Category Archives: Psychiatry

Depression: Symptoms, Aetiology and Treatment Options

Symptoms 

Depression is a serious affective disorder that affects millions of people in the world, approximately 5% of the population. In the United States alone approximately 33 million people will suffer from depression at some point in their life (Bear, 2007). In addition, the disorder is the leading cause of suicide. Despite its high prevalence, however, stigma still also remains high. A primary reason for the stigma surrounding any mental disorder is a misunderstanding of the symptoms and causes.

depressed

Even though depression strikes people differently, the cardinal symptoms are lowered mood and feelings of dejection, a lack of pleasure or interest rather than sadness. Accompanying symptoms include changes in appetite, fatigue, insomnia or hypersomnia, diminished concentration, feelings of worthlessness and/or guilt and recurrent thoughts of death and/or suicide (Bear, 2007). Depression can be one half of bipolar disorder but also occur on its own and in varying degrees of severity. Usually, for a diagnosis of major depression, the cardinal symptoms of depression must be present every day for approximately 2 weeks. Importantly, the cause of depression cannot be linked to a bereavement. This clear distinction is what separates depression from sadness.

Types of depression include chronic depression of dysthymia, major or clinical depression, atypical depression and manic depression. Chronic depression or dysthymia is usually less severe than major or clinical depression; however, it can be more disabling in that the symptoms are long-term (2 years+) or recurrent throughout a lifetime. Major or clinical depression is more severe; however, the symptoms do not last longer than 2 years and is not typically recurrent. Approximately 17% of sufferers have chronic symptoms.  It is important to note, however, that when depression is left untreated, recurrence is far more likely. Manic depression is found in bipolar disorder, to find out more click here. Finally, atypical depression is when a person suffers from the accompanying symptoms rather than the cardinal symptoms.

Aetiology and Treatment Options 

Biological basis 

Affective or mood disorders such as depression alter the typical function of the brain. Many different parts of the brain are usually affected at the same time, but the major system involved is the hypothalamic-pituitary-adrenal system (HPA). Exaggerated activity in the HPA system is common in people with anxiety and affective disorders. Specific to depression, blood cortisol levels are heightened as is the concentration of corticotropin-releasing hormones (CRH) in the cerebrospinal fluid.

Monoamine hypothesis

The monoamine hypothesis of depression states that a deficit in monoamines causes mood disorders. Monoamines include serotonin and catecholamines (inc. dopamine, noradrenaline, norepinephrine).  Current anti-depressants focus on this theory of depression. Anti-depressants inhibit the re-uptake of of monoamines, increasing the concentration of them in the synaptic cleft. The great benefit of anti-depressants is that they promote long-term, adaptive changes in the brain reducing the possibility of another depressive episode. Unfortunately, not all depressed people find anti-depressants effective. This can mean that either the treatment does not work for them at all or they require a greater dosage. Furthermore, it can takes week for depressants to take affect. Lastly, anti-depressants can raise levels of norepinephrine, which makes anti-depressants less effective. As anti-depressants are not always effective,  patients with prolonged depressive episodes may seek alternative treatment. Electroconvulsive therapy (ECT) and therapy are both options. ECT is mainly used in extreme cases because it can offer immediate relief. However, ECT is controversial due to the danger of memory loss. This is not surprising considering ECT is a localised seizure controlled by keeping the patient under anaesthesia. It is unknown exactly how ECT works; however, the hippocampus has been implicated. The hippocampus is involved in regulating CRH levels and the HPA system.

Types of anti-depressants include: selective serotonin re-uptake inhibitors, serotonin-noradrenaline re-uptake inhibitors, tricyclic anti-depressants and monoamine oxidase inhibitors. For people with bipolar disorder, lithium is also used to stabilise mood primarily the mania but has been shown stabilise mood overall.

Diathesis-Stress hypothesis 

The diathesis-stress hypothesis proposes that mental disorders have a genetic component that predisposes us to mental illness. Certain life stressors then makes us susceptible to mental illness actually presenting themselves. As such, traumatic childhoods full of abuse and/or neglect can leave a child at high risk for developing mental disorders. Tragically, children whose poor treatment is due to mentally ill caregivers, this cycle becomes hard to break. However, according to the diathesis-stress model, a trigger is not enough to bring forth mental illness without a genetic foundation. This genetic foundation goes hand in hand with the HPA system. Of course this does not mean that only traumatised children will suffer from mental health disorders. Individuals that have experienced a highly stressful life even such as divorce, moving away from home, changing schools, becoming ill, etc. will also be at risk are they predisposed to mental health issues.

depressed2

In a healthy individual, cortisol activates hippocampal glucocorticoid receptors, which inhibit the the HPA system. However, in a depressed individual there is a flaw in the feedback system. On a molecular level there is a diminished hippocampal response to cortisol due to reduced number of  glucocorticoid receptors. Here the genetic component of depression comes into play; glucocorticoid receptors are the product of gene expression. Hence, an individual with few glucocorticoid receptors is more susceptible. Fittingly, the amount of glucocorticoid receptors are epigentically influenced, early sensory experience can alter the number as well. This means that a childhood where we are well looked after, loved, cared for, kept safe and happy can protect us from developing depression even if we disposed to at birth. This illustrates how important the interaction of nature and nurture is. Think Voldemort vs Harry Potter. Despite the traumatic death of his parents, the one year of unconditional love and Lily’s sacrifice protected him not just magically but neurologically. Interestingly, in an interview with Oprah Winfrey, JK Rowling discuss this exact point.

 

Citation 

Antidepressants . (n.d.). Antidepressants. Retrieved July 18, 2014, from http://www.nhs.uk/conditions/Antidepressant-drugs/Pages/Introduction.aspx

Bear, M. F., Connors, B. W., & Paradiso, M. A. (Eds.). (2007). Neuroscience(Vol. 2). Lippincott Williams & Wilkins.

Pinel, J. P. (2010). Biopsychology (8th ed., International ed.). Harlow: Pearson Education.

What the Heck is an HPA Axis & What Does it Have to do with Stress?. (n.d.). About.com Fibromyalgia & Chronic Fatigue. Retrieved July 18, 2014, from http://chronicfatigue.about.com/od/cfsglossary/g/hpa_axis.htm

Bipolar Disorder

My most recent post showcased the artist Isti Kaldor who has bipolar disorder. This post will explain the basics of the disorder. Quite a few celebrities have come forward stating they have bipolar disorder including Catherine Zeta Jones, Demi Lovato and Stephen Fry. If you want to know the true scope, there is a wikipedia page dedicated to celebrities known to have it. Despite their very public work lives, with our limited insight into their personal lives it is difficult to really know much about the disorder. Stephen Fry, however, did a brilliant documentary on his experiences dealing with his bipolar disorder called Stephen Fry: The Secret Life of the Manic Depressive, which is available in full on YouTube.

Symptoms and Types 

As the title says, bipolar disorder is sometimes also called manic depression, but bipolar disorder is its official name. Characterised as a recurrent mood disorder, it consists of repeated episodes of mania interchanged with episodes of depression. The depressive episodes include similar but less severe symptoms of major depression such as changes in appetite, insomnia or hypersomnia, fatigue, feelings of worthlessness, guilt, inability to concentrate and suicidal thoughts. As such, the symptoms can be managed with anti-depressants. The manic periods, however, are the opposite in some respects. Symptoms consist of grandiosity, decreased need for sleep, talkativeness, flight of ideas, short attention span, and impaired judgement. It is believed that the correlation between bipolar disorder and celebrities is that those with the disorder usually experience these manic highs with bursts of creativity and inspiration. Unfortunately, the manic period can also result in promiscuity and complete loss of inhibition much like the effects of alcohol. As with any disorder, the range and complexity of symptoms varies greatly from person to person.

Bipolar comes in two general forms: type I and type II. Type I is marked by manic episodes (with or without incidents of major depression), and occurs in about 1% of the population, equally among men and women. Type II is marked by hypomania (milder form of mania that is not associated with marked impairments in judgment of performance) and is always followed by milder depressive periods.

Aetiology 

Numerous twin studies and most notably the one conducted by McGuffin and colleagues (2003) have shown that there is a high concordance between monozygotic twins with “67% MZ vs. 19% DZ.” Also, even though there is a high correlation with depression and mania, the manic component appears to be significantly more heritable in monozygotic twins. We do know that bipolar disorder affects our neurochemical pathways as treatment of lithium and anti-depressants do help alleviate the drastic mood swings. However, the actual structural component is yet to be properly determined. Studies by Bearden et al., 2001 admit that even though “dysfunction is implicated in bipolar illness patients supported by reports of relatively greater impairment in visuospatial functioning, lateralization abnormalities, and mania secondary to RH lesions” there is still not enough conclusive evidence to draw a clear link between right hemisphere dysfunction and bipolar disorder.

Strakowski et al., 2005 on the other hand using MRIs have found compelling examples of damage to the prefrontal cortical areas, striatum and amygdala that predates that onset of symptoms, which suggests that abnormal brain structure could in fact play a quintessential role in onset of the disease. Furthermore, if further studies can confirm these findings, it could offer psychiatrists and neurologists a revolutionary way of pre-symptomatic diagnosis. As of 2012, Strakowski et al. have reached a “general consensus” that bipolar type I occurs due to abnormalities within networks that control emotional behaviour such as the prefrontal cortex and limbic area, specifically the amygdala.

Treatment 

To date the most effective treatments for bipolar disorder include lithium (used to target the manic episodes), anti-depressants such as SSRIs, monoamine oxidase and tricyclics. Other types of medication such as anti-anxieties and anti-psychotics are used in some cases depending on the severity of the symptoms. In addition to medication, therapy has also been proved to significantly reduce the psychological stress of the disorder.

Citations:

Bear, Mark F., Barry W. Connors, and Michael Paradiso. Neuroscience: Exploring the Brain. Baltimore, MD: Lippincott Williams & Wilkins, 2006. Print.

Bearden, C. E., Hoffman, K. M. and Cannon, T. D. (2001), The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disorders, 3: 106–150. doi: 10.1034/j.1399-5618.2001.030302.x

Malliaris, Yanni,. “1.7 Aetiology of Bipolar Disorder.” 1.7 Aetiology of Bipolar Disorder. BipolarLab.com, 20 Aug. 2010. Web. 03 Aug. 2013.

Strakowski, S. M., Adler, C. M., Almeida, J., Altshuler, L. L., Blumberg, H. P., Chang, K. D., DelBello, M. P., Frangou, S., McIntosh, A., Phillips, M. L., Sussman, J. E. and Townsend, J. D. (2012), The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disorders, 14: 313–325. doi: 10.1111/j.1399-5618.2012.01022.x

TED Talk – Jim Fallon: Exploring the mind of a killer

The other day I was listening to SciFri’s online podcasts and I stumbled upon an interview with Dr. Jim Fallon. Jim Fallon is a neuroscientist and professor emeritus at the University of California Irvine. In the interview with NPR’s Ira Flatow, Dr. Fallon tells the tale of how he discovered he has the brain of a psychopath. In this TED talk Fallon does not speak about how he found this out, but he does talk about his family history which does include many murders and in particular, one very famous one. Both video and audio podcast delve into how genetics play into the making of a criminal but also how our environment can to a large extent prevent many from ever veering into criminality.

ADHD/ADD: Symptoms, Aetiology and Treatment Options

Symptoms

In 2012, CDC data showed that 11% of school children in the US had been diagnosed with ADD/ADHD. It remains unclear why these figures are rising. Perhaps any or all of theses things are contributing: constant changes in diagnostic criteria that are expanding the symptomology, a greater acceptance of neurological disorders has prompted more people to step forward and accept a diagnosis, a shift in society that is actually increasing the rate of ADD/ADHD or even just misdiagnosis. One of the major changes in the DSM-V diagnosis is the recognition of adults with ADD/ADHD. Previously, ADD/ADHD has merely focused on the symptoms observed in childhood onset. In fact, the majority of children that develop the disorder go on to experience a variety of difficulties into adulthood. Being able to recognise ADHD as a long-term condition will hopefully improve the level of care for adults with a childhood diagnosis.

ADD

The symptoms of diagnosis can be broken down into two major categories: inattention and hyperactivity with impulsivity. Classic examples of these behaviours include: difficulty to failure to pay attention to details, difficulty organising tasks, fidgeting, excessive talking and inability to remain still or seated for a prolonged period. In order to be diagnosed with ADD/ADHD according to DSM-V guidelines, a child must present with six symptoms in either or both the inattention criteria and hyperactivity and impulsivity categories. Accordingly, the disorder can present in three ways: combined, predominately inattentive and predominately hyperactive-impulsive presentative. Adults (over the age of 17) must be present with a minimum of five symptoms. For both children and adults, these symptoms must be present for 6 months prior to diagnosis and should interfere with normal, daily life. Finally, these symptoms should be present in two or more settings, before the age of 12 and not singularly in conjunction with any other mental disorder.

Inattention Symptom – Taken directly from the DSM-V

  • Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other activities.
  • Often has trouble holding attention on tasks or play activities.
  • Often does not seem to listen when spoken to directly.
  • Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g., loses focus, side-tracked).
  • Often has trouble organising tasks and activities.
  • Often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time (such as schoolwork or homework).
  • Often loses things necessary for tasks and activities (e.g. school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
  • Is often easily distracted
  • Is often forgetful in daily activities.

Hyperactivity and Impulsivity Symptoms 

  • Often fidgets with or taps hands or feet, or squirms in seat.
  • Often leaves seat in situations when remaining seated is expected.
  • Often runs about or climbs in situations where it is not appropriate (adolescents or adults may be limited to feeling restless).
  • Often unable to play or take part in leisure activities quietly.
  • Is often “on the go” acting as if “driven by a motor”.
  • Often talks excessively.
  • Often blurts out an answer before a question has been completed.
  • Often has trouble waiting his/her turn.
  • Often interrupts or intrudes on others (e.g., butts into conversations or games)

I was very fortunate to receive permission to use a first hand report of how ADHD/ADD feels. Below are his experiences in his own words. Please check out the Reddit post where he discusses his experiences with ADHD/ADD. It is linked in the reference section under the author Jonathan Michael. His personal experience really helped my understanding of what these symptoms feel like, not just what they are.

“ADD is almost like having a regulator switch turned off in my head…I feel like my mind is racing at 90 miles per hour, constantly thirsting to take in information and sense perception all around me.”

“It’s not that I can’t “pay attention”, it’s that I’m paying attention to almost everything around me and can’t consciously order which is “most important” to pay attention to fast enough, or sometimes at all.”

“ADD isn’t about “becoming bored”, it’s about losing the natural instinct to be able to prioritize what should be focused on instead of what shouldn’t be…For us, we literally lose chunks of time because we were so wrapped up in something else.”

Psychiatrist Edward M. Hallowell, M.D. describes ADHD/ADD as such, and Jonathan Michael mentioned in his post that he found it a very accurate metaphor for the disorder. 

“In ADD, time collapses. Time becomes a black hole. To the person with ADD it feels as if everything is happening all at once. This creates a sense of inner turmoil or even panic. The individual loses perspective and the ability to prioritize. He or she is always on the go, trying to keep the world from caving in on top.”

Aetiology and Treatment Options 

Genetics

Researchers suggest a strong correlation between genetics and ADD/ADHD. A meta-analysis of 20 international twin studies revealed a heritability estimate of 0.76 for ADHD, making it the most heritable psychiatric disorder (2). However, despite a high concordance rate between monozygotic twins (72-83%) and fraternal twins (21-45%), pinpointing what genes are different has proven difficult. One of the main reasons it has been so hard to map the genetic component to the disorder is because many genes seem to be implicated. This makes sense because ADD/ADHD is so complex that it is far more likely the phenotypes found result from the additive characteristics of many different genes. Not only that but the variation in symptoms suggests the possibility that ADD/ADHD involves endophenotypes. In other words, ADHD has hereditary characteristics associated with it but that are not a direct symptom of  it or dependent upon it.

ADD Brain

Natalie M. Zahr, Ph.D., and Edith V. Sullivan, Ph.D. “Translational Studies of Alcoholism Bridging the Gap” Alcohol Research & Health, Volume 31, Number 3, p.215- (2008)[1]

The Brain 

As with genetic factors, the brain regions involved in ADHD/ADD are not completely clear either. One region that appears to be most involved is the prefrontal cortex. The prefrontal cortex’s main role is executive function – planning, self-control and attention. Catecholimanergic (dopamine and noradrenaline) neurotransmitter pathways in the prefrontal cortex have been implicated. Symptoms of ADD/ADHD reflect problems in executive function. Drug therapies prescribed to individuals target these catecholaminergic pathways by inhibiting the re-uptake of dopamine and noradrenaline to increase the levels of these neurotransmitters in the synaptic cleft. Common drug treatments that act as a reuptake of inhibitor of dopamine an/or noradrenialine have methylphenidate, dexamfetamine or atomoxetine as an active ingredient. These active ingredients are stimulants which may seem counterintuitive when treating a hyperactivity disorder. However, as dopamine and noradrenaline in the prefrontal cortex increase self-control, attention, planning, etc. stimulating the release of these neurotransmitters is suitable. Unfortunately as with all drugs, those used in treatment of ADD/ADHD have side effects that sometimes outweigh the benefits of the treatment for some. Common side effects of Ritalin f.eg. includes depression, irritability, anxiety, aggression, reduced sex drive, heart palpitations and more. Other options include behavioural therapy which works on central executive tasks such as goal setting, impulse control, planning and organisation.

Common ADHD/ADD drugs:

  • Concerta XL (methylphenidate)
  • Dexamfetamine
  • Elvanse (lisdexamfetamine)
  • Equasym XL (methylphenidate)
  • Medikinet (methylphenidate)
  • Ritalin (methylphenidate)
  • Strattera (atomoxetine)

Diet and Environment

Researchers suggest that damage or trauma to a foetus’ brain or trauma in early childhood can in some cases lead to the development of ADHD/ADD later in life. A  foetus exposed to drugs, alcohol, cigarettes and/or high levels of stress due to their mother’s habits or environment whilst in the womb are more likely to develop ADHD. From birth into childhood, brain diseases or infection, trauma during birth, head injury or exposure to secondhand smoke are also seen as risk factors. Some parents argue that diet or supplements reduce the symptoms of or prevent ADHD; however, little evidence supports this belief. A few studies have found that children with ADHD have lower levels of fatty acids, but it remains unclear whether this actually plays any role in the pathogenesis of the disorder. A poor family environment, a difficult upbringing or many life upheavals in early life are found more often in children with ADHD, but as of yet there is no way of knowing whether a difficult family environment acts as a stressor or if related genes in ADHD put the family at risk for more familial conflicts and unlawful behaviour. Importantly, as with any disorder or even personality a poor familial or social environment aggravates any imperfect aspects of our character. As I emphasise with any post on mental health, the key is to recognise the true severity of the disorder and to respect those who fight through it on a daily basis.

For those seeking help for ADD/ADHD:

  • Contact your local GP
  • Speak to a family member or friend
  • http://www.nhs.co.uk/ (UK)
  • http://www.youngminds.org.uk/ (UK)
  • http://www.mentalhealth.org.uk/ (UK)
  • http://www.help4adhd.org/ (US)
  • http://www.addhelpline.org/ (Global)
  • http://www.cdc.gov/ (US)

References

American Psychiatric Association. (2013). The Diagnostic and Statistical Manual of Mental Disorders: DSM 5. bookpointUS.

Attention Deficit Hyperactivity Disorder. (2012, January 1). Retrieved November 10, 2014, from http://www.nimh.nih.gov/health/publications/attention-deficit-hyperactivity-disorder/index.shtml#pub5

Faraone SV, Perlis RH, Doyle AE, et al.: Molecular genetics of attention deficit hyperactivity disorder. Biol Psychiatry 2005, 57:1313–1323.

Hallowell, E.M (2012). What’s it Like to Have ADHD?. [ONLINE] Available at: http://www.huffingtonpost.com/edward-m-hallowell-md/what-adhd-feels-like_b_1627463.html. [Last Accessed 10 November 2014].

Khan, S. A., & Faraone, S. V. (2006). The genetics of ADHD: a literature review of 2005. Current Psychiatry Reports, 8(5), 393-397.

Michael, J. (2014). My husband was diagnosed with ADD because he can’t focus on reading or similar tasks. I can read a book all day but simply *cannot* focus on a movie or a TV show. My mind will not stay focused. How come he has ADD and I don’t?. [ONLINE] Available at: http://np.reddit.com/r/NoStupidQuestions/comments/2b6bt9/my_husband_was_diagnosed_with_add_because_he_cant/cj2e6a6. [Last Accessed 20 July 2014].

Millichap, J. Gordon, and Michelle M. Yee. “The diet factor in attention-deficit/hyperactivity disorder.” Pediatrics 129.2 (2012): 330-337.

Rutherford, D. (2014, January 24). What causes ADHD? Retrieved November 10, 2014, from http://www.netdoctor.co.uk/adhd/whatcausesadhd.htm

Symptoms and Diagnosis. (2014, September 29). Retrieved November 10, 2014, from http://www.cdc.gov/ncbddd/adhd/diagnosis.html