The Frontal Lobes and Antisocial Behavior

One cannot take an introductory psychology or neuroscience class without hearing about the railway construction worker, Phineas Gage. In 1848 while blasting rock in Vermont an ill-fated crowbar was propelled through the left-side of Gage’s face and out the top of his skull. Remarkably, Gage never lost consciousness and managed to survive another 12 years with his cognitive skills reportedly intact, but as the story goes Gage’s personality was never the same after the incident (Costandi, 2010). Before the bilateral laceration to Gage’s frontal lobes, coworkers described Gage as personable, but that shortly after the event he began to exhibit psychopathic personality traits. It is said Gage lost all social inhibition and grew violent physically and sexually, all while maintaining his intellect (Costandi, 2010).

Over a hundred years before neuroimaging, the story of Phineas Gage gave scientists and medical professionals their first look in to functional neuroanatomy. Gage’s story indicated that personality was held in a different part of the brain than intellect and motor control. Today, it is widely accepted that the frontal lobes primarily control mood, decision making, judgment and inhibition (Scott, 2013). Phineas Gage was not the only person in history to have their frontal lobes physically altered bringing forward a change in personality. Between the 1940s and 1960s, around 40,000 patients underwent the psychosurgery popularized by Walter Freeman and James Watt called the frontal lobotomy: In which slender metal rod was inserted through a drilled hole in the skull or behind the eye socket and pivoted around two centimeters into the frontal lobes (Pressman). The surgery was done to correct many psychological ailments; from depression, schizophrenia, and anxiety to disruptive behavior, pain and moodiness (Pressman). The practice of lobotomizing patients ceased in the early 1960s as patients were seen to lack emotional expression and to have little to no energy or drive (Dewey, 2007).  Additionally, some patients appeared to be ‘stimulus-bound’ responding to pleasurable things around them such a eating and masturbation, with no regard to consequence and exhibited an inability to set goals (Dewey, 2007).

My question is, why did Phineas become a violent and cruel person after the severing of his frontal lobes, while the thousands of lobotomy patients merely listless after having an ice pick swirled through their frontal lobes? The answer might lie in the area between the orbital frontal cortex (OFC) and the amygdala. The orbital frontal cortex, is a part of the brain that controls decision making and impulsivity. The OFC also receives external stimuli and projects them to the amygdala, which is the center of the brain that control fear. Both the OFC and the amygdala have reduced volume and activity in patients with ASPD (James, 2003). Could Phineas Gage have had the projection pathways from his OFC to his amygdala altered by his deep lesion, while the lobotomy patients only had their OCT changed by their more superficial lesions? According to the picture below, one could see that this could be the case…

 

Orbital Frontal Lobe. (Wikipedia, 2015)

The Amygdala. (Davis, 2011)

The frontal lobotomy. In this photo one can see that a frontal lobotomy would affect the Orbital Frontal Cortex (OFC). (Freeman, 2010)

Gage (Keuchenius, 2014)

Here one can see that the rod could have damaged the OFC and the area between the OFC and the amygdala, destroying the projection pathway between the two areas.  Could the damage between these two parts of the brain lead to psychopathic behavior exhibited by Gage, by blocking communication between the impulse control center and the fear control center of the brain, leading anti-social behavior? If so, what future research question should scientists be asking?

Currently, there is no efficacious pharmacological or psychotherapy treatment options for disruptive behavior disorders such as oppositional defiant disorder, conduct disorder, antisocial personality disorder, or psychopathy (Uptodate, 2015). Currently, prescribers will recommend therapy and give an atypical antipsychotic or mood stabilizer to reduce violent behavior, but neither therapy nor drugs have not been shown to change the underlying personality that promotes social irresponsibility and guiltless behavior (Uptodate). Is it time medical researchers started looked to neuroanatomy to alter personality?  Neuroscientist have ways to mechanically stimulate the OFC and the amygdala using deep brain stimulation, but with a possibly poor connection between the two parts of the brain this stimulation might not improve behavior.

We need to look for ways to strengthen the pathway Phineas Gage had severed, the connection that may be underactive in ASPD patients between their OFC and amygdala. Neuroscience has taught us that neurogenesis occurs throughout the adult lifespan. Through intensive and early therapy focusing on fear conception and impulsivity, practitioners might be able to ‘rewire’ the brain to strengthen the connection between the impulse center and the fear centers of the brain. Also in the past decade there have been medical advances made targeting neural pathways such as vagus nerve stimulation and prescribing pharmaceutical agents such as D-cycloserine during therapy to enhance synaptic activity (Wikipedia, 2015). While at this time practitioners have no perfect way to strength brain circuits, neurosciences research in this field could change the future treatment of not only personally disorders, but many psychiatric conditions.

 

 

 

Works Cited

Costandi, M. (2010, November 8). Phineas Gage and the effect of an iron bar through the head on personality. Retrieved March 11, 2015, from http://www.theguardian.com/science/blog/2010/nov/05/phineas-gage-head-personality

Davis, L. (2011, September 1). Arguing with Your Spouse: The Emotional Hijacking. Retrieved March 12, 2015, from http://www.psychologicalgrowth.com/arguing-wtih-your-spouse/

Dewey, R. (2007, January 1). Effects of Lobotomies | in Chapter 02: Human Nervous System | from Psychology: An Introduction by Russ Dewey. Retrieved March 11, 2015, from http://www.intropsych.com/ch02_human_nervous_system/lobotomy_effects.html

Freeman, S. (2010, January 1). How Lobotomies Work. Retrieved March 12, 2015, from http://science.howstuffworks.com/life/inside-the-mind/human-brain/lobotomy1.htm

James, R. (2003, January 2). Neurobiological basis of psychopathy | The British Journal of Psychiatry. Retrieved March 11, 2015, from http://bjp.rcpsych.org/content/182/1/5

Keuchenius, K. (2014, October 31). Phineas-Gage. Retrieved March 12, 2015, from http://www.united-academics.org/magazine/mind-brain/mind-blowing-brain-cases-the-man-with-a-hole-in-his-head/attachment/phineas-gage/

Ressler, Kerry J., and Helen S. Mayberg. “Targeting Abnormal Neural Circuits in Mood and Anxiety Disorders: From the Laboratory to the Clinic.” Nature Neuroscience 10.9 (2007): 1116-124. Web. 8 Apr. 2015. http://www.nature.com/neuro/journal/v10/n9/abs/nn1944.html

Orbitofrontal cortex. (2015, January 1). Retrieved March 12, 2015, from http://en.wikipedia.org/wiki/Orbitofrontal_cortex

Pressman, M. (n.d.). Frontal Lobotomy and Ethical Questions of Psychosurgery. Retrieved March 11, 2015, from http://neurology.about.com/od/Neurosurgery/a/Frontal-Lobotomy.htm

Scott, T. (2013, January 1). Frontal Lobe – The Brain Made Simple. Retrieved March 11, 2015, from http://brainmadesimple.com/frontal-lobe.html

“UpToDate.” UpToDate. N.p., 11 Feb. 2015. Web. 11 Feb. 2015. <http://www.uptodate.com/home>.

“Wikipedia.” Wikipedia. N.p., 11 Feb. 2015. Web. 11 Feb. 2015. <http://www.wikipedia.com/home>.

Deep Brain Stimulation: A Solution to Severe Tourette’s Syndrome?

Tourette’s syndrome is a neurological disorder that is characterized by tics or, involuntary movements and verbalizations. For quite some time, the underlying etiology of Tourette’s syndrome was unknown. Studies had failed to find a particular brain abnormality through imaging, post mortem procedures, or genetic testing (Robertson, 2000). More recently, however, newer research has focused on two different neurologic mechanisms at play: dysfunction in the cerebral cortex and the brain pathways underlying the tics that characterize the disease itself (Segawa, 2003).

Both investigational approaches have implicated the basal ganglia as a central area of dysfunction in the brains of those suffering from Tourette’s syndrome. The basal ganglia is made up of several, smaller brain regions: the striatum, the globus pallidus, the nucleus accumbens, the substantia nigra, and the subthalmic nucleus. The basal ganglia is largely responsible for controlling movement. More specifically, “the motor circuits within the striato-pallidal complex are thought to facilitate desired movement and inhibit unwanted movement through their influence via thalamus, mainly on precentral motor cortical regions” (Marsden & Obeso, 1994). The level of dysfunction within the basal ganglia extends even beyond the motor circuits. That is, even non-motor basal ganglia-thalamocortical circuits are involved in the pathophysiology of Tourette’s syndrome (Segawa, 2003). Put simply, the etiology of Tourette’s is now widely recognized as a defect in the cortical-basal-ganglia-thalamo-cortical neuronal circuit. This abnormality has been linked to different neurotransmitters: decreased function in dopamine neurons (due to increased dopamine receptor sensitivity) and decreased function of serotonin neurons within the brainstem (Segawa, 2003).

Though our understanding of the neural mechanisms underlying Tourette’s syndrome has increased, our ability to treat Tourette’s syndrome specifically is still limited. There are various treatment modalities (pharmacological, behavioral, procedural) that have been utilized to help improve the symptoms associated with Tourette’s syndrome. Pharmacologically, neuroleptics (e.g. haloperidol and pimozide) are often prescribed to help suppress tics. Behaviorally, awareness and competing response training have both been shown to help reduce tic symptoms. However, these interventions are not helpful for everyone.

In cases where tics are severe and intractable to other treatment, deep brain stimulation might be an option worth pursuing. Deep brain stimulation or, “DBS,” is a procedural treatment in which electrodes are surgically placed within different, specific brain regions. These electrodes are connected to a small generator that is implanted within the chest wall. DBS works by electrically altering the abnormal function in the surrounding brain regions. It has often been referred to as the “brain pacemaker” because it delivers consistent pulses of electrical charge that work to return brain rhythms to normal (Deep Brain Stimulation for Movement Disorders, 2015). DBS can vary from individual to individual in that it almost entirely depends on electrode placement. For the treatment of severe Tourette’s syndrome, various brain regions have been identified as targets for DBS.

Cannon, Silburn, Coyne, O’Maley, Crawford, and Sachdev (2012) identified nine different brain regions that have been targeted via DBS. These neural targets were located in the thalamus, pallidum, ventral caudate, and anterior internal capsule. However, in their specific study, they were able to isolate a single region as an effective target for DBS in the treatment of Tourette’s syndrome: the anteromedial globus pallidus. The anteromedial globus pallidus was initially selected “because it is the main output regulator of the basal ganglia and appears to play a role in controlling motor function and behavior” (Cannon et al., 2012).

In their study, 11 patients with severe and treatment-refractory Tourette’s syndrome had DBS electrodes placed bilaterally in the anteromedial globus pallidus. Ten of the eleven patients (i.e. 91 percent of their sample) endorsed having an effective response to DBS within 3 days of their surgical procedure. Specifically, they reported having decreases in the quantity, severity, frequency, and intensity of tics. Many of the patients also experienced obsessive-compulsive symptoms prior to DBS. Of those who reported having such symptoms, there was a significant decrease (59%) in scores (on the scale used to quantify OCD-related symptoms) following DBS.

As with any surgical procedure, DBS does not come without its associated risks. While in surgery, a patient could suffer from hemorrhage, stroke, infection, or cardiac complications (Deep Brain Stimulation, 2015). There are even side effects that could take place after surgery. These include, but are not limited to, seizure, infection, headache, insomnia, and memory impairments (Deep Brain Stimulation, 2015). It is for this reason that is important to utilize and exhaust other treatment modalities before turning to DBS. However, severe, treatment-refractory Tourette’s syndrome and its corresponding symptoms can be debilitating for an individual. Consider, for example, a life where you frequently lose control of your body or the things that you say. Such symptoms can significantly impact a person’s functioning in all facets of life – socially, occupationally, academically. It is in these severe cases that the benefits of DBS might outweigh the risks and, more generally, could be a practical solution to Tourette’s syndrome.

References

Cannon, E., Silburn, P., Coyne, T., O’Maley, K., Crawford, J.D., & Sachdev, P.S. (2012). Deep brain stimulation of anteromedial globus pallidus interna for severe Tourette’s syndrome. The American Journal of Psychiatry, 169(8), 860-66.

Deep brain stimulation for movement disorders. Neurological Surgery. (University of Pittsburgh, 2015). Retrieved from http://www.neurosurgery.pitt.edu/centers-excellence/epilepsy-and-movement-disorders-program/deep-brain-stimulation-movement-disorders

Deep brain stimulation. Tests and Procedures. (2015, Mayo Clinic). Retrieved from http://www.mayoclinic.org/tests-procedures/deep-brain-stimulation/basics/risks/prc-20019122

Marsden, C.D. & Obeso, J.A. (1994). The functions of the basal ganglia and the paradox of stereotaxic surgery in Parkinson’s disease. Brain, 117(4), 877-97.

Robertson, M.M. (2000). Tourette syndrome, associated conditions and the complexities of treatment. Brain, 123(3), 425-462.

Segawa, M. (2003). Neurophysiology of Tourette’s syndrome: pathophysiological considerations. Brain and Development, 25(1), S62-S69.

Shapiro, A.K. & Shapiro, E. (1981). The treatment and etiology of tics and Tourette syndrome. Comprehensive Psychiatry, 22(2), 193-205.

Tourette syndrome fact sheet. National Institute of Neurological Disorders and Stroke. (2012). Retrieved from http://www.ninds.nih.gov/disorders/tourette/detail_tourette.htm

The Basics in Learning to Fear

Living through dangerous situations and learning to avoid them in the future have forever been key elements in human survival and evolution. The human brain is naturally equipped with mechanisms – subconscious reactions commonly referred to as “fight or flight” responses (Higgins & George, 2013) that are largely regulated by the amygdala and prefrontal cortex. This startle response and fear learning – “conditioning” – can save us from true danger, but also has the potential to overwhelm and impair normal daily functioning, resulting in various degrees of distress or psychiatric disorders (Krystal, 2011). This blog post will present the fundamentals of how the brain forms memory and learns fear, and will introduce the implications of impaired memory consolidation on the brain suffering from post-traumatic stress disorder.

What is a memory? It seems like a basic question, however the development, the storage, and the maintenance of memories within the brain are only loosely understood within the field of neuropsychology. The scientist Donald Hebb discovered in 1949 that memories are associated with tightly knit clusters of rapidly firing neurons within various regions of the brain associated with memory, those regions including the hippocampus, amygdala, and various regions of the cortex. Hebb’s Postulate suggests that learning changes the physical structure of the brain by inducing dendritic spine formation, projections that reach out to nearby neurons.

“When an Axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.” (Hebb, 1949)

Hebb rephrased it simply: “neurons that fire together, wire together”. More connections increase the frequency, intensity, and duration of signal transmission to postsynaptic neurons, thus increasing the potential for gene expression causing dendritic growth, and enduring plasticity.

Once memories are formed, they undergo a process called consolidation, “the process by which sensory information…solidifies into fully-formed memories to be stored for the long term.” (Romm 2014).  Main structures involved in memory system consolidation and storage are the hippocampus, the parahippocampal gyrus, the cortex, and the cingulate gyrus. Recent memories are formed initially in the hippocampus and, as they are consolidated, they are transferred to various layers and regions throughout the cortex to be stored. Of course, not all memories are long-lasting. As space is limited, the brain has many tools for making room for more important information. For example, it is possible for superfluous information to “passively decay” over time; with less use, signals between neurons become weaker (Higgins & George, 2013).

The fate of memories is also influenced by “interference” experienced during memory consolidation, which has potential to impair future recall (Higgins & George, 2013). This may result in memory loss or inaccurate recall of details or sequence. Disruptions during memory consolidation are believed to lay the groundwork for dysregulated, pathological fear learning and response that is manifested by several PTSD symptoms.

In PTSD, interference affecting the acquisition of new information could be caused by hyper-arousal of the amygdala and the subsequent flooding of stress hormones in reaction to a traumatic event. The exact consequences of interference are, again, unknown, however effects manifest as symptoms that include distorted interpretation of events, sequential and spatial recall, as well as inability to remember important details. Examples of DSM-V criteria that represent the effects of interference on memory consolidation include:

  • Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).
  • Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative amnesia and not to other factors such as head injury, alcohol, or drugs).
  • Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame himself/herself or others. (5th ed.; DSM-5; American Psychiatric Association, 2013).

Understanding the significance of impaired memory in PTSD and the brain’s enormous capacity for change and growth guides treatment interventions. Just as fear is conditioned, it can also be extinguished through a process called “extinction”. Extinction is achieved by learning new information about feared stimuli after repeated exposure without negative repercussions. Old memories are not erased, however newer, stronger, and more accurate memories may be formed. (Krystal, 2011). This concept is the basis for Cognitive Processing Therapy (CPT), a widely adopted form of evidence-based cognitive and behavioral modification therapy – a variation of Cognitive Behavioral Therapy (CBT) – that purposefully re-exposes traumatized patients within a safe environment. Repeated exposure to a feared stimulus without experiencing the feared outcome may eventually diminish the strength of the memory, leading to extinction. This exposure therapy along with processing the emotions, thoughts, and behaviors associated with the original beliefs is effective in diminishing inaccurate cognitive distortions in traumatic memory (Rabalais, Resick, & Sobel, 2009). According to the VA’s website geared toward PTSD public education, CPT is such an effective treatment for PTSD in veterans that the VA’s Office of Mental Health Services has pushed for a national therapist training campaign in order to provide CPT to all veterans in need.

Memory formation, maintenance, somatic associations, alterations and distortions are all abstract and enigmatic phenomena in neuropsychology. The elements of interference, distortion, and distress in traumatic memory add even more to the list of mysteries.

 References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental Disorders: DSM-5. Washington, D.C: American Psychiatric Association.

Cognitive Processing Therapy (2014). Retrieved from: http://www.ptsd.va.gov/public/treatment/therapy-med/cognitive_processing_therapy.asp

Higgins, E., George, M., (2013). The Neuroscience of Clinical Psychiatry (2nd ed.). Philadelphia, PA. Lippincott Williams & Wilkins. p. 260-262.

Krystal, J. [via tildecafe]. (2011, October 22). Stress, resiliency, and PTSD: from Neurobiology to treatment [Video file]. Retrieved from: https://www.youtube.com/watch?v=-tyMJ0rRdkE

Lu, S. (2014). Erasing bad memories. Retrieved from: http://www.apa.org/monitor/2015/02/bad-memories.aspx

Rabalais, AE., Resick, PA., Sobel, AA. The effect of cognitive processing therapy on cognitions: impact statement coding. Journal of Traumatic Stress. 2009. 22(3): 205-211. doi:  10.1002/jts.20408

Romm, C. (2014). Changing memories to treat PTSD. Atlantic. Retrieved from: http://www.theatlantic.com/health/archive/2014/08/changing-memories-to-treat-ptsd/379223/