress disorder (PTSD), research suggests that areas of the brain that inhibit the activity of the amygdala (such as the ventral medial prefrontal cortex) are themselves less active. Neuroimaging studies vary, however, in terms of whether structures considered abnormal in anxiety disorders, such as the amygdala and the prefrontal cortex, show increased or decreased activity—which may be due to the use of different experimental tasks and other variables.
Multiple neurotransmitters, including norepinephrine, serotonin, glutamate, and GABA, appear to have a part in anxiety disorders, but not necessarily in straightforward ways. For example, increased activation of the serotonin system may promote or dampen anxiety, depending on the part of the brain where it happens. Meanwhile, a high level of activity in the norepinephrine system has been linked to some anxiety disorders.
How does addiction change the brain?
With repeated use of pleasure-inducing drugs, the patterns of use become reinforced through changes in the brain. The neurotransmitter dopamine, which is involved in the reinforcement of behaviors more generally, is thought to play an important part in the development of addiction. Research has found that most addictive drugs can cause sudden surges of dopamine in a brain area called the nucleus accumbens. With recurring surges of dopamine due to drug use, the brain is encouraged to repeat the pleasurable behavior (and to associate it with related cues in the environment), and it becomes more automatic.
Over time, habitual substance use can alter the brain’s reward circuit in ways that make it less sensitive to the drug, inducing the user to seek increasing amounts in order to experience the same sense of reward. These alterations include reductions in the amount of neurotransmitters produced and the number of receptors for those chemicals.
Researchers have observed lower activity, among those who abuse alcohol, cocaine, and other substances, in brain areas involved in inhibition and emotion control: the orbitofrontal cortex, cingulate gyrus, and dorsolateral prefrontal cortex. Abnormal dopamine function connected to these regions could help explain key aspects of addiction such as reduced control over drug-seeking behavior.
Are some brain differences related to more than one disorder?
While scientists commonly link brain characteristics to specific disorders, some aspects of brain structure and function appear related to a variety of conditions. This may reflect overlap in the characteristics and symptoms of different psychiatric disorder categories.
For example, elevated activity in parts of the brain key to emotional processing and diminished activity in parts of the frontal lobe have been linked to multiple conditions, including anxiety disorders and schizophrenia. And a recent analysis found evidence of neural commonalities among those with mood disorders and anxiety disorders: similarly, lower activity in a brain circuit related to cognitive control and higher activity in some emotion-related areas such as the amygdala. Mood and anxiety disorders are diagnosed separately but frequently co-occur and have shared features.
Characteristics of the brain’s wiring also appears to be related to risk for mental illness across diagnostic categories. An analysis of white-matter pathways (which connect different areas of the brain) found that a specific pattern involving two such pathways was associated with measures of psychopathology in adolescents—suggesting that structural connectivity is related to multiple conditions.
