Synaptic Loss and the Pathophysiology of PTSD: Implications for Ketamine as a Prototype Novel Therapeutic
PTSD + Ketamine Treatment
Studies of the neurobiology and treatment of PTSD have highlighted many aspects of its pathophysiology that might be relevant to treatment. The synaptic deficits associated with PTSD, as a result of the chronic stress caused by persisting symptoms, may contribute to its complex profile of symptoms and functional impairments. Synaptic disconnection syndrome, particularly involving regions of the brain associated with fear, may play a significant role in the pathophysiology of PTSD and partially explain why compromised neuroplasticity impairs healing.
About the study
This study identifies ketamine as an effective treatment to improve neuroplasticity, and therefore aid in the treatment of PTSD. Ketamine demonstrates abilities to increase synaptic connectivity, modulate glutamatergic pathways, and increase brain-derived neurotrophic factor (BDNF), which all play a role in enhancing neuroplasticity. These positive impacts on one’s neurophysiology may partially explain the rapid-acting antidepressant effects that individuals with depression and PTSD experience with ketamine treatments.
The persisting potentiation of neuroplasticity of ketamine suggests a novel role in the treatment of PTSD: to enhance the efficacy of progressive exposure, cognitive processing therapy (CBT), eye movement desensitization and reprocessing (EMDR), or other exposure-based therapies. Ketamine shows promise as a tool in treating PTSD, as research continues to explore its synergy with other methods.
