Self-Concept and Personal Attributes

by Jen L’Insalata

The question ‘who am I?’ is at the fundamental core of humanity (Broderick, & Blewitt, 2010). One’s self concept is how seeks to answer that question by formulating a description and mental representation of that individual (Niepel, Brunne, & Preckel, 2014). William James discussed the differences of “I” and “Me” when discussing the self-system. He made the distinction that “me” centers on defining an individual’s self-concept and who they project to others (Broderick, & Blewitt, 2010).

Charles Cooley’s looking-glass-self metaphor is derived from the idea that we gain a sense of self, and therefore self-concept by observing the appraisals or criticisms from others, particular attachment figures. The influence of such interactions impact outward behaviors and social awareness (Broderick, & Blewitt, 2010). Within a culture there are varying themes including gender roles, social connections, academic, and career expectations that shift and impact an individual’s self-concept (Broderick, & Blewitt, 2010. & Wagner, Gerstorf, Hoppmann, & Luszcz, 2013).

Self-concept internally as an external description of features, characteristics and attributes through interactions with others (Broderick, & Blewitt, 2010). The role of early care givers is important in establishing self-concept in that secure attachments allow a child to develop positive self-worth and self-concept (Broderick, & Blewitt, 2010). Studies show that there is a strong correlation between self- concept and achievement. Individuals with a positive self-concept show tendencies toward continued self-enhancement and motivation in several domains throughout life (Niepel, Brunne, & Preckel, 2014). On the contrary, individuals with poor self-concept show trajectories toward maladaptive behaviors, delinquency, and substance abuse (Steiger, Allemand, Robins, & Fend, 2014).

Self-concept possess elements of stability and change throughout an individual’s lifespan and eventually begins to differentiate form others with maturity (Broderick, & Blewitt, 2010). Adolescence is marked by a period of rapid changes throughout multiple domains. Transitions such as those in adolescence are marked by shifts in domain competencies and the development of new skills that shape social interactions and identity (Wagner, Gerstorf, Hoppmann, & Luszcz, 2013).

Self-concept cannot completely be isolated from the self-system. Self-concept helps to shape and formulate self-esteem and self-regulation. The interaction of biopsychosocal and spiritual domains continues to impact fluctuations in the self-system (Broderick, & Blewitt, 2010). Individuals with a positive self-concepts show tendencies toward an overall higher self-esteem and self-regulation through transitional life phases (Steiger, Allemand, Robins, & Fend, 2014).


Broderick, P. C., & Blewitt, P. (2010). The lifespan: Human development for helping professionals (3rd. ed.). Boston, MA: Allyn & Bacon.

Niepel, C., Brunner, M., & Preckel, F. (2014). The longitudinal interplay of students’ academic self-concepts and achievements within and across domains: Replicating and extending the reciprocal internal/external frame of reference model. Journal Of Educational Psychology, doi:10.1037/a0036307

Steiger, A. E., Allemand, M., Robins, R. W., & Fend, H. A. (2014). Low and decreasing self-esteem during adolescence predict adult depression two decades later. Journal Of Personality And Social Psychology, 106(2), 325-338. doi:10.1037/a0035133

Wagner, J., Gerstorf, D., Hoppmann, C., & Luszcz, M. A. (2013). The nature and correlates of self-esteem trajectories in late life. Journal Of Personality And Social Psychology, 105(1), 139-153. doi:10.1037/a0032279

Considering Socioeconomic Status in Treatment

By Jen L’Insalata

Socioeconomic status encompasses more then just income. It includes aspects of ownership, wealth, and class identity. Social gradients between rich and poor showcase varying degrees of well-being linked to mental and physical health outcomes, access to resources, opportunity, and education, and provide a pathway to power through the existence of a status-driven western economy (Wilkinson, & Pickett, 2017).

Individuals residing in a higher socioeconomic status have access to healthcare and education which present opportunities for global wellbeing. Education and career endeavors associated with higher income offer a sense of prestige that is often unavailable to those of lower socioeconomic standing (Wilkinson, & Pickett, 2017). Individuals in lower socioeconomic classes are often considered ‘disadvantaged’ in terms of health outcomes, access, and opportunity. The association with being ‘disadvantaged’ leads to social isolation and alienation (Smith, 2005).

Poverty is complex and can be addressed from framework spanning several disciplines including psychology. However psychological services often fall short when providing services for low income populations. Classism and negative biases often influence the service provider and distinctions between white collar and blue-collar mentalities are not acknowledged in the therapeutic setting. This further exacerbates alienation and leads to a breakdown in understanding between the therapist and the client (Smith, 2009).

Historical movements have attempted to provide access to psychological services to lower income individuals through means of community mental health programs. Clinicians trained through higher education observed that individuals from lower socioeconomic status appeared unable to “grasp” concepts addressed through therapy (Smith, 2009). Misconceptions surrounding relatability and priority further alienate the client from the therapist.

When developing psychological services for lower income populations, once can utilize Maslow’s Hierarchy of needs as a framework. Maslow suggests that in order for individuals to address higher level concerns, basic needs must be satisfied (Wedding, & Corsini, 2014). In application, psychologists must recognize that individuals at lower socioeconomic statuses often struggle to secure basic needs such as food and shelter. Thus, priorities differ from individuals who have obtained security in low level needs and are able to focus on higher level motivators such as belonging, emotional wellbeing, and self-actualization.

Strength based client centered approaches are likely benefit those at lower socioeconomic levels as the focus on a client’s strengths rather then limitations and encourage the client to take an active role in the course of their program. Strength based client focused approaches rely heavily on collaboration when treatment planning and recognizing that clients may experience challenges unforeseen to the therapist. Strength based approaches also place the client in the position as the expert shifting the power differential between client and psychologist (Snyder & Lopez, 2006).

Similarly, family systems theory incorporates both the systemic and structural framework when working with low income individuals. Family systems therapy addresses poverty as it effects the individual and conceptualizes a client’s relationship to poverty when formulating a treatment approach (Smith, 2005). The therapist becomes aware of their interactions as a component of the system structure and thus the impact on the client.


Smith, L. (2005). Psychotherapy, Classism, and the Poor: Conspicuous by Their Absence. American Psychologist, 60(7), 687–696.

Snyder C.R. & Lopez, S.J.(2006). Positive Psychology: The Scientific and Practical Explorations of Human Strengths” SAGE.

Wedding, D., & Corsini, R. J. (Eds.). (2014). Current psychotherapies (10th ed.). Belmont, CA: Brooks/Cole. ISBN: 9781285083711.

Wilkinson, R. G., & Pickett, K. E. (2017). The enemy between us: The psychological and social costs of inequality. European Journal of Social Psychology, 47(1), 11–24.

A Historical Perspective of Schizophrenia

schizophrenia1by Jen L’Insalata

Schizophrenia cannot be explained in its entirety by one particular theoretical model and the underlying neurobiological foundation for the disease is still relatively unknown.  Rather it is the descriptions and observations of the primary psychotic symptoms that have allowed several theories surrounding schizophrenia to evolve (Mishara, & Schwartz, 2013). Historically, schizophrenia was considered to be constructive in which anomalous experiences provide the construct of one self. Early clinical observations emphasized subjective self-experiences and altered self-awareness. The concept of self-experience is still referenced in modern work with schizophrenia. (Parnas, & Henriksen, 2014).

The earliest depictions of schizophrenia were recorded in France during the 12th century but were not linked to any particular disorder. Writing described individuals who deviated from what was considered to be normal self-perception; anomalous self-experiences. In many cases writing illustrate a disunity of consciousness in which a person’s thinking, perception, movement, and vision were disjointed and incongruent with presented stimuli (Parnas, & Henriksen, 2014).

The modern understanding of schizophrenia rose form the work of Emil Krapelin, an influential German psychiatrist working in the late 19th and early 20th century. Krapelin research surrounding the combination of symptoms and psychiatric illness from a biological origin highlighted two forms of psychosis; manic depression and dementia praecox (Ebert, & Bär, 2010). The disturbance known as Krapelin’s dementia praecox consisted of the phenomenon currently recognized as schizophrenia. During his research, Krapelin described the deterioration of what he believed to be perception and attention in combination with muscular tension (Mishara, & Schwartz, 2013).

Throughout the late 1800’s and early 1900’s core symptoms were studied by individuals from a psychodynamic perspective such as Carl Jung, Josef Berze, and Hans Walter Gruhle. Many of these theorists called attention to various cognitive and affective characteristics of the disorder. Jung in particular was fascinated by patients displaying confused speech which he described as a state of sleep-drunken-ness and confusion. Their theories critiqued by many other early psychotheorists and the phenomenon later was renamed schizophrenia in 1908 by Eugen Bleuler (Mishara, & Schwartz, 2013).

Bleuler theorized individuals with schizophrenia experienced a general loose association with a fissure personality which was highly influenced by Jung’s work. Bleuler believed that such loose associations allowed aspects of the unconscious to invade the consciousness and lead to an ego disorder. The unconscious invasion would erode the functioning of the ego to the level in which it exists in dreams. Gruhle added to Bleuler’s work and theorized that the primary symptoms of schizophrenia operated independently and observed a dysfunction between the cognitive and the affective components of the disorder (Mishara, & Schwartz, 2013).

Josef Berze criticized Jung’s work and theories believing that the symptoms were due to a reduction in mental activity rather than attention. He theorized that mental activity is more closely related to consciousness than affect and highlighted the concept of a disruption in self as the essences of schizophrenia. Berze also noted diminished mental activity in goal setting, linguistic coherence, and the ability to access the autobiographical self. Much of his work was inspired by emerging neurobiological research. He theorized that schizophrenia symptoms originated at a subcortical area, specifically the thalamus which gave rise primitive drives and motivations (Mishara, & Schwartz, 2013).

Jaspers integrated and critiqued his predecessors work in his book General Psychopathology published in 1913. (Mishara, & Schwartz, 2013). Highly influenced by the philosopher Descartes, he solidified the concept of self-experience pertaining to schizophrenia. Jaspers recognized that an individual may have and recognize experiences that are invalid and referred to positive symptoms as first person symptoms (Parnas, & Henriksen, 2014).

During the 1940s Freud’s psychoanalytic work continued to influence much of the theories surrounding schizophrenia and emphasized an etiological root stemming from early relationships. Psychoanalytic writers produces detailed descriptions of the schizophrenic experience including disruptions in interpersonal relationships and the self-experience due to the psychosis (Hamm, & Lysaker, 2016).

Writers such a Freud and Searles illustrate individuals that were detached from the world and redirected psychic energies inward during psychosis. Such writings provide the concept of an altered self-experience from which the schizophrenic individual is unable to integrate life experiences. Psychodynamic approaches took a pessimistic view of schizophrenia treatment which failed to produce empirically supported and measurable treatment modalities. Eventually, such treatment modalities fell out of favor and were replaced by psychosocial and cognitive behavioral perspectives (Hamm, & Lysaker, 2016).

With the publication of the ICD 8 and 9, Schizophrenia was recognized as a disturbance of personality and involved disorder concepts of individual uniqueness and self-direction. During that time the term personality referred to a subjective self rather than the personality descriptions used in contemporary psychology. Research surrounding a subjective self could be measured using systematic approached however lacked reliability in its methods. This notion soon fell out of favor and was replaced with an operational model following the publication of the DSM-III in 1980 (Parnas, & Henriksen, 2014).

The DSM-III emphasized behavioristic components of schizophrenia which stress observable features over the subjectivity and inference of previous theories. Biological concepts such as genetics in the etiology of schizophrenia were highlighted and lead to the emergence of a spectrum of observable features and predictors. Among the most noted were deficits in emotion, eccentricity, and thought disorder which caused interpersonal difficulties in social and occupational function. The inclusion of the diathesis stress model illustrated how core vulnerability combined with environmental stressors and produce cognitive changes observed in schizophrenia (Parnas, & Henriksen, 2014).



Asenjo Lobos, C., Komossa, K., Rummel-Kluge, C., Hunger, H., Schmid, F., Schwarz, S., & Leucht, S. (2010). Clozapine versus other atypical antipsychotics for schizophrenia. The Cochrane Database of Systematic Reviews, (11), CD006633. Advance online publication.

Ebert, A., & Bär, K.-J. (2010). Emil Kraepelin: A pioneer of scientific understanding of psychiatry and psychopharmacology. Indian Journal of Psychiatry, 52(2), 191–192.

Hamm, J. A., & Lysaker, P. H. (2016). Psychoanalytic phenomenology of schizophrenia: Synthetic metacognition as a construct for guiding investigation. Psychoanalytic Psychology, 33(1), 147-160. doi:10.1037/a0038949

Mishara, A. L., & Schwartz, M. A. (2013). Jaspers’ critique of essentialist theories of schizophrenia and the phenomenological response. Psychopathology, 46(5), 309-19. doi:

Parnas, J., & Henriksen, M. G. (2014). Disordered Self in the Schizophrenia Spectrum: A Clinical and Research Perspective. Harvard Review of Psychiatry, 22(5), 251–265.

Spencer, E. K., & Campbell, M. (1994). Children with schizophrenia: Diagnosis, phenomenology, and pharmacotherapy. Schizophrenia Bulletin, 20(4), 713-725.

Psychotropic Medications and Children

childrenpills-e1463156827980by Jen L’Insalata

Historically children’s psychiatric treatment was comparable to those of adult populations. Diagnostic features were assumed to take on the same aspects of adult psychiatric features and therefore treatment was approached in the same manner. Contemporary views observe that emotional stress experienced by children and adolescents is due largely to situational experience. In these cases non-medication based treatment and psychotherapeutic interventions produce the best outcomes. However, research does take into consideration that many adult psychological and psychiatric disorders have their onset during childhood and can result in progressive neurobiological impairment. In the case of Bipolar disorder, Schizophrenia, and attention deficit/hyperactivity disorder (ADHD), pharmaceutical intervention is necessary to prevent neurological degradation (Preston, O’Neal, & Talaga, 2013).

Research surrounding the efficiency of two or more psychotropic medications is still limited and often time children are prescribed a combination of pharmaceutical agents to medicate disorders. The most common polypharmacy regimens include an antidepressant and a stimulant in combination with an antipsychotic and relate to the co-occurrence of a mood disorder and ADHD (Comer, Olfson, & Mojtabai, 2010).

Controversial Aspects

When medicating children there is no true informed consent and it is often the parents who facilitate the decision for medication treatment. In such instances, it becomes easier for parents to view the disorder as a chemical imbalance and ignore environmental components such as family dysfunction. Parents may rule out the need for psychological treatment in exchange for an easy chemical solution (Preston, O’Neal, & Talaga, 2013).

Many psychotropic medications have adverse side effects including addiction, which at an early age can lead to lifelong struggles with prescription abuse.  Stimulants such as Ritalin used to treat ADHD and benzodiazepines such as Xanax used to treat anxiety (Preston, O’Neal,  & Talaga, 2013) are among the most commonly abused prescription drugs among children and adolescents.

Pre-pubescent children have a higher hepatic rate then children who have entered puberty. Medication dosages prior to puberty are often metabolized faster and require a higher dose. Once a child enters puberty the dosage must continue to be monitored closely for toleration and side effects (Preston, O’Neal, & Talaga, 2013).

Parents often ignore the child’s beliefs and views surrounding medication and may have private consultations regarding treatment with doctors. When working with children it is important to address the child’s concerns surrounding psychotropic medication and mental health stigma (Preston, O’Neal, & Talaga, 2013). Doing so no only ensures that the child will comply with medication treatment, but also provide education and awareness to the outcome of their disorder.

Integrated treatment

The use of psychotropic medication in children is on the rise and in conjunction, doctors are moving toward a polypharmaceutical regime to manage childhood psychological distress. This is largely due to an emphasis of symptom reduction and the increasing number of psychiatrists specializing in pharmacotherapy. Emphasis and access to psychosocial interventions is sometimes limited, expensive (Comer, Olfson, & Mojtabai, 2010), and time consuming.

The Affordable Care Act of 2010 established the health home program for children with emotional disorders aimed at helping children meet both health and developmental goals. Aspects focus on behavioral health, education, child-welfare, and juvenile justice to create a continuum of care that care child and family focused. Policies aim at prevention and continued care while also controlling the cost of child psychiatric care. Aspects emphasize substance abuse and mental health issues that are common among children and adolescents and aim to prevent complications leading to behavioral health problems as adults (de Voursney, & Huang, 2016).

It is estimated that childhood mental health problems cost aproxamiatly 12.2 billion dollars annually and are some of the most prevalent concerns surrounding health, productivity, and crime. Conditions such as oppositional defiant and conduct disorder, substance abuse, post-traumatic stress disorder, anxiety and depression, and bipolar disorder (de Voursney, & Huang, 2016) lead to involvement in criminal and illegal activity, as well as social and societal dysfunction.

Stigmas surrounding the diagnosis of childhood mental health concerns inhibit the identification of children who may be at higher risk and the improper or inadequate treatment. The goal of the Affordable Care Act is to ensure continuity between a child’s home and school life to ensure therapeutic intervention as well as medical intervention (de Voursney, & Huang, 2016).



Comer, J. S., Olfson, M., & Mojtabai, R. (2010). National Trends in Child and Adolescent Psychotropic Polypharmacy in Office-Based Practice, 1996–2007.Journal of the American Academy of Child and Adolescent Psychiatry, 49(10), 1001–1010.

de Voursney, D., & Huang, L. N. (2016). Meeting the mental health needs of children and youth through integrated care: A systems and policy perspective. Psychological Services, 13(1), 77-91. doi:10.1037/ser0000045

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

Benzodiazepines and Anxiety

overmedicated-pharmaby Jen L’Insalata

Benzodiazepines, sometimes referred to as anti-anxiety medications, are intended for the use in treating severe rehabilitating panic attacks and panic disorder. However all too often, benzodiazepines are prescribed for generalized anxiety disorder. From a biological etiology, anxiety is the result of stimuli triggers that activate a series on neurochemical and hormonal responses that prepare the body and mind for immediate activation. This sequence is commonly referred to as the fight or flight response and the limbic system and amygdala become activated. The excitatory hormones cortisol, adrenaline, and norepinephrine are released and the locus coeruleus or gated chloride ion channels are excited (Preston, O’Neal, & Talaga, 2013).

Generalized anxiety disorder is the low level chronic stress experienced throughout an individual’s life. This differs from panic attack in that there is a persisting anticipation of stressful or dangerous events. The limbic system is kept on a lower level of alert but does not cross the threshold into full activation of the fight or flight response.

Panic disorder is characterized by a series of reoccurring panic attack which may appear to be unprovoked. There is strong evidence suggesting the biological etiology of panic attacks stem from hypersensitive neurons within the limbic system, specifically when concerning GABA (Preston, O’Neal, & Talaga, 2013).  This causes individuals to experience dizziness, nausea, chest palpitations, shortness of breath, and profuse sweating that accompany and intense fear.

Benzodiazepines bind to chloride ion channels enhancing the flow of negative chloride ions. This inward flow of negatively charged chloride ions decreases neuron excitation and produces a calming effect on the brain. Benzodiazepines work by interacting with benzodiazepine receptors during presynaptic inhibition. By binding with the receptor sites, the calming effects of the influx of negative chloride ions as well as the effects of GABA are enhanced (Preston, O’Neal, & Talaga, 2013).

The first Benzodiazepine, chloriazepoxide was developed in 1957 for anxiety and insomnia. Since then several other forms of the drug have been developed with varying degrees of anti-anxiety and hypnotic properties. Benzodiazepine gained popularity in pharmisudical anxiety treatment due to its rapid effectiveness. Therapeutic effects can be experienced in as little as 30 minutes. Additionally, benzodiazepines are well tolerated by most individuals (Preston, O’Neal, & Talaga, 2013).

Although considered relatively non-addictive, I have seen numerous cases of benzodiazepine abuse while working with addictions. Many individuals utilizes benzodiazepine to escape unwanted generalized anxiety symptoms and do not have adequate coping skills. Such coping skills can be developed through psychotherapeutic means.

I have observed the use of benzodiazepines to alleviate anxiety cause by other drugs, withdrawal, and the lack of healthy coping skills. Many individuals use benzodiazepines as an intermediary drug or for relaxation purposes. I often observe the illicit use of benzodiazepine coupled with various forms of opiates, a combination that can often be fatal.

For this reason, I question and caution the frequent and over use of benzodiazepines as a primary pharmaceutical treatment for anxiety. As they are effective to reduce dehabilitating anxiety quickly, this medication should be reserved for panic attacks and panic disorder. If prescribed, the duration should be limited and quantity should begin at a low dosage.



Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

Medicating Mood Disorders

adderallby Jen L’Insalata

 Mood disorders are a broad category with symptoms ranging from mild dysphoria and grief to chronic and intense clinical depression. Symptoms include both psychological and physical components and can emerge as a reaction to stimuli or spontaneously. Psychological symptoms include diminished self-esteem, sadness, and diminished self-worth; while physical symptoms include alterations in sleep, appetite, and fatigue (Preston, O’Neal, & Talaga, 2013).

Psychological based depression is often reactive, stemming from a stressor either known or unknown to the individual. Biologically based depression does not develop as a response to a stimuli, rather a number of neurobiological conditions are altered which effect neurotransmission within the limbic system. While prolonged reactive depression can lead to biological changes, often individuals show predisposed vulnerability and biological markers (Preston, O’Neal, & Talaga, 2013).

Psycho therapeutic intervention is a primary treatment for reactive depression through which the individuals learns coping skills and is able to address the underlying factors.  Vegetative and neurovegitatve conditions observed in the physical manifestations such as diminished concentration, psychomotor agitation, and changes to sleep and appetite alert practitioners to biological depression (Preston, O’Neal, & Talaga, 2013).  Treatment for biological components of depression includes medication to help stabilize symptoms.

Biological Etiology

Depression symptoms are brought about by the malfunction of norepinephrine, serotonin and dopamine transmission thought out the neurons of the limbic system and hypothalamus. It is believed that a depletion of these neurotransmitters leads to symptom manifestation. The monoamine hypothesis suggests that neurotransmitter depletion can occur in several ways (Preston, O’Neal, & Talaga, 2013).

Excessive reuptake can deplete levels of norepinephrine, serotonin, and dopamine. In this instance, significant amounts of the neurotransmitter are released by the presynaptic neuron into the synapse. The neurotransmitters are rapidly reabsorbed by the presynaptic neuron resulting in a diminished quantity of neurotransmitters reaching and binding with receptors on the opposing postsynaptic nerve (Preston, O’Neal, & Talaga, 2013).

Another instance suggests that there is a decrease number of neurotransmitters released into the synapse. This is possibly due to the reduction of neurons being synthesized, the inability of the vesicle to adequately store or migrate neurons across the membrane of the presynaptic neuron (Preston, O’Neal, & Talaga, 2013). Still a final instance of neurotransmitter abnormalities can occur when the naturally occurring levels of monoamine oxidase become too active. This shouts down and degrades the neurotransmitters themselves (Preston, O’Neal, & Talaga, 2013) resulting in depression symptoms.


Antidepressants are used to treat the biological aspect of depression. When combined with psychotherapy, the pharmisudical treatment of depression is highly effective. There are many medications used to treat depression but the most commonly prescribed fall into three categories; Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs), and Tricyclic Antidepressants (TCAs).

Tricyclic Antidepressants (TCAs)

Tricyclic Antidepressants were first developed as an antipsychotic for the treatment of schizophrenia. The original TSA imipramine did not produce the desired antipsychotic effects but produced marked improvement with depressive symptoms. TSAs have a diverse philological profile and are considered a superior form of medicinal depression treatment. Action occurs at the two receptor transporters and three receptor proteins. This inhibits presynaptic reuptake of norepinephrine, serotonin, and blocks post synaptic adrenergic, muscarinic, and histamine H receptors (Hillhouse, & Porter, 2015).

For this reason, the medications prove effective and target many receptors on both end of the synapse. However there are many adverse side effects including unpleasant dry mouth and skin, blurred vison, bladder issues and even death. Additional symptoms involve a quick drop in blood pressure and light headedness. TCAs are considered toxic and can be lethal if the dosage is not accurate (Preston, O’Neal, & Talaga, 2013).

Selective Serotonin Reuptake Inhibitors (SSRIs)

Selective Serotonin Reuptake Inhibitors were developed in the 1960s with the aim of increasing the concentration in the synapse by the inhibition of the reuptake mechanisms of the presynaptic neuron. SSRIs bind the the reuptake receptors on the presynaptic neuron allowing adequate serotonin to bind with receptors on the post synaptic neuron (Hillhouse, & Porter, 2015).

SSRIs targets the serotonin receptor s and have very little effects on other receptors. This allows them to be as effective as TCAs with significantly fewer side effects. Most of the side effects observed have to do with the increase of serotonin and include mild nausea, insomnia, sedation, and restlessness. Over time, patients may experience a recurrence of symptoms that are similar to the initial depression they are being treated for. Patients may experience loss of energy, passivity, and decreased pleasure. Additional medication may be needed to augment some of the unwanted effects (Preston, O’Neal, & Talaga, 2013).

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) were developed and introduced in the early 1990s and are considered duel action antidepressants. As the name suggests, SNRIs target and inhibit the reuptake of both serotonin and norepinephrine. For this reason it is possible that SNRIs may be more effective then SSRIs in the treatment of depression but studies how there are significantly more unwanted side effects (Preston, O’Neal, & Talaga, 2013, & Hillhouse, & Porter, 2015).



Hillhouse, T. M., & Porter, J. H. (2015). A brief history of the development of antidepressant drugs: From monoamines to glutamate. Experimental And Clinical Psychopharmacology, 23(1), 1-21. doi:10.1037/a0038550

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.


Artwork by Toby Allen

By Jen L’Insalata

Stress has been cited for many adverse physical and mental health conditions and is linked to the proliferation of non-communicable disease epidemics in recent years. During the 1800’s most deaths were related to poor sanitary and hygienic conditions. Most deaths were attributed to outbreaks of cholera, Influenza, typhoid, and tuberculosis spread through unsanitary drinking water (Shern, Blanch, & Steverman, 2016).

In the 21st century, public health is still at risk. The US ranked 36th out of 194 for life expectancy in 2012 with the vast majority of deaths related to obesity, coronary heart disease, lung disease, and substance abuse. Most contemporary chronic illness has its roots in stress and it is estimated that nearly half of Americans will develop resulting mental health and addiction issues at some point during their lifetime (Shern, Blanch, & Steverman, 2016).

It is widely understood that a combination of genetic predisposition coupled with environmental influence shape over all human development. Many alterations in genetic material correlate with environmental stressors. In other words, genetic mutation and expression is strongly influenced by the environments which people are exposed to.

While manageable stress is considered important for healthy human development, toxic stress is not. Frequent, intense, and prolonged exposure to adversity including but not limited to physical and emotional abuse or violence, neglect, and economic hardship account for the source of much toxic stress. Acute or chronic exposure to traumatic events including death and sexual abuse also fall into the toxic stress category as does the persistence of less sever stressors including family instability and income insecurity (Shern, Blanch, & Steverman, 2016).

Stress alters development   over the course of a lifetime. Prenatal exposure to stress impacts developing structures of the fetus leading to adverse effects on memory and cognition. Early childhood stress often results in diminished behavioral, emotional, and impulse control. Individuals exposed to toxic stress during late adolescence and early adulthood develop a heightened fear response and are hyper responsive to stress stimuli (Shern, Blanch, & Steverman, 2016). Additionally, stress amplifies the aging process on both the brain and the body as a whole.

Stress causes structural remodeling of the brain and weakens neuro-connections within in the brain. Exposure to stress activates stress hormones and raises cortisol levels. Persistent elevation of cortisol levels increases the adverse effects on the connective structures within the amygdala; a structure commonly linked to cognitive and emotional regulation (Shern, Blanch, & Steverman, 2016 & Pagliaccio, Luby, & … Barch, 2015).

Genetic mutations occur throughout the short alleles of the serotonin transport promoter and produced heightened monoamine oxidise A activity. Heightened activity along the Hypothalamic-Pituitary-Adrenal Axis greatly effects the monoamine/serotonin structures and leads to additional cortisol release. It is the relationship between cortisol and amygdala connectivity that is believed to be a foundational component of internalizing pathology (Pagliaccio, Luby, & … Barch, 2015).

Internalizing pathology such and depression and anxiety contribute additional stress to an individual’s life. Symptoms of both disorders have dehabilitating effects on one’s ability to function in a socioeconomic capacity and produce feeling of dependency on unhealthy relationships and substances. Thus the cycle of stress, cell malfunction, and disorder is perpetuated.



Pagliaccio, D., Luby, J. L., Bogdan, R., Agrawal, A., Gaffrey, M. S., Belden, A. C., & … Barch, D. M. (2015). Amygdala functional connectivity, HPA axis genetic variation, and life stress in children and relations to anxiety and emotion regulation. Journal Of Abnormal Psychology, 124(4), 817-833. doi:10.1037/abn0000094

Shern, D. L., Blanch, A. K., & Steverman, S. M. (2016). Toxic stress, behavioral health, and the next major era in public health. American Journal Of Orthopsychiatry, 86(2), 109-123. doi:10.1037/ort0000120


A General Diagnostic Understanding: Schizophrenia and Related Psychotic Disorders

schizophreniaJen L’Insalata

Schizophrenia is a psychotic disorder characterized by the disruption of an individual’s sense of self and perception. Psychotic symptoms manifest in the form of auditory, visual, and sensational hallucinations, disordered or delusional thoughts, and disruptions in language and communication. An individual with schizophrenia is not always incoherent. Most individuals experience periods of active symptoms and symptom remission, while many experience at least one period of relapse (NIMH, 2009).

Schizophrenia is sometimes confused with having a split of multiple personality which are characteristic of another disorder. Diagnosing in an emergency room setting can be difficult as symptoms manifest differently in varying individuals. Involuntary hospitalization can only occur legally if a professional witnesses psychotic behavior which can take the form of the vocalization of delusional thoughts (NIMH, 2009).

295.90 (F20.9) Schizophrenia is characterized by delusions, hallucinations, disorganized speech that is easily derailed or incoherent, grossly disorganized or catatonic behavior, and negative symptoms including flat affect and diminished emotional expression. The symptoms must be severe enough to impact normal day to day function such as interpersonal relationships and self-care (APA, 2013). In an emergency room scenario it may be difficult to assess the impact of the symptoms on education and employment. It may be easier to visually assess the appearance of the individual to gather the extent of the symptoms on daily functionality. Schizophrenia can be distinguished from other psychotic disorders based on severity and length of duration of the symptoms. In schizophrenia the symptoms persist continuously for six months and meet the full diagnostic criteria for at least one month. If the duration and severity of the symptoms is less than the diagnostic criteria, a diagnosis of schizophrenipform disorder may be more appropriate. Additionally, if the active phase of psychosis includes depressive symptoms, a diagnosis of schizoaffective disorder may be warranted (APA, 2013).

Schizoaffective Disorder is similar to schizophrenia and symptoms include hallucinations, delusions, disorganized thought, and negative symptoms. In addition to the psychotic features present, individuals with schizoaffective disorder also exhibit features of depressive disorders and bipolar disorders. Coding for schizoaffective disorder is based on the mood episodes exhibited. 295.70 (F25.0) Schizoaffective Disorder, Bipolar type indicated there is a manic phase to the mood disturbances indicative of bipolar disorder. In 295.70 (F25.1) Schizoaffective Disorder, Depressive type, the individual experiences mood symptoms congruent with major depressive disorder (APA, 2013).

298.8 (F23) Brief Psychotic Disorder is characterized by the presence of delusions, hallucinations, disorganized speech and grossly disorganized or catatonic behavior. Symptoms last for at minimum, one day and at maximum, one month. Typically the onset is sudden and an individual goes from a non-psychotic to a psychotic state within two weeks. The differentiation between Brief psychotic disorder and other forms of psychotic disorder focuses on the length of time and onset of the symptoms. If the symptoms last longer that one month, the diagnosis of schizophrenipform disorder is more appropriate. Additionally, individuals who experience brief psychotic disorder do not meet the full DSM criteria for schizophrenia and show no disturbance in mood or affect. Individuals who experience brief psychotic disorder do not often show negative symptom that are common in schizophrenia. If mood congruent symptoms are present, schizoaffective disorder is a more appropriate diagnosis (APA, 2013).

The exact cause of schizophrenia is still unknown. It is believed that there is genetic, biological, and environmental links that correspond with the disorder and provide risk factors. Schizophrenia shows a genetic component and runs within families. Having a first degree relative with schizophrenia increases a person’s likelihood to develop the disorder themselves. Environmental factors such as exposure to prenatal viruses, malnutrition, and complications during birth also increase the risk of schizophrenia (NIMH, 2009). According to the diathesis stress model, individuals inherit a high or low genetic risk for schizophrenia. Varying psychosocial factors throughout the lifespan such as stressors and experiences influence the trajectory and development of the disorder (U.S. Department of Health and Human Services, 1999).

Several genes have been linked to schizophrenia and individuals with schizophrenia have a higher rate of gene mutation than healthy individuals. Brain physiology also differs in individuals with schizophrenia. Ventricles in the center of the brain are often larger in schizophrenic patients and individuals have decreased amounts of gray matter than healthy individuals. Genes that code for the chemicals associated with the development of higher brain function, neurotransmitters such as dopamine and glutamine are also effected which cause changes to the neuropathways that develop during puberty (NIMH, 2009).

Individuals with schizophrenia who receive treatment have a better outcome than individuals who do not. One halt to two thirds of individuals who receive treatment recover or show significant improvement over time (U.S. Department of Health and Human Services, 1999). Treatment for schizophrenia includes both psycho-pharmisudical and psychotherapeutic interventions that focus on eliminating the symptoms and developing coping strategies.

During the 1950’s antipsychotics were developed to treat schizophrenic symptoms. This first generation of antipsychotics consisted of medications including Chlorpromazine (Thorazine), Haloperidol (Haldol), Perphenazine (Etrafon, Trilafon), Fluphenazine (Prolixin), and Clozapine (Clozaril). Each individual responds to treatment differently, however Clozapine appeared to be most effective in the most varied cases. Clozapine also had a side effect that reduced white blood cell count requiring patients using the medication to receive blood screening every two weeks (NIMH, 2009).

During the 1990’s a second generation of antipsychotics were developed that had reduces side-effects. These include Risperidone (Risperdal), Olanzapine (Zyprexa), Quetiapine (Seroquel), Ziprasidone (Geodon), Aripiprazole (Abilify), Paliperidone (Invega); which are more commonly prescribed today. Side effects to antipsychotics may include drowsiness, dizziness, blurred vision, rapid heartbeat, sensitivity to the sun, and skin rashes. In women, menstrual problems may occur. Additional side effects may be physical in nature and long term use of antipsychotics may cause loss of neuromuscular control. Once a compatible antipsychotic is found patients may see improvements in as little a few days, with an overall reduction in psychotic symptoms in as little as six weeks (NIMH, 2009).

In addition to pharmisudical treatment, psychotherapy is important to an individual’s recovery.  Therapy provides prosocial, interpersonal, vocational skills, and education that helps prevent relapse of symptoms. Family and community based therapy helps to build a support system that also helps improve the individual’s prognosis. Psychosocial and Cognitive Behavioral Therapy address the disruptive thoughts and perceptions that are symptomatic of schizophrenia. CBT helps develop coping skills that allow the individual to test the legitimacy of their delusions or hallucinations and implement healthy behavioral alternative to actin on such thoughts. Prosocial components address areas of daily self-care, occupational, and educational skills that help schizophrenic patients live healthy and functioning lives (U.S. Department of Health and Human Services, 1999, & NIMH, 2009).

Schizophrenia effects men and woman and displays cultural equality, however not all symptoms manifest the same. Misdiagnosis can occur if the culture to which a patient differs from that of the diagnosing clinician.  Many cultural sub groups participate in religious experiences where hearing voices or seeing vision is acceptable. In other cultures, affect and avoidance can be misinterpreted as paranoia or other negative symptoms. It is important to understand the culture from which an individual comes from to determine if the symptoms are due to psychosis or cultural misinterpretation (U.S. Department of Health and Human Services, 1999, & NIMH, 2009).



American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author. ISBN: 9780890425558.

National Institute of Mental Health. (2009). Schizophrenia. Retrieved from

U.S. Department of Health and Human Services. (1999). Mental health: A report of the surgeon general. Retrieved from