Until recently, the cerebellum, often referred to as “the little brain,” was thought to regulate motor movements, balance, and coordination. However, according to an article published in 2009, the cerebellum has 70 billion neurons (compared to the 25 billion in the cerebral cortex) giving it 2.5 times more neurons than the brain region responsible for executive functioning. Additionally, the cerebellum projects into several brain regions including the pons, medulla, reticular formation, and thalamus. These regions are responsible for functions such as consciousness, sleep, respiration, and alertness. Therefore, it is hard to believe that this complicated, neuron-rich, and highly communicative structure is solely involved in movement.

Recently, much research has focused on the involvement of the cerebellum in different psychiatric disorders, including attention deficit hyperactivity disorder (ADHD), autism spectrum disorders (ASD), schizophrenia, and anxiety disorders. A review conducted by Phillips et al. in 2015 concluded that damage to the structural integrity of the cerebellum may result in a lower cerebellar volume in most of these psychiatric disorders.

In ADHD, loss of cerebellar volume increases with age, starting in adolescence and tapering in adulthood. Interestingly, patients who use psychostimulants (which are highly effective in the treatment of ADHD) have an increase in cerebellar volume over time compared to untreated ADHD patients. The size of the vermis, the medial part of the cerebellum, also seems to play a role in the outcome of ADHD, where patients with a smaller vermis having poorer outcomes, resulting in more severe attention problems. Similar size irregularities have been found in ASD.

One of the defining symptoms of ASD is stereotyped (repetitive and/or aimless) movements—a behavior controlled by the cerebellum. Cerebellar damage in infants positively correlates with the occurrence of autism. Notably, animal studies demonstrate decreased cerebellar volume leads to abnormal social behaviors, suggesting that the cerebellum is also involved in social interactions. There are also fewer Purkinje cells (a class of inhibitory neurons in the cerebellum) found within the cerebellum of animal models of autism. With loss of inhibitory input from Purkinje cells, the cerebellum could become overexcited. The overexcitation, in turn, may contribute to issues in social interaction and cognitive deficits. Interestingly, a similar pattern seems to be implicated in schizophrenia.

Cognitive deficits are linked to cerebellar dysfunction and abnormal connections with the cerebral cortex in schizophrenia. When doing memory recall tasks, there was lower cortico-thalamic-cerebellar activity in patients with schizophrenia compared to healthy individuals. In addition to reduced volume, there also seems to be less blood flow to the cerebellar cortex and vermis when completing cognitive tasks, which could suggest an underlying issue with communication to other brain regions. Interestingly, even though there is decreased volume and blood flow in the cerebellum, the number and integrity of Purkinje cells do not seem to differ between healthy individuals and patients with schizophrenia.

As for anxiety disorders, the neural pathways affected are not yet fully understood by scientists. Some studies suggest that anxiety disorders may also be characterized by less blood flow to the cerebellum and lower cerebellar volume, as seen in other psychiatric disorders. PTSD patients re-experiencing a traumatic event have increased cerebellar activity. Patients with panic disorders showed a similar increase in cerebellar activity, as indicated by an increase in glucose metabolism.

Overall, the research shows that the cerebellum plays a key role in many psychiatric disorders. However, there is still a lot to explore and learn about the little brain with a big potential. 

By Mariam Melkumyan