Tag Archives: insomnia

Comorbidity of Personality Disorders and Substance Abuse Disorders

There are an estimated 44%-60% of people who have been diagnosed with substance use disorder who also qualify with symptoms pertaining to a minimum of one personality disorder.  Personality disorders include antisocial personality disorder, avoidant personality disorder, borderline personality disorder, obsessive-compulsive personality disorder and schizoid personality disorder.  Each of these personality disorders have their own symptoms and characteristics, but generally speaking any personality disorder affects people cognitively, which is the way people look at themselves and the world in general, affectation, which is the level of reaction to any one thing, as well as interpersonal functioning and the level of impulse control a person has.  A person can suffer from mood swings, anger outbursts or alcohol or substance abuse.

A person who is diagnosed with a personality can also have a second diagnosis of substance abuse disorder.  This is defined as:







“A complex behavioral disorder characterized by preoccupation with obtaining                     alcohol or other drugs (AOD) and a narrowing of the behavioral repertoire towards          excessive consumption and loss of control over consumption.  It is usually also           accompanied by the development of tolerance and withdrawal and impairment in social and occupational functioning.” (www.cdad.com)

A patient must present with certain symptoms in order to be diagnosed with substance abuse disorder, the symptoms are the behaviors someone would expect from anyone with a substance abuse disorder, but they are not usually so obvious to the patient.  The symptoms include a tolerance of the substance or a need for more and more of the substance because it is harder and harder to feel the effects of the substance, withdrawal when the substance is not used on a regular basis, the substance being used for longer than the patient thought they would be using it for, the patient having a continuous desire to control the habit of using the substance but is unsuccessful at doing so, the patient spending a lot of time trying to find or use the substance or coming off of the substance, the patient giving up activities in multiple areas of their life in order to have the opportunity to use the substance, and continuing use even though it is causing health problems to the patient.

The diagnosis of substance abuse disorder comes about when the patient has become increasingly more tolerant and dependent on their chosen substance.  After the body becomes accustomed to having that substance available on a regular basis, the body will react with withdrawal symptoms which can include headaches, insomnia, and hallucinations and could include aggression, paranoia or promiscuous behavior.  Most patients live in denial when it comes to admitting they have a problem and have to get past that denial in order for any type of treatment to help them.

When a patient is diagnosed with both of these disorders at the same time it is considered co-morbidity of substance abuse disorder and personality disorder.  A little over half of patients who have been seen for substance use disorder have also been diagnosed with a minimum of one personality disorder.

There are two treatments that have been established for this type of co-morbidity.  One is called dual focus schema therapy and it combines different life skills such as functional analysis and coping skills training.  This treatment involves 24 sessions and plans for two stages.  The first of these stages is called early relapse prevention and helps the patient develop life skills that will aid the patient in dealing with temptation or actual relapses.  The second stage is called schema change therapy and coping skills work, this stage helps the patient make the changes more concrete and helps the patient develop methods for coping once abstinence is achieved.

Looking at co-morbidity of substance abuse and personality disorders has shown how difficult it can be to diagnose a patient with multiple disorders, especially when it involves substance abuse because substance use is so common and it seems there really is a fine line between the two.


Netherton, S.D., Holmes, D., Walker, C.E. (1999). Child and Adolescent Psychological Disorders.  New York, NY: Oxford University Press.

(Retrieved 2009, October 28). Co-occurring Mental Health and Substance Abuse Disorders. www.dshs.wa.gov.com.   http://www.dshs.wa.gov/pdf/hrsa/mh/cobestpract.pdf

(Retrieved 2009, October 28). Axis II Personality Disorders and Mental Retardation.  Psyweb.com.   http://psyweb.com/Mdisord/DSM_IV/jsp/Axis_II.jsp

(Retrieved 2009, October 28). Frequently Asked Questions (FAQ’s) About Substance Abuse Disorders.  www.cdad.org  http://www.cdad.org/FAQSubstanceUseDisorders.htm

Dysthymic Disorder

My choice of Dysthymic Disorder for purposes of this essay was both personal and professional.  First and foremost, I was attracted to this disorder because it resides in the gray area somewhere between an Axis I disorder and a personality disorder.  Because of this unique diagnostic positioning I feel as though I could reasonably justify techniques that are traditionally associated with all of the major schools of psychotherapy I have studied to date: Behavior Therapy, Cognitive Behavior Therapy, Schema Therapy, Existential Psychotherapy, and/or (perhaps most importantly) my own personal brand of psychotherapy that shall remain unnamed.  With some amalgamation of techniques derived from the above, as dictated by individual client needs, I have confidence I would have a reasonable chance of having “success” (however we mutually choose to define that) with the majority of clients that present with Dysthymic Disorder.  Secondly, it seems to me a young clinician’s time is best spent on the disorders he is mostly likely to encounter.  Prevalence rates of Dysthymic Disorder could be as high as 6% in a nationally representative sample, and as high as 22% in outpatient mental health settings.  (Dougherty, Klein, & Davila, 2004)  It’s extremely unlikely that I will not encounter Dysthymic Disorder during the course of my professional life.  Third and finally, this disorder is close to me because someone I love endured it for the better part of 10 years.  Thankfully – I can report at this time that it is in full remission.  The journey to full remission was one that tested all of our capacities for change and growth.  This essay represents a personal and professional journey that is has led to significant gains in my own understanding of mood disorders.  Successfully navigating through the dark forest that is Dysthymic Disorder is no easy task.  It is my hope that my clients don’t have to endure the dark thoughts any longer than is absolutely necessary.

The essential feature of Dysthymic Disorder is a chronically depressed mood that occurs for most of the day, more days than not, for at least two years.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 376)  During periods of depressed mood, at least two of the following additional symptoms are present: poor appetite or overeating, insomnia (sleep too little?) or hypersomnia (sleep too much?), low energy or fatigue, low self-esteem, poor concentration or difficulty making decisions, and feelings of hopelessness.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 377)  In my example case the individual was laden with hypersomnia, fatigue, and poor concentration.  It is noteworthy that are over 700 different combinations of symptoms that any single individual could potentially present with and still have the same diagnosis of Dysthymic Disorder.  As a result, it bears mentioning that the following analysis is in no way suggesting that this is the only right way to treat the disturbance.  Manualized treatment is probably doomed to failure when it comes to treating Dysthymic Disorder.  Any reasonable attempt to work toward complete remission of Dysthymic Disorder should be guided by a professional.

Differential diagnosis can be a challenge with Dysthymic Disorder.  “This is the way it’s always been” is not an unexpected response from patients whom suffer from Dysthymic Disorder.  There is no rest for the wicked: During the two year period of the disturbance, the individual may not have been without the qualifying symptoms in for more than 2 consecutive months.  Furthermore, no major depressive episode should be present during the first two years of the disturbance and the disturbance cannot be better accounted for by the diagnoses of chronic Major Depressive Disorder, or Major Depressive Disorder, In Partial Remission.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 380)  Double depression, or the comorbid combination of Major Depressive Disorder and Dysthymia, is also a very real consideration since major depressive episodes are often superimposed on mild chronic depression.  (Dougherty et al., 2004, p. 1012; Morrison, 2007, p. 139)  There should never have been a manic, hypomanic, or mixed episode that would be contraindicative of Dysthymic Disorder and indicative of either Cyclothymic Disorder or Bipolar Disorder (I or II).  The disturbance should not occur exclusively during the course of a chronic psychotic disorder (like schizophrenia, for example) or be the direct physiological effects of a substance (like methamphetamine, for example) and/or general medical condition (like a traumatic brain injury, for example).  As is the case with most DSM diagnoses, the disturbance should cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 381)  This differential diagnosis quandary is further exacerbated by the fact that depression “shares borderlands with bereavement and other losses, problems of living, and adjustment disorders.”  (Morrison, 2007, p. 127)  A thorough investigation of antecedents and mitigating factors is absolutely critical to accurately “anchor your boat” so you can “wade into the river” with a correct diagnosis.

Family history is an important consideration when determining the hypothetical etiology of a disturbance, especially in the case of mood disorders.  “Family history is more useful in starting the train of diagnostic thought than in determining its final destination.”  (Morrison, 2007, p. 133)  Research suggests that the strongest predictors for Dysthymic Disorder include a history of sexual abuse, quality of the patient’s relationship with both parents, and higher familial loadings for drug abuse and ‘Cluster A’ personality disorders.  Unfortunately, we could use that same laundry list of antecedent events for just about every personality disorder in the DSM-IV-TR… so that doesn’t tell us much.  Childhood adversity and familial psychopathology and have greater predictive utility for Dysthymic Disorder when compared with demographic and clinical variables.  (Durbin, Klein, & Schwartz, 2000)  Translation: nurture appears to trump nature.  Nature continues to play a significant role in the development and maintenance of the disturbance, however.  A patient with a parent (or parents) with unipolar depression exhibited significantly higher rates of Affective/Mood Disorders including Major Depressive Disorder and Dysthymic Disorder – yet another marker that can guide the patient-clinician dyad in the right direction.  (Klein, Clark, Dansky, & Margolis, 1988)

A full exploration of the potential therapeutic interventions is beyond the scope of this paper, but there are a few empirically supported treatments that are noteworthy.  Supportive therapies, coupled with cognitive behavioral interventions, have been effective in extinguishing negative verbalizations and normalizing daily functioning.  (Elligan, 1997)  This is consistent with my “necessary but not sufficient” position when it comes to person centered therapies practiced by the late great Carl Rogers (1902-1987).  Although I concede that the research I found doesn’t specifically point to Schema Therapy as a potential treatment modality for Dysthymic Disorder, I would consider it based in part on event-related brain potential research.  (Yee, Deldin, & Miller, 1992)  Processing deficits including selective attention may be modified and corrected vis-à-vis Schema therapy.  Since research suggests that resource allocation is the issue, not resource capacity, the goal of Schema Therapy would be to allow for attention resources to be more effectively and efficiently focused on task performance.  (Yee & Miller, 1994)  Pharmacological interventions have been less effective on Dysthymic Disorder when compared with other mood disorders, so I would not consider this to be a first line of defense except in cases of Double Depression or in cases where talk therapy would be otherwise unproductive without the value added by antidepressant medications.  Other noteworthy psychological treatments that have garnered empirical support for the treatment of clinical depression include Behavior Therapy (Behavioral Activation), Cognitive Therapy, Cognitive Behavioral Analysis System of Psychotherapy, Interpersonal Therapy, Problem-Solving Therapy, Self-Management/Self-Control Therapy, Acceptance and Commitment Therapy, Behavioral Couples Therapy, Emotion-Focused Therapy (Process-Experiential), Reminiscence/Life Review Therapy, Self-System Therapy, and Short-Term Psychodynamic Therapy.  (Hayes & Strunk, n.d.)  In the end, the choice is one that will be made based on the training and expertise of the respective therapist and the needs of the individual patient.  Not all therapists are created equal.  In the end, every clinician should know a little about most of the treatment options above so they can make a referral if your particular variant of Dysthymia will not be well served by the treatment modalities that your clinician is versed in.

Knowing nothing about my potential client, I would begin the treatment from a cognitive behavioral perspective because I believe that it is the “best bang for the buck” in a brief therapy environment.  The most likely scenario for a first session could be summed up in the word “triage.”  Something brought the client into therapy and we need to “stop the bleeding.”  Behavioral activation in the form of cognitive behavioral homework is absolutely critical to get the ball rolling.  Although we can only speculate without a specific case study to reference, we would likely begin with some simple behavioral activation like “going on a walk with a friend for one hour, once a week.”  Ideally the target behavior would be specific, measurable, and relatively easy to complete (at least at the beginning).  Reversing that “downward spiral” as soon as is possible is an important first step in the treatment of Dysthymic Disorder.  (Beck, 2011, p. 80)  After identifying avoidance behaviors and potential reinforcing activities, I would endeavor to implement some form of self-reinforcement whereby transfer, generalization, and long-term maintenance of the desired behavior can be established and maintained.  (Spiegler & Guevremont, 2010, p. 135)  It should be a foregone conclusion but it bears mentioning that the homework should be customized for the specific patient and, if deemed necessary, “contracted” to increase the likelihood of compliance.

Furthermore, I would work to identify chronic stressors that appear to be contributing to the maintenance and onset-recurrence of the disturbance.  (Dougherty et al., 2004, p. 1012)  I typically engage in a series of assessments including interviews, behavioral checklists, assessments (ex: Beck Depression Inventory), and direct ecological observation to obtain both direct and indirect data regarding the antecedent variables and functional relations that serve to perpetuate the disturbance.  (Cooper, Heron, & Heward, 2007, p. 50)  I would pay particular attention to social, medical, family circumstances in the past, present, and anticipated future.  I would also make certain to note any vested friends and family without whom behavior change cannot be successful.  (Cooper et al., 2007, p. 51)  Parallel to that search for natural supports, I would engage in a systematic search for pool of appropriate people whom the individual could potentially model.  (Cooper et al., 2007, p. 413)  Finally, it bears mentioning that the continued inclusion of data from multiple sources (people) and situations (cultural contexts and mediating factors) makes the process of culturally competent cognitive behavioral therapy a possible since “identification of important, controllable, causal functional relationships” is an intimately subjective process laden with unique cultural issues and challenges.  (Hays & Iwamasa, 2006, p. 255-256)

The next logical step after the aforementioned behavioral interventions is a series of cognitive interventions that help the patient establish a bridge between automatic thoughts and behavior.  The cognitive elements of belief modification may need to be undertaken in parallel with behavioral interventions if the patient isn’t “buying the rationale” or is repeatedly unable to traverse unforeseen cognitive obstacles.  (Beck, 2011, p. 295)  The process of teaching a patient to identify and monitor automatic thoughts is of paramount importance for long term success and maintenance.  If the patient-clinician dyad comes to consensus about a longer treatment course, Schema Therapy would be my personal tool of choice since we can reasonably anticipate it will take at least 12-24 months to modify an individual’s core belief system.

There are a number of anticipated complications that we can reliably predict before treatment commences.  The first and most obvious complication is that negative self talk and poor self image are so much a part of the typical patient with Dysthymic Disorder that compliance is likely to be a huge issue.  Resistance is likely to be moderate to high, especially once core issues are identified.  Metaphorically, we are talking about convincing someone that gravity doesn’t exist… it’s sure to be an uphill battle.  By virtue of the fact that I have endured the disorder myself, countertransference is a real and pertinent issue.  I would personally address this by attending my own individual sessions to ensure that I don’t get in the way of the best interest of my patient.  Finally, it must be noted that an individual with Dysthymic Disorder should be considered extremely vulnerable and handled with the utmost care.  For example, individuals with Dysthymic Disorder often exhibit symptoms such as fatigue and low self-esteem.  These symptoms may lead to tension in interpersonal relationships, thereby increasing the probability of terminating therapy.  Although these life events may appear to be the “cause” a major depressive episode, the episode is often predated by deficits in informational processing that lead to pre-morbid deterioration of the relationship.  (Harkness & Luther, 2001)

Because Dysthymic Disorder is largely defined and distinguished by its protracted course, longitudinal studies are uniquely positioned to investigate the prognosis of the disorder.  Due to the staggering costs associated with longitudinal studies, few have been conducted on the naturalistic course of Dysthymic Disorder.  (Klein, Norden, Ferro, Leader, & Kasch, 1998)  The overall consensus is that success treating Dysthymic Disorder is better addressed on a case by case basis – making a generalization about expected treatment outcomes and prognosis is probably ill advised.  However, we can reasonably expect that there will be some measure of improvement in cognitive functioning, motivation, mood, and affect.  I would be cautious about setting expectations for full recovery or total remission until the underlying core beliefs are identified.  Assuming I could obtain permission from the patient, I would endeavor to track relevant data over the course of treatment as we consider the transition to schema therapy together, if applicable.  Individuals whom suffer from Dysthymic Disorder often find that the minor daily hassles that happen to everyone may spiral into more serious life events that trigger depression.  (Harkness & Luther, 2001, p. 570)  Tracking those hassles seems to a reasonably simple way to measure the effectiveness of the therapy being provided and adjusting it if necessary.


American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Beck, J. S. (2011). Cognitive behavior therapy: Basic and beyond (2nd ed.). New York, NY: Guilford Press.

Cooper, J. O., Heron, T. E., & Heward, W. L. (2007). Applied Behavior Analysis (2nd ed.). Upper Saddle River, NJ: Pearson Education.

Dougherty, L. R., Klein, D. N., & Davila, J. (2004, Dec). A growth curve analysis of the course of dysthymic disorder: The effects of chronic stress and moderation by adverse parent-child relationships and family history. Journal of Consulting and Clinical Psychology, 72(6), 1012-1021. doi: 10.1037/0022-006X.72.6.1012

Durbin, E. C., Klein, D. N., & Schwartz, J. E. (2000, Feb). Predicting the 21/2-year outcome of dysthymic disorder: The roles of childhood adversity and family history of psychopathology. Journal of Consulting and Clinical Psychology, 68(1), 57-63. doi: 10.1037/0022-006X.68.1.57

Elligan, D. (1997). Culturally sensitive integration of supportive and cognitive behavioral therapy in the treatment of a bicultural dysthymic patient. Cultural Diversity and Mental Health, 3(3), 207-213. doi: 10.1037/1099-9809.3.3.207

Harkness, K. L., & Luther, J. (2001, Nov). Clinical risk factors for the generation of life events in major depression. The Journal of Abnormal Psychology, 110(4), 564-572. doi: 10.1037/0021-843X.110.4.564

Hayes, A., & Strunk, D. (n.d.). Depression. Retrieved May 28, 2012, from http://www.div12.org/PsychologicalTreatments/disorders/depression_main.php

Hays, P. A., & Iwamasa, G. Y. (Eds.). (2006). Culturally responsive cognitive-behavioral therapy. Washington DC: American Psychological Association.

Klein, D. N., Clark, D. C., Dansky, L., & Margolis, E. T. (1988, Aug). Dysthymia in the offspring of parents with primary unipolar affective disorder. The Journal of Abnormal Psychology, 97(3), 265-274. doi: 10.1037/0021-843X.97.3.265

Klein, D. N., Norden, K. A., Ferro, T., Leader, J. B., & Kasch, K. L. (1998). Thirty-month naturalistic follow-up study of early-onset dysthymic disorder: Course, diagnostic stability, and prediction of outcome.. The Journal of Abnormal Psychology, 107(2), 338-348. doi: 10.1037/0021-843X.107.2.338

Morrison, J. (2007). Diagnosis made easier: Principles and techniques for mental health clinicians. New York: Guilford Press.

Spiegler, M. D., & Guevremont, D. C. (2010). Contemporary Behavior Therapy (5th ed.). Belmont, CA: Wadsworth: Cengage Learning.

Yee, C. M., & Miller, G. A. (1994, Nov). A dual-task analysis of resource allocation in dysthymia and anhedonia. The Journal of Abnormal Psychology, 103(4), 625-636. doi: 10.1037/0021-843X.103.4.625

Yee, C. M., Deldin, P. J., & Miller, G. A. (1992, May). Early stimulus processing in dysthymia and anhedonia. The Journal of Abnormal Psychology, 101(2), 230-233. doi: 10.1037/0021-843X.101.2.230

Sleep Disorders in Childhood

There are a number of theories regarding the purpose of sleep.  “Sleep may provide a period of restoration in which deficits in somatic and central nervous system tissues are repaired.”  (Netherton, Holmes, & Walker, 1999, p. 415)  What I question is… wouldn’t we be able to detect that process (cellular creation/division)?

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It has been suggested that sleep facilitates information processing and memory consolidation.  This, too, seems plausible given the effects of sleep deprivation.  “Fatigue, excessive sleepiness, decreased attention, decline in perceptual, cognitive, and psychomotor capabilities and performance, regressive behavior, and disoriented though may result from prolonged sleep deprivation.  (Netherton et al., 1999, p. 415)

The “cycle of sleep” is a concept I found helpful to be able to conceptualize the process that takes place during sleep.

“While psychopathology is often comorbid with sleep disorders in adults, it is rarely so in children.”  (Netherton et al., 1999, p. 420)  NHW throws this out as a fact, but they don’t really give a reason why that is the case?

With regard to assessment, I very much approve of the use of sleep diaries as an effective way to document the course of events in a sleep-wake cycle.  We currently employ this tool with a couple clients of mine with a great deal of success.  One individual, in particular, had to take “the long way around” (which was particularly hard for the night staff I might add) but eventually we got them on a schedule that was amiable for all.

“Treatment of sleep disorders is designed to address both the symptoms and the causal factors of the disturbance; therefore, it is essential to cast a broad net in assessment to identify the likely etiology of a sleep disruption.”  (Netherton et al., 1999, p. 420)  I’m not sure it can be said better than that, great piece of writing in my opinion.

With insomnia, you sleep too little… with hypersomnia, you sleep too much.  Just FYI.

With regard to treatment, it would appear that the first and most important step is to regulate sleep hygiene.  This means we set and enforce a bedtime routine, and we foster the development of an environment that is conducive to sleep.  Eating and drinking (especially liquids that contain caffeine) should be limited close to bedtime.  (Netherton et al., 1999, p. 428)  We should assess all medications and determine if any possess stimulant qualities.  A “bedtime ritual” should be established and adhered to, including grooming and personal hygiene, flossing and brushing teeth, and using the bathroom.  Although this may be the case for some people, I personally disagree with the concept that bathing is a stimulant.  Personally, I have difficulty sleeping if I don’t bathe at night… it’s relaxing.  Matter of fact, sitting in the hot tub on a cold winter night is the sure fire way to make sure I get a great night of sleep.

I was also particularly interested in the relaxation training suggestion.  One method in particular that I was taught as a child, and that I endorse, is conceptualizing first that your lower extremities (starting with your feet) are “falling asleep.”  I progressively work my way “up” until I reach my head.  Usually, but the time I get to my arms, I am out like a light.  Mileage may vary, but it is one relaxation technique that worked for me as a kid.

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Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Sleep/Wake Disorders

Historically, sleep disorders have long been commonly recognized within the context of other psychopathological conditions, but they have been frequently minimized or otherwise ignored as distinct entities or stand-alone psychopathological situations.  Research supporting the current DSM-IV-TR classification system is extremely limited, despite the common sense approach (in my opinion) of grouping sleep disorders primarily on the basis of underlying constellation of symptoms.

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Primary insomnia is the hallmark diagnosis in this category.  It is “characterized by chronic difficulty initiating and/or maintaining sleep or persistent poor-quality sleep.”  (Blaney & Millon, 2009, p. 508)  Individually commonly suffer from mild anxiety, mood disturbances, concentration/memory dysfunction, somatic concerns, and general malaise… but these conditions are generally viewed as symptoms rather than causes.  Insomnia prevalence increases with age, in contrast with sleep onset difficulties are more common in young adults.  It has also been suggested that, generally speak, women are more susceptible than men.  Societal prevalence is between 1% and 2%.  (Blaney & Millon, 2009, p. 508)

I was intrigued by the statement that “the majority of insomnia sufferers tend to overestimate the time it takes them to fall asleep and to underestimate the time they actually sleep to some degree.”  (Blaney & Millon, 2009, p. 510)  This might give some basis to a cognitive-behavioral approach if we can reset those expectations.  A stated by the text, the main problem is that most clinicians don’t have access to the raw data to confirm or refute this subjective complaint.  My question… is it out of the realm of possibility for us to send a client home with a measurement device so we can accumulate that data?

Narcolepsy is characterized by recurrent, irresistible day time sleep episodes.  The “classic tetrad” indicative of narcolepsy includes excessive daytime sleepiness and unintended sleep episodes during situations where most persons could stay awake, abrupt and reversible decrease or loss of muscle tome (without loss of consciousness, also known as cataplexy), and/or awakening from nocturnal or diurnal sleep with an inability to move (sleep paralysis), and finally vivid images and dreams that are evoked just as sleep develops (hypnagogic hallucinations).  (Blaney & Millon, 2009, p. 510)  Narcolepsy generally first appears during adolescence or young adulthood, and is believed to be genetically predisposed.   Life events may precipitate the onsite of this disorder… although it is not clear to me whether they are causes or effects?

Breathing related sleep disorders encompass what is widely known as sleep apnea.  This condition manifests as loud snorting, pauses in breathing, gasping for breath during sleep, headaches on wake, and automatic behaviors during wakefulness or excessive daytime sleepiness.  The headaches on waking part turned my head because I get that all the time… although I haven’t really noticed any other signs or symptoms.  Odd…

Circadian Rhythm Sleep Disorders (CRSDs) represent a mismatch between natural sleep/wake rhythms and the schedule imposed by occupational or social demands.  (Blaney & Millon, 2009, p. 512)  Individuals typically report insomnia at certain times of the day (generally when they want to be sleeping) and excessive sleepiness at other times (generally when they should be awake).

Parasomnias encompass nightmares, night terrors, and sleepwalking.  Nightmare disorder is characterized by repeated awakenings by disturbing dreams.  Sleepwalking and Night Terrors both occur early in the sleep period and appear to represent incomplete arousals from the deepest states of sleep (states 3-4), known as slow wave sleep (SWS).  All of the above are more prevalent in children when compared with adults, and more common in males than in females. (I honestly would have expected it to be more common in females?)

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Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.