All the confusion about defining “mental disorder” makes sense when one thinks about the term more carefully. Mental has to do with mind and disorder is often (though not always) a euphemism for disease. So, another way to think about mental disorder is as some kind of “mind disease.” Of course, as Thomas Szasz (1974) pointed out, mind or perception are products of our brain but – unlike brain – are not tangible, and so, in a literal sense, they cannot be afflicted by diseases.

Mental disorders fall into two likely categories: (a) everyday problems in living that warrant professional attention but are not diseases, and (b) suspected brain diseases whose aetiologies may one day be uncovered but currently remain unknown.

Given a commitment to an atheoretical position on etiology, the prospect of changing the definition of mental disorder to one that explicitly defines disorders as “psychobiological dysfunctions” is big news indeed because doing so is overtly theoretical. Psychobiology conceptualises human psychology as something that can be reduced to and explained exclusively in biological terms. As such, the proposed new definition of mental disorder contends that all diagnostically defined disorders have biological causes.

Moving in an openly biological direction might make sense, but only if the diagnostically defined mental disorders are restricted to disorders where the underlying biological causes are known. As Thomas Szasz said “I have tried to show that for those who regard mental symptoms as signs of brain disease, the concept of mental illness is unnecessary and misleading. For what they mean is that people so labeled suffer from diseases of the brain; and, if that is what they mean, it would seem better for the sake of clarity to say that and not something else.” In other words, if there will be a shift from an atheoretical to a psychobiological stance, it should probably have pretty clear evidence that the mental disorders it contains can be diagnosed using biological tests or markers. Yet, this is not the case, while all diagnostic manuals explicitly refer to the current unknown causality of the defined mental disorders.

In cases where mental disorders are diagnosed and treated successfully with medication, we cannot say whether there is a specific underlying biological cause and whether is being remedied. Improved mood notwithstanding, whether we have cured something remains the subject of speculation because, when it comes down to it, we just don’t know enough to say with certainty what the underlying biological cause of any given mental health condition actually is in the first place. We must keep in mind that changing a person’s experience and behaviour (for example regulation of stress, sleep, diet) doesn’t necessarily mean we have corrected a psychobiological dysfunction. To feel confident that medication cures an underlying disorder, we need to know whether the mental disorder can be solely attributed to biological etiology and how medication “fixes” that etiology.

However, human mentality and behaviour is constantly in dynamic interaction with biological processes and altogether, these are in constant dynamic interaction with past, present and projected in time external and internal stimuli. Therefore, even in cases that medication works sufficiently upon symptomatology of a disorder, the individual still needs to engage in psychotherapy in order to explore and resolve past, present and projected into the future learned cognitive patterns, emotions and behaviour in relation to his own self, to others and to the world. These have been continuously forming in us while we are growing in our social environments, and are in timeless constant interaction with biological processes; dynamically influencing autonomic biological processes and being dynamically influenced by autonomic biological processes.

Schizophrenia Disorder is a mental illness that occurs worldwide, affecting 21 million of people. The lifetime prevalence of schizophrenia is estimated to be 0.3% – 0.7% approximately, varying across countries (DSM-5; American Psychiatric Association, 2013). Incidents per year are about 1.5 per 10.000 people, while it is more common among men than among women (ratio 1.4:1) (McGrath, Saha, Chant & Welham, 2008). In spite of its relatively low prevalence, schizophrenia is ranked the 8th most disabling illness among all illnesses of the age range of 15-44, contributing significantly into the global illness burden (World Health Organization [WHO], 2001). People with Schizophrenia Disorder are 2 to 2.5 times more at risk of premature death mainly due to comorbiding chronic conditions such as diabetes, hypertension, cardiovascular and pulmonary illnesses. Stigma pertaining to schizophrenia and to other psychotic disorders is possibly the worst among other illnesses, however schizophrenia is also treatable, from which the majority of patients (approximately 80%) fully recover or can lead meaningful and productive lives (AlAqeel & Margolese, 2012; Harding, C. M., 1988). Effective treatment is usually the integration of pharmacotherapy, psychotherapy and psychosocial support interventions.

Schizophrenia and other psychotic disorders are characterized by the presence of the namely “positive” (delusions or/and hallucinations) and “negative” symptoms. The “positive symptoms” of psychosis are called “positive” because these can be conceptualized as being exerted levels of normal functions. Common positive symptoms include delusions of persecution and auditory hallucinations. Accordingly, the “negative symptoms” can be considered as diminution of normal functioning, as is anhedonia (inability to feel pleasure), avolition (diminished volition), alogia (diminished speech) and flattened affect. Negative symptoms are also present in other psychopathological conditions, such as in Major Depression Disorder and plenty others (Hovington & Lepage, 2012). The assessment of symptoms and diagnosis of psychotic disorders require mental health clinical expertise.

References

AlAqeel, B. & Margolese, H. C. (2012). Remission in schizophrenia: critical and systematic review. Harvard Review of Psychiatry, 20(6), pp. 281-297. doi: 10.3109/10673229.2012.747804

American Psychiatric Association. (2013). Diagnostic and statistical 
manual of mental disorders (5th ed.) Washington, DC; London, England: American Psychiatric Publishing.

Harding, C. M. (1988). Course types in schizophrenia: An analysis of European and American studies. Schizophrenia Bulletin, 14(4), pp. 633-643. doi: 10.1093/schbul/14.4.633

Hovington, C.L. & Lepage, M. (2012). Neurocognition and neuroimaging of persistent negative symptoms of schizophrenia. Expert Rev Neurother, 12(1), 53-69. doi: 10.1586/ern.11.173.

McGrath, J., Saha, S., Welham, J., El Saadi, O., MacCauley, C. & Chant, D. (2004). A systematic review of the incidence of schizophrenia: the distribution of rates and the influence of sex, urbanicity, migrant status and methodology. BMC Medicine, 28, pp. 2-13. doi: 10.1186/1741-7015-2-13

World Health Organization. (2001). The world health report 2001. Mental Health. New Understanding. New Hope. Geneva WHO. Retrieved from http://www.who.int/whr/2001/en/

Depression is a leading worldwide cause of illness burden affecting more than 300 million people and is the 4th leading cause of disability of all ages according to the World Health Organization, while projected estimates suggest that by 2020 depression will be the 2nd leading cause of disability worldwide (World Health Organization [WHO], 2001). Year prevalence in U.S. is approximately 7% (DSM-5; American Psychiatric Association, 2013; Kessler, Wai, Demler & Walters, 2005) and in Europe approximately 4% (Alonso, 2004). In cross-sectional design researches, prevalence varies across countries and studies. A recent meta-analytic study, which included cross-sectional studies from all five continents, reports that on average the prevalence of Major Depression Disorder or subthreshold depression symptoms is approximately 27% (Wang et al., 2017). Oppositely to schizophrenia, Major Depression Disorder occurs significantly more among women than among men, whereas significantly higher at risk of depression are the age groups 30-40, elderly population and people who suffer from chronic physical illnesses. Although occurrence of depression and subthreshold depressive symptomatology in younger population (<30 years old) is found to be the lowest, prevalence is still as high as 20% (Wang et al. 2017).

The symptoms of depression differ from usual sadness or mood changes that people experience in their everyday lives. People with Major Depression Disorder experience depressed mood for almost all day or all day and everyday or almost everyday, or experience severely diminished interest/pleasure in all or almost all activities, as well as a series of other symptoms, such as fatigue, psychomotor retardation, agitation, inability to concentrate, inappropriate guilt, feelings of worthlessness. Symptoms of depression may also include anhedonia (inability to feel pleasure), avolition (diminished volition), alogia (diminished speech) and flattened affect. In addition, Major Depression may be presented with psychotic features (DSM-5). The assessment of symptoms and diagnosis of depression require mental health clinical expertise. Depending on the severity of depression, treatment may involve from psychoeducational interventions to low or high intensity psychological intervention, medication and combined therapy for patients with chronic physical illnesses.

References

Alonso, J. et al. (2004). Prevalence of mental disorders in Europe: results from the European Study of the Epidemiology of Mental Disorders (ESEMeD) project. Acta Psychiatrica Scandinavica, 109 (Suppl. 420), pp. 21–27. doi: 10.1111/j.1600-0047.2004.00327.x

American Psychiatric Association. (2013). Diagnostic and statistical 
manual of mental disorders (5th ed.) Washington, DC; London, England: American Psychiatric Publishing.

Kessler, R. C., Chiu, W. T., Demler, O. & Walters, E. E., (2005). Prevalence, Severity, and Comorbidity of 12-Month DSM-IV Disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 6, pp. 617-627. doi: 10.1001/archpsyc.62.6.617

Wang, J. (2017). Prevalence of depression and depressive symptoms among outpatients: a systematic review and meta-analysis. British Medical Journal, 7(8). doi:10.1136/bmjopen-2017-017173

World Health Organization. (2001). The world health report 2001. Mental Health. New Understanding. New Hope. Geneva WHO. Retrieved from http://www.who.int/whr/2001/en/

Bipolar Disorder is slightly more common among men than in women and one year prevalence of type I and II is found from 0.0% to approximately 1% across different countries (DSM-5; American Psychiatric Association, 2013; Fajutrao, Locklear, Priaulx & Heyes, 2009). Bipolar disorder type I is characterized by the occurrence of manic, hypomanic and depression episodes. Bipolar II disorder is characterized by the absence of manic episodes but patients experience hypomanic and depression episodes. Patients may also experience mixed episodes, characterized by manic and depression symptomatology. Between episodes, there may be periods of normal emotional functioning (DSM-5). Manic and hypomanic episodes are periods of time during which the individual experiences an extraordinary abnormal elevated energy – not necessarily “joy” – along with symptoms such as pervasive distractibility, extremely racing thoughts, abnormal reduced need of sleep or incapability to sleep. Patients may also experience psychotic symptoms. Symptoms pertaining at least four consecutive days, for most of the day, are considered as of an hypomanic episode, while symptoms persisting at least one week are considered as of a manic episode (DSM-5). The assessment of symptoms and diagnosis of Bipolar Disorder require mental health clinical expertise. Treatment involves pharmacotherapy, psychological interventions and psychosocial support programs.

References

American Psychiatric Association. (2013). Diagnostic and statistical 
manual of mental disorders (5th ed.) Washington, DC; London, England: American Psychiatric Publishing.

Fajutrao, L., Locklear, J., Priaulx, J. & Heyes, A. (2009). A systematic review of the evidence of the burden of bipolar disorder in Europe. Clinical Practice and Epidemiology in Mental Health, 5(3). doi:10.1186/1745-0179-5-3

In most cases, an Anxiety Disorder is a chronic illness and strongly related to subsequent onset of Major Depression and other severe mental disorders as well as with physical illnesses, such as ulcer, especially if remained untreated (Kessler & Greenberg, 2002). In an international meta-analytic study the pooled twelve-month and lifetime prevalence of anxiety disorders in overall is estimated to be10.6% and 16.6%, respectively (Somers, Goldner, Waraich & Hsu (2006). Women compared to men are twice (ratio 1.9:1) at risk (Remes, Brayne, van der Linde & Lafortune, 2016). Anxiety disorders have very early onset with median age less than 15 years old and prevalence has been sharply rising among youth (Remes, Brayne, van der Linde & Lafortune, 2016; Kessler & Greenberg, 2002). It has been estimated that only 13.3% of affected population receives early or efficient treatment and in most cases among children and youth, Anxiety Disorders remain untreated for approximately a decade (Kessler & Greenberg, 2002).

People feel fear or anxiety in a wide range of stressful situations that they might encounter in everyday life. However, Anxiety Disorders are characterized by abnormal worry, anxiety, hyperarousal and excessive fear and involve specific persistent symptomatology for several months, which markedly interferes with the individual’s everyday activities and behaviour. Anxiety disorders include Specific Phobia, Panic Disorder, Agoraphobia, Social Anxiety Disorder and Generalized Anxiety Disorder, among others, which differ in the type of the objects/situations that cause anxiety and differ in related cognitive inferences and distortions (DSM-5; American Psychiatric Association, 2013). The symptoms include persistent fear, anxiety and avoidance behaviours as well as physical symptoms such as trembling/shaking, palpitation, shortness of breath, sweating, dizziness, feeling of chocking, chest pain, paresthesias, derealization (DSM-5).  Assessment of symptoms and diagnosis of Anxiety Disorders require mental health clinical expertise. Treatment involves psychotherapy, other psychological interventions and possibly pharmacotherapy.

References

American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.) Washington, DC; London, England: American Psychiatric Publishing.

Kessler, R. C., and Greenberg, P. E. (2002) The economic burden of anxiety and stress disorders. In Davis, K. L., D. S. Charney, J. T. Coyle and C.

Nemeroff (eds.), Neuropsychopharmacology: The fifth generation of progress (pp. 981-992).  Lippincott Williams & Wilkins, Philadelphia.

Remes, O., Brayne, C., van der Linde, R. & Lafortune, R. (2016). A systematic review of reviews on the prevalence of anxiety disorders in adult populations. Brain and Behavior, 6(7). doi: 10.1002/brb3.497

Post Traumatic Stress Disorder (PTSD) is a Trauma and Stressor Related Disorder (previously included in Anxiety Disorders). Patients with PTSD have experienced or witnessed serious life-threatening event(s) or death, severe injury or sexual violence and suffer from intrusion symptoms re-experiencing the trauma (recurring thoughts, dreams, dissociative reactions, psychological distress or psyhcological reactions at exposure to stimuli that symbolize the traumatic event) as well as from persistent avoidance of memories (or loss of specific memories about the event), avoidance of emotions and stimuli associated to the traumatic event (eg. places, people, activities, objects, situations), cognitive distortions (self-blame, negative beliefs about self, others and the world), negative mood related to the event (persistent diminished ability to feel positive emotions, diminished interest in important activities, persistent horror, fear, anger, shame, guilt, feelings of detachment/estrangement from others), and significant changes in arousal (exhibiting irritability, anger outbursts, startle, concentration problems, sleep disturbance, self-destructive behaviour, hypervigilance), (DSM-5; American Psychiatric Association, 2013). One year prevalence in U.S. is estimated to be about 3.5% and in Europe 0.5%-1%, however prevalence rates increase among war veterans, individuals who have experienced rape, combat, captivity, genocide and individuals whose occupation involves higher risk of exposure at traumatic events (DSM-5). It has been estimated that approximately 40% of population affected by war or large scale natural disasters suffer from mental disorders or sub-threshold symptoms, whereas the most common diagnoses have been PTSD, Depression and Anxiety Disorders (World Health Organization [WHO], 2001). Recognition of symptoms and assessment of symptoms and diagnosis of PTSD require mental health clinical expertise, interdisciplinary team work and screening programs, especially in regions that suffer a major disaster (National Institute for Clinical Excellence, 2005 [NICE], 2005). Treatment involves trauma-focused psychological interventions by specialized mental health professionals and possibly pharmacotherapy (NICE, 2005).

References

American Psychiatric Association. (2013). Diagnostic and statistical 
manual of mental disorders (5th ed.) Washington, DC; London, England: American Psychiatric Publishing.

National Institute for Clinical Excellence (2005). Post-traumatic stress disorder: management. NICE Clinical Guideline 26. Available at https://www.nice.org.uk/guidance/cg26. [NICE guideline]

World Health Organization. (2001). The world health report 2001. Mental Health. New Understanding. New Hope. Geneva WHO. Retrieved from http://www.who.int/whr/2001/en/

Obsessive Compulsive Disorder (OCD) is characterised by persistent and recurrent obsessions to which the individual respond with effort to ignore, suppress or neutralise them with other thoughts or actions (compulsions). Obsessions are thoughts, urges or images that are felt as intrusive and unwanted, which cause the individual marked distress. The individual respond with devoting considerable time on compulsions, such as repetitive acts (eg. washing, ordering, repeating words, counting, checking, praying) in order to reduce anxiety, whereas these behaviours are not realistically connected to the nature of the external or internal situation to be avoided/neutralised or they are markedly excessive. The prevalence of OCD is estimated to be about 1.2% in U.S. and 1.1-1.8% worldwide (DSM-5; American Psychiatric Association, 2013). OCD onset is higher among individuals in the age range of 18-29 than all other age groups and chances of onset declines as age increases, whereas significantly more women than men are affected (ratio 2:1) by the disorder (Ruscio, Stein, Chiu & Kessler, 2010). Assessment of symptoms and diagnosis of OCD require mental health clinical expertise. Depending on the severity of the disorder and patient’s responsiveness to therapy, treatment involves psychological interventions of low to high intensity and possibly pharmacotherapy.

References

American Psychiatric Association. (2013). Diagnostic and statistical 
manual of mental disorders (5th ed.) Washington, DC; London, England: American Psychiatric Publishing.

Ruscio, A. M., Stein, D. J., Chiu, W. T. & Kessler, R. C. (2010). The epidemiology of obsessive-compulsive disorder in the
national comorbidity survey replication. Molecular Psychiatry, 15(1), pp. 53–63. doi:10.1038/mp.2008.94

As psychology is the science of behavior, health psychology is focused on behavior related to health and illness, including individuals who confront chronic physical illness and psychosocial difficulties.

Health psychology views health and illness on a continuum and according to the positivistic definition of health by the World Health Organization as being a complete state of physical, psychological, and social wellness.  Health psychology views illness as a state on a continuum, which can be behaviourally influenced. Neither sickness circumscribes well-being, nor does health. According to the World Health Organization, health is not defined as the absence of a disease and it includes psychological and social well-being. The biopsychosocial model of health and illness was developed in an effort to address the psychological and social factors which contribute to the causality and outcome of health and illness.

Research in health psychology is dedicated to understanding the processes of health behavior change and understanding how this change can be better promoted and maintained. Studies are focused on the identification and understanding of health-risk factors and health-protective behaviors as well as on the investigation of the psychological impact of acute and chronic diseases on individuals. Research interventions often have the form of psychoeducation and target teaching patients of acute and chronic illness self-management and coping techniques.

Studies and interventions have been aiming at sedentary lifestyles, dietary intake, smoking cessation, prophylaxis, and sexual behavior.  Health psychologists work closely with other health professionals and often in interdisciplinary teams in order to design and implement an intervention, from developing the budget plans and designing the training process of front-line personnel to assessing implementation gaps and re-adjusting. This process might involve cooperation with professionals of different domains such as dieticians, physiotherapists, occupational therapists, social workers, and management or administration professionals. 

Psychotherapeutic procedures depend largely on the background of each practitioner, however usually, in health psychology operant – cognitive behavior techniques are employed. Psychotherapy with patients with chronic illness might be more focused on patients’ felt insecurity, changes in self-image, changes in relationships, grief, and fear of loss and death. With patients who suffer from chronic pain, psychotherapy aims at the enhancement of the patient’s understanding of the bio-psychological interaction of factors that might maintain or exacerbate distress through the use of the appropriate techniques. Also, health psychologists often work with patients whose relatives suffer from a chronic disease. In all circumstances, the ethical standards of good practice apply, including the clear psychotherapeutic contract and confidentiality.

References

Engel, G. L. (1980). The clinical application of the biopsychosocial model. The American Journal of Psychiatry, 137(5), 535-44. 10.1176/ajp.137.5.535

French, D., Vedhara, K., Kaptein, A.A. & Weinman, J. (2007). Health psychology: introduction to second edition. (2nd Ed.). Health psychology. Malaysia: BPS Blackwell.

Gurung, R.A.R. (2014). Health Psycholody. A cultural approach. US: Wadsworth Cengage Learning.

Marks, D.F. (2002). A brief history of health psychology. The health psychology reader. UK: Sage Publications.

Mattarazzo, J.D. (1982). Behavioral health’s challenge to academic, scientific and professional psychology. American psychologist. 37, 1-14. Retrieved from http://www.ncbi.nlm.nih.gov

Okifuji, A.& Turk, D. C. (2015). Behavioral and cognitive – behavioral approaches to treating patients with chronic pain : thinking outside the pill box. Journal of rational-emotive & cognitive-behavior therapy, 33(3) 218-238.  doi.org/10.1007/s10942-015-0215-x

Amyotrophic Lateral Sclerosis (ALS) management requires multidisciplinary teams of health professionals including health psychologists, nutritionists, physical therapists and speech therapists, who work closely with physicians and nursing care, with the aim to provide enhanced health care support, improve patients overall quality of life and reduce rate of disease progress (Zarei et al., 2015).

ALS is a devastating, rare and progressive neuron degenerative disease that appears rather uniformely worldwide, affecting 1-2 individuals in every 100,000 population (Mitsumoto, 2009). Symptoms include limbic, bulbar, truck and respiratory weakness. The disease is causing the progressive loss of muscles, leading to difficulties in moving, speech, swallowing and respiration and can be extended to non-motor neuron degeneration, causing cognitive impairment and dementia. After appearance of the first symptoms the average survival is approximately 3 to 5 years (Zarei et al, 2015), however in some people ALS appears with a very slow progress of several decades.

The cause of the disease remains uncertain. Approximately 5%-10% of cases of ALS occurrence are familial and the rest are sporadic with no previous family history of the disease (Wijesekera & Leigh, 2009). Riluzole and enderavone are the only FDA approved drugs, which in clinical trials have shown that may help in prolonging survival and and improve daily functioning (Miller, Mitchell, & Moore, 2012; Takahashi, 2009). Furthermore, treatment is limited to drug prescriptions for the management of symptoms, such as cramps, excessive saliva, insomnia, anxiety, depression as also to enteral feeding and oxygen to support malnutrition and respiratory dysfunction, accordingly (Wills, 2009;  Mitsumoto, 2009). A substantial amount of research has been devoted on numerous risk factors including immunity dysfunction, neuronal metabolism dysfunction, excitoxicity, genetic abnormalities, heavy metals, toxic agents and exposure, infections, inflammation and nutritional disorders, such as vitamins deficiencies (Mitsumoto, 2009).  It has been suggested that a combination of genetic and environmental factors may trigger the disease onset (Mitsumoto, 2009). 

Patients with ALS suffer from chronic pain. ALS secondary symptoms, such as weakness, fatigue, loss of dexterity, loss of appetite, insomnia and anxiety can mask symptoms of depression, which is highly under-diagnosed (Atassi et al., 2011). Chronic pain and pain intensity significantly influences patients’ quality of life and clinical attention to depressive symptomatology is highly recommended. It has been suggested that the influence of pain on patients’ quality of life remains only at the presence of depressive symptomatology. For example, the findings of a pilot study suggest that the worsening of the Quality of Life (QOL) of patients with intense pain occurs only in the presence of depressive symptomatology and also that depression directly deteriorates the QOL of patients with ALS; an effect irrespective of pain intensity (Pizzimenti, Aragona, Onesti, & Inghilleri, 2013).

In addition, clinical attention to depressive symptomatology is recommended by robust evidence from national studies for the occurrence of depression preceding ALS onset (Euesben, Danese, Lewis, & Maughan, 2017). For example, the results of a recent longitudinal study with a national sample – conducted in Sweden and included 1,752 and 8,760 controls – suggested that individuals who initially did not have ALS, but the disease was developed later, had increased risk of depression prior to the diagnosis of ALS – particularly, during the year before the diagnosis of ALS – as compared to participants in the control group. The study also found that after receiving the diagnosis of ALS, patients presented increased risk of depression, especially during the first year after (Roos et al., 2016), suggesting the need of psychological interventions and support for those patients receiving ALS diagnosis.

In terms of the contribution of dietary intake, research suggests that mitochondrial dysfunction and progressive failure to produce energy may play a key role in ALS onset and progression. There has been substantial amount of research evidence showing that Ketogenic diet – a diet that brings the metabolism in a state at which it burns fat rather than carbohydtrates – is protecting neuron cells’ energy production efficiency. Also, there has been evidence that malnutrition, which is common among ALS patients due to the difficulties that degeneration causes, plays an important role in disease progression in both humans and mice (Paganoni & Wills, 2013). Based on those findings, numerous diet animal models for ALS have been developed, intervening high daily intake in fat, 50%-60%, 20%-40% carbohydrates, 15%-20% protein and reported reduced risk of ALS and improved rate of disease progression. However, randomized control clinical trials (RCT’s) are needed to explore whether ketogenic diet can ameliorate symptoms and disease progression in humans (Zhao 2006; Paganoni & Wills, 2013). Physical activity (Pupillo et al., 2014) and Mediterranean diet rich in monosaturated fat may also be protective against the disease (Sofi, Macchi & Casini, 2013). Also, there has been some evidence from few exercise intervention trials and animal model studies that some types of exercise, may improve patients functional ability, delay decline and decrease disability, however more RCT’s are needed to explore to what extent exercise is beneficial and which types of exercise (Dal Bello-Has & Florence, 2013). Moreover, insufficient level of physical activity and avoidance may further contribute into muscle weakness, contractures and pain, as well as cause cardiovascular and respiratory dysfunction (Lunetta et al., 2016). 

References

Atassi, N., Cook, A., Pineda, C. M. E., Yerramilli-Rao, P., Pulley, D., & Cudkowicz, M. (2011). Depression in amyotrophic lateral sclerosis. Amyotrophic Lateral Sclerosis, 12(2), 109-112. doi:10.3109/17482968.2010.536839

Cwick, V. A. (2009). What is Amyotrophic Lateral Sclerosis? In H. Mitsumoto (Ed.), Amyotrophic Lateral Sclerosis. A Guide for Patients and Families (pp. 3-22).New York: Demos Medical Publishing

Dal Bello-Haas V., & Florence J. M. (2013). Therapeutic exercise for people with amyotrophic lateral sclerosis ormotor neuron disease. Cochrane Database of Systematic Reviews, 5(5). doi: 10.1002/14651858.CD005229.pub3.

Euesden, J., Danese, A, Lewis, C. M, & Maughan, B. (2017). A bidirectional relationship between depression and the autoimmune disorders: New perspectives from the National Child Development Study. PLoS ONE, 12(3). doi:10.1371/journal.pone.0173015

Wijesekera, L. C., & Leigh, P. N. (2009). Amyotrophic lateral sclerosis. Orphanet Journal of rare Diseases, 4(3). doi:10.1186/1750-1172-4-3

Lunetta, C., Lizio, A.,  Sansone, V. A.,  Cellotto, N. M., Maestri, E.,  Bettinelli, M., …  Corbo, M. (2016).  Strictly monitored exercise programs reduce motor deterioration

in ALS: preliminary results of a randomized controlled trial. Journal of Neurology, 263, 52-60. doi: 10.1007/s00415-015-7924-z

Miller, R., Mitchell, J. D., & Moore, D. H. (2012). Riluzole for amyotrophic lateral sclerosis (ALS)/motor neuron disease (MND). Cochrane Database of Systematic Reviews, 14(3). doi: 10.1002/14651858.CD001447.pub3

Paganoni, S., & Wills, A. M., (2013). High-Fat and Ketogenic Diets in Amyotrophic Lateral Sclerosis. Journal of Child Neurology, 28(8), 989-992. doi:10.1177/0883073813488669

Pizzimenti, A., Aragona, M., Onesti, M., & Inghilleri, M. (2013). Depression, pain and quality of life in patients with amyotrophic lateral sclerosis: a cross-sectional study. Functional Neurology, 28(2), 115-119. doi: 10.11138/FNeur/2013.28.2.115.

Pupillo, E., Messina, P., G., Biold, G. G.,  Logroscino, G., Zoccolella, S., Chίo, A., … the EURALS Consortium, (2014). Physical activity and amyotrophic lateral sclerosis: a European population-based casecontrol study. Annals of Neurology, 75, 708-716. doi: 1 0.1002/ana.24150

Roos,E., Mariosa, D.,  Ingre, C., Lundholm, C.,  Wirdefeldt, K.,  Roos, P. M., & Fang, F. (2016). Depression in amyotrophic lateral sclerosis. Neurology, 86(24), 2271-7. doi: 10.1212/WNL.0000000000002671

Takahashi, R. (2009). Edaravone in ALS. Experimental Neurology, 217, 235-236. doi: 10.1016/j.expneurol.2009.03.001

Wills, A. M., Hubbard, J. Macklin, E. A., Glass, J., Tandan, R., Simpson, E. P., … the MDA Clinical Research Network, (2014). Hypercaloric enteral nutrition in Amyotrophic Lateral Sclerosis: a randomized double-blind placebo-controlled trial. Lancet, 383(9934), 2065–2072. doi:10.1016/S0140-6736(14)60222-1.

Zarei, S., Carr, K.,  Reiley, L., Diaz, K., Guerra, O., Altamirano, P. F., Chinea, A. (2015).  A comprehensive review of amyotrophic lateral sclerosis. Surgical Neurology International, 6(171). doi: 10.4103/2152-7806.169561

Sofi, F., Macchi, C., & Casini, A. (2013). Mediterranean Diet and Minimizing Neurodegeneration. Current Nutrition Reports, 2, 75-80. doi: 10.1007/s13668-013-0041-7

Osteoarthritis (OA) is a degenerative joint disease that creates painful joints’ and bones’ deformities, stiffness, synovial inflammation and swelling. Rheumatoid Arthritis (RA) is a progressive autoimmune disease with unpredictable pain and produces inflammation around joints and organs.

Arthritis is expected to become the world’s fourth cause of disability by the year 2020 (Woolf & Pfleger, 2003) and is already the first cause of disability in adults in U.S.A (Centers for Disease Control and Prevention [CDC], 2015) and in UK (Arthritis Research UK, 2013). Prevalence of OA is 9.6% for male and 18% for female and prevalence of RA is 0.3% to 1% (Saloni, 2004).  Prevalence of OA and RA increases by age and is consistently greater among women (Saloni, 2004). High health care direct costs – 80.8 billion dollars in US for the year 2003 (Yelin, 2007) and 8 billion pounds in UK, yearly (National Rheumatoid Arthritis Society [NRAS], 2010) – reflect the high prevalence rates.

There has been a substantial amount of research that relates stress with arthritis in both cause and effect layers – related to neuroendocrine and immune procedures (Irwin, 2008; Walker et al., 1999). In parallel, depression is more prevalent among older people and people who have lost valuable activities (Keefe & France, 1999; Kool &Geenen, R.2012), reaching 20% among patients of RA, who are diagnosed with Major Depression (Irwin, 2008).

It is important for practitioners to conceptualize the dynamic interaction between stress and feelings of inadequacy, pain and dysfunction (Strating, Schuur, & Suurmeijer, 2006). Chronic pain changes the psychological and social presence of patients (Roy, 2004; Sperry, 2014).  Patients with arthritis are at risk of early retirement, of being downsized at work and being bullied at work (Kivimäki, Vahtera, Ferrie, Hemingway, & Pentti, 2001; Schofield et al., 2013; Fattori et al., 2015). Losing societal/familial roles, sense of control, self-efficacy and social support, as opposed to maladaptive beliefs, guiltiness, catastrophizing and depression – they all have been related to pain experience (Keefe & France, 1999; Cross, March, Lapsley, Byrne, & Brooks, 2006; Roy, 2008; Okifuji & Turk, 2015).

Suffering in chronic illness is not only about pain and disability but also grief for what is lost by pain (Roy 2008). A study on 3,844 individuals measuring health related quality of life (HRQOL) among patients with arthritis as opposed to individuals with no arthritis has  concluded that patients with arthritis had consistently lower HRQOL scores in all 6 indexes and in all gender/age groups (Khanna et al., 2011).  Furthermore, a large study with 18.531 participants, has reported that individuals with higher scores of pain were comparable in functionality to individuals which were 2 or 3 decades older but with lower scores of pain (Covinsky,Lindquist, Dunlop, & Yelin, 2009).

Health Behaviours: the role of physical activity and appropriate nutrition:
Over-protective coping strategies and activities’ avoidance in response to pain causes muscle atrophy, arthritis’ deterioration and further pain (Fordyce as cited in Okifuji, 2015; Plasqui, 2008).  Muscles mass protection and retention of joints’ flexibility are of vital importance. The sensitivity of muscle mass to limited physical activity in response to pain is probable (Plasqui, 2008). The sensitivity of muscles’ atrophy to physical inactivity is well depicted (Plasqui, 2008).

Exercise and in specific intensive exercise has been proved better in illness deterioration and is strongly recommended in OA (Booth, Roberts, & Laye, 2012; NICE, 2014; NICE,  2009). However, it is very important for patients to know that exercise by itself is not enough. In fact, in one study the proportion of sedentary time and the occurrence of metabolic syndrome have been found significant – independently of the rest physical activity (Bankoski et al, 2011).

Adipose tissue (body fat) has been consistently related to increased production of the pro-inflammatory cytokines (interleukin) in OA (Nelson, 2012) and balanced diet has been associated with reduced inflammation in RA (Kjeldsen-Kragh & Haugen, 1991).  A diet – longitudinal intervention with 34 participants with RA, followed for a year and being in fasting and vegetarian diet, found significantly related improvements in a wide range of measures compared to control group.  Participants in fasting and vegetarian diet condition improved in biological measurements such as erythrocyte sedimentation rate, c-reactive protein (measures of level of inflammation) and white blood cell, in pain level, swelling and stiffness (Kjeldsen-Kragh & Haugen, 1991). When patients are overweight then weight loss in OA is highly advised, (NICE, 2014), however, these findings suggest that interventions must be rich in nutritional information – not focused solely to weight control (Nelson, 2012). 

On the top of that, arthritis has been strongly related to metabolic syndrome (Nelson, 2012), while the disease most commonly comorbid with cardiovascular diseases (Lima-Martinez et al., 2014; CDC, 2015). The relationship of sedentary lifestyles and the metabolic syndrome is widely proposed (Bankoski et al, 2011). However, in any case, exercise and weight control are of vital importance in arthritis course, as depicted by studies on body fat and arthritis disease activity.

References

Bankoski, A., Harris, T. B., McClain, J. J., Brychta, R. J., Caserotti, D., Chen, K. Y., … Koster A. (2011). Metabolic syndrome independent of physical activity. Diabetes care, 34, 497-503. doi: 2337/dc10-0987

Booth, F. W., Roberts, C. K., & Laye, M. J. (2012). Lack of exercise is a major cause of chronic diseases. Comprehensive physiology, 2(2), 1143-1211. doi: 10.1002/cphy.c110025

Centers for Disease Control and Prevention. (2015). Arthritis. Retrieved from http://www.cdc.gov/arthritis/index.htm

Covinsky, K. E., Lindquist, K., Dunlop, D. D., & Yelin, E. (2009). Pain, functional limitations, and aging. Journal of American geriatrics Society, 57(9), 1556-1561. doi.org/10.1111/j.1532-5415.2009.02388.x.Pain

Cross, M. J., March, L. M., Lapsley, H. M., Byrne, E., & Brooks, P. M. (2006). Patient self-efficacy and health locus of control: relationships with health status and arthritis-related expenditure. Rheumatology, 45(1), 92-96. doi.org/10.1093/rheumatology/kei114

Fattori, A., Neri, L., Aguglia, E., Bellomo, A., Bisogno, A., Camerino, D., … Favaretto, G. (2015). Estimating the Impact of Workplace Bullying : Humanistic and Economic Burden among Workers with Chronic Medical Conditions. Biomed research international,15(1), 1-12. doi.org/10.1155/2015/708908

Irwin, M. R., Davis, M., & Zautra, A. (2008). Behavioral Comorbidities in Rheumatoid Arthritis: A Psychoneuroimmunological Perspective. Psychiatric Times, 25(9).  PMCID: PMC2707019

Keefe, F. J. & France, C. R. (1999). Pain : Biopsychosocial Mechanisms and Management.Current directions in psychological science, 8(5), 137-141. Retrieved from https://www.researchgate.net/

Kivimaki, M, Vahtera, J., Ferrie, J.., Hemingway, H., & Pentti, J., (2001). Organizational downsizing and musculoskeletal problems in employees: a prospective study. Occupational and environmental medicine, 58, 811-817.  10.1136/oem.58.12.811 

Khanna, D., Maranian, P., Palta, M., Kaplan, R. M., Hays, R. D., Cherepanov, D., & Fryback, D. G. (2011). Health-related quality of life in adults reporting arthritis: analysis from the National health measurement study. Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation, 20(7), 1131-40. doi: org/10.1007/s11136-011-9849-z

Kjeldsen-Kragh, J., & Haugen, M. (1991). Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet, 118(8772).   doi: 10.1016/0140-6736(91)91770-U

Kool, M. B. & Geenen, R. (2012). Loneliness in patients with rheumatic

diseases: the significance of invalidation and lack of social support. The journal of psychology, 146(1-2), 229-241. 10.1080/00223980.2011.606434 

Lima-Martínez, M. M., Campo, E., Salazar, J., Paoli, M., Maldonado, I., Acosta, … Iacobellis, C. (2014). Epicardial fat thickness as cardiovascular risk factor and therapeutic target in patients with rheumatoid arthritis treated with biological and non-biological therapies. Arthritis. doi: 10.1155/2014/782850

National Rheumatoid Arthritis Society [NRAS], 2010). Employment and Rheumatoid Arthritis in Scotland. A national picture.  Retrieved from https://www.nras.org.uk

Nelson, F. R. T. (2012). Osteoarthritis and metabolic syndrome. Journal of American orthopaedic surgeons, 20(4), 259-260. doi: 10.5435/JAAOS-20-04-259 

Okifuji, A. & Turk, D. C. (2015). Behavioral and cognitive – behavioral approaches to treating patients with chronic pain : thinking outside the pill box. Journal of rational-emotive & cognitive-behavior therapy,33(3) 218 -238. doi.org/10.1007/s10942-015-0215-x

NICE (2009). Rheumatoid arthritis in adults: management. NICE Clinical Guideline 79. Available at https://www.nice.org.uk/guidance/cg79 [NICE guideline]

NICE (2014). Osteoarthritis: care and management. NICE Clinical Guideline 177. Available at https://www.nice.org.uk/guidance/cg/79[NICE guideline]

Plasqui, G. (2008). The role of physical activity in rheumatoid arthritis. Physiology & Behavior, 94, 270-275. doi:10.1016/j.physbeh.2007.12.012

Roy, R. (2004). Chronic pain, loss and suffering. CA: University of Toronto press.

Roy, R. (2008). Psychosocial interventions for chronic pain: in research of evidence. NY: Springer science & business media.  doi: 10.4236/psych.2015.610124

Saloni, T. (2004). Osteoarthritis: opportunities to address pharmaceutical gaps. Archives of the World Health Organization. Retrieved from http://archives.who.int/prioritymeds/report/background/osteoarthritis.doc

Sperry, L. (2014). Treating patients with arthritis: the impact of individual, couple,

and family dynamics. The family journal: counseling and therapy for couples and families, 17(3), 236-266. doi: 10.1177/1066480709338288

Strating, M. M. H., Schuur, W. H., & Suurmeijer, T. P. B. M. (2006). Contribution of Partner Support in Self-Management of Rheumatoid Arthritis Patients. An Application of the Theory of Planned Behavior. Journal of behavioral medicine, 29(1). doi.org/10.1007/s10865-005-9032-5

Walker, J. G., Littlejohn, G. O., McMurray, N. E., & Cutolo, M. (1999). Stress system response and rheumatoid arthritis: a multilevel approach. Rheumatology, 38(11), 1050-1057. doi.org/10.1093/rheumatology/38.11.1050

Woolf, A. D. & Pfleger, B. (2003). Burden Of Major Musculoskeletal Conditions. Bulletin Of The World Health Organization, 8, 646-569. Retrieved from http://www.who.int/bulletin/volumes/81/9/Woolf.pdf

Yelin, E. (2007). National and State Medical Expenditures and Lost Earnings Attributable to Arthritis and Other Rheumatic Conditions. Morbidity and mortality weekly report, 56(01), 4-7. Retrieved from http://www.cdc.gov/mmwr/

Multiple sclerosis (MS) is an autoimmune, inflammatory, demyelinating and sometimes neurodegenerative disease of the central nervous system that cause physical disability (Peterson & Fujinami, 2007). Prevalence rates vary significantly across the world, affecting from 2 individuals per 100,000 population in regions of sub-Saharan Africa and Eastern Asia, to 100 individuals per 100,000 population in regions of North America and Europe (Leray, Moreau, Fromont , & Edan, 2016). Also, studies report more than three to six fold increase of prevalence rates with increased latitude, suggesting a strong influence of environment and possible differences in climate, diet, and infectious agents (Van Der May, Ponsonby, Blizzard, & Dwyer, 2001). Females are more frequently affected than male, at a rate approximately of 2:1, and in the relapsing-remitting form of the disease at a rate of 3:1 in 2000’s from 2:1 in 1950’s and 1960’s (Leray,et al., 2016).

MS is a devastating disease with a wide range of symptoms that cause disability, including fatigue, meaning that patients find themselves struggling to carry out the simplest activities, dizziness, spasms, muscle stiffness, tremor, imbalance, temporary loss of vision, colour blindness, incontinence, constipation, numbness in different parts of the body and feelings of burning or needles, musculoskeletal pain, speech difficulty, swallowing difficulty and cognitive dysfunction. 

Approximately 10% of patients suffer from a continuous deterioration of symptoms, with no remission periods; a form of the disease that is called primary progressive MS. Gradual worsening of symptoms along with periods marked by sudden deterioration appears in 5% of patients (Progressive-relapsing MS). The majority of patients, approximately 85%, experience periods of exacerbation of symptoms, followed by periods of symptoms improvement or disappearance (relapsing-remitting MS). At some point in time, about 5% of these patients may experience a progressive deterioration of symptoms, followed by periods of remission or with absence of remission (secondary progressive MS) beyond that point (Goldenberg, 2012).

The unpredictability and change of symptoms put patients at risk of anxiety and depression, denial and hopelessness. Nurses, neurologists, psychologists, physiatrists, nutritionists, physical therapists, urologists and speech therapists are needed to work closely together and react fast to changing symptoms, in order to provide co-ordinated information, medical, technical, and psychological support and facilitate easy access to available resources, primary health care, inpatient rehabilitation and community MS groups (Gibson, 2002). Other patients with different forms of the disease or at different phases may offer important support. Also, psychologists need to work closely with social workers and ensure psychosocial support and vocational rehabilitation in collaboration with employers in order to protect patients jobs and employability (Gibson, 2002; Khan, & Turner-Stokes, 2009).

The need of assessment and treatment for depression and anxiety (early as well as regular screening) is crucial for the course of MS and patients well-being. Symptoms unpredictability triggers anxiety and depressive symptomatology and often elicit chronic sorrow and grief. Up to 50% of patients with MS are affected by depression and anxiety (Landro, Celius, & Sletvoid, 2004), whereas lifetime prevalence is estimated to be approximately 24% and 21.9% (Marrie et al., 2015), accordingly. Unfortunately, it is estimated that depression is under-diagnosed in around 23%-30% of patients (Horwitz, Cutter, Tyry, Campagnolo, & Vollmer, 2009; McGuigan & Hutchinson, 2006). Also, studies report varying rates of untreated depression ranging from 20% to as high as approximately 66% of the patients as for example a study that included 260 patients with MS, which found that only 3.1% of those with depression received sufficient treatment for depression (Mohr, Hart, Fonareva, & Tasch, 2006).

Moreover, depression and fatigue, which affects up to 90% of patients with MS, directly influences patients’ cognitive function, including attention and working memory, processing speed, ability to memorize and learn new information, abstract reasoning and executive function (Chiaravalloti, & DeLuca, 2008). Fatigue and fatigue-associated difficulties in cognitive function produce additional anxiety to the individual and further compounds cognitive dysfunction and depression.  In turn, depression and anxiety reduces patients adherence to medication (DiMatteo, Lepper, & Croghan, 2000), adherence to vital exercise for MS and deteriorate rehabilitation (Gibson & Frank, 2002) and quality of life (QOL) of patients (Janssens, vanDoorn, deBoer, Kalkers, vanderMeche, & Passchier, 2003).

Adherence to exercise is important in MS. Limited physical activity and lack of exercise due to MS symptoms such as spasticity, muscle stiffness and fatigue as well as overprotection (avoiding exercise), which is exacerbated by anxiety and depression, deteriorates rehabilitation, can lead to muscular weakness, cardiovascular dysfunction and disease (Gibson & Frank, 2002). Exercise contributes significantly to muscle strength and walking speed, fatigue, cognitive function and overall QOL, whereas there is also some evidence coming from research in humans and animal models that exercise has neuroprotective effects, however more control trials are needed (Giesser, 2015; Heine, van de Port, Rietberg, van Wegen, Kwakkel, 2015).  In addition, a healthy diet, rich in low fat protein, in unsaturated fat and fibre is always beneficial and offers protection from cardiovascular and neurodegenerative diseases (Paoli, Bianco, Damiani, & Bosco; Stafstrom & Rho, 2012). In MS, more research is needed; however, the results of few studies suggest that diet, especially rich in polyunsaturated fat and vitamins, may have a positive impact on MS outcome (Farinotti, Vacchi, Simi, Di Pietrantonj, Brait, & Filippini, 2017).

References

Chiaravalloti, N. D., & DeLuca, J. (2008). Cognitive impairment in multiple sclerosis. The Lancet Neurology, 7, 1139–51. doi: 10.1016/S1474-4422(08)70259-X

DiMatteo, M. R., Lepper, H. S., & Croghan, T. W. (2000). Depression is a risk factor for noncompliance with medical treatment: meta-analysis of the effects of anxiety and depression on patient adherence. Archives of Internal Medicine Journal, 160(14), 2101-2107.  doi: 10.1001/archinte.160.14.2101

Farinotti, M., Vacchi, L., Simi, S., Di Pietrantonj, C., Brait, L., & Filippini, G. (2012). Dietary interventions for multiple sclerosis. Cochrane Database of Systematic Reviews, 12. doi: 10.1002/14651858.CD004192.pub3.

Gibson, J. (2002). Supporting individuals with disabling multiple sclerosis

Journal of the Royal Society of Medicine, 95, 580-586. doi: 10.1258/jrsm.95.12.580

Giesser, B. S. (2015). Exercise in the management of persons with multiple sclerosis. Therapeutic Advances in Neurological Disorders, 8(3), 123-130. doi: 10.1177/1756285615576663

Goldenberg, M. M. (2012). Multiple sclerosis review. Pharmacy and Therapeutics, 37(3), 175-184. PMC3351877

Heine, M., van de Port, I., Rietberg, M. B., van Wegen, E. E. H., Kwakkel, G. (2015). Exercise therapy for fatigue in multiple sclerosis. Cochrane Database of Systematic Reviews, 9. doi: 10.1002/14651858.CD009956.pub2

Janssens, A. C., van Doorn, P. A., de Boer, J. B., Kalkers, N. F., van der Meche, F. G., Passchier, J., & Hintzen, R. Q. (2003). Anxiety and depression influence the relation between disability status and quality of life in multiple sclerosis. Multiple Sclerosis, 9(4), 397-403. doi: 10.1191/1352458503ms930oa

Khan,  F, Ng, L., & Turner-Stokes, L. (2009). Effectiveness of vocational rehabilitation intervention on the return to work and employment of persons with multiple sclerosis. Cochrane Database of Systematic Review, 1, doi: 10.1002/14651858.CD007256.pub2.

Landro, N. I., Celius, E. G., & Sletvoid, H. (2004). Depressive symptoms account for deficient information processing speed but not for impaired working memory in early phase multiple sclerosis. Journal of Neurological Sciences, 217, 211–216. doi: 10.1016/j.jns.2003.10.012 

Leray, E., Moreau, T., Fromont, A., & Edan, G. (2016). Epidemiology of multiple sclerosis.  Revue Neurologique, 172(1), 3-13. doi: 10.1016/j.neurol.2015.10.006.

Marrie, R. A., Horwitz, R., Cutter, G., Tyry, T., Campagnolo, D., & Vollmer, T. (2009). The burden of mental comorbidity in multiple sclerosis: frequent, underdiagnosed, and undertreated. Multiple Sclerosis, 15(3), 385-392. doi: 10.1177/1352458508099477

Marrie, R. A., Reingold, S., Cohen, J., Stuve, O.,Trojano, M., Sorensen, P. S., & Reider, N., (2015). The incidence and prevalence of psychiatric disorders in multiple sclerosis: a systematic review. Multiple Sclerosis 21(3), 305-317. doi: 10.1177/ 1352458514564487

McGuigan, C. & Hutchinson, M. (2006). Unrecognised symptoms of depression in a community-based population with multiple sclerosis. Journal of Neurology, 253(2), 219-223. doi: 10.1007/s00415-005-0963-0

Mohr, D. C., Hart, S. L., Fonareva, I., & Tasch, E. S. (2006). Treatment of depression for patients with multiple sclerosis in neurology clinics. Multiple Sclerosis, 12(2), 204-208.  doi: 10.1191/135248506ms1265oa

Paoli, A., Bianco, A., Damiani, E., & Bosco, G. (2014). Ketogenic diet in neuromuscular and neurodegenerative diseases. BioMed Research International, 474296, doi: 10.1155/2014/474296

Peterson, l. K. & Fujinami, R. S. (2007). Inflammation, demyelination, neurodegeneration and neuroprotection in the pathogenesis of multiple sclerosis. Journal of Neuroimmunology, 184(1-2), 37-44. 10.1016/j.jneuroim.2006.11.015

Stafstrom, C. & Rho, J. M. (2012). The ketogenic diet as a treatment paradigm for diverse neurological disorders. Frontiers in Pharmacology, 3(59). doi: 10.3389/fphar.2012.00059

Van Der May, I., Ponsonby, A. L., Blizzard, L., & Dwyer, T. (2001). Regional variation in multiple sclerosis prevalence in Australia and its associations with ambient ultraviolent radiation. Neuroepidemology, 20, 168-174. doi: 10.1159/000054783