Complex Integrated Primary Health and Psychiatric Disorders

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Table of Contents

Background Information
Substance Use Disorder
Depression
Co-occurrence of Depression and SUDs
Case Scenario
Assessment
Conclusion
References

People are said to have co-occurring disorders or conditions if they have a combination of any mental health conditions, or any substance use or addictive behavior and physical disease (Dinwiddie, 2017). Historically, individuals with co-occurring disorders (COD) experienced limited success in healing, wasted a lot of finance and time in treatment programs. That was because the wrong approach was employed by mental health specialists; they used to handle each condition separately. Currently, individuals with symptoms of mental health or addiction can be screened for COD in any psychiatric health facility. The high incidences of substance use disorders (SUDs) and other psychiatric disorders are well recognized. The group of people with COD is diverse, and the frequency of comorbidity varies by a diagnostic group (Pettinati, O’Brien, & Dundon, 2013). The consequences of comorbidity are extensive and pose challenging questions yet to be answered.

For instance, why are substance use and other psychiatric diseases so frequently co-occur? Are there genetic influences or neurobiological links between these conditions that drive comorbidity? Do various mental disorders have different associations with several types of substances of abuse? Knowledge of the association between SUDs and psychiatric illness is essential for effective prevention and treatment. The rapid progress of technical innovations in neurosciences has demystified signal transduction mechanisms, neural circuitry, and neurotransmitter systems participating in SUDs and psychiatric illness (Sadock, Sadock, & Ruiz 2014). This paper focuses on co-occurrence between substance use and depression/mood disorders because research concerning neurobiology and the mechanistic association between these conditions is predominantly active. A case study is also presented.

Background Information

SUDs are quite frequent among young people in the US, with incidence rates ranging from ~ 8 – 35% (Dinwiddie, 2017). Frequently, they co-occur with additional mental ailments. The 2010 national statistics on drug use and health revealed that 21.1% of teenagers 12-17 years old with a profile of drug abuse or dependence had a major depressive attack in the same timespan (SAMHSA, 2017). Around 8.9 million people out of the total US population suffer from depression and substance use dependence (SAMHSA, 2017). Among the adults who at one time used injectable drugs, evidence disclose a higher rate of lifetime major depressive disorder in women than in men (SAMHSA, 2017). The average age of occurrence is 40 years. The economic burden of drug abuse has been estimated at $180.9 billion, while the overall cost of alcohol and drug abuse summed around $246 billion (SAMHSA, 2017). These comprise healthcare expenses, crime costs, and productivity losses.

Although there is convincing evidence confirming a secure connection between depression and SUDs, the nature of this association is complex and varies depending on the substance used (Stubbs et al., 2017). Depression may predispose a person to SUDs or may exacerbate the effects of SUDs (Stubbs et al., 2017). Drugs and their psychotropic features are used to manage emotional distress. Depression and other mental conditions have been hypothesized as prolonged distress states associated with neurobiological modulations in the brain stress circuits. Conversely, chronic substance use is linked with neuroadaptations in the CNS reward pathway that elicit secondary psychiatric symptoms during severe and extended withdrawal states (Stubbs et al., 2017). Neuroadaptations in stress and reward pathways ensue with increased addiction, and these may cause the elevated emotional distress frequently connected with SUDs (Stubbs et al., 2017).

Substance Use Disorder

The misuse of drugs of all kinds is common, and it presents with it a myriad of problems connected to the substance taken, route of administration, and addiction. Dependence on and misuse of both prescribed and illegal drugs is a global problem. Drugs abused include alcohol, sedatives (benzodiazepines, opiates, and barbiturates), stimulants (amphetamines and cocaine), hallucinogens (cannabis and LSD), and organic solvents (Sharpe & Lawrie, 2014). They produce a broad spectrum of effects in the body from dependence, respiratory depression, seizures, withdrawal syndrome, schizophrenia, acute and paranoid psychotic episodes, confusion, severe intoxication, to death (Sharpe & Lawrie, 2014).

The etiology of substance misuse disorder depends on factors such as availability of the drugs, the social patterns of use, and cultural pressures, especially within a peer group. Most likely, the genetic factors play a role in predisposition to dependence. Medical over prescription and a relative decline in the price of illegal drugs increase the availability of these substances. Diagnosis of SUDs may be obtained from history or made once a patient presents with a complication (Sharpe & Lawrie, 2014). Screening of samples of blood and urine to detect the presence of drugs is a valuable confirmatory diagnosis, especially if patients persist in denying. From a mental health standpoint, substance use disorders not only cause significant morbidity and mortality, but also interfere with and obstruct the course of treatment of CODs such as anxiety, depression, and psychotic conditions (Sharpe & Lawrie, 2014).

Numerous substance use screening tools are available. These comprise the alcohol dependence scale (ADS), the drug abuse screening test (DAST), and CAGE. Others include the Dartmouth assessment of lifestyle instrument (DALI), screening-brief intervention-referral to treatment (SBIRT), the Simple screening instrument for substance abuse (SSI), etc., (American Psychiatric Association, 2014). These instruments measure several parameters related to substance abuse. Factors considered when endorsing specific screening tools include observed evidence supporting the consistency and authenticity of the device, relative cost of the apparatus, ease of administration, and a history of application (American Psychiatric Association, 2014). Instruments which align closely with the new DSM-5 criteria, that allow a continuous transition to the current classification system, and which can be integrated within the SBIRT approach are recommended for screening SUDs (American Psychiatric Association, 2014).

Depression

The major depressive disorder has a prevalence rate of 5% in the general population and roughly 10% in persistently ill medical outpatients (Stubbs et al., 2017). It is a primary cause of disability and suicide. If it co-occurs with a physical health condition, it magnifies disability, reduces compliance to treatment and rehabilitation programs, and eventually shortens life expectancy (Sadock et al., 2014). Early onset depression has an element of genetic predisposition. Several genes have been implicated, with serotonin transporter gene being the leading candidate (Sharpe & Lawrie, 2014). Childhood emotional deprivation and adversity may lead to depression. Also, stressful life events – the death of a loved one and medical illnesses- trigger depressive episodes. Symptoms of depressive disorders are both mental and somatic.

Psychological symptoms include depressed mood, reduced self-esteem, pessimism, psychomotor agitation and retardation, indecisiveness, guilt, loss of interest (anhedonia), and suicidal thinking. Contrariwise, the physical signs include reduced appetite, weight change, loss of libido, insomnia, and bowel disturbance (Sharpe & Lawrie, 2014). Diagnosis of comorbid depression is based on careful assessment of the core mental symptoms, i.e., persistently lowered mood and anhedonia. The occurrence of five or more of these signs for over two weeks is a reliable diagnostic indicator of a major depressive disorder. Differential diagnosis is made to differentiate depression from adjustment disorders with depressed mood; self-limiting responses to adversity which are momentary and require only general support (Sharpe & Lawrie, 2014). Likewise, many psychiatric conditions, i.e., psychotic, anxiety, and personality disorders are characterized by depressive symptoms. Thus, it is essential to distinguish between these conditions to achieve a correct diagnosis and for proper treatment. Getting an in-depth history, performing a physical examination, and requesting relevant laboratory studies are significant in the assessment of new onset of depression (Miller & Prosek, 2013). Similarly, diagnosis entails thoughtful inquiry into suicidal thoughts and plans.

Tools for screening and assessing of depression include the center for epidemiological studies – depression scale (CES – D), brief symptom inventory (BSI), and Beck scale for suicidal ideation (BSS) (American Psychiatric Association, 2014). The instruments examine the magnitude of depression and suicidality (American Psychiatric Association, 2014). Global appraisal of individual needs (GAIN) and psychiatric diagnostic screening questionnaire (PDSQ), are some instruments that can be used to monitor and diagnose depression that co-occurs with SUDs (American Psychiatric Association, 2014).

Co-occurrence of Depression and SUDs

Epidemiological research reported prevalence rate ranges of 32 -54% for co-occurrence of SUDs with depression. People suffering from major depression have an increased probability of developing SUDs. Similarly, people with SUDs are at a higher risk of manifesting with moodiness when compared with the whole population (Dinwiddie, 2017). Depressive signs are often observed during acute, chronic withdrawal of drugs of abuse. Inability to sleep, irritability, unease, and inattentiveness are connected with both prolonged withdrawal states and depression. Perhaps, neurobiological resemblances between depression and SUDs are liable for the many incidences of comorbidity and symptom similarity (Dinwiddie, 2017). The extrahypothalamic corticotropin release factor (CRF) and hypothalamic-pituitary-adrenal (HPA) axis dyscrasia and changes in the catecholamines, 5-HT, GABA, and glutamate pathways are associated with depression (Sharpe & Lawrie, 2014).

Comparatively, neuroadaptations related to protracted substance misuse are linked to these neurotransmitter systems, particularly during severe drug deprivation states (Sharpe & Lawrie, 2014). CRF/HPA reaction in acute drug withdrawal is similar to withdrawal-related distress and signs of depression. Studies on SUDs patients, with or without features of depression, have confirmed a considerably reduced ACTH and mineralocorticoids reaction to excitation by CRF than in healthy individuals (Sharpe & Lawrie, 2014). This observation of abnormal neuroendocrine response to demanding challenges in SUDs endorses the clinical reports that patients with SUDs have trouble dealing with traumatic events and circumstances of emotional anguish and usually deteriorate when faced with these conditions (Sharpe & Lawrie, 2014). CNS scans have identified changes in frontal-limbic CNS pathway in moodiness and SUDs. A decline in metabolic reactions in the frontal and anterior cingulate regions and increased activities within the amygdala has been found in patients with SUDs and major depression when compared with healthy individuals (Sharpe & Lawrie, 2014). These observations agree with autopsy histological inquiries that revealed decreased cell compactness and gray matter content in persons screened with depression (Sharpe & Lawrie, 2014).

Case Scenario

The case study presents a patient who experiences severe low mood and diminishing of function. A 45-year-old man reports to his doctor with a mental state of hopelessness, melancholy, and helplessness. On being interviewed by the GP, he says that he cries for no reason, and experiences trouble in sleeping. He informs the doctor that he noticed the onset of the problems around six weeks ago, and has not been able to discard them. He has ceased going to work and currently drinks alcohol and smokes more than usual. When lonely he admitted that he contemplated on going to a river nearby to drown himself. He also informs the GP that two years ago, he suffered from a stroke episode. On the review of the man past medical history, the GP establishes that indeed the man had experienced bleeding in one of the cerebral blood vessels of the left brain.

Assessment

Several questions ought to be answered to synthesize the above information and arrive at a meaningful conclusion. These regard to the likely differential diagnosis, the evidence in the history that supports the diagnosis and any other confirmatory information, the essential etiological factors, the role of a post-stroke event in the generation of symptoms the man experienced, available treatment options, and prognosis. In this scenario, the preferential diagnosis is a severe depressive disorder. Alternative diagnoses include substance misuse, physical illnesses, e.g., HIV, influenza, stroke, endocrine or neoplastic disorders, and prescribed medication. The patient complains of four significant signs of depression – low mood, lack of energy, loss of interest, and insomnia. Other confirmatory information that the GP can obtain by taking the patient history includes loss of appetite, weight loss, reduced sexual drive, a diurnal variation in mood, and cognitive symptoms discussed above.

An interview with a family member assists to confirm the story while the review of the past medical records helps to reveal previous episodes, physical illnesses, and aids in staging effective treatment approaches. A substance misuse history excludes this as a primary diagnosis. Physical examination, urinalysis, and routine blood tests are performed to absolve physical illness and substance misuse from the causes of the symptoms. The critical etiological factors that might have predisposed the man to depression are a family history of mood disorder and atypical premorbid personality (Jørgensen et al., 2016). Precipitating factors include a life event, stressor or physical illness, such as stroke. Persisting social stressor, high alcohol intake, or loneliness may prevent rapid resolution of depression, but instead maintain it (Jørgensen et al., 2016).

Treatment of depression involves selecting the setup where it takes place and dealing with physical, psychological, and social implications of the disorder (Jørgensen et al., 2016). Usually, depression is best treated at home where the family provides support to the patient. However, in situations of loneliness or risk of self-harm at home, it becomes necessary to confine the patient at the hospital. Physical treatment involves prescription of antidepressant medication, followed by symptomatic management with a benzodiazepine or a hypnotic for anxiety (Jørgensen et al., 2016). Antidepressants are useful in treating post-stroke depression, although some tricyclics lead to confusion (Jørgensen et al., 2016).

Therefore, selective serotonin reuptake inhibitors (SSRIs) or any other medicine with better tolerability should be considered. Psychological management will involve educating the patient and the family about the nature of depression, its cause and the likely period of resolution (Jørgensen et al., 2016). Also, cognitive therapy is recommended to counter the ideas of guilt, worthlessness, and pessimism. Since the patient does not report to work, advice about financial hardships, support with time off from employment, and resolving of housing difficulties all help to speed up the healing process (Jørgensen et al., 2016). The temporary prognosis of episodes of mood is good with ~ 75% of cases responding favorably to simple antidepressant treatment (Jørgensen et al., 2016). Unfortunately, a majority of depressive patients undergo a recurrent experience at some point in their life, while 10 -15% of them proceed to commit suicide.

Physical ailments increase the risk of suffering from severe depressive episodes. The cognitive or psychological mechanism to explain this situation is that any acute or chronic illness presents a danger to a person’s sense of purpose and meaning in life (Sadock et al., 2014). The ailment provides the life event or stressor that generates a depressive incidence in a susceptible person. Therefore, a physical dysfunction may be a component of the complex genetic or non-genetic pathway that determines the onset of depression (Sadock et al., 2014). For post-stroke depression, the specific locality of the brain lesion influences the risk of subsequent mood disorder. Past studies on stroke patients established an association between depression and the injuries in the left basal ganglia (Sadock et al., 2014).

Advanced age, female gender, primary educational attainment, solitude, history of moodiness, and multiple comorbidities are potential socio-demographic and health issues that may precipitate the onset of depression in individuals with or without stroke (Jorgenson et al., 2016). The level of risk of developing post-stroke depression depends on the current smoking status and the severity of stroke. Conversely, alcoholic indulgence by both genders causes an insignificant effect on the generation of post-stroke moodiness. Studies have shown a surge in the detection of depression within three months after the stroke incident, then again the risk declines, but remain significantly higher than that in non-stroke subjects after one year (Jorgenson et al., 2016). Currently, there is weak study evidence associating depression with increased mortality in stroke patients.

The rise in the prevalence of depression within the period immediately following stroke diagnosis and the weak associations with the known predisposing factors for moodiness and the subsequent mortality implies that post-stroke depression contrasts from that which is not connected with a physical illness (Jorgenson et al., 2016). As discussed above, theories of injury location, angiogenic depression, inflammation, neurotransmitter, neuroplasticity, and HPA axis activation have been postulated to explain the role of the brain physiology in the etiology and pathogenesis of post-stroke depression (Jorgenson et al., 2016). Higher numbers of post-stroke depression reports may also be because of increased sensitization due to screening programs and preventive management with antidepressants (Jorgenson et al., 2016). However, both of these explanations have a limited and conflicting evidence base.

The appropriate diagnosis of post-stroke depression (PSD) should be based on a semi-structured psychological health examination and clinical criteria such as DSM – 5 or the International Classification of Diseases (ICD 10) (Ojagbemi, Owolabi, Akinyemi, & Ovbiagele, 2017). Currently, there is no formal tool for identifying depression in PSD patients. However, tools like the Hospital Anxiety and Depression Rating Scale (HADS), the Health-Related Quality of Life in Stroke patients (HRQOLISP-26), and HRQOLISP-E are psychometrically adequate in stroke population and are suitable for screening and evaluation of a medical scenario presented above (Ojagbemi et al., 2017).

Conclusion

In summary, this paper has described two psychiatric conditions: depression and SUDs. The mental states were investigated independently and in a comorbid scenario to single out any difference in the neurobiological mechanisms of onset, prevalence, symptomatology, and diagnostic approaches in each situation. Similarly, a hypothetical scenario of a patient presenting with a severe depressive incidence that is complicated by other factors – physical ailment, substance abuse, etc., was simulated. The study shows that depression rarely occurs singly, but in association with other mental or physical conditions. The demographic factors involved in single depressive episodes slightly vary from those in co-occurring moodiness, suggesting that different neurobiological pathways and neural circuitry play a role in the etiology of the mental conditions.

References

American Psychiatric Association. (2014). Diagnostic and statistical manual of mental disorders, DSM-5 (5^th ed.). Washington, DC: American Psychiatric Association Publishing.

Dinwiddie, S. H. (2017). Psychiatric comorbidity in people who inject drugs. Psychiatric Annals, 47(1), 27-32.doi: 10.3928/00485713-20161206-02

Jørgensen, T. S. H., Wium-Andersen, I. K., Wium-Andersen, M. K., Jørgensen, M. B., Prescott, E., & Maartensson, S., …Olser, M. (2016). Incidence of depression after stroke, and associated risk factors and mortality outcomes, in a large cohort of Danish patients. JAMA Psychiatry, 73(10), 1032-1040. Web.

Miller, R., & Prosek, E. A. (2013). Assessment & diagnosis: Trends and implications of proposed changes to the DSM-5 for vulnerable populations. Journal of Counseling & Development, 91(3), 359-366. Web.

Ojagbemi, A., Owolabi, M., Akinyemi, J., & Ovbiagele, B. (2017). Proposing a new stroke-specific screening tool for depression: Examination of construct validity and reliability. eNeurologicalSci, 9(2), 14–18. doi: Web.

Pettinati, H. M., O’Brien, C. P., & Dundon, W. D. (2013). Current status of co-occurring mood and substance use disorders: A new therapeutic target. Am J Psychiatry 170(1), 23-30. Web.

Sadock, B. J., Sadock, V. A., & Ruiz, P. (2014). Kaplan and Sadock’s synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11^th ed.). Philadelphia, USA: Walters Kluwer.

Sharpe, M. C., & Lawrie, S. M. (2014). Medical psychiatry. In R. N. Colledge et al. (Eds.), Davidson’s principles and practice of medicine (22nd ed.) (pp. 230-252). Edinburg, UK: Elsevier Limited.

Substance Abuse and Mental Health Services Administration. (2017). Key substance use and mental health indicators in the United States: Results from the 2016 National Survey on Drug Use and Health (HHS Publication No. SMA 17-5044, NSDUH Series H-52). Web.

Stubbs, B., Vancampfort, D., Veronese, N., Kahl, K. G., Mitchell, A. J., Lin. P. Y., …Koyanagi, A. (2017). Depression and physical health multimorbidity: primary data and country-wide meta-analysis of population data from 190 593 people across 43 low- and middle-income countries. Psychological Medicine, 47(12), 2107-2117. Web.

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