Insomnia and reducing suicide - the importance of sleep

The risk of suicide in people with insomnia could be reduced if they are able to get more sleep. 

Suicide is one of the major leading causes of death. Approximately 1 million people die each year worldwide from suicide. Suicidal behaviour is complex. Relevant risk factors vary with age, gender, and ethnic group and may even change over time. However, more than 90% of people who kill themselves have depression or another diagnosable mental or substance abuse disorder, often in combination with other mental disorders. Prior suicide attempt, family history of mental disorder or substance abuse, family history of suicide, family violence, including physical or sexual abuse, firearms in the home, incarceration and exposure to the suicidal behaviour of others are among the risk factors ( Agargun, M. Y., Lütfullah Beşiroğlu, 2005).

A very recent study found a relationship between sleep duration and suicidal thoughts in people with insomnia (Linden Oliver, University of Pennsylvania). Specifically, researchers discovered that every one-hour increase in sleep duration was associated with a 72 percent decrease in the likelihood of moderate or high suicide risk.

“We were surprised by the strength of the association between sleep duration and suicide risk,” said primary author Linden Oliver, M.A., clinical research coordinator for the University of Pennsylvania Behavioural Sleep Medicine Research Program.

“A 72 percent decrease in the likelihood of moderate or high suicide risk with a one-hour increase in sleep is interesting given the small sample size.”

Everyone’s individual sleep needs vary. In general, most healthy adults are built for 16 hours of wakefulness and need an average of eight hours of sleep a night. However, some individuals are able to function without sleepiness or drowsiness after as little as six hours of sleep. Others can't perform at their peak unless they've slept ten hours.

Earlier studies have also found that people with insomnia are up to twice as likely to commit suicide as people who don't have such difficulties sleeping. A 2011 study in teens found that those who had sleep problems at ages 12 to 14 were 2.5 times more likely to have suicidal thoughts in their late teen years.

Depending on the person, insomnia could be a cause or an effect of depression. Insomnia can lead to a very specific type of hopelessness, and hopelessness by itself is a powerful predictor of suicide ( Dr. W. Vaughn McCall).

Every cell in our bodies runs on a 24-hour clock, tuned to the night-day / light-dark cycles. It can be said that the brain acts as timekeeper, keeping the cellular clock in sync with the outside world so that it can govern our appetites, sleep, moods and much more. The research also shows that the clock may be broken in the brains of people with depression even at the level of the gene activity inside their brain cells (Proceedings of the National Academy of Sciences, the University of Michigan Medical School).

In a normal brain, the pattern of gene activity at a given time of the day is so distinctive that the authors could use it to accurately estimate the hour of death of the brain donor, suggesting that studying this "stopped clock" could conceivably be useful in forensics. By contrast, in severely depressed patients, the circadian clock was so disrupted that a patient's "day" pattern of gene activity could look like a "night" pattern and vice versa. 

Sleep is essential for a person’s health and well-being. Sleeping poorly increases the risk of poor mental health and physical health. As such, it is important to recognise the link between sleep and mental health and to highlight a dire need for people to begin to take sleep seriously as a health concern.

Understanding Psychosis

 

The word psychosis is used to describe a mental health problem that can affect the brain, so that there is a loss of contact with reality. When someone develops a mental health problem in this way it is called a psychotic episode. According to Rethink Mental Illness charity, about 3 out of every 100 people will experience a psychotic episode, making psychosis more common than diabetes. Most people make a full recovery from the experience.

The word ‘psychotic’ relates to ‘psychosis’, which is a psychiatric term, and describes experiences, such as hearing or seeing things or holding unusual beliefs, which other people don’t experience or share. Psychotic experiences are surprisingly common, but can also lead to diagnosis such as schizophrenia, bipolar disorder, schizo-affective disorder, paranoia, several depression or puerperal psychosis (a very severe form of postnatal depression).

One sign of psychosis is that a person lacks insight into their own state of mind. Psychosis distorts the senses, making it very difficult for the ill person to tell what is real from what is not real. Someone experiencing a first-episode psychosis may not understand what is happening. Symptoms are unfamiliar and frightening, leaving the person confused and distressed. If they do not know the facts and have no real understanding about mental illness, their distress may be increased by negative myths and stereotypes.

A psychotic episode occurs in 3 phases: (1) Prodrome, (2) Acute, (3) Recovery.

1. PRODROME - refers to the early symptoms and signs of an illness that precede the characteristic manifestations of the acute, fully developed illness. It is defined as the period of time from the first change in a person until development of the first frank psychotic symptoms.

2. ACUTE - clear psychotic symptoms are experienced, such as disorganised thinking, hallucinations or delusions.

3. RECOVERY - psychosis is treatable and most people recover, however, the pattern of recovery varies from person to person.

CAUSES OF PSYCHOTIC EXPERIENCES

Almost anyone can have a brief psychotic episode. In general, psychotic experiences may be caused by:

• Physical causes, such as illness: For example through a lack of sleep or high fevers (including malaria, pneumonia, other viral infections). They can also be a result of damage to the brain or dementia, lead and mercury poisoning, or changes in blood sugar levels.
• Drug use: Alcohol, street drugs, prescription medication (including steroids) can result in a psychotic experience that may continue even if the drug has worn off.
• Changes in brain chemistry: It’s not clear though whether these changes are the cause or the effect of the psychotic experience.
• Inherited vulnerability: However, no single gene has been found to be responsible, though, and the majority of people who have these experiences have no known family history.
• Traumatic events such as abuse: Many people who have psychotic experiences have been physically, emotionally, or sexually abused, and feel a need to push their feelings and memories away, because they are so painful. Psychotic experiences may be an expression of these overwhelming feelings and forbidden thoughts, and a way of coping with trauma.

TREATMENT OF PSYCHOSIS

Treating psychosis involves education, medication, close monitoring of symptoms, stress management and creating a strong, supportive environment. These treatments all help to speed up the recovery process and promote good quality of life for both the person and the family. 

RECOVERY

Some of the most recent and hopeful news in psychosis research is emerging from studies in the field of Early Intervention. New studies challenge several long held myths in psychiatry about the inability of people with psychosis to recover. It now appears that such myths, by maintaining an overall pessimism about outcomes, may significantly reduce a persons opportunities for improvement and/or recovery. After three decades of empirical study, it is now clear that early intervention is an important part of the treatment strategy. Furthermore, the importance of family input for treatment and the benefits of supportive partnerships between clinicians and families are well established (Rethink Mental Illness Charity).

Cognitive Enhancers in Schizophrenia: non-pharmacological approach

This post is a follow up part to the previous post, which introduced the pharmacological approach to the enhancement of cognition in schizophrenia.

With no major clinical success to date in targeting cognitive deficits in schizophrenia, attention shifted to behavioural, neuro-cognitive interventions. These approaches are based on the assumption that a broad and intensive activation of neural processing systems can stimulate neural resources to improve their functioning. It is believed that intense activation of cognitive (mental) systems damaged in patients with schizophrenia could effectively lead to a general and lasting functional improvement. As a result, several cognitive training strategies have been developed and these can generally be divided into either (1) COGNITION-ENHANCING or (2) COMPENSATORY approaches. The former approaches train patients with laboratory tasks designed to improve specific abilities in various cognitive domains, such as perception, learning, or memory. On the contrary, the latter approaches attempt to bypass cognitive deficits and teach strategies to compensate for them by relying on aids or other processes (Tomás, Roder, & Ruis, 2010).

1) COGNITION-ENHANCING PROGRAMMES

• Cognitive Remediation Therapy (CRT)
• Cognitive Enhancement Therapy (CET)
• Integrated Psychological Therapy for Schizophrenia (IPT) 

CRT aims to improve attention, working memory, cognitive flexibility, planning and executive functioning. CRT is usually administered via use of a computer, with the tasks appearing on the monitor. Research to date demonstrates small to moderate durable effects of CRT and that irrespective of therapy characteristics CRT can provide benefits to patients with cognitive difficulties. Although having more symptoms is associated with smaller effects, all participants were shown to benefit from CRT.

CET is a recovery-phase intervention for symptomatically stable schizophrenic out-patients with reduced relapse risk (Hogarty et al., 2004). This programme tackles areas and disabilities of a wider functional range. For example, specifically designed exercises target analytic logic, decision making, strategic and foresightful planning, as well as the intuitive thinking that supports social cognition (thinking). CET is a small-group approach that combines approximately 75 hours of progressive software training exercises in attention, memory and problem solving with 1.5 hours per week of social cognitive group exercises. Consistent positive results are fund in processing speed and verbal memory. A drawback of this approach is that it is only applicable to patients with a certain intellectual level (with an IQ above 80) who are psychopathologically stable (Tomás et al., 2010).

IPT integrates neuro-cognitive and psychosocial rehabilitation methods.IPT is administered to groups and consists of five, hierarchically organised sub-programs: cognitive differentiation, social perception, verbal communication, social skills and interpersonal problem solving. Studies typically reveal the largest improvements in neuro-cognitive functioning, however, effects on psychosocial functioning tend to be smaller (Roder et al., 2006). More research is currently needed to evaluate the effectiveness of this approach.

2) COMPENSATORY REHABILITATION PROGRAMMES

• Errorless Learning (EL)
• Cognitive Adaptation Training (CAT)

EL involves two main procedures: prevention of errors during the learning phase and automation of perfect task execution (Terrace, 1963). It refers to teaching procedures that are designed in such a way that a learner/patient does not have to - and does not- makes mistakes as she/he learns new information and new procedures.

CAT uses environmental supports and various clues such as signs, check-lists or alarmed drug packaging. It also encourages organisation of belongings and the sequencing of appropriate routines.

In effect, compensatory strategies work to some extent, however, they do not succeed in achieving pre-morbid levels of performance (Tomás et al., 2010). Moreover, they are aimed at people with significant cognitive impairment that is difficult to restore and thus renders them less suitable for people with recent illness who are more intact.

References

Roder, V., Mueller, D. R., Mueser, K. T., & Brenner, H. D. (2006). Integrated psychological therapy for schizophrenia: is it effective? Schizophrenia bulletin, 32 Suppl 1, S81-93. doi:10.1093/schbul/sbl021 

Terrace, H. S. (1963). Discrimination learning with and without errors. Journal of the Experimental analysis of Behaviour, 6, 1-27.

Tomás, P., Roder, I. F. V., & Ruiz, J. C. (2010). cognitive Rehabilitation Programs in Schizophrenia: Current Status and Perspectives. International Journal of Psychology and Psychological Therapy, 10(2), 191-204.

Enhancing Cognition in Schizophrenia - pharmacological approach

Cognitive impairment is a core feature of schizophrenia, with more than 80% of patients showing significant impairments (Keefe & Fenton, 2007). The range of cognitive impairments in individuals with schizophrenia is broad, with the more robust and replicable deficits typically found in the domains of processing speed, episodic memory, working memory and executive function. These impairments have been shown to be associated with various impaired functional outcomes and thus development of new therapies to enhance cognition has become one of the most pressing challenges. Cognitive deficits persits throughout the course of the illness and as such, negatively affect daily functioning, work outcomes and treatment adherence. While anti-pscyhotic medications can control psychotic symptoms for the majority of patients, such improvements do not automatically transfer into the functional outcome, such as community functioning. Additionally, anti-psychotic drugs that are currently the main form of treatment in schizophrenia demonstrate only a modest positive effect on cognition.

Despite a large number of compelling rationales and significant body of preclinical data, there are no dramatic or consistent results that any one medication has the power to increase cognitive skills to the level of normal functioning. While a wide range of cholinergic, dopaminergic, glutamatergic and cannabinoid compounds have been developed, the Food and Drug Administration (FDA) has not yet approved any of the drug development programmes specifically aimed at treating cognitive impairments in schizophrenia.

Pharmacological approach: Potential Cognitive-Enhancing Drugs in Schizophrenia

1. Antipsychotic Drugs (APDs)

While numerous studies have demonstrated the dramatic efficacy of APDs in suppressing psychotic symptoms and preventing their recurrence, they have also revealed their inability to alleviate the negative and cognitive symptoms of the illness. There are, however, some studies that suggest that some of the newer atypical antipsychotics e.g. aripiprazole, clozapine, quetiapine, olanzapine, risperidone and ziprasidone, may provide minimal benefits in certain specific areas of cognition.

2. Donepezil, Rivastigmine, Galantamine

Researchers sometimes focus on drugs that have proved effective in other cognitively impaired conditions, such as in dementia. Several drugs approved for dementia stimulate acetylcholine by blocking its breakdown, which has been shown to improve cognition and slow cognitive decline. Donepezil belongs to this type. The results in schizophrenia field, however, are not very encouraging, with only a few studies showing somewhat minimal memory improvement.

Rivastagime has also been investigated but only in smaller-scale studies. No significant findings have been reported to date.

Evidence of cognitive benefit with galantamine has been mixed so far. The overall trend indicates that at lower doses galantamine exerts a positive effect on cognition but at higher doses it is consistently associated with negative results. The most effective dosage is yet to be established.

3. Nicotine and nicotinic receptors

It is now widely accepted that nicotinic receptor abnormalities are present in schizophrenia. The vast majority of studies found some positive effects, improvements were frequently recorded in working memory and attentional/executive control functions and in episodic memory. However, nicotine did not improve every measure examined in each study and the magnitude of the effects was not large. Additionally, nicotine as a therapeutic agent may be limited by tachyphylaxis.

4. Modafinil

Modafinil is a wakefulness-promoting agent, shown to be effective in enhancing cognition in sleep-deprived and healthy individuals, as well as in some psychiatric disorders. While having effect on many neurotransmitter systems, modafinil has an uncertain mechanism of action. Results at this stage appears to be inconclusive. Benefits demonstrated by early studies were not replicated by larger-scale studies.

NB: Non-pharmacological applications will be reviewed in a future post

Reference

Keefe, R. S. E., & Fenton, W. S. (2007). How should DSM-V criteria for schizophrenia include cognitive  impairment? Schizophrenia bulletin, 33(4), 912-20. doi:10.1093/schbul/sbm046