SAN FRANCISCO – Hoarding disorder is characterized by a distinct pattern of serotonergic dysfunction different from that seen in obsessive-compulsive disorder (OCD) or major depression, Sanjaya Saxena, MD, reported at the annual conference of the Anxiety and Depression Association of America.
He presented the findings of the first-ever study to examine neurotransmitter function in patients with hoarding disorder. In contrast to hoarding disorder, the neurobiology of OCD is among the most extensively studied and best understood of any psychiatric disorder, with Dr. Saxena having made important contributions to this body of knowledge.
Bruce Jancin/Frontline Medical News
Dr. Sanjaya Saxena
The findings underscore the prescience of the authors of DSM-5 in removing hoarding disorder from under the umbrella of OCD and giving it its own separate diagnostic category.
“Our study provides more evidence suggesting that OCD and hoarding disorder are two separate disorders that do sometimes occur together in patients, but not necessarily more often than other disorders do. OCD is found in only about 15% of patients with hoarding disorder, and vice versa. Depression is much more commonly comorbid, and [attention-deficit/hyperactivity disorder] is present in about one-quarter of hoarding disorder patients,” according to the psychiatrist.
His study included 8 patients with hoarding disorder and 14 age- and sex-matched normal controls who underwent positron emission tomography with carbon-11-labeled DASP, a ligand that binds with high selectivity to the brain serotonin transporter. The serotonin transporter is a neuronal membrane protein whose main function is to recycle serotonin from synapse back into the neuronal cell body. The serotonin transporter also is the primary site to which serotonin reuptake inhibitor medications bind. Serotonin transporter binding is associated with fear conditioning, amygdala reactivity, the cortisol response, and state anxiety.
Subjects with hoarding disorder proved to have significantly greater serotonin transporter binding than healthy controls in the bilateral amygdala, nucleus accumbens, putamen, and right caudate nucleus. In contrast, their serotonin transporter binding was significantly diminished, compared with controls, in the bilateral retrosplenial posterior cingulate cortex. Severity of hoarding symptoms was correlated with serotonin transporter binding in the right anterior cingulate cortex and right orbitofrontal cortex, but negatively correlated with serotonin transporter binding in the bilateral posterior thalamus, Dr. Saxena reported.
“The binding pattern is almost opposite that seen in OCD,” he observed.
The new study of serotonergic function in hoarding disorder, taken together with earlier brain imaging studies of regional glucose metabolism and functional MRI studies conducted by Dr. Saxena and other research groups, point to a couple of areas of the brain as being strongly implicated in the pathophysiology of hoarding disorder – most notably, the anterior and posterior cingulate cortex.
Particularly intriguing, in Dr. Saxena’s view, is the retrosplenial posterior cingulate cortex, located in Brodmann areas 29 and 30. The retrosplenial posterior cingulate cortex, part of the default mode network, is involved in emotional functioning, learning, planning, navigation, as well as autobiographical, episodic, and visuospatial memory.
“Abnormalities of all those functions are found in hoarding disorder patients, so the retrosplenial posterior cingulate cortex is a candidate for further study,” according to Dr. Saxena.
His neurotransmitter study was funded by the university’s department of psychiatry. He reported having no financial conflicts.