I always was an excellent student. “A” grades in every subject, at any level of school. But since high school, high school performance had to be related with lack of sleep, use of (mild, legal) stimulats, nicotine, caffeine, but then I discovered pemoline in university days. At the same time, just like Sherlock holmes who used cocaine when he was looking for misteries to solve andthen stayed clean when solving them, and then again he used morphine after the problem was solved, I became addicted to several drugs, either street drugs or prescription ones. I stopped and became fully clean and sober after 4 years of activeaddiction, I stayed clean for 12 years, then my life presented me challenges too hard to face: divorce, loss of money, depression, exploitation and brainwashing by a pseudo-psychotherapic cult. I started being treated by a psychiatrist, he gave me fluoxetine, then venlafaxine, then reboxetine (all of them together) because my depression was severly damaging my relationships and my work. Im those months I also hadashort (3-4 months) relapse in the use of heroin, which was resolved with a methadone maintenance program.
None the less, all the SSRI and the SNRI caused a switch in my brain:
After 2 years of depression treatment the bipolar disorder came out… I had a mixed episode, angry, irritable, verbally abusive, sleeping 2-3 hours per night and strongly convinced that no onecouldunderstand me, help me or give proper advice: everyone seemed stupid to me! I tried to committ suicide, quite seriously, (I won’t explain what I ingested not to suggest anything).
They started therapy with strong doses of sodium valproate (1500mg/die), then they eliminated it because it wastoxic for myliver. I’m currently on quetiapine (175mg/die) and I’m happy with it. I can do my job with a new strong awareness of what happens in a bipolar mind. I obviously work under strict supervision, but I believe we shoul make astudy on the effectiveness of therapist who had (and positively solved) a mental disease or problem:
Strength or weakness?
I wish further resarch will address this, but not on students… on valid professionals who see their disease as a plus or as a minus.
Carlo Fornesi

This post was submitted by Dr. Carlo Fornesi.

Hypomania in depressed patients is under-recognised and bipolar disorder is consequently under-diagnosed. Important information can be collected by self-assessment screening questionnaires, such as the Hypomania Checklist-32 (HCL-32).

The objective of the BRIDGE study is to investigate transcultural differences in the self-perceived symptoms and consequences of hypomania using the HCL-32.

Across cultures the two-factor structure of the HCL-32 can be confirmed. The HCL-32 is partially measurement invariant (i.e. its items measure the underlying factors of hypomania in the same way across cultures), but shows some item variation depending on the cultural context, especially regarding the use of substances.
Northern Europeans expressed more the active/elated aspects of hypomania, whereas Eastern Europeans more the irritable, risk-taking and substance-use aspects. The HCL-32 is suitable as a screening instrument across cultures.
I welcome comments and discussion from individuals regarding the utility of this questionnaire and its results in the clinic.

This post was submitted by Prof Jules Angst.

Bipolar disorder does not occur in isolation but instead is associated with numerous co-occurring conditions that strongly impact the course of the illness, including risk of relapse and even suicidal behavior, and functional outcomes. Anxiety, impulsivity and substance use occur in the majority of patients with bipolar disorder and do not necessarily resolve when mood symptoms improve. The issue of comorbidity between bipolar anxiety, impulse control, substance use and personality disorders is very complex and prone to different pathogenetic interpretations. It is likely that the affective dysregulation of bipolar disorder extends beyond elation and depression to include, among others, such negative affective arousal states as anxiety, panic, irritability, impulsivity and mood lability.

The identification of differential patterns of comorbidity may provide important information in distinguishing more homogeneous clinical subtypes of affective disorders from the genetic and therapeutic point of view. As concern treatment perspective, anxiety disorders are highly prevalent in bipolar disorder and confer poor outcomes. Treatment challenges, particularly the use of antidepressants in this population, will be highlighted. Lithium and atypical antipsychotics seems to be not effective in controlling panic anxiety. On the contrary, Valproate seems to provide benefit in treating both mood instability and anxiety in patients with co-morbid bipolar and panic disorder. Bipolar disorder is associated with the highest rates of substance use disorders of any Axis I illness. However, until recently minimal research has focused on the treatment of this important subgroup and patients with substance use are still generally excluded from bipolar disorder clinical trials. Recent placebo-controlled clinical trials in patients with bipolar disorder and comorbid alcohol and substance abuse indicate a possible efficacy of valproate. In conclusion, in patients with bipolar disorder psychiatric comorbidity, other than clinical presentation and course of the illness, strongly influences treatment response to different mood stabilizers.

This post was submitted by Dr Giulio Perugi.

HIGH SUPPORT SERVICE
THERAPEUTIC ENVIRONMENT:
A THERAPEUTIC ENVIRONMENT IS ESTABLISHED BY MEANS OF THERAPEUTIC INTERVENTIONS AND SUPPORT
Core services establish a recuperative environment by means of therapeutic interventions and support.
The framework for Therapeutic intervention work from the following models:
1. Cognitive Behavioural Therapy
2. Solution-Focused Therapy
3. Narrative Therapy
MANAGEMENT OF ATTACHMENT DISORDERS
A two pronged approach is utilised:
1. Psycho-education:
Importance will be given to the involvement of family members
Planned Work with the family through
Parenting interventions
Relationships building with parent-child, siblings
Planned work with the child e.g. anger management, stress management, emotional regulation
2. Psychotherapy:
Cognitive behavioural Therapy: how thoughts affect behaviour and actions and exploring underlying negative thought patterns etc
Solution focused therapy: Working with the young persons strengths, empowering the child through ‘up-skilling’ of emotional regulation
Narrative Therapy: exploring the client’s life story and experiences
ON CALL PSYCHOLOGY TEAM
Role : to support young person and care team in a crisis
An on call Clinical Psychologist for any therapeutic advice required before, during and after a crisis. Dr. Clare Brady B. A (Hons), M. A, D. Psych Sc. (Clin. Psych) will provide this support service. Dr. Brady is available outside of working hours and including weekends for crisis management and staff consultation.
Please watch the details in below links provided:
Psychological Disorders : OCD Symptoms in Children

Behavioral Treatment for ADHD Children

Depression and Suicide – Pictures and facts

Contact Info: Lark Cottage, New Road, Donabate Co. Dublin info@corestaffing.ie www.corestaffing.ie T: 01 8359747 F: 01 8359750

This post was submitted by robert123 Cor.

Although full clinical recovery and good quality of life for the patients is the ideal target in the everyday clinical practice, suicidal behaviour is the most important (and most visible) treatment outcome in patients with psychiatric, disorders. Untreated and unsuccessfully treated major major mood disorder (particularly the acute major depressive episode) is the main cause of attempted and completed suicide, particularly in the presence of comorbid Axis I/Axis II psychiatric disorders and other (psycho-social) suicide risk factors. Since the majority of mood disorder patients never commit or attempt suicide, other clinically explorable suicide risk factors in major depressive episode (like high level of severity, hopelessness, aggressive/impulsive personality features, prior suicide attempt, family history of suicide, adverse life situations etc.) also play a contributory role.

A relatively newly recognised important proximate suicide risk factor in major depressive episode might be the depressive mixed state (3 or more simultaneously co-occuring non-euphoric intra-depressive hypomanic symptoms = DMX-3) since the frequency of past suicide attempts and current suicidal ideations is much higher among mixed than nonmixed unipolar and bipolar major depressives. A most recent study have also found a significantly higher rate of DMX-3 among the 29 bipolar (I+II) depressive and 60 unipolar depressive suicide attempters (90% vs 62% respectively) than in nonsuicidal 241 bipolar (I+II) and 104 unipolar major depressive outpatients (59% vs 29% respectively). On the other hand, however, suicidal behaviour in bipolar patients is not exclusively restricted to depressive episodes since mixed (major) affective episode (meeting the full syndromal criteria for mania and major depression in the same time) and dysphoric mania (full mania and 3 or more depressive symptoms) also increases the risk of attempted and completed suicide.

The recognition of depressive mixed states as possible suicide risk factor has important implications for suicide prevention, since antidepressant monotherapy (unprotected by mood stabilizers) in depressed patients with unrecognised bipolarity can worsen depression via augmenting mixed depression or generating de novo mixed states.

Balázs J, et al, J Affect Disord, 2006, 91: 133-138.
Benazzi F, Psychother Psychosom, 2005, 74: 61-62.
Benazzi F. and Aksikal HS, Curr Opin Psychiat, 2003, 16 (Suppl.2): 71-78.
Perugi G, et al, J Affect Disord, 2001, 67: 105-114.
Rihmer Z, Clinical Neuropsychiatry, 2005, 2: 48-54.
Rihmer Z, Aksikal HS. J Affect Disord, 2006, 94: 3-13.

This post was submitted by Prof Zoltan Rihmer.

Untreated and unsuccesfully treated major major mood disorder (particularly the acute, severe major depressive episode) is the main cause of attempted and completed suicide, particularly in the presence of comorbid Axis I/Axis II psychiatric disorders and other (psycho-social) suicide risk factors. Since the majority of mood disorder patients never committ or attempt suicide, other clinically explorable suicide risk factors in major depressive episode (like high level of severity, hopelessness, agitation, aggressive/impulsive personality features, prior suicide attempt, familiy history of suicide, adverse life situations etc.) also play a contributory role in the self-destructive behaviour.

A relatively newly recognised important proximate suicide risk factor in major depressive episode is the depressive mixed state (3 or more simultaneoulsy co-occuring non-euphoric intra-depressive hypomanic symptoms = DMX-3), and the most common hypomanic symptoms of mixed depression are irritability, psychomotor agitation, mental overactivity (flight of ideas, racing thoughts, crowded thoughts), and more talkativeness. Frequency of mixed depression is around 60% in bipolar II and 30% in unipolar major depressive episode, and there are several evidences that depressive mixed state and agitated depression are greatly overlapping phenomena. Several prior studies have found that the rate of past suicide attempts and current suicidal ideations is much higher among mixed than nonmixed unipolar and bipolar major depressives. On the other hand, however, one of our recent study have found a significantly higher rate of DMX-3 among the 29 bipolar (I+II) depressive and 60 unpolar depressive suicide attempters (90% vs 62% respectively) than in nonsuicidal 241 bipolar (I+II) and 104 unipolar major depressive outpatients (59% vs 29% respectively). These findings suggest that suicide attempters come mainly from mixed depressives with predominantly bipolar II base, and can explain, at least in part, why bipolar II patients carry the highest risk of suicidal behaviour in patients with major mood disorders.

The recognition of depressive mixed states as possible suicide risk factor has important implications for suicide prevention, since antidepressant monotherapy (unprotected by mood stabilizers or atypical antipsychotics) in depressed patients with unrecognised bipolarity can worsen depression via augmenting mixed depression or generating de novo mixed states.

Balázs J, et al, J Affect Disord, 2006, 91: 133-138.
Benazzi F, Curr Opin Psychiat, 2006; 19: 1-8.
Rihmer Z, Akiskal HS, J Affect Disord, 2006; 94. 3-13

This post was submitted by Prof Zoltan Rihmer.

Bipolar disorders are quite prevalent, but frequently underreferred, underdiganosed and undertreated illnesses. The early recognition and appropriate treatment is particularly important, since untreated bipolar disorders carry extremely high risk of both attempted and committed suicide. Recent studies clearly show that suicidal behaviour in patients with bipolar disorders is state and severity dependent that means that suicidality markedly decreases or vanishes after clinical recovery from major depressive episode or from dysphoric mania. However, since the majority of bipolar patients never committ and around half of them never attempt suicide, special clinical characteristics of the illness as well as some familial and psycho-social factors should also play a contributory role. Considering the clinically explorable suicide risk factors in patients with bipolar disorders (family and/or personal hisotry of suicidal behaviour, early onset, severe depressive episode/hopelessness, agitated/mixed depression, bipolar II diagnosis, rapid cyling course, dysphoric mania, mixed affective episode, comorbid Axis I and Axis II disorders, adverse life situations, lack of social and medical support), in the majority of cases, suicidal behaviour is predictable with a good chance. There are also several evidences that (succesful) acute and long-term treatment of bipolar patients (with mood stabilizers and with antidepressants/antipsychotics) substantially reduces the risk of attempted and completed suicide, even in this high-risk population. Supplementary psycho-social interventions (psychoeducation, targeted psychotherapies) further improve the results.

This post was submitted by Prof Zoltan Rihmer.

Previous studies, performed mainly in the second half of the last century, focused primarily on the two extreme clinical manifestations of major mood disorders (i.e., unipolar major depression and “classical” bipolar I disorder), and found marked differences in almost all clinical features and diagnostic validators, virtually supporting the strict categorical distinction between unipolar major depressive disorder and “bipolar” disorder. However, a number of recent studies clearly support the original “unitary” concept of Emil Kraepelin on the continuity between unipolar depression and manic-depressive illness. Nowdays it is well accepted that bipolar I (major/minor depression with a history of mania) and bipolar II (major depression with a history of hypomania but not with mania) disorders represent two prominent clinical phenotypes at the “bipolar edge” of the full unipolar-bipolar spectrum with several similarities and differences. Phenomenologically, bipolar II disorder is more close to bipolar I disorder than to unipolar depression, and, particularly if the subthreshold cases of hypomania are also considered, bipolar II is the most common form of bipolar disorders both in clinical settings and in the general population. While the basic similarity between bipolar I and bipolar II is the two different (“positive” and “negative”) pathological levels of mood and activity, there are several important differences between them, such as: 1, Familiy history of specific mood disorders, 2, Affective temperament, 3, Cross-sectional clinical picture of depression, 4, Long-term course, 5, Psychiatric and medical comorbidity, 6, Gender ratio, 7, Long-term course and 8, Suicidal behavior.

Although there is no fundamental difference in the acute and long-term pharmacotherapy between bipolar I and bipolar II disorders, because of the more complex clinical presentation and more recurrent nature of bipolar II, its pharmacological treatment is also more complex.

Prophylactic lithium therapy seems to exert greater anti-suicidal potential in bipolar II patients.

This post was submitted by Prof Zoltan Rihmer.

I was diagnosed as bipolar with psychotic features at age 41. I had several psychotic episodes over a period of several years before I discovered that adding a large quantity of salt to my diet could halt my illness. I was never diagnosed as being hyponatremic while in the hospital so I’m guessing that my low sodium level was an intermittent problem. After purchasing a commercial salt concentration meter, I discovered that my urinary salt level rose substantially during the evening. The level was normal during the daytime and while I was asleep. This is an indication that my body actively got rid of salt during the evening and my sodium blood level dropped at this time. I believe that low testosterone may be the culprit because of its circadian rhythm and effect on sodium reabsorption in the kidneys. I have yet to determine how low sodium levels effected my brain, but for the past three years I’ve had no psychotic episodes. All of my other mental and some physical symptoms have been eliminated as I’ve optimized the salt level. Currently I’m consuming about 14 grams of salt and a total of 1.9 liters of water for my body weight of 85 kg. Fortunately my blood pressure has not increased. Before my illness struck I had only been consuming a couple grams of salt a day. From my reading, I’ve found that about 10.5% of psychiatric patients are diagnosed as also being hyponatremic upon admission to a hospital. This is more than ten times the number of all other hospital admissions. My guess is that many more are hyponatremic the evening before admission. Currently hyponatremia is thought of as a symptom of polydipsia, an additional mental illness. From my experience, I believe it should be looked at as possible cause of bipolar disorder and possibly several other mental illnesses.

This post was submitted by Mr. Marlow .

The Hypothalamic-Pituitary-Adrenal (HPA) axis is one of the main physiological systems which allow the organism to respond to environmental “stress”. The HPA axis is influenced by early life experiences and is responsive to acute life events and furthermore has long been thought to be dysfunctional in mood disorders. Recent work has shown that subtle alterations in levels of corticosteroids (the main hormonal output of the HPA axis) may profoundly interfere with the actions of serotonergic antidepressants (Gartside et al, 2003). Corticosteroids may also be important for the cognitive impairment which is present in both unipolar and bipolar mood disorders (Porter et al, 2003; Thompson et al, 2005). Remission of certain domains of cognitive impairment may provide an important marker for remission in Mood Disorders (Gallagher et al, 2007). Lastly, the prospects of novel treatments for mood disorders which directly act on the HPA axis will be reviewed.

Keywords: mood disorders; HPA Axis; cognition; drug treatments.

References

(1) Gartside SE, Leitch MM, Young AH. Altered glucocorticoid rhythm attenuates the ability of a chronic SSRI to elevate forebrain 5-HT: implications for the treatment of depression.

Neuropsychopharmacology. 2003 Sep;28(9):1572-8.

(2) Porter RJ et al, Neurocognitive impairment in drug-free patients with major depressive disorder. Br J Psychiatry. 2003 Mar;182:214-20.

(3) Thompson JM et al, Neurocognitive impairment in euthymic patients with bipolar affective disorder. Br J Psychiatry. 2005 Jan;186:32-40.

(4) Gallagher P et al, Neurocognitive function following remission in major depressive disorder: potential objective marker of response? Aust N Z J Psychiatry. 2007 Jan;41(1):54-61.

(5) Young AH et al, Improvements in neurocognitive function and mood following adjunctive treatment with mifepristone (RU-486) in bipolar disorder. Neuropsychopharmacology. 2004 Aug;29(8):1538-45.

This post was submitted by Prof Allan Young.