Psychiatry needs neurosciences

It challenges our intuition to think that brain neurons like these are responsible for all of our thoughts, emotions and mental disorders—but they are. Credit: Nephron Wikimedia (CC BY-SA 3.0) 
Earlier this month, JAMA Psychiatry published a groundbreaking addition to their journal’s line-up: an educational review intended to educate psychiatrists about neuroscience. A group of psychiatrists led by David Ross described how and why post-traumatic stress disorder (PTSD) should be clinically evaluated from a neuroscience framework. The fact that this editorial was published in one of psychiatry’s leading journals is no small feat.

Psychiatry houses a large and powerful contingency that argues neuroscience has little clinical relevance. The relevance of neuroscience to psychiatry was the subject of a recent Op-Ed debate in the New York Times: “There’s Such a Thing as Too Much Neuroscience” was rebutted with “More Neuroscience, Not Less.” This specific debate—and the dense politics as a whole—exists because competing frameworks are vying for competing funding, a conflict that pre-dates Freud’s departure from neurology.

That the relevance of neuroscience to psychiatry is still questioned is blatantly outlandish: what organ do psychiatrists treat if not the brain? And what framework could possibly be more relevant than neuroscience to understanding brain dysfunction?

In his review, Ross tactfully presented his case for neuroscience, describing the obvious choice for a clinical framework as one “perspective,” making a delicate intellectual curtsey while supporting his case with data.

Ross discussed five “key neuroscience themes” (read: lines of evidence from burgeoning sub-fields) relevant to understanding and treating PTSD: fear conditioning, dysregulated circuits, memory reconsolidation, and epigenetic and genetic considerations. Each theme accounts for the diverse biological, psychological and social factors involved in PTSD—which is to say, these factors all have some affect on the brain mechanisms. Most importantly, Ross describes how a mechanistic approach allows clinicians to trace the specific causes of PTSD to specific treatments that can target those causes.

The delicate balancing act Ross performs reflects a conflict between competing clinical frameworks, which in turn, boil down to two different worldviews: one worldview is intuitive, the other is data-driven.How and why these worldviews clash is better felt than explained: perhaps I may explain the way I once felt.

The first time I saw a Purkinje cell, I was a high school sophomore in A.P. Biology. My teacher, Mr. Francom, had just explained that the Purkinje cell is a brain neuron and, from a central nub, its arms splay throughout the cerebellum connecting with other neurons. Similar connections throughout the brain formed the hardware for mental phenomenon—our ability to move, think, love, remember, etcetera. Experiments and data were involved.

Following this teaser Mr. Francom slid the Purkinje cell transparency onto the projector with a magician’s élan, revealing an eerie monstrosity: a fluorescent green cell. With its long dendritic tentacles, it seemed less like something you’d find between your ears and more like War of the Worlds meets the Kraken.

I’m sure I blurted out, “That thing lets me think?”

The Purkinje cell was an uncomfortable disconnect from my intuition of what makes me Me. Were my thoughts and feelings and memories all some extension of a tentacled neuron?

There was a palpable threat to realizing that my mental behavior, the phenomenon of Me, was produced by venomous-looking neural hardware—as if someone had pulled back the magician’s sleeve to reveal my own secret, destroying the beauty of my mental life.

Of course, that was just adolescent silliness. The beauty of the brain remains that it actually works, that combinations of lipid membranes, salt water, and proteins actually do produce the love I feel towards my wife or my experience of a sunset while zipping home on my Vespa. And yet it isn’t intuitive at all that this neural hardware exists—would you have assumed your thoughts came from a Purkinje cell?

Knowledge of the brain’s hardware is even more relevant when things go awry, especially to understand specific phenomena that patients report as symptoms in mental illness.

In their recent Molecular Psychiatry article, Michael Treadway and Chelsea Leonard discussed the distinction between a patient’s reported symptom and a patient’s underlying neural hardware, which they refer to as “neural substrate.” More than a scholastic exercise, this distinction is a clinical tool that allows greater clinical precision because symptoms can have multiple causes.

Imagine it is 3AM and a patient enters the emergency room reporting “chest pain.” This is a serious symptom and, without question, the emergency room staff will rush to sort out the underlying cause of the chest pain. They will immediately examine the patient and order an electrocardiogram to see if the heart’s electrical activity has changed, revealing a heart attack. They will draw blood to look for evidence of heart damage or clot formation. They will order a chest X-ray to rule out pneumonia or a broken rib. The emergency doctors know that chest pain is a phenomenon with many causes and to treat the patient, they must correctly diagnose and treat the underlying cause.

Anxiety is also a cause of chest pain. Imagine that, after ruling out life-threatening causes, the doctors learned that while in the food court at a local mall the patient broke out in a sweat, her vision blurred, and her chest tightened. If she further reported that this happens every time she goes to a large public space, the doctors might diagnose her with a panic attack produced by agoraphobia, a fear of open public spaces.

But consider if our patient recently immigrated from Syria and, last year, was shopping with her family in a city marketplace when a car bomb exploded. Post-traumatic stress disorder (PTSD) now becomes the leading diagnosis.

And yet PTSD, agoraphobia, and panic attack are not causes. They are phenomena. Anxiety is a symptom, an anthromorphism of the phenomenon produced by a network of millions if not billions of tentacled neurons firing together.

Ross helps us understand that patients with PTSD have an overactive sympathetic nervous system, which contributes to symptoms such as hyperarousal, hypervigilance, and accentuated startle response, symptoms that can spiral into a panic attack. Further refining our scope to the overproduction of adrenaline in the hypothalamic-pituitary-adrenal axis guides the clinician to prescribe propranolol and prazosin. These medications block aspects of the adrenergic system, thus targeting specific mechanisms that alleviate PTSD symptoms.

Treadway and Leonard would view Ross’s system as substrate-centered, one wherein mental phenomena are followed to and treated at their root cause.

Treating a person by focusing on a single receptor—in the case of prazosin, the alpha-1-adrenergic receptor subtype!—is not a cold, dehumanizing abstraction. By looking beyond the phenomena of our inner experience, to the Purkinje cells hard at work, we can create a pragmatic, nuts and bolts method of understanding and healing ourselves.

Plus, studies show that it works.

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