ADHD and Adults

Attention deficit hyperactivity disorder (ADHD) is one of the most commonly diagnosed and recognized psychiatric disorders among school-age children but there seems to be disconnect when it comes to diagnosing adults. William-Orlando (2011) suggest that as many as 10% of children in the United States are diagnosed with ADHD, while Kessler et al. (2006) estimate that 4.4.% of the US adult population has ADHD with only 10.9% in treatment. Though this disorder has been traditionally been diagnosed in children, there has been an ongoing paradigm shift in the field of psychiatry and psychiatric nursing with an alteration in the treatment options across the full range of ADHD symptoms for both children and adults. As healthcare providers, it is essential to understand the diagnostic criteria of ADHD as a neurodevelopmental disorder and educate ourselves in the multidimensional causes, symptoms, and treatment modalities associated with ADHD in children and adults alike.

ADHD consists of a trio of symptoms that are defined by the DSM-5 as inattention, hyperactivity, and impulsivity. According to the DSM-5 (2013), when diagnosing individuals with ADHD, there needs to be a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development with several inattentive or hyperactive-impulsivity symptoms that were present before the age of 12 and symptoms that are present in two or more settings (such as school, work, home, or socially). As a neurodevelopmental disorder, ADHD is caused by a combination of genetics, brain size, gray matter thickness, childhood experiences, environmental factors, and the interaction and distribution of chemical receptors and neurotransmitters. Many of the symptoms present in ADHD are linked with abnormalities of various circuits involving the striatum and the prefrontal cortex, more specifically the dorsolateral prefrontal cortex (DLPFC), dorsal anterior cingulate cortex (dACC), orbitofrontal cortex (OFC) and the prefrontal motor cortex. As one of the most prominent symptoms of inattention in ADHD, inefficient processing in the DLPFC results in executive dysfunction and problems with selective attention. In addition, individuals with ADHD either fail to activate or there exists dysfunction of the dorsal anterior cingulate cortex (dACC). Dysfunction and failure to activate the dACC results in individuals experiencing problems sustaining attention. Impulsivity in individuals with ADHD is linked to the orbitofrontal cortex (OFC) while hyperactivity is associated with the prefrontal motor cortex.

Taken from Stahl's Essential Psychopharmacology

In addition to dysfunction of the PFC and striatum, studies conducted by Shaw, et al (2006) at the National Institute of Mental Health have shown that children with ADHD had smaller total brain volumes (in all four cerebral lobes, including white matter and gray matter, as well as the cerebellum) by approximately 5% compared with controls. In a follow-up study, Shaw (2006) also found that children with ADHD had global thinning of all the gay matter compared with the controls, and there was predominate thinning of gray matter in the PFC. As the individuals from this study grew into adolescence and showed the usual pruning of total gray matter, the children who remained impaired at follow-up had thinner gray matter in the medial PFC at the beginning of the study and children who grew out of the disorder showed a normalization of the gray matter thickness in the right parietal cortex.

There appears to a narrow-mindedness that occurs in psychiatry when diagnosing adults for ADHD, especially since this has been considered a predominantly child disorder. But what happens when the child diagnosed with ADHD grows up—do they simply grow out of the disease as well? Evidence suggests that the young individual with ADHD does not necessarily grow out of the problem, and symptoms tend to persist, although adolescents usually become more goal directed and less impulsive (Cipkala-Gaffin, 1998; Pelham et al, 1998). The presenting symptoms of a child with ADHD vary significantly from those of an adult, and it is the role of the clinician to provide a thorough and substantial analysis of the patient’s presenting symptoms and retrospective assessment to ensure appropriate diagnosis and evaluation. In a review on the diagnosis of adult ADHD, Primich and Iennaco (2012) discuss the risk for misdiagnosis and ineffective treatment because of the presence of symptoms and impairments held in common mood and anxiety disorders. Barkley (1990) writes that while children are typically referred to a clinician for diagnosis of ADHD by school officials and parents, most adult patients self-present which may explain the low percentage of adults receiving treatment for ADHD.

One of the major difficulties that clinicians face when assessing the adult is differentiating and understanding the presentation of inattention, impulsivity, and hyperactivity. Among adults, only 50% report symptoms of hyperactivity–impulsivity while 90% report prominent symptoms of inattention (Wilens & Dodson 2004). The common symptoms of hyperactivity found in children are less prominent in adults and evolve into a sense of inner restlessness, which can be demonstrated by shifting in seat, difficulty relaxing, and an inability to sit throughout a meeting (Primich & Iennaco, 2012). As the individual matures and ages, quantifiable problems that may have existed in their youth and adolescence, as measured by declining school performance, become more difficult to measure due to compensation of deficiencies. Primich and Iennaco (2012) write that direct and collateral information regarding such areas as the quality and character of interpersonal relationships, ability to routinely pay bills on time and keep promises and/or appointments can yield insight into the patient’s profile. Due to the retrospective criteria necessary for diagnosing an adult with ADHD, consulting family and friends of the individual as collateral can be helpful in determining the longitudinal scope of their symptoms and behavior.


American Psychiatric Association. (2013) Diagnostic and Statistical Manual of Mental Disorders, Fifth edition (DSM-5). Arlington, VA: American Psychiatric Association.

American Psychiatric Association. (2000). Diagnostic Criteria from DSM-IV-TR. Arlington, VA: American Psychiatric Association.

Barkley R.A. (1990) Attention Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. The Guilford Press, New York, NY.

Cipkala-Gaffin, J. (1998). Diagnosis and treatment of attention-deficit/hyperactive disorder. Perspective Psychiatric Care 34, 18.

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

Kessler R.C., Adler L., Barkley R., et al. (2006) The prevalence and correlates of adult ADHD in the United States: results from the national comorbidity survey replication. American Journal of Psychiatry 163, 716–723.

Primich, C., & Iennaco, J. (2012). Diagnosing adult attention-deficit hyperactivity disorder: The importance of establishing daily life contexts for symptoms and impairments. Journal of Psychiatric and Mental Health Nursing, 19, 362-373. doi:10.1111/j.1365-2850.2011.01845.x

Shaw P, Lerch J, Greenstein D, et al. (2006). Longitudinal mapping of cortical thickness and clinical outcome in children and adolescents with attention-deficit/hyperactivity disorder. Arch Gen Psychiatry 63, 540-549.

Wilens T.E. & Dodson W. (2004) A clinical perspective of attention-deficit/hyperactivity disorder into adulthood. Journal of Clinical Psychiatry 65, 1301– 1313.

Williams-Orlando, C. (2011). Patient beliefs on children’s attention-deficit hyperactice disorder. Integrative Medicine: A Clinician’s Journal, 10(2), 16-21.

Autism and “Mirror Neurons”

“Marissa, Marissa. Listen to me, Marissa. I can’t do this right now! I am just TOO busy! I need to save the princess from the dark one. Go shoe, shoe”. Picture this: first thing in the morning at the lockers. One hand on the hip and the other pointed towards me, waving. Eyes on the floor, face scrunched, eyes narrowed, and grimacing (“angry”). My job is to look away, fold my hands and ignore this behavior until he responded to with the socially appropriate response. He quickly comes around and follows his social script:  “OK..” (Deep breathes, hands folded, face changed to a smile and blinking eyes, waiting for my eye contact to return, changes voice to “happy”) “Good morning, Marissa. Can I go use the bathroom now?”. “Of course! See you in a minute B”. “Marissa? It’s going to be a great day. Thumbs up?”.

 When I make this face


Autism is one of the most devastating (DiCicco-Bloom, 2006) and talked about childhood disorders. There is a great deal of anticipation for research discovering a single, medically treatable, cause. However, this disorder that affects social, emotional, and cognitive aspects of an individual cannot be so easily summed up as other disorders such as the extra chromosome of Down Syndrome. Many researchers are looking into different pathways and brain areas that contribute to the disease. One popular pathway is the “mirror neurons”. This pathway in the brain activates when observing an “object or goal directed action” (Perkins, Stokes, McGillivray, & Bittar, 2010). In other words when you build a “Lego” set and when you see a friend build a “Lego” set, the same areas of the brain are activated. This area is connecting your movement, and also interpreting the motivation of movements by your friend. This quickly became a popular belief because many assumed that the connection of interpreting motivation of behaviors, as well as mirroring social and emotional states is diminished or absent in autism (Perkins et al., 2010).

Multiple studies using meta-analysis have shown that the data is inconsistent for “mirror neurons” and their role in autism deficits. Hamilton (2013) shows through the interpretation of 25 different imaging studies, that there may be differences in this network but there are also differences across the brain structures. The MRI data, however, do support that there may be a connection specifically between lack of emotion processing and the mirror neuron system (Hamilton, 2013).  From this it is not hard to believe that other MRI studies show that there is lack of activity in the amygdala related to social perception tasks, emotional engagement and arousal (DiCicco-Bloom, 2006). Together, the lack of activity in the amygdala and mirror neurons may support one deficit of autism. Hamilton (2013) also point out that there are also many other tasks which individuals with autism struggle with such as: predicting the next part in a sequence of a task, difficulty answering ‘why’ compared to ‘what’ questions, and reduced imitation during tasks. These tasks however are difficult to point directly to the mirror neuron system, and not the global deficits in autism. These tasks are further exacerbated by the features of autism behavior such as: echolalia (repeating exactly what is heard), and echopraxia (involuntarily imitating someone’s movements exactly). These features actually seem to improve imitation during testing (Hamilton, 2013). However exactly repeating words and movements, and understanding their social meaning and implication are very different.  Overall the research is still conflicted on the usefulness of the mirror neuron pathway as the main dysfunction in autism.

There are other areas of research that are promising. As stated earlier, for example, the role of the amygdala in emotional processing. Research studies show that upon longitudinal study the increased size of the right amygdala at age 3-4 is associated with worse outcomes at age 6 (Munson, 2006). Another theory is “failing to deactivate”, or the brain actually changing the areas that are active when a mental task is ceased. In autism there is no deactivation period, which implies that there is an interruption in processing at the prefrontal cortex (Kennedy, 2006). When asked to make reflections of other people or themselves, the right-temporal parietal junction was observed to have atypical activation in individuals with autism. This points to another theory of autism ‘mind blindness’, in which there are deficits in reciprocal social interactions (Lombardo, 2011).  The current state of research is that many areas of the brain are unequally interrupted in autism. The posterior superior temporal sulcus has reduced activity in joint attention tasks, the amygdala in emotion regulation, the medial prefrontal lobe in taking another persons perspective, and that the mirror neurons may have their best role empathy deficits (DiCicco-Bloom, 2006).  The brain of an individual with autism is a very complex. There are many areas of the brain that are not activating or connecting, correctly. The mirror neurons have one role in these deficits, however they do not necessarily offer insight into treatment. A multi-disciplinary approach to autism treatment is required, and ideal for the many different aspects that these disorder can take.


One of the most positive assessment and treatment techniques for autism is behavior modification training. There is a whole specialized field of professionals dedicated to its implementation, and it would be difficult to sum up all of its benefits in one small page. The field of applied behavior analysis is based on the idea that learning takes place when there is a positive reward to an agreeable behavior and will likely be repeated, and also shaping rewards to reduce behaviors that interfere with learning (AutismSpeaks, 2014). In one example of its benefit, Grindle and colleagues (2012) studied the applied behavioral analysis (ABA) techniques in a small group classroom for 11 children over 2 years. The children also participated in mainstream classroom setting part of the day with their ABA therapist.  The therapists used ABA techniques such as shaping, chaining, prompting, fading, modeling, discrimination learning, task analysis, functional analysis, and differential reinforcement to teach children new skills and reduce problem behaviors. These techniques were started in a one to one setting and then generalized to the larger classroom, and parents were encouraged to continue the techniques at home. After one year the children in this setting had moderate to large increases in standardized test scores, and after 2 years scores for daily living and social skills were even greater (Grindel et al. 2012). In addition work with children with autism requires a whole team approach: ABA therapist, teachers, counselors and 1:1 aides, speech language pathologists, reading and math specialists, as well as classrooms conducive to implementing the many interventions.

Anecdotally, my experience in a specialized school with an ABA learning environment, the children I worked with made huge strides in behavior and social skills. A typical day consisted of shaping behaviors using social scripts, rewards for appropriate responses, identifying emotions using specialized language (“oh, yelling in the classroom is unexpected”), and verbally reflecting reactions. One child I worked with, through consistent utilization of ABA techniques, on going in-service training, constant modification of planning, and a whole team of dedicated and passionate professionals- this child went from many hours outside of the classroom daily for unsafe or disruptive behavior management, to a few times a week, and even three weeks without a single episode of disruption. In an even better moment for teachers and his family, this child was able to build a friendship over the course of a year.



AutismSpeaks. (2014). Applied Behavior Analysis (ABA). Retrieved Oct 26, 2014,from AustismSpeaks: 

Cook, J. L., & Bird, G. (2012). Atypical social modulation of imitation in autism spectrumconditions. Journal of Autism and Developmental Disorders, 42, 1045-1051. doi:10.1007/s10803-011-1341-7 [doi]

DiCicco-Bloom, E. (2006). The developmental neurobiology of autism spectrum disorder. The Journal of Neuroscience, 26, 6897; 6897-6906; 6906. Retrieved from psyc5; Ovid database.

Grindle, C. F., Hastings, R. P., Saville, M., Hughes, J. C., Huxley, K., Kovshoff, H., Griffith, G. M., Walker-Jones, E., Devonshire, K., & Remington, B. (2012). Outcomes of a behavioral education model for children with autism in a mainstream school setting. Behavior Modification, 36, 298-319. doi:10.1177/0145445512441199 [doi]

Grossberg, S. (2010). How do children learn to follow gaze, share joint attention, imitate their teachers, and use tools during social interactions? Neural Networks, 23, 940; 940-965; 965. Retrieved from emed9; Ovid database.

Hamilton, A. F. (2013). Reflecting on the mirror neuron system in autism: A systematic review of current theories. Developmental Cognitive Neuroscience, 3, 91-105. doi:10.1016/j.dcn.2012.09.008 [doi]

Kennedy, D. P. (2006). Failing to deactivate: Resting functional abnormalities in autism. Proceedings of the National Academy of Sciences – PNAS, 103, 8275; 8275-8280; 8280. Retrieved from psyc5; Ovid database.

Lombardo, M. V. (2011). Specialization of right temporo-parietal junction for mentalizing and its relation to social impairments in autism. NeuroImage (Orlando, Fla.), 56, 1832; 1832-1838; 1838. Retrieved from psyc8; Ovid database.

Mak-Fan. (2014). Structural and functional aspects of brain development in children with an autism spectrum disorder (ASD). Dissertation Abstracts International.B.the Sciences and Engineering, 74, No; No-Pagination Specified; Pagination Specified. Retrieved from psyc11; Ovid database.

Mills, K. L. (2014). Developmental changes in the structure of the social brain in late childhood and adolescence. Social Cognitive and Affective Neuroscience, 9, 123; 123-131; 131. Retrieved from psyc11; Ovid database.

Munson, J. (2006). Amygdalar volume and behavioral development in autism. Archives of General Psychiatry, 63, 686; 686-693; 693. Retrieved from psyc5; Ovid database.

Perkins, T. (2010). Mirror neuron dysfunction in autism spectrum disorders. Journal of Clinical Neuroscience, 17, 1239; 1239-1243; 1243. Retrieved from emed9; Ovid database.

Perkins, T., Stokes, M., McGillivray, J., & Bittar, R. (2010). Mirror neuron dysfunction in autism spectrum disorders. Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia, 17, 1239-1243. doi:10.1016/j.jocn.2010.01.026 [doi]

Pineda, J. A. (2008). Positive behavioral and electrophysiological changes following neurofeedback training in children with autism. Research in Autism Spectrum Disorders, 2, 557; 557-581; 581. Retrieved from emed8; Ovid database.

Ruysschaert, L. (2014). Exploring the role of neural mirroring in children with autism spectrum disorder neural mirroring in children with ASD. Autism Research, 7, 197; 197-206; 206. Retrieved from psyc11; Ovid; Ovid database.


The Autism Spectrum and Oxytocin

Autism Spectrum Disorder has recently been favored with an increase in media attention. With increase of ASD diagnoses in recent years has generated an increase in research surrounding the disorder. ASD has been redefined by the DSM-V as “persistent deficits in social communication and interaction across multiple contexts…restricted, repetitive patterns of behavior, interest, or activities…symptoms must be present in the early developmental period…causing clinically significant impairment in social, occupational, or other important areas of current functioning”  (American Psychiatric Assosciation , 2013). As evident from the description however, the diagnosis is a compilation of behaviors. There is no definitive test that proves a person falls within the autism spectrum. Although science has yet to be able to find a cause of autism, neuroimaging has been noted to be of particular significance. With sensitive neuroimaging techniques, it is possible to get a better picture the brain of each person on the ASD spectrum and with that information on hand are able to make suggestions about treatment options, efficacy, and trajectory of the disorder (Westpphal & Pelphrey, 2011). With research in neuroimaging growing, especially neuroimaging surrounding the autism spectrum, it has been hypothesized that research might be able to find specific neural signatures related to ASD. Currently, data shows that ASD is four to five times more often diagnosed in males (Autism Speaks Inc. , 2014). Research also shows that the rate of diagnosis of an autism spectrum disorder has drastically increased, currently it is estimated that 1 in every 68 children are diagnosed on the spectrum (Autism Speaks Inc. , 2014). Only a portion of the rise in diagnosis can be attributed to increased awareness.

Autism, because of its still unknown origins, is treated somewhat differently than many other neural disorders. Treating the cause of the disorder is not applicable in ASD, instead practitioners treat the subsequent behaviors associated with an ASD diagnosis. There are numerous behavioral therapy options that do not include medication. Applied behavioral analysis is the approach of understanding how the environment effects behavior and vice versa (Autism Speaks Inc. , 2014). Applied behavioral analysis has been shown to help patients with ASD better adapt to their environments. Medication is often part of the treatment plan for someone diagnosed on the autism spectrum. Risperidone has been found to be effective in management of irritability, aggression to self/others and decreasing repetitive behaviors (McDougle & Posey, 2011). There are also many anecdotal therapies that families have said help decrease certain behaviors in their autistic children. An example of a type of these treatment options is modifying a child’s diet; although there has been little research done on whether diet is actually an effective treatment modality or not.

One of the main distinguishing characteristics of ASD are the abnormalities within social interactions and attachment. Westphal and Pelphrey refer to social perception as “the initial stage of evaluating the intentions and psychological dispositions of others using gaze direction, body movements, hand gestures, facial expressions, and other biological motion cues” (Westpphal & Pelphrey, 2011). It has been shown using eye tracking, that persons with ASD do not show preference to other’s biological motion cues, thus impairing their social interaction (Westpphal & Pelphrey, 2011). This aspect of ASD is the current focus in research with regards to intranasal oxytocin.  Oxytocin is a hormone whose significant impact on feelings of attachment have been well studied. Oxytocin has been shown to play a pivotal role in the neuroanatomy of social attachment, intimacy, and sexual reproduction. Recent studies have looked at oxytocin’s role in social recognition and pair bonding (Preti, et al., 2014).

We know that oxytocin is made by the hypothalamus, stored and secreted by the posterior pituitary gland, and targets peripheral tissues including: the uterus, mammary gland, ovaries, kidneys, heart and endothelial cells. Donaldson and Young in 2008 were able to demonstrate that oxytocin was involved in the formation of mother-infant and adult-adult pain bonds, separation distress, and recognition (Preti, et al., 2014). An additional study performed by Levine et al. in 2007 was able to show the correlation between increased salivary levels of oxytocin when positive behaviors within the child-parent relationship were present (Preti, et al., 2014).  An especially significant study done by Kirsch et al. in 2005 was shown that oxytocin administration improved recognition of facial expressions. This study was able to be recreated two other times in 2010 with similar findings (Preti, et al., 2014). All the above studies show how oxytocin plays a role in social recognition, something that people with a diagnosis on the autism spectrum have increasing difficulty with. Through a systematic review of research and literature on oxytocin and its effect on ASD, Preti et al. were able to conclude that while current research shows that intranasal oxytocin could benefit patients on the autism spectrum by increasing their social recognition, there have not been enough studies done in conjunction with other treatment modalities. The possibility that intranasal oxytocin could bolster effectiveness of many behavioral therapies already in place for many children on the autism spectrum has not been studied at great length. Long-term administration studies also need to be conducted, so as to see the efficacy over time. There is a definite need for further research on the subject, especially considering the dramatic increase of ASD diagnosis in recent years.




American Psychiatric Assosciation . (2013). Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA: American Psychiatric Publishing.

Autism Speaks Inc. . (2014). Autism FAQ. Retrieved from Autism Speaks:

McDougle, C., & Posey, D. (2011). Assessment and Treatment of Autistic and Other Pervasive Developmental Disorders. In A. Martin, S. L, & C. Kratochvil, Pediatric Psychopharmacology (pp. 547-560). Oxford University Press.

Preti, A., Melis, M., Siddi, S., Vellante, M., Doneddu, G., & R, F. (2014). Oxytocin and Autism: A Systematic Review of Randomized Controlled Trials. Journal of Child and Adolescent Psychopharmacology, 54-68.

Westpphal, A., & Pelphrey, K. (2011). Neurobiology of Autism Spectrum Disorder: Implications for Improving Pharmacotherapy. In A. Martin, L. Scahill, & C. Kratochvil, Pediatric Psychopharmacology (pp. 200-210). Oxford University Press .



Neuroscientific Underpinnings of Aggression

Circuitry of the Brain

There are a multitude of factors that contribute to the display of aggression and violence. In addition to theoretical perspectives such as social learning (Bandura, 1977), self determination theory (Ryan & Deci, 2000), script theory (Huesmann, 1986), cognitive neoassociation theory (Berkowitz, 1989), and others, there exists a complex web of neuroscientific underpinnings to the etiology of aggression.

Studies have shown that the prefrontal cortex plays an important role in modulating primal instinct. One of the most famous case studies describe a man, Phineas Gage, who, prior to the accident, possessed a pleasant disposition. During a railroad accident, a rod pierced his skull through the orbital frontal cortex. After the traumatic incident, he became angry, irritable, and socially disinhibited (Damasio, Grabowski, Frank, Galaburda, & Damasio, 1994). In addition to lesions of the frontal cortex, a reduction in the volume of the prefrontal gray matter (the area consisting of neuronal cell bodies) has been linked to antisocial personality disorder, a psychiatric diagnosis characterized by aggressive and violent tendencies (Narayan et al., 2007). Given these findings, one could postulate that any deficit to the prefrontal cortex, whether organic or trauma-related, would potentiate aggression. In support of this hypothesis, scientists have found decreased glucose metabolism in the temporal and frontal cortices of psychiatric patients with a history of violence, a finding that extends to those who have committed a violent crime (Raine et al., 1998).

The temporal lobe has also been implicated in the manifestation of aggression. In a review by Bufkin and Luttrell (2005), temporal lobe anomalies in the form of reduced left temporal lobe volume and/or activity were found in adult subjects with a history of violence. Pediatric patients with temporal lobe epilepsy were also found to be more aggressive than children with epilepsy originating from other structures of the brain (Juhasz, Behen, Muzik, Chugani, & Chugani, 2001). Part of the limbic system, the area researchers have pinpointed as the center of emotional regulation is called the amygdala. It has been heavily implicated in aggression along with the ventral and orbital medial prefrontal cortex. In animal models, stimulation of that region of the brain produces heightened aggression (Adamec, 1991). The display of reactive aggression (characterized by impulsivity based on emotion, usually anger) has been associated with lesions in that area or atrophy of that structure along with damage to the orbitofrontal cortex (Izquierdo, Suda, & Murray, 2005).

Neurochemistry of the Brain

The neurochemistry of the brain is also involved in the production of aggressive tendencies. It has been well established in both human and animal subjects that serotonin plays a key role in modulating aggression (Mehlman et al., 1994; Caramaschi, de Boer, & Koolhaas, 2007; Brown et al., 1982). Since the original research began linking serotonin with aggression, newer studies have also investigated the interplay between nitric oxide and serotonin in modulating aggression. In particular, it has been shown that inhibition of nitric oxide producing enzyme elicits elevated aggression in male mice (Chiavegatto & Nelson, 2003). Although the exact nature of the interplay is unclear, there is a connection between nitric oxide synthase, the enzyme responsible for producing nitric oxide, serotonin, and serotonin receptor function (5-HT1A and 5-HT1B). What we do know is that nitric oxide appears to be important in the maintaining proper serotonin activity.


A number of therapies have been shown to be moderately to significantly effective for aggression.  In order to evaluate the mode of therapy, researchers distinguished between various forms of issues surrounding aggression. The categories included driving anger, anger suppression (difficulty expressing pent up anger), and anger expression (ie. explosive and impulsive anger) difficulties. Four therapies were examined (cognitive-behavioral therapy, cognitive therapy, relaxation therapy, and other, which included process group counseling, social skills training, etc.). The positive effects were noted after twelve or less treatments, which is promising as it suggests that aggression may be amenable in a short amount of time. Driving anger seemed particularly amenable to cognitive therapy, anger expression is best addressed with cognitive-behavioral therapy, and anger suppression was most improved by cognitive therapy (Del Vecchio & O’Leary, 2004). Dialectical behavioral therapy, the front line psychotherapy used to treat borderline personality disorder, also shows promise in reconditioning anger responses to cultivate healthier emotional expression (Fruzzetti & Levensky, 2000).

Pharmacological treatments such as selective-serotonin reuptake inhibitors (SSRIs) enhance inhibition of subcortical areas such as the amygdala via increasing serotonin in the orbitofrontal cortex (New et al., 2004). In addition, anticonvulsants and mood stabilizers alter the balance of GABA and glutamate (with the result of potentiating GABAnergic activity or lowering glutamate activity), resulting in less impulsivity (Hollander et al., 2003; Pavlovic, 2008; Cooney, Murphy, Tessema, & Freyne, 2013.)




Adamec, R.E. (1991). Individual differences in temporal lobe sensory processing of threatening stimuli in the cat. Physiol Behav, 49(3), 455-464.

Bandura, A. (1977). Self-efficacy: toward a unifying theory of behavioral change. Psychological Review, 84(2), 191-215.

Berkowitz, L. (1989). Frustration-aggression hypothesis: examination and reformulation. Psychology Bulletin, 106, 59-73.

Brown, G.L., Ebert, M.H., Goyer, P.F., Jimerson, D.C., Klein, W.J., Bunney, W.E., & Goodwin, F.K. (1982) Aggression, suicide, and serotonin: relationships to CSF amine metabolites. Am J Psychiatry, 139, 741–746.

Bufkin, J.L., & Luttrell, V.E. (2005). Neuroimaging studies of aggressive and violent behavior: current findings and implications. Trauma Violence Abuse, 6, 176–190.

Caramaschi, D., de Boer, S.F., & Koolhaas, J.M. (2007). Differential role of the 5-HT1A receptor in aggressive and nonaggressive mice: an across-strain comparison. Physiol Behav, 90, 590–601.

Chiavegatto, S., & Nelson, R.J. (2003). Interaction of nitric oxide and serotonin in aggressive behavior, Horm Behav, 44, 233–241.

Cooney, C., Murphy, S., Tessema, H., & Freyne, A. (2013). Use of low-dose gabapentin for aggressive behavior in vascular and mixed vascular/alzheimer dementia. The Journal of Neuropsychiatry and Clinical Neurosciences25(2), 120-125.

Damasio, H., Grabowski, T., Frank, R., Galaburda, A.M., & Damasio, A.R. (1994). The return of Phineas Gage: clues about the grain from the skull of a famous patient. Science, 264, 1102–1105.

Del Vecchio, T., & O’Leary, K. D. (2004). Effectiveness of anger treatments for specific anger problems: A meta-analytic review. Clinical Psychology Review, 24, 15–34.

Fruzzetti, A.E., & Levensky, E.R. (2000). Dialectical behavior therapy for domestic violence: rationale and procedures. Cognitive and Behavioral Practice, 7(4), 435-447.

Hollander, E., Tracy, K.A., Swann, A.C., Coccaro, E.F., McElroy, S.L., Wozniak, P., Sommerville, K.W., & Nemeroff, C.B. (2003). Divalproex in the treatment of impulsive aggression: efficacy in cluster B personality disorder. Neuropsychopharmacology, 28, 1186–1197.

Huesmann, L.R. (1986). Psychological processes promoting the relation between exposure to media violence and aggressive behavior by the viewer. J. Soc., 42, 125–40.

Izquierdo, A., Suda, R.K., & Murray, E.A. (2005). Comparison of the effects of bilateral orbitofrontal cortex lesions and amygdala lesions on emotional responses in rhesus monkeys. J Neurosci, 25, 8534–8542.

Juhász, C., Behen, M.E., Muzik, O., Chugani, D.C., & Chugani, H.T. (2001). Bilateral medial prefrontal and temporal neocortical hypometabolism in children with epilepsy and aggression. Epilepsia, 42, 991–1001.

Mehlman, P.T., Higley, J.D., Faucher, I., Lilly, A.A., Taub, D.M., Vickers, J., Suomi, S.J., & Linnoila, M. (1994). Low CSF 5-HIAA concentrations and severe aggression and impaired impulse control in nonhuman primates. Am J Psychiatry, 151, 1485–1491.

Narayan, V.M., Narr, K.L., Kumari, V., Woods, R.P, Thompson, P.M., Toga, A.W., & Sharma. T. (2007). Regional cortical thinning in subjects with violent antisocial personality disorder or schizophrenia. Am J Psychiatry, 164, 1418–1427.

New, A.S., Buchsbaum, M.S., Hazlett, E.A., Goodman, M., Koenigsberg, H., Lo, J., Iskander, E., Newmark, R., Brand, J., O’Flynn, K., & Siever, L. (2004). Fluoxetine increases relative metabolic rate in prefrontal cortex in impulsive aggression. Psychopharmacology, 176, 451–458.

Pavlovic, Z.M. (2008). Lamotrigine for the treatment of impulsive aggression and affective symptoms in a patient with borderline personality disorder comorbid with body dysmorphic disorder. The Journal of Neuropsychiatry and Clinical Neurosciences, 20, 121-122.

Raine, A., Meloy, J.R., Bihrle, S., Stoddard, J., LaCasse, L., & Buchsbaum, M.S. (1998). Reduced prefrontal and increased subcortical brain functioning assess using positron emission tomography in predatory and affective murderers. Behav Sci Law, 16, 319–332.

Ryan, R. M., & Deci, E. L. (2000). Self-Determination theory and the facilitation of intrinsic motivation, social development, and well-being. American Psychologist, 55, 68–78.