By Prof. Rony Paz, Department of Brain Sciences
After experiencing a life-threatening or high-stress situation—anything ranging from exposure to combat, physical or sexual assault, accidents, natural disasters, or the loss of a close family member—many people will exhibit symptoms of acute stress disorder, such as difficulty sleeping, anxiety, and nightmares.
While for most people, these symptoms will subside with time, in some cases, the symptoms persist, accompanied by hyperarousal, negative thoughts and mood, avoidance behavior, and intrusive and unwanted memories of the event, such as flashbacks. This phenomenon is known as post-traumatic stress disorder (PTSD), a debilitating condition that can derail daily functioning, result in loss of one’s social connections and job, and even lead to suicidal behavior.
PTSD affects approximately 5-9% of the adult population, with cycles of remission and recurrence over a person’s lifetime. In some cases, the onset of symptoms is delayed until months or even years after the initial triggering experience. Although there are known genetic and environmental risk factors, the truth is that anyone who goes through a traumatic event in their lifetime—as much as 70% of the world’s population—is at risk of developing PTSD.
Current treatment strategies, such as cognitive-behavioral therapy, offer limited relief. Pharmacological and biological treatments are also of limited effectiveness, focused mainly on managing the symptoms. Indeed, clinicians prescribe the same drugs for PTSD that they prescribe for depression or anxiety; there is no treatment specifically tied to the physiological origin of PTSD.
Because it develops after intense events, PTSD is considered to be a disorder of emotional learning: Instead of learning an adaptive behavioral response in the face of danger, the brain learns to overreact to this emotional event, and sees danger everywhere and anytime. Modern neuroscience approaches have unveiled the brain and neural circuits that underlie this emotional learning and are now attempting to clarify why these networks fail to modulate the emotional response and allow traumatic memories to resurface.
Neuroimaging studies have shown that a set of brain regions—chiefly the amygdala, the prefrontal cortex, and the hippocampus—exhibit abnormal activity in PTSD patients. Recent behavioral models explain the symptoms as an inability to extinguish the original memory combined with an overgeneralization of the memory to daily, “safe” situations. My lab group in the Department of Brain Sciences has identified the specific neural network that “encodes” the trauma, and how that network contributes to these two processes (inability to extinguish memories and overgeneralization). The next steps in our research will involve targeting the specific representation in the network with advanced methods such as precision molecular biology and brain stimulation.
RONY PAZ IS SUPPORTED BY:
- Irene and Jared M. Drescher Fund for Clinical Research on Mood Disorders
- Irene and Jared M. Drescher Center for Research on Mental and Emotional Health
- Azrieli Institute for Brain and Neural Sciences
- Manya Igel Chair of Neurobiology
- The Sam and Frances Belzberg Research Fellow Chair in Memory and Learning supports a Staff Scientist in Prof. Paz’s lab
