Pattern & Legal Consequences in Hospitalised Drug Abusers more

JOURNAL OF MENTAL HEALTH AND HUMAN BEHAVIOR 2007: VOL 12, NO. 2 CONTENTS Editorial Deliberate self harm in adolescents Priti Arun Review Article Mood Disorders And Anxiety Disorders: How Much Is The Overlap? And What Are The Implications? Munish Aggarwal, Debasish Basu Original Article Pattern & Legal Consequences in Hospitalised Drug Abusers RK Solanki, DR Swami, Paramjeet Singh, Ravi Gupta, Navendu Gaur Cannabis induced psychosis – A Phenomenological perspective Ajeet Sidana, Mamta, BS Chavan Emotional Maturity: Therapeutic Implications Harprit Kaur, Parwinder Singh, Varinderjeet Singh Effect of maternal employment on children’s temperament and behavior Priti Arun, Jaspreet Kaur, Sophia Tinku, Lok Raj Study of Psychiatric Patients in Pingla Ashram Rahul Jindal, Kuldip C Sharma, Jagjeet Singh Case Conference Narcolepsy: clinical presentation, differential diagnosis and management Sandeep Grover, Swapnil Gupta Case Report Alcohol Dependence With Seasonal Bipolarity And Self-Medication For Psychotic Symptoms: A Case Report Anindya Banerjee, Surendra Kumar Mattoo, Munish Aggarwal 106-108 100-105 72-76 77-80 81-87 88-94 95-99 59-71 57-58 EDITORIAL Deliberate self harm in adolescents Mental health problems are a substantial cause of morbidity and mortality among adolescents. The high prevalence of mental health problems and the potential risk for serious consequences are strong arguments for early detection and appropriate management of adolescents’ mental health problems. The term ‘deliberate self-harm’ (DSH) is generally used to cover all acts of self-harm, self-injury or attempted suicide. Acts of deliberate self-harm may not always involve the intention to die. Self-injury can be quite different in intent from attempted suicide, because the injuries are generally inflicted in order to enable the person to carry on living, or to cope with difficult feelings, rather than to end their life. It is widely accepted that self-injury is the result of profound emotional pain. The injuries can release feelings of self-hatred, anger and anxiety, and can provide a means of self-punishment or of taking control. The most common form of self-injury is cutting but it can also include bruising, scraping, burning and other self-inflicted wounds. . In a study from UK 7%-14% of adolescents were reported to self harm at some time in their life, and 20%-45% of older adolescents report having had suicidal thoughts at some time.1 In an Indian study lifetime prevalence of suicidal ideation was 21.7%, and one-year prevalence was 11.7%. 2A survey of 11000 high school students in Kerala between fourteen and seventeen years age revealed that 27%had thought about suicide , 16% had a specific plan, 8% had made an attempt and 2% had made attempts requiring medical attention.3 In a study of 2404 school children from class 6th to 12th prevalence of suicidal ideas was found to be 1.04% in Chandigarh..4 Early gender specific risks for suicidal ideation included preschool behaviors that are counter to typical gender norms, such as aggressive behavior in females and dependence in males.5Isolation from peers leads to lower estimation of self worth and self-confidence. It has been seen that one’s friends should be friends with each other.6 Occasional DSH was associated with school type, poor academic achievement, and family related variables. Psychological factors like body image problems as well as self perception of having problems was related with repetitive DSH.7 In Indian studies, the risk factors for non-fatal suicidal behavior reported are failure in examination, anticipated punishment, social conflict, physical illness, and impending loss of love object.2 Factors suggestive of high risk of repetition of DSH include circumstances of attempt like degree of isolation, potential lethality of means used, precautions to avoid detection, and leaving a suicide note. Other factors are presence of psychiatric disorder and a past history of deliberate self-harm. However there is a strong association between attempted suicides, deliberate self-harm and subsequent successful suicide, and thus all incidents of self-harm should be handled with extreme care. There is a need to understand the underlying issues and low self-worth associated with selfinjury. It is suggested that adequate psychosocial assessment should be offered to all individuals attending hospital accident and emergency departments following incidents of deliberate self-harm. This is not only important for the risk of subsequent suicide, but also because the degree of physical trauma is not a reliable indication of the degree of psychological distress being experienced. Most teenagers will reveal that they are suicidal or have emotional problems for which they might Journal of Mental Health & Human Behavior, 2007 57 request emotional help. Many studies have shown that adolescents are more willing to share suicidal thoughts with a peer than a school staff member. Talking about suicide in the classroom provides with an avenue to talk about their feelings, thereby enabling them to be more comfortable with expressing suicidal thoughts and increasing their chances of seeking help from a friend or school staff member. When issues concerning suicide are taught in a sensitive, educational context they do not lead to, or cause, further suicidal behaviors. In a study where such measures were adapted it led to improvement in students’ knowledge of and attitudes toward depression and suicide, help-seeking behavior, suicidal ideation. 8 It is important to include awareness about DSH in school mental health. Rating scales can be used to assess suicidal intent. Practical methods such as reducing the availability of the means of self-harm can be helpful on individual and societal level. Underlying psychiatric disorder should be identified and treated. Other predisposing or precipitating factors should be addressed wherever possible. Priti Arun REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. Hawton K, James A. suicide and deliberate self harm in young people. BMJ 2005;330:891-894 Sidhartha T, Jena S. Suicidal behaviors in adolescents. Indian J Pediatrics 2006;73:783-788 Seethalakshmi George: Suicide and attempted suicide in childhood and adolescence, in George Joseph et. al, 1995, Suicide in Perspective with Special Reference to Kerala, CHCRE-HAFA, Kalamassery, p.55 Arun P, Chavan BS. Study of academic and behavioral problems in school children. Report submitted to department of Science and Technology, Chandigarh, 2006 Reinherz HZ, Giaconia RM, Silverman AB et al. Early psychosocial risks for adolescent suicidal ideation and attempts. J Am Acad Child Adolesc Psychiatry 1995;34(5):599-611 Bearman PS, Moody J. Suicide and friendship among American adolescents. Am J Public Health 2004;94(1):89-95 Brunner R, Parzer P, Haffner J et al. Prevalence and psychological correlates of occasional and repetitive self harm in adolescents. Arch Pediatr Adolesc Med 2007; 161: 641-649 Aseltine RH, Jr, James A, Schilling EA et al. Evaluating the SOS suicide prevention program: a replication and extension. BMC Public Health 2007; 7 : 161. Journal of Mental Health & Human Behavior, 2007 58 REVIEW ARTICLE Mood Disorders And Anxiety Disorders: How Much Is The Overlap? And What Are The Implications? Munish Aggarwal, Debasish Basu Abstract : Ever since Kraepelinian times, the distinction between anxiety and depressive states remains an ongoing subject of debate. Although conceptually different, all clinicians and researchers alike are struck by the common co-occurrence of depressive and anxiety symptoms in the same patients. This review aims to update our current knowledge in this clinically and conceptually important area. It focuses on several areas of “overlap” between mood and anxiety disorders: diagnostic, nosological, etiological, and management overlap, and also the correlates and consequences of such overlap (i.e., their implications). There is a large co-occurrence of syndromal diagnoses of both mood and anxiety disorders, presence of symptoms not meeting the syndromal criteria of one in the presence of syndromal diagnosis of other, and presence of both mood and anxiety symptoms and none of them meeting the syndromal criteria. Etiologically, it has been postulated that same areas of brain and same neurotransmitters are involved in both mood and anxiety disorders. There has been linkage between mood and anxiety disorder in family studies, and similar psychological and environmental factors contribute to the development of mood and anxiety symptoms. Patients with comorbid bipolar and anxiety disorders have younger age of onset, more pernicious course in terms of increased prevalence of suicide, increased number of psychotic and mixed features, poor quality of life, higher rate of substance abuse and worse response to treatment. Finally, drugs initially used for mood disorders now constitute the first-line major group of drugs to treat anxiety disorders. Some drugs initially used for anxiety disorders are used in the treatment of mood symptoms especially in the initial part. INTRODUCTION The distinction between anxiety and depressive states remains an ongoing subject of debate. Kraepelin described mixed states of manicdepressive insanity as ‘depressive or anxious mania… a morbid state… composed of flight of ideas, excitement, and anxiety… mood is anxiously despairing’. He also described ‘excited depression… great restlessness… mood is anxious, despondent, lachrymose, irritable, occasionally mixed with a certain self-irony’.1 Some investigators think that the two disorders occur along a single continuum with different patients manifesting different symptoms Journal of Mental Health & Human Behavior, 2007 along a spectrum of disorders. Others believe that anxiety and depression are clearly separate entities. 2 Mood and anxiety disorders have traditionally been classified separately in the standard nosological systems. During the past two decades the relationship between the mood and anxiety disorders has been examined closely. This review aims to update our current knowledge in this clinically and conceptually important area. For this purpose, we conducted multiple internet searches on PubMed, Google Scholar and other relevant search engines, using several combinations of key words such as mood disorders, anxiety disorders, comorbidity, dual 59 Aggarwal & Basu : Overlap between mood & anxiety disorders diagnosis, mixed anxiety & depression, bipolar, bipolar affective disorder (BPAD), depression, panic, phobia, post traumatic stress disorder (PTSD), obsessive compulsive disorder (OCD), generalized anxiety disorder (GAD), and overlap. We followed the lead from key relevant articles and searched the links to related articles from there. Wherever possible, we accessed the full text of the articles, either by manual search in the library or by electronic means. The voluminous data thus obtained were then categorized, for the purpose of this review, into several areas of “overlap”: namely, diagnostic, nosological, etiological, and management overlap, and also the correlates and consequences of such overlap (i.e., their implications). OVERLAP DUE TO DIAGNOSTIC ISSUES It is generally accepted that approximately two thirds of patients with depression have a comorbid anxiety disorder and one third or more of patients with panic disorder or generalized anxiety disorder (GAD) also have depression.3 SYNDROMAL COMORBIDITY 1. Comorbid Anxiety in Depressive Disorder The WHO collaborative study found that depression was 9 times more likely to develop in patients with anxiety disorders compared with no mental illness, with 39% of patients with current depression also having an anxiety disorder.4 Two studies 5,6 found lower rate of comorbid generalized anxiety disorder, phobic anxiety and especially panic attacks in depressed elderly subjects than found in similar studies involving the younger adults.7,8 One study found that 38% of 45 elderly outpatients with major depression also met the DSM-III-R criteria for anxiety disorder.9 In the National Comorbidity Survey database, 58% of respondents with major depression also had an anxiety disorder. The rates of comorbidity in depressed patients were 24.3% (simple phobia), 27.1% (social phobia), Journal of Mental Health & Human Behavior, 2007 17.2% (GAD), and 9.9% (panic disorder).10 Data from the Munich Follow-Up Study revealed that 44% of patients diagnosed with major depression also met the criteria for at least one anxiety disorder.11 2. Comorbid Anxiety in Bipolar Affective Disorder (BPAD) According to one study the prevalence of any anxiety disorder comorbidity in BPAD was 54% when meeting the criteria of BPAD.12 In the univariate analysis, panic disorder, OCD and GAD were more common among individuals with BPAD compared with those with major depressive disorder (MDD). With the multivariate logistics model, a lifetime diagnosis of panic disorder and current GAD were also both significantly more common among persons with BPAD.13 In the Epidemiologic Catchment Area (ECA) study, among patients with BPAD, 21.0% had lifetime panic disorder and 21.0% had lifetime OCD, as compared to 0.8% and 2.6%, respectively, in the general population group.14 In another study of 149 inpatients with affective disorders, it was found that 35% of 37 patients with bipolar disorder had comorbid OCD, which was similar to the prevalence of OCD among patients with unipolar depression.15 In the National Comorbidity Survey (NCS), 92.9% of the persons who met criteria for lifetime bipolar I disorder also met criteria for a lifetime anxiety disorder, as compared to 24.9% of the general population sample. Further, 47.2% of persons with bipolar I disorder were found to have comorbid social phobia, as compared to 13.3% of the general population group.16 In the same survey, the estimated lifetime prevalence of any anxiety disorder in BPAD was estimated at 92.9% versus 72.0% for alcohol abuse. Specific phobia was the most prevalent anxiety disorder comorbidity (66.6%) while panic disorder was the least prevalent (33.1%).17 According to the ECA study the lifetime rates of OCD were significantly 60 Aggarwal & Basu : Overlap between mood & anxiety disorders higher in the BPAD versus the MDD group (21.0% and 12.8%, respectively, versus 2.5% in the general population).17,18 An analysis of the ECA survey database also reported that the lifetime prevalence of panic disorder was significantly higher amongst persons with BPAD (20%) versus MDD (10.0%) and the general population (0.8%).19 3. Comorbid Depression in Anxiety Disorders The WHO collaborative study found that 44% with a current anxiety disorder have a comorbid depression.4 In another study of elderly major depression was more common in panic disorder and OCD (50% and 44.4%, respectively) than in general anxiety disorder and social phobia (30.3% and 25.0%, respectively).20 4. Comorbid BPAD in Anxiety Disorders According to one study the prevalence of BPAD (3.5%) was not significantly increased amongst patients with social phobia in contradistinction to MDD (70.2%).21 The estimated prevalence of bipolar spectrum disorders in the general population is approximately 2–4%.22 The rate of BPAD-II was more frequently associated with social phobia (21.1%) and OCD (17.7%) than with panic disorder (5.0%). SUB-SYNDROMAL COMORBIDITY 1. Comorbid Anxiety in Depression In a study of 200 patients who were diagnosed with major depressive disorder (MDD) using Research Diagnostic Criteria, 72% had moderate to severe levels of worry, 62% had moderate to severe levels of psychic anxiety, 29% reported panic attacks, and 19% had phobic symptoms of at least moderate severity.23 An earlier study found 88% of the patients reported either persistent or episodic tension, 28% had agoraphobic symptoms, and 17% had panic attacks.24 Symptoms commonly associated with anxiety states that may emerge in depressed patients include panic attacks, depersonalization, derealization, emotional lability, sleep disturbances, and agitation.25 In a study of elderly nursing home residents, 65% of those with major depression also displayed concurrent symptoms of anxiety, but very low rate of panic attacks were seen.26 In another retrospective study involving 336 elderly inpatients and out patients with major depression, one third to one half had severe anxiety symptoms, but 8% had only diagnosable anxiety disorder.27 2. Comorbid Anxiety in BPAD According to one study the prevalence of any anxiety disorder comorbidity in BPD was 54% when not meeting the syndromal criteria of BPAD.12 In a recent study of 316 inpatients with DSM-III-R manic or mixed episodes, 39% were rated as having some degree of anxiety.28 NOSOLOGICAL OVERLAP Till the advent of ICD-10, there was no nosological overlap category between mood and anxiety syndromes in any official classificatory system. ICD-10, for the first time, introduced such a category, viz., Mixed Anxiety Depressive Disorder (MAD), where an individual has both anxiety and depressive features that are a cause for clinical concern, but neither set of symptoms meets the criteria for an independent mood or anxiety disorder. Mixed anxiety-depressive disorder may occur in 1 to 4% of primary care patients.29,11,3 Estimates of community prevalence have been relatively low, ranging from 1 to 13%, 11,30-33 although there seems little doubt that these patients are quite common in primary-care settings. 11,30,31,34 Furthermore, these patients may demonstrate a relatively poor prognosis and significant disability;35 subsyndromal cases appear to be at greater risk of developing syndromal illnesses in Journal of Mental Health & Human Behavior, 2007 61 Aggarwal & Basu : Overlap between mood & anxiety disorders follow-up studies.30,36 In a report from the DSM-IV field trial, Zinbarg et al.37 concluded that patients with mixed anxiety-depression are characterized by less prominent symptoms of pervasive anhedonia and low interest or motivation compared with patients with major depression and less pervasive worry than patients with GAD. The validity of mixed anxiety depression as a formal diagnostic category has been debated for many years,37-40 and although it was added as a formal diagnostic category in ICD-10,41 it appears in the appendix of DSM-IV. In studies of MAD, prevalence rates for subthreshold symptoms of anxiety and depression vary from 0.8% in the Munich Follow-Up Study11 to 11.7% in mental health outpatients in the DSM-IV field trial for MAD.37 Weisberg et al.42 found that 0.2–0.6% of primary care patients in their sample qualified for a DSM-IV diagnosis of MAD. Approximately 70% of these patients remitted by the 6-month followup, and 80% remitted by 12 months after the initial interview. One additional published study43 based on the ICD-10 investigated the course of MAD and found that MAD is not a stable diagnosis. Only 1.2%of patients with a MAD diagnosis at baseline qualified for a MAD diagnosis at followup. Approximately 49% of patients had no ICD10 diagnosis after a year, 27% had a depressive or anxiety disorder diagnosis, and 22% of patients had a diagnosis other than depressive or anxiety disorder.43 ETIOLOGICAL OVERLAP A. Biological Overlap 1. Neurotransmitter systems Noradrenaline In bipolar disorder, noradrenergic activity has been demonstrated to be higher in mania than in depression across patient groups44 and within an individual.45 Also, indices of noradrenergic activity have been correlated with the severity of mania, and not with psychomotor agitation.46 Moreover, in a study of 22 medication-free acutely manic patients,47 patients had significant elevations in cerebrospinal fluid (CSF) nor epinephrine concentrations compared with depressed and euthymic patients and with normal volunteers, and the degree of elevation correlated significantly with the degree of manic dysphoria, anger, and anxiety. Investigators demonstrated increased norepinephrine turnover, as estimated by the ratio of neither MHPG (3-methoxy-4-hydroxyphenylglycol) to nor epinephrine, in specific brain regions of patients with bipolar disorder irrespective of affective state.48 DOPAMINE Regarding bipolar disorder, increased CSF, plasma, and urinary levels of the dopamine shown to be present in acute mania.49 Regarding anxiety disorders, an elevated growth hormone response to apomorphine, a dopamine agonist, in panic disorder suggests dopaminergic overactivity.50 GAMMA-AMINO BUTYRIC ACID (GABA) Gerner et al.51 found that GABA levels were significantly lower in the depressed group than in the manic, schizophrenic, or control groups. No significant differences in GABA levels were found between unipolar and bipolar depressed patients, and between manic patients and controls. Other investigators have found decreased GABA levels in patients with acute depression.52 Roy et al.,53 found no significant differences in CSF GABA levels when 25 patients with depression (unipolar and bipolar), were compared with controls. However, when the data were further analyzed, a subgroup of patients with unipolar melancholic depression had significantly lower levels. Benzodiazepines, which act on GABA receptors, have been proven effective in generalized, panic, and social anxiety. Enhancing GABA transmission has been suggested to promote anxiolysis.54 Journal of Mental Health & Human Behavior, 2007 62 Aggarwal & Basu : Overlap between mood & anxiety disorders SEROTONIN There are data to suggest reduced levels of the major serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in post mortem brain regions of bipolar patients.48 Other studies, however, have shown no trait abnormalities in CSF levels of 5-HIAA.55 In panic disorder the most compelling hypothesis is that of reduced central serotonin levels56 and subsequent hypersensitivity of postsynaptic serotonin receptors.57 In OCD, there does not seem to be any basal serotonin abnormalities as reflected in normal CSF levels of 5-HIAA as compared to controls. Strong support for involvement of the serotonergic system in anxiety disorders in general is provided by the increasing number of controlled trials showing that serotonin reuptake inhibitors are efficacious treatments for OCD,58 panic disorder,59 social phobia,60 GAD,61 and PTSD.62 2. Neurobiological Overlap Targum63 demonstrated that significantly more patients with panic disorder (65%) or major depressive disorder with comorbid panic disorder (56%) experienced an anxiogenic reaction to intravenous lactate infusion when compared with patients with major depressive disorder alone (19%) or with controls (0%) (p<0?.035). It is hypothesized that there is a continuum from normal arousal to anxiety to depression. Normal arousal occurs by increasing the excitability and firing rates of neurons in the serotonin, GABAergic, and noradrenergic systems. Sustained arousal may deplete neurotransmitters in critical forebrain areas, which might precipitate the emotional and somatic symptoms of depression.64 Up to 50% of patients with major depression demonstrate HPA axis dysregulation and subsequently do not suppress cortisol after dexamethasone administration. Approximately 30% of patients with GAD and 10% of patients with panic disorder also are nonsuppressors.65 Gray66 proposed a neuroanatomical model suggesting that threatening experiences activate noradrenergic cells in the locus coeruleus and ventral bundle; rising efferents from these sites in turn activate both the septohippocampal system and the hypothalamus, signaling the need for an appropriate behavioral response. Gray further suggested that anxiety is the product of the stimulation of the septohippocampal system by the locus coeruleus, while depression is secondary to the exhaustion of noradrenergic input to the hypothalamus (resulting in the vegetative symptoms of depression). This noradrenergic exhaustion occurs as a result of repeated stimulation of the neuronal cell bodies— a process that, if sustained, depletes neurotransmitter stores. Gray hypothesized that should the environmental stressor continue, septohippocampal noradrenergic transmission also ultimately fails. This hypothesis nicely fits the clinical data on comorbidity of anxiety and depression in that (a) it predicts that anxiety is an integral part of depression as sequelae of chronic stress and (b) when the stress is unremitting and noradrenergic input to the septohippocampal system “crashes,” a state of relatively pure depression emerges. This prediction is reminiscent of the previously reviewed dimensional data in mixed anxiety-depression, suggesting that the two syndromes can be most readily differentiated at the extremes of pathology. 3. Genetic Overlap Patients with comorbid depression and GAD have twice as many relatives with depression as patients with either depression or GAD alone.67 Relatives of patients with major depression alone also exhibit a higher incidence for developing anxiety disorders.64 Weissman et al.68 found rates for GAD to be twice as high in the relatives of probands with major depressive disorder (MDD) vs. control. Angst et al.69 utilizing epidemiological proband sample found increased rates of anxiety Journal of Mental Health & Human Behavior, 2007 63 Aggarwal & Basu : Overlap between mood & anxiety disorders and depression in parents of subject who had anxiety only, depression only, and depression and anxiety. According to Kendler et al.70 no evidence could be found for genes that specifically affect symptoms of depression without influencing the symptoms of anxiety. There are some environmental risk factors for MDD and GAD that is shaired in common; a substantial portion of factors is unique to each other. Common or familial environment played no role in the etiology of MDD and GAD and therefore could not possibly influence their co-occurrence and individual specific environmental risk factors are solely responsible for the differentiation between MDD and GAD. MacKinon et al. 71 analyzing chromosome 18 linkage data on 28 families with Bipolar Disorder, found that linkage scores for 5 consecutive 18q marker loci were highest in the families with the probands with comorbid panic disorder. B. Psychological Overlap Increased negative and decreased positive affect during agonistic social interactions may have their counterparts in specific clinical syndromes that may either occur alone or in combination with each other. When an individual competes for a secure place in society (e.g. vying to be chosen as a lover, teammate, or employee) and fails, or when he/she is involved in an agonistic encounter that carries a risk of injury, the triggering of a negative affect serves to warn him/her about the risks involved with continuing the struggle. Conversely, a low positive affect serves to decrease the individual’s motivation to continue to meet the challenge. Both of these affects are capable of triggering disengagement and preventing a renewed conflict or struggle from arising. When there is a failure of reconciliation, or when flight is not possible, the mechanisms associated with low positive affect or high negative affect may go into overdrive and become maladaptive by operating at a greater intensity and/or over a prolonged period of time. For this reason, individuals with Separation Anxiety may continue to pursue reconciliation, even when it is inappropriate, people with Panic Disorder are intent on escape, even in the absence of obvious danger, and people with social anxiety and depression find it difficult to assert themselves with people of equal or higher status. On the other hand, the person facing inevitable defeat may remain in ‘fight mode’ because he/she feels a sense of injustice, or unfairness.72 In many patients with atypical depression and bipolar II disorder, interpersonal sensitivity and mood overreactivity with cyclothymic-anxious-impulsive temperamental disposition might represent the mediating common denominator in the complex syndromic pattern of mood, anxiety and impulsive disorders.53 TRIPARTITE MODEL Clark and Watson73 reviewed the relevant literature and proposed a tripartite model. In this model, symptoms of depression and anxiety are subdivided into three broad groups. First, many symptoms of both constructs are strong markers of a general distress or negative affect factor and are, therefore, relatively nonspecific. In other words, these symptoms are commonly experienced by both anxious and depressed individuals. This nonspecific group includes both anxious and depressed affect, as well as other symptoms (e.g., insomnia, restlessness, irritability, poor concentration) those are prevalent in both types of disorder. In the tripartite model, these nonspecific symptoms are primarily responsible for the strong association between measures of anxiety and depression.73 In such a model, anxiety is viewed as an enduring trait. The high degree of correlation between anxious and depressive symptoms, as well as the increased correlation observed with time is explained by the presence of a stable core of anxiety symptoms embedded within fluctuating levels of affective Journal of Mental Health & Human Behavior, 2007 64 Aggarwal & Basu : Overlap between mood & anxiety disorders symptoms, which, unlike the relatively stable symptoms of chronic anxiety, may completely remit. The intensity of the anxiety, as well as the depression, likely varies according to life events occurring over the course of time. Life events have been shown to precipitate major depressive episodes,74,75 perhaps through the effects of such events on gene transcription and, ultimately, on neuronal structure and function as hypothesized by Post.76, 77 Symptoms reflecting anhedonia and the absence of positive emotional experiences (e.g., feeling disinterested in things, lacking energy, feeling that nothing is enjoyable, having no fun in life) are relatively specific to depression. In contrast, manifestations of somatic tension and arousal (e.g., shortness of breath, feeling dizzy or lightheaded, dry mouth, trembling or shaking) are relatively specific to anxiety.73 C. Social Overlap Environmental risk factors for the development of anxiety disorders as well as depression are poverty, exposure to violence, social isolation, and repeated losses of interpersonal significance.78 However, research in this area is very meager. CONSEQUENCES & CORRELATES OF OVERLAP Age of Onset The NIMH-sponsored large multicentre study on bipolar disorder from the USA, entitled ‘Systematic Treatment Enhancement Program for Bipolar Disorder’ (STEP-BD), has generated valuable data on the bipolar-anxiety comorbidity and its correlates.79-82 It showed that bipolar participants with a lifetime anxiety disorder had a significant lower age at onset (mean = 15.6 years) than subjects without anxiety (mean = 19.4 years).79 Course and Severity In a prospective study, again from the STEP-BD as mentioned above, anxiety disorder comorbidity in bipolar patients was associated with the estimated loss of 39 days of being well relative to patients without anxiety comorbidity; further, patients with anxiety disorders assessed during a period of recovery relapsed into a new mood episode more quickly.80 Bipolar subjects with OCD were more likely than those without OCD to have higher lifetime rates of thoughts of death and suicide, of wanting to die, of suicide attempts, and of panic disorder also. Unlike OCD patients without bipolar disorder, those with bipolar disorder reported a more gradual onset of OCD, a more episodic course of OCD symptoms, a greater frequency of concurrent major depressive episodes, higher rates of sexual and religious obsessions, and a lower rate of checking rituals.83 In a prospective study the presence of anxiety disorder (primarily social phobia) enhanced the risk of persisting depression for patients who were depressed at study entry.83 Depressed patients with panic attacks are significantly more likely than those without panic attacks to manifest such core depressive symptoms as guilt, terminal insomnia, anorexia, anhedonia, agitation, lack of reactivity, dysphoria, negative self-evaluation, fatigue, and difficulty concentrating.77 It does not appear that such findings are unique to panic disorder. In the Epidemiologic Catchment Area study, while 20% of the individuals with a lifetime diagnosis of panic disorder reported a history of suicide attempts, 18% of the patients with panic and 12% of those with social phobia reported such a history. Both studies concluded that the increased risk of suicide attempts in anxious patients was in part due to coexisting depression, although the magnitude of this effect was uncertain.77 SUBSTANCE ABUSE AND SUICIDAL BEHAVIOR STEP-BD data suggested that alcohol and substance abuse are common among patients with bipolar disorder but that of alcohol Journal of Mental Health & Human Behavior, 2007 65 Aggarwal & Basu : Overlap between mood & anxiety disorders dependency was doubled in the presence of an associated anxiety disorder (17.7% Vs 35.0%) and of substance abuse markedly increased (15.9% Vs 25.1%).79 Similarly, recent data from the same group showed that a lifetime diagnosis of any anxiety disorder more than doubled the odds of a past suicidal attempt in bipolar patients, and current anxiety comorbidity again more than doubled the odds of having current suicidal ideation in these patients.81 In another recent publication, this link was attributed primarily to the endless depressive ruminations seen in anxious bipolar patients.82 QUALITY OF FUNCTIONING LIFE AND SOCIAL and chlordiazepoxide in terms of anxiolytic activity. According to results of two meta-analyses, clomipramine (a TCA with potent serotonergic properties) is efficacious in the treatment of OCD.87 Monoamine oxidase inhibitors (MAOIs) The MAOIs are very effective in the treatment of depression and anxiety disorders, including panic disorder, and are superior to TCAs in the treatment of atypical depression. Selective serotonin reuptake inhibitors (SSRIs) SSRIs are effective in the management of anxiety disorders, such as panic disorder and OCD (88). SSRIs are now clearly established as the first line pharmacological treatment for most anxiety disorders. Lithium No controlled studies of lithium could be found in GAD, panic disorder, PTSD, or social phobia, However, two double blind trials of lithium augmentation (one with lithium and the other with thyroid hormone) in patients with OCD who were treatment resistant to SSRI therapy were negative .88 Divalporex A preliminary controlled crossover trial, divalporex may decrease panic symptoms. Panic attack and generalized anxiety improved significantly more with divalporex in patients who received divalporex as there initial therapy compared with those who received placebo as their initial treatment.88 Carbamazepine Carbamazepine was not effective in a study of 14 patients with panic disorder. Carbamazepine was associated with reduced frequency of panic attacks in 40% of patients, but it had no effect on 10% of patients and was associated with an increase in panic attack in 50% of patients.88 66 In a prospective study current anxiety comorbidity was associated with poorer quality of life and role functioning over the course of the year.80 Comorbid anxiety disorders with bipolar disorders are associated with poor quality of life as determined by the quality of life and enjoyment scale. 79 Bipolar and comorbid anxiety can have a major economic and social impact on patients, their families and social associates. Patients can experience work, family and social impairment and made to contend with increased health care costs and strains on social support.84 TREATMENT ISSUES Patients with bipolar disorder and comorbid anxiety have poor response to pharmacological and psychotherapeutic treatments.79 Anxiety disorders are usually treated with antidepressants, which, not infrequently trigger hypomanic and mixed states in patients with bipolar diathesis.85 MANAGEMENT OVERLAP Tricyclic antidepressants More than 40 years ago, imipramine was recognized to be an effective antipanic agent.86 Migraine also appears to be similar to alprazolam Journal of Mental Health & Human Behavior, 2007 Aggarwal & Basu : Overlap between mood & anxiety disorders Atypical antipsychotics In a study of 19 patients with combat related PTSD minimally responsive to 12 weeks of SSRI treatment, olanzapine augmentation was superior to placebo in specific measures of PTSD symptoms. Olazapine addition was associated with significant improvement in Clinician Administered PTSD Scale (CAPS) score, sleep disorder symptoms and depressive symptoms. As measured by Clinical Global Impression (CGI), response rates for to the olanzapine augmentation were relatively low (30%) and not statistically superior to placebo.88 Olanzapine also did not produce a better treatment response than placebo in a randomized, double blind 10-week study in 15 patients with PTSD. In a study of 73 patients with chronic combat related PTSD, risperidone or placebo was added to stable psychotropic medication. Risperidone treated patients who completed their study had significantly greater reduction in their CAPS scores compared to placebo. In a study risperidone (N=20) or placebo (N=16) was given to patients with OCD who were refractory to12 weeks of treatment with an SSRI. Among patients who completed the study, 9 (50%) of the patients in the risperidone group responded compared to none in the placebo group. Response was defined as 35% or greater improvement in Yale-Brown Obsessive Compulsive Scale (YBOCS) score and final score less than equal to 16. Similarly, 20 patients receiving quetiapine as adjunctive therapy had significantly greater improvement in YBOCS scores compared to the placebo group, as well as higher percentage of responders, 55% vs. 10%.88 Gabapentin It has been found to be effective in the treatment of social anxiety and panic disorder. Benzodiazepines Benzodiazepines have not been shown to have acute antimanic or long-term mood stabilizing properties, they are helpful for managing agitation, anxiety, insomnia, catatonic symptoms associated with bipolar disorder. Benzodiazepines are effective in panic disorder and GAD, but there have been no controlled studies of the use of these agents in bipolar disorder complicated by panic disorder or GAD. CONCLUSION It can be seen that there is a large co-occurrence of syndromal diagnoses of both mood and anxiety disorders, presence of symptoms not meeting the syndromal criteria of one in the presence of syndromal diagnosis of other, and presence of both mood and anxiety symptoms none meeting the syndromal criteria. It has been postulated that same areas of brain and same neurotransmitters are involved in both mood and anxiety disorders. There has been linkage between mood and anxiety disorder in family studies, and similar psychological and environmental factors contribute to the development of mood and anxiety symptoms. It can be concluded that patients with comorbid bipolar and anxiety disorders have younger age of onset, more pernicious course in terms of increased prevalence of suicide, increased number of psychotic and mixed features, poor quality of life, higher rate of substance abuse and worse response to treatment. Finally, drugs initially used for mood disorders now constitute the first-line major group of drugs to treat anxiety disorders. Some drugs initially used for anxiety disorders are used in the treatment of mood symptoms especially in the initial part. REFERENCES 1. Kraepelin E. Manic-depressive insanity and paranoia. Edinburgh: E & S Livingstone, 1921. Reprinted in: Carlson ET, ed. Dementia praecox and Journal of Mental Health & Human Behavior, 2007 67 Aggarwal & Basu : Overlap between mood & anxiety disorders paraphrenia together with manic-depressive insanity and paranoia. Birmingham: Classics of Medicine Library, 1989. 2. Gorman JM. 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The association of comorbid anxiety disorders with suicide attempts Journal of Mental Health & Human Behavior, 2007 70 Aggarwal & Basu : Overlap between mood & anxiety disorders and suicidal ideations in outpatients with bipolar disorder. J Psychiatry Res 2007; 41: 255-264. 82. Simon NM, Pollack MH, Ostacher MJ, et al. Understanding the link between anxiety symptoms and suicidal ideations and behaviors in outpatients with bipolar disorder. J Affect Disord 2007; 97: 9199. 83. Freeman MP, Freeman SA, McElroy SL. The comorbidity of bipolar and anxiety disorders: prevalence, psychobiology, and treatment issues. J Affect Disord 2002; 68: 1–23. 84. Post RM. The impact of bipolar depression. J Clin Psychiatry 2005; 66(suppl 5): 5-10. 85. Perugi G, Toni C, Akiskal HS. Anxious-Bipolar Comorbodity: Diagnostic and Treatment challenges. Psychiatr Clin N Am 1999; 22: 565-583. 86. Klein DF, Fink M (1962) Psychiatric reaction patterns to imipramine. Am J Psychiatry 119: 432–438. 87. Greist JH, Jefferson JW, Koback KA, et al. Efficacy and tolerability of serotonin transport inhibitors in obsessive-compulsive disorder. A meta-analysis. Arch Gen Psychiatry 1995; 52:53–60. 88. McElroy SL. Diagnosing and Treating Comorbid (Complicated) Bipolar Disorder. J Clin Psychiatry 2004; 65 (suppl 15): 35-44. Munish Aggarwal, Junior Resident Debasish Basu, Addl. Professor Department of Psychiatry Postgraduate Institute of Medical Education & Research Chandigarh 160012 Corresponding Address : Dr D Basu, Addl. Professor Department of Psychiatry Postgraduate Institute of Medical Education & Research Chandigarh 160012 db_sm2002@yahoo.com Journal of Mental Health & Human Behavior, 2007 71 ORIGINAL ARTICLE Pattern & Legal Consequences in Hospitalised Drug Abusers RK Solanki, DR Swami, Paramjeet Singh, Ravi Gupta, Navendu Gaur Abstract: The present study includes the sample from the Deaddiction Ward, SMS Hospital, Jaipur. The patients were admitted, assessed on socio-demographic basis & substance abuse and then results were drawn. 70% patients were found to be alcoholics, while 20% were multiple substance abusers. 64% of patients were belonging to age group 31-50 years. All were male. 70% belonged to urban area. 10% of patients were found to abuse newer drugs. History of violence was present in 26% of the patients and among them 18% were alcoholics. 6% of patients had faced the legal consequences. Key Words: Substance use, legal problems INTRODUCTION The history of drug-addiction is going hand in hand with the history of human civilization. The abbrient drug has a place in our mythology also, where it has been described as Somrasa. With the technical development of human civilization the form of drug has changed a lot. Previously the crude drugs were in use while with the availability of new instruments for processing of these crude chemicals, the drugs are now available in more potent and concentrated form. The abuse of drug is also influenced by the availability of the drug, abuser’s psychological state, economical condition, social status social beliefs and community norms in which he lives. The NSDUH suggests that nearly 6 million individuals in the US experience an arrest annually and that nearly half meet criteria for Substance Used Disorder. 1 Varying courses of offending may have plausible causal effects on young adult outcomes beyond the effects of an underlying propensity for crime. 2 Considering all these facts, the following study was planned with following aims : 1. To study the socio-demographic variables of the drug-abusers; 2. To study the pattern of Journal of Mental Health & Human Behavior, 2007 drug abuse; 3. To study legal consequences associated with drug addiction. METHODOLOGY This study was conducted with subjects from the Deaddiction ward, a unit of Dept. of Psychiatry, S.M.S. Medical College, Jaipur. This ward is situated in the main building of S.M.S. Hospital while the Department of Psychiatry is situated away from this building. The faculty members of this department along with the Resident Doctors run this unit. This is a 20-bedded unit where those patients are kept for detoxification that does not respond to ambulatory treatment. This study includes 100 consecutive patients admitted in this ward. The patients were diagnosed as per ICD-10 criteria3. They were assessed in detail at the time of admission regarding their socio-demographic data and pattern of drug abuse. The subjects upon admission if found to have previous or concurrent psychiatric illness were not included in the study. The finding were recorded in a specially designed semi-structured proforma and kept for the future reference. From the information thus obtained, the observations were drawn & tabulated. 72 Solanki et al : Legal consequences in Drug Abusers Table 1 Socio-Demographic Profile of Drug Abusers Variable Alcohol (N=50) Cannabis (N=2) Opium (N=12) Multiple (N=20) (N=4) Age (in yrs) 21-30 31-40 41-50 > 50 Marital Status Unmarried Married Divorced/ Separated Widow/ Remarried Education Illiterate Upto 8th 9 to 12th Graduate/ P.G. Religion Hindu Muslim Origin Rural Urban 14 (28%) 36 (72%) 2 (100%) 4 (33.3%) 8 (66.6%) 4 (20%) 16 (80%) 4 (100%) 2 (100%) 4 (40%) 6 (60%) 30 (30%) 70 (70%) 46 (92%) 4 (8%) 2 (100%) 10 (83.3%) 2 (16.6%) 20(100%) 4 (100%) 2 (100%) 10(100%) 94 (94%) 6 (6%) 2 (4%) 8 (16%) 18 (36%) 22 (44%) 2 (100%) 6 (50%) 2 (16.6%) 4 (33.3%) 4 (20%) 2 (10%) 14(70%) 4 (100%) 2 (100%) 6 (60%) 4 (40%) 8 (8%) 16 (16%) 30 (30%) 46 (46%) 8 (16%) 38 (76%) 4 (8%) 2 (100%) 10 (83.3%) 2 (16.6%) 2 (10%) 18(90%) 4 (100%) 2 (100%) 10 (100%) 24 (24%) 70 (70%) 4 (4%) 2 (2%) 4 (8%) 24 (48%) 18 (36%) 4 (8%) 2 (100%) 6 (50%) 2 (16.6%) 2 (16.6%) 2 (16.6%) 2 (10%) 14 (70%) 4 (20%) 0 4 (100%) 0 2 (100%) 0 10 (100%) 0 30 (30%) 40 (40%) 24 (24%) 6 (6%) Nicotine (N=6) Tobacco Gutkha (N=2) Others (N=10) Total (N=100) All Patients were male, Multiple drug abuse category as per ICD-10 criteria. Table 2 Types of Legal Offences in Different types of Drug Abusers (N = 100) S. No. Legal consequences 1. 2. Violence Present Apprehended by police A. For Traffic rules B. For theft 4 4 0 Alcohol 18 (18%) (4%) (4%) 2 Opium 6 2 (6%) (2%) 0 (2%) 2 0 0 0 Multiple (2%) 6 4 2 Total 26 (26%) (6%) (4%) (2%) Journal of Mental Health & Human Behavior, 2007 73 Solanki et al : Legal consequences in Drug Abusers RESULTS 50% of patients were pure alcoholics while 20% were abusing multiple drugs. All the multiple drug abusers were alcoholic. Hence we can see that 70% of total patients were alcoholic. Isolated cannabis abuse was found only in 2% of patients while 40% of multiple drug abusers were consuming cannabis thus total cannabis abuse comes to be 10% of total sample. 12% patients were abusing only opium. Among multiple drug abuse 100% were alcoholics along with the other drugs, while 50% were addicted to Benzodiazepines along with other drugs. 10% of the total sample was suffering from addiction to pharmacotherapeutic agents for example Alprazolam, Codeine, Dextropropoxyphene, and Diazepam. Overall, most abusers were in the age group of 21 to 40 years. 84% of alcoholics were belonging to the age group of 31-50 years. Multiple drug abuse was most common (70%) in the age group of 31-40 years. Pharmacotherapeutic agent’s addiction shows little age variation with 100% cases in the age group of 21 to 30 years. 76% of alcoholics, 83.33% of opium addicts, 90% of multiple drug abusers and 100% of pharmacotherapeutic agent abusers were married. 80% of alcoholics were well educated while 50% opium addicts were illiterate. 70% of multiple drug abusers were graduate/post graduate. Most of the cases followed Hindu religion, rest were Muslims. 72% of alcoholics, 66.66% of opium addicts, 80% of multiple-drug abusers were belonging to urban area with total of 70% of the sample size Legal consequences were present in 38% of total sample. 26% of patients were involved in violent activities among them 18% were alcoholics. A total of 6% were apprehended. Among these, 4% were those who broke traffic rule and were found to be alcoholic. Journal of Mental Health & Human Behavior, 2007 DISCUSSION In our study the maximum number of abusers was belonging to the age group of 31-40 years while others found that the maximum number of abusers were in the age group of 20-29 years. The sequential or concomitant use of drugs has a correlation with age and reflects the increasing time and opportunity for contacts with drugs in elder groups.5-9 Previously it was found that married persons were most commonly abusing the drugs,4 so is the finding of this study, because with marriage and social responsibilities the stress also increases. Our study found that substance abuse increases with the increase in educational level 4. Possible explanation may be that they are more prone to stress, which leads them to abuse these substances. These people also understand the harmful effect of these drugs thus they come across the medical detoxification facilities frequently. In some studies most of the patients were tobacco abusers4,9 while one study showed that alcohol, tobacco and painkillers were most commonly used substances. 10 In our study most of the patients were alcoholics. This difference can be seen due to the different study settings, since our study is based on the sample that presents for detoxification in the hospital. Generally tobacco abusers are managed on an OPD basis. Isolated cannabis abuse was found in only two patients in our study. The social acceptance and lack of physical and psychological dependence on this substance is responsible for such a low admission rates in the special ward for the purpose of detoxification. All the multiple drug abusers show alcohol addiction, which reflects the easy availability of this substance as compared to the others. 74 Solanki et al : Legal consequences in Drug Abusers Among the multiple drug abusers this study found that both the opium dependent patients were alcoholics which is similar to some earlier reports that say that in the case of non-availability of opioids this substance was used to control physical withdrawal, craving and/or feeling of emptiness. 9,11 Among the “others” group all the drugs, which the patients consumed, have a sure addiction liability and are mostly available as OTC (over the counter) drugs, at least In India. These drugs are refined chemicals. This shows the changing trends from the crude substances to concentrated forms or those refined chemicals that have a potential to exert a similar effect. This is very clear from our study that 26% of patients are involved in violent activities which is very close to the observation of earlier studies.12,13 Among these 18% are alcoholics showing the neuropharmacological effects of this substance on the person. The other reason for this high number may be the easy availability of this drug. Subjects with alcohol or drug use disorders were more than twice as likely as those with schizophrenia to report violent behavior.14 The criminal justice system in UK is heavily burdened with people withserious problems: 60% of people arrested tested positive for illegal drugs, nearly 20% of them for opiates. At a conservative estimate, the general costs to the criminal justice system of drug relatedcrime are at least £1 billion every year. 15 A total of 6% patients faced the legal consequences of this violence. 66.6% of these persons were alcoholics and were involved in breaking traffic laws. Remaining 33.3% of these, 6% were legally involved subjects, and opium user that were involved in theft, as they needed money for drug purchase. This might be due to the effect of craving, the fear of the withdrawal symptoms of opium or both. Thus we can conclude that the pattern of drug abuse has changed a lot in past few years with more frequency among urban males and in the vulnerable age that makes them prone to various types of stresses. REFERENCES 1. Sheryl PK, Cynthia LA, James AS, et al. Treatment at the front end of the criminal justice continuum: the association between arrest and admission into specialty substance abuse treatment. Sub Abuse Treat Prev Policy 2006;1: 20. Wiesner M, Kim HK, Capaldi DM. Developmental Trajectories of Offending: Validation and Prediction to Young Adult Alcohol Use, Drug Use, and Depressive Symptoms. Dev Psychopathol 2005;17(1): 251-70. 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Violence and psychiatric disorder in the community: evidence from the Epidemiologic Catchment Area Surveys. Hosp Community Psychiatry 1990;41:761-770. 15. Farrell M, Strang J. Britain’s new strategy for tackling drugs misuse. BMJ 1998;316: 1399-1400. RK Solanki, Professor and Unit Head DR Swami, Junior Specialist Paramjeet Singh, Asso. Professor Ravi Gupta, Formerly Resident Doctor Navendu Gaur, Resident Doctor Department of Psychiatry S.M.S. Medical College and Hospital, Jaipur Corresponding Address : Dr RK Solanki Professor and Unit Head Department of Psychiatry S.M.S. Medical College and Hospital, Jaipur Journal of Mental Health & Human Behavior, 2007 76 ORIGINAL ARTICLE Cannabis induced psychosis – A Phenomenological perspective Ajeet Sidana, Mamta, BS Chavan Abstract: Cannabis abuse is a growing health concern. Cannabis dependence is associated with two-fold increase in psychotic symptoms. The current study is an attempt to highlight the phenomenology of cannabis-induced psychosis and its temporal correlation with heavy cannabis intake in 20 patients of cannabis dependence syndrome. The mean age of the patients was 24 years with average duration of 4 years for cannabis abuse. The average interval between heavy cannabis intake and psychosis was 24-48 hours. Majority of the patients had delusional thinking (90%), followed by delusion of grandiose identity of Lord Shiva (65%), delusion of persecution (60%) and reference (30%). Key words: Cannabis, psychosis and phenomenology INTRODUCTION There has been a recent increase in the use of cannabis in many developed societies.1 Recent studies suggest that up to two-thirds of young people use cannabis at least once, with nearly 10% developing cannabis dependence.2,3 The increased use of cannabis has led to growing research interest to study the effects of heavy use of cannabis on health.4 The most heated debates in cannabis research is the possibility of existence of distinct nosological entity i.e. cannabis psychosis. In fact the existence of this entity has been dismissed by various authors for the poor quality of information on cannabis use, temporal correlation, premorbid and family history.5-8 However, there are number of case reports in the literature showing evidence of ‘cannabis induced psychosis’ describing the ways in which the onset of psychotic episodes was preceded by the heavy use of cannabis.9 A study has shown that cannabis psychosis is to be short lasting with predominant polymorphic picture, presence of more odd and bizarre behaviour, violence, panic attacks with reactive and congruent affect and less evidence of schizophrenic formal thought disorder and generally there is complete recovery as compared to schizophrenia. 10 It means that cannabis psychosis is an independent entity. However, cannabis use is associated with an increased risk of experiencing schizophrenia like symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for, indicating that cannabis use is not secondary to a pre-existing psychosis.11 In a study the authors reported a comparison of 15 “bhang” users with psychotic symptoms with 10 bhang users without psychosis and found that the patients of bhang users with psychotic symptom were more likely to be uncooperative and had symptoms of excitement, hostility, grandiosity, hallucinations, disorientation and unusual thought content.12 A retrospective study compared the prevalence of hallucinations, delusions and hospitalizations between the active cannabis users and psychotic patients who had never used cannabis.13 There was high rate of continuous hallucinations and delusions, and more hospitalizations among active cannabis users. Journal of Mental Health & Human Behavior, 2007 77 Sidana et al : Cannabis induced psychosis Psychiatric disturbances associated with cannabis use range from minor psychological responses such as anxiety and panic attacks 14, depressive disorders 15 to more serious mental illnesses such as the putative cannabis psychosis 16, acute functional psychosis 17 and poorly validated entity of “amotivational syndrome” 18. Whilst considerable attention has been paid to the association between cannabis use and psychotic disorders 10,19,20 relatively little is known about the impact of cannabis abuse on phenomenology of psychotic symptoms. Moreover there is no clear cut time interval between heavy cannabis intake and onset of psychosis. So, this study is an attempt to evaluate the hypothesis that heavy cannabis use is associated with psychosis having distinct phenomenology and it is closely associated with heavy cannabis intake. The study was planned with the aims: 1. To study the clinical presentation and phenomenology of cannabis induced psychosis. 2. To study the temporal correlation between heavy consumption of cannabis and onset of psychosis. METHODOLOGY A total of 20 patients who visited the psychiatry department, Government Medical College & Hospital, Sector-32, Chandigarh were included in the study Inclusion Criteria : 1. Patients fulfilling the criteria of DSM-IV 21 for cannabis-induced psychosis[ICD-10 also has similar information under the heading of substance induced psychotic disorder (F12.5)]. 2. Recent use of cannabis i.e. within past 30 days. 3. Age 18 or more. Exclusion Criteria : 1. Patient with history of past psychiatric illness. 2. Patients having co-morbid psychiatric illness, co-exiting personality disorder and consumption of substance other than cannabis. However, nicotine use was not the exclusion criteria. 3. History of psychiatric illness in family. 4. Mental retardation and other organic disorders. Table 1 Socio-demographic and clinical variables Variables Age of patient Education Age of onset of cannabis use Duration of continuous cannabis use Mean (Years) 24 10.1 18.9 4 Range 18-35 years 8th - 12th 15-27 years 2 days20 years Table 2 Temporal correlation and phenomenology Phenomenological variables (n=20) Delusional thinking Delusion of Grandiosity Percentage 90 75 (65% had delusion of Bhola Shankar) 60 30 24-48 hrs. Delusion of persecution Delusion of reference Interval between heavy consumption of cannabis and onset of psychosis RESULTS All the patients were male; in the age group of 18-35 years and majority were matriculate. The mean age of starting cannabis was 18.9 years and mean duration of cannabis use was 4 years (range 2 days – 20 years). Out of the 20 patients, 40% (n=8) gave recreational and experimental reasons for using Journal of Mental Health & Human Behavior, 2007 78 Sidana et al : Cannabis induced psychosis cannabis; another 40% cited peer pressure and 20% used it for elevation of mood. Display of abnormal behavior in the form of violent and aggressive behavior, excessive talks observed by family members were the reasons for establishing contact with the clinical services in all the cases. The treatment lag i.e. time period between onset of psychosis and seeking help was 6.5 months (Mean). Out of 20 patients, 85 % (n=17) required hospitalization for the control of symptoms and rest were managed on OPD basis only. There was an average gap of 24 to 48 hours between heavy cannabis intake and onset of full-blown psychosis. On Mental State Examination, it was noticed that delusional thinking was present in 90% of cases; delusion of grandiosity was present in 75%, followed by persecutory (60%) and referential (30%) delusions. Out of patients reporting delusions of grandiosity, 65% cases showed distinct over- religiosity with content related to Bhola Shankar Nath (Lord Shiva). However, none of patients reported any cognitive deficits i.e. disorientation to time, place, person and forgetfulness. All the patients recovered completely with antipsychotic treatment within one month. DISCUSSION The findings of current study suggest that all these patients did not have any past or family history of psychosis and might not have developed psychosis if they had not used cannabis. It means that cannabis psychosis is an independent entity and which has been reported by other authors too 9,10,16,19,20. The finding that 20% of patients who restarted cannabis again developed cannabis psychosis, further substantiates the diagnosis. Majority of the patients were younger and required hospitalization for control of psychotic symptoms, and recovered completely with achieving abstinence or with anti-psychotic treatment which is in accordance with other studies 10,22,24. It has been mentioned in the literature that psychosis develops after heavy intake of cannabis but exact temporal relationship has not been defined 5,10,16,19,20. In the current study, the authors found strong correlation between heavy dose of cannabis and onset of psychosis with the average gap of 1-2 days without any signs of confusion or disorientation. Out of the total sample, 75% (n=15) of patients had manic symptomatology in the form of delusions of grandiosity (overreligiosity), and out of that, 65 % of patients had delusional identity of Bhola Shankar (Lord Shiva). None of the patient showed any formal thought disorder. The current study showed predominantly manic symptomatology, which is similar to some earlier studies 19,23 but contrary to few studies 14,15. The distinct delusion of identity of Bhola Shanker is reported first time in this study only. The following may be possible reasons for this- firstly; all the patients were Hindu and had belief in Shiva Bhakti. Lord Shiva is a Hindu god and synonymous with power and fulfilling the desire of devotee easily. Secondly; bhang (cannabis) is used as Prasad (holly sweet) in Shiva temple and bhang is religiously associated with Shiva bhakti. This might be a possible reasons for the delusional identity with Lord Shiva, that god had given them special power for their worship. Probably this is why we do not see too many patients of cannabis abuse from other religious communities. Additionally, 60% of the patients had referential delusions and 30% had auditory hallucinations (commanding type), which is similar to another study 12. Limitations of the present study are, it was a retrospective analysis and no formal assessment was done for severity of dependence. Sample size was small. Journal of Mental Health & Human Behavior, 2007 79 Sidana et al : Cannabis induced psychosis REFERENCES 1. 2. Hall W, Solowij N. Long-term Cannabis use and Mental Health. Br J Psychiatry 1997; 171:107-108. David M, Fergusson L, Horwood J. Does cannabis use encourage other forms of elicit drug use? Addiction 2000; 95 (4): 505–520. Poulton RG, Brooke M, Moffitt TE et al. Prevalence and correlates of cannabis use and dependence in young New Zealanders. New Zealand Med J 1997;110: 68–70. Hall W, Babor T. Cannabis and public health: assessing the burden. Addiction 2000; 95: 485-490. Thornicroft G, Meadows G, Politi P. Is “cannabis psychosis” a distinct category? European psychiatry 1992;7:277-282. Gruber AJ, Pope HG. Cannabis psychotic disorder. Does it exist? Am J Addiction 1994;3:72-83. Poole R, Brabbins C. Drug induced psychosis. Br J Psychiatry 1996,168:135-138. Schukit M.A. Can marijuana cause a long-lasting psychosis? Drug Abuse Alcoholism Newsletter 1994; 23:1-4. Núñez LA, Gurpegui M. Cannabis-induced psychosis: A cross-sectional comparison with. Acute schizophrenia. Acta Psychiatr Scand 2002, 105: 173– 178. 13. Negrete J C, Knapp W P, Douglas D E et al. Cannabis affects the severity of schizophrenic symptoms: Results of a clinical survey. Psychol Med 1986;16:515–520. 14. Thomas H. Psychiatric symptoms in cannabis users. Br J Psychiatry 1993;163: 141–149. 15. Troisi A, Pasini A, Saracco M et al. Psychiatric symptoms in male cannabis users not using other illicit drugs. Addiction 1998; 93: 487–492. 16. Talbott J A, Teague J W. Marijuana psychosis. J Am Med Asso 1969; 210: 299-302. 17. Johns A. Substance misuse: a primary risk and a major problem of comorbidity. Int J Psychiatry 1997; 9: 233-241. 18. Hall W, Solowij N, Lemon J. The Health and Social Consequences of Cannabis Use. National Drug Strategy Monograph Series no 25. Canberra: Australian Government Publishing Service, 1994. 19. Thacore V R, Shukla S R P. Cannabis psychosis and paranoid schizophrenia. Arch Gen Psychiatry 1976;33: 383-386. 20. Chopra G S, Smith J W. Psychotic reactions following cannabis use in East Indians. Arch Gen Psychiatry 1974; 30: 24-27. 21. Harold I, Kaplan MD. Comprehensive Text Book of Psychiatry. VIth Ed. 1994,814. 22. Linszen DH, Dingemans PM, Lenior ME. Cannabis abuse and the course of recent onset schizophrenic disorders. Arch Gen Psychiatry 1994; 51: 273–279. 23. Rottemberg DR, Robins AH, Ben-Arie O et al. Cannabis associated psychosis with hypomanic features (ii). Lancet 1982;1364-1366. 24. Basu D, Malhotra A, Varma VK Cannabis related psychiatric syndromes: A selective review. Indian J Psychiatry 1994;36:121-128. 3. 4. 5. 6. 7. 8. 9. 10. Basu D, Malhotra A, Bhagat A et al. Cannabis psychosis and acute schizophrenia: a case-control study. European Add Res 1999;5:71- 73. 11. Louisa D, George C, Patton, Carolyn C. Cannabis use and mental health in young people: cohort study, Br Med J 2002; 325:1195-1198. 12 Chaudry H R, Moss H B, Bashir A et al. Cannabis psychosis following bhang ingestion. Br J Addiction 1991; 86: 1075 –1081. Ajeet Sidana, Senior Lecturer Mamta, Senior Resident BS Chavan, Professor & Head Department of Psychiatry Government Medical College & Hospital, Sector-32, Chandigarh. Corresponding Address : Dr. Ajeet Sidana, Senior Lecturer Department of Psychiatry, Government Medical College & Hospital, Sector-32, Chandigarh, E-mail. ajeetsidana@hotmail.com Journal of Mental Health & Human Behavior, 2007 80 ORIGINAL ARTICLE Emotional Maturity: Therapeutic Implications Harprit Kaur, Parwinder Singh, Varinderjeet Singh Abstract : Alexithymia is characterized by difficulty in recognizing and describing emotions. Emotional Maturity is the ultimate goal for optimum psychological functioning in any individual that can be attained only if one is able to recognize and describe one’s emotions. The current study aimed to assess alexithymia among high emotionally mature and low emotionally mature individuals. 74 males and 74 females of the age groups (22-25 years) were selected and assessed with the help of Emotional Maturity Questionnaire and Toranto Alexithymia Scale. The sample was divided into two equal halves i.e. 74 low emotionally mature and 74 high emotionally mature by applying median split half technique on emotional maturity score. A 2x2 analysis of variance with 2 levels of emotional maturity and 2 levels of gender was applied to evaluate the differences. There was significant difference on alexithymia in high and low emotionally mature individuals. No gender differences were observed. It can be observed from the results that persons who are emotionally mature, experience less difficulty in identifying and communicating feelings as compared to low emotionally mature individuals. The implications of management of alexithymia for efficient therapeutic intervention and steps for same are also proposed. Key words: Alexithymia, emotional maturity Alexithymia refers to a personality construct that is characterized by, a difficulty in identifying and communicating feelings; a difficulty in distinguishing between feelings and bodily sensations; impaired symbolization, as evidenced by paucity of fantasies and other imaginative activity; and a preference for focusing on external events rather than inner experiences.1, 2 It has been suggested that the features comprising the alexithymia construct reflect deficits in the cognitive processing and regulation of emotions.3 It is not that the alexithymics are unable to express emotions verbally or that they fail to acknowledge that they experience emotions. The distinguishing factor is their inability to elaborate beyond a few limited adjectives such as “happy” or “unhappy” when describing these feelings.4 The core issue is that alexithymics have poorly differentiated emotions limiting their ability to distinguish and describe them to others.5 Thus the range and depth of emotionality are adversely affected. The concept evolved from clinical observations to empirical quantification in psychosomatic patients. Later it was evident even among patients with a variety of psychiatric disorders that involve disturbances in emotion regulation, including substance use disorders, posttraumatic stress disorder, panic disorder, somatoform disorders, and eating disorders3, 6, 7. Alexithymia has also been associated with hypertension,8 inflammatory bowel disease, 9 functional gastrointestinal disorders, 10 somatoform disorders,11 panic disorder 12 and eating disorders .13 As an individual difference, alexithymia overlaps conceptually with the emotional intelligence construct. Latter encompasses the ability to perceive and appraise one’s own and other’s feelings and emotions, the ability to access and use feelings to guide one’s thinking and action, and the ability to regulate 81 Journal of Mental Health & Human Behavior, 2007 Kaur et al : Emotional maturity emotions to promote emotional and intellectual growth.14 There is empirical evidence that the two constructs are strongly and inversely related.15, 16 Emotional maturity means, controlling one’s emotions rather than allowing emotions to control the individual. It is a relative freedom from the constellation of inferiority, egotism and competitiveness. The important attribute of maturity is a sense of reality. Its characteristics are flexibility and adaptability. 17 The more mature the individual is the more stable and flexible his/her adjustment is. Emotionally mature person has the capacity to withstand delaying in satisfaction of needs. He/she has ability to tolerate a reasonable amount of frustration.18 He/she has belief in long term planning and is capable of delaying or revising his expectations in terms of demands of situations. He has the courage to express his/her feelings and convictions, balanced with consideration for the feelings and convictions of other people.19 Emotional maturity is a significant predictor of the level of success that an individual would achieve in his lifetime. It also predicts general level of happiness, self confidence, success in relationships, the level of wellbeing in terms of emotional and physical health, the health of one’s family, degree of leadership and responsibility taken in one’s community and the world as a whole.20 Emotional maturity is thus the ultimate goal for every individual aspiring for positive mental health. Yet the presence of alexithymia would be a significant deterrent towards that goal as it would not be possible to master emotions when the insight into it is limited. The objectives of the current study were (1) to assess alexithymia among high emotionally mature and low emotionally mature post graduate students; (2) to study the relationship between emotional maturity and alexithymia. METHODOLOGY The sample of the study comprised of 148 post graduate students (74 males & 74 females), selected randomly from various teaching departments (including science and arts faculties) of Punjabi University, Patiala , between the agerange of 22-25 years. All participants were unmarried and belonged to urban background. The participants were assessed individually using Emotional Maturity Questionnaire20 and Toranto Alexithyima Scale (TAS-20).21 The sample was further divided into two equal halves (74 high emotionally mature and 74 low emotionally mature individuals) by applying median split half technique on emotional maturity scores. A 2 X 2 Analyses of Variances, with 2 levels of Emotional Maturity and 2 levels of Gender, was applied to evaluate the differences. Tools Toronto Alexithymia Scale (TAS-20, Hindi Adaptation) 21 : It is 20-item, 5-point likert type scale. It has three-factors namely: (a) Factor 1 – difficulty identifying feelings and distinguishing them from bodily sensations of emotion (b) Factor 2 – difficulty describing feelings, and (c) Factor 3 – externally-oriented thinking. Evidence of reliability and factorial validity has been well established. It has been demonstrated to be a psychometrically sound measure of alexithymia.22 The TAS and TAS-20 are now the most widely used measures of alexithymia. 7 The Hindi standardized version was used in the current study. Emotional Maturity Questionnaire20 : Emotional Maturity Questionnaire is a 40-item, 3-point likert type scale ranging from ‘Rarely’ to ‘Often’, measuring emotional maturity quotient. Subjects are to respond according to the applicability of each item in their life. ‘Rarely’, ‘sometime’ and ‘Often’ responses get ‘1’, ‘0.5’ and ‘0’ marks respectively and by adding up the marks, total EMQ score is obtained. 82 Journal of Mental Health & Human Behavior, 2007 Kaur et al : Emotional maturity Table- 1 Means and Standard Deviations (SD) of Alexithymia in relation to emotional maturity and gender. VARIABLES LEVELS TAS-20 TOTAL MEAN (SD) 45.54 (9.14) 56.08 (7.63) 51.12 (7.36) 50.495 (9.41) TAS-20 FACTOR 1 MEAN (SD) 13.98 (4.66) 19.84 (4.94) 16.95 (4.36) 16.87 (5.24) TAS-20 FACTOR 2 MEAN (SD) 11.43 (2.99) 14.73 (3.46) 12.89 (3.27) 13.27 (3.19) TAS-20 FACTOR 3 MEAN (SD) 19.58 (3.87) 22.58 (4.06) 21.36 (4.56) 20.79 (3.37) EMOTIONAL MATURITY HEM* LEM** GENDER MALE FEMALE *HEM- High Emotionally Mature; **LEM- Low Emotionally Mature; Factor 1- Difficulty in identifying feelings and distinguishing them from bodily sensations of emotion; Factor 2- Difficulty in describing feelings; Factor 3- Externally-oriented thinking. Table- 2 Summary of Analysis of variance for Alexithymia in relation to emotional maturity and gender ALEXITHYMIA TAS-20FACTOR 1 SS MS F-ratio TAS-20FACTOR 2 SS MS F-ratio TAS-20FACTOR 3 SS MS F-ratio TAS-20TOTALSCORES SS MS F-ratio EMOTIONAL MATURITY (A) 1266.82 1266.82 54.772** 402.27 402.27 30.889** 333.00 333.00 17.828** 4110.8 4110.8 56.29** GENDER (B) 0.17 0.17 0.007 (NS) 5.30 5.30 0.407 (NS) 11.92 11.92 0.638 (NS) 14.3 14.3 0.196 (NS) AB 86.28 86.28 3.730 (NS) 0.11 0.11 0.008 (NS) 0.43 0.43 0.023 (NS) 87.8 87.8 1.202 (NS) 10515.8 73 2689.68 18.68 1875.35 13.02 ERROR 3330.59 23.13 * p< .05; ** p< .01; NS- Non-Significant; Factor 1- Difficulty in identifying feelings and distinguishing them from bodily sensations of emotion; Factor 2- Difficulty in describing feelings; Factor 3- Externally-oriented thinking. RESULTS Results revealed that less emotionally mature individuals scored more on alexithymia (total scores), (M=56.08) as compared to high emotionally mature individuals (M=45.54) Table 1. It implies that those individuals who are emotionally mature tend to be less alexithymic. Table II provides the summary of Analysis of Variance for alexithymia (total scores, Factor1, Factor 2 & Factor 3) in relation to emotional maturity and gender. There was significant difference (F=56.29, p<0.001) between high emotionally mature and low emotionally mature individuals on alexithymia. High emotionally mature individuals were significantly lower on alexithymia as compared to low emotionally mature individuals. Same results were evident when high emotionally mature individuals were Journal of Mental Health & Human Behavior, 2007 83 Kaur et al : Emotional maturity compared with low emotionally mature individuals on the three factors of alexithymia separately. As evident in Table 2 high emotionally mature individuals scored less on all the three factors of TAS-20 as compared to low emotionally mature individuals. There was significant difference between high emotionally mature and low emotionally mature individuals on Factor 1 (F=54.772, p< 0.001), on Factor 2 (F=30.889, p< 0.001) and on Factor 3 (F= 17.828, p<0.001). The mean score on alexithymia of male participants came out to be 51.12 and females’ mean score was 50.495. There was no significant difference between males and females on alexithymia. DISCUSSION From the results, we can observe that the mean score on alexithymia of male participants came out to be 51.12 and females’ mean score was 50.495. These mean alexithymia scores closely resemble the findings of Pandey et al. on Indian young adults which were 49.57 and 52.46 for males and females respectively.21 Parker et. al. in a comparative work with psychiatric population found that the normal controls scored less than or equal to 51 on TAS-20.23 The scores thus are comparable with the Indian sample; indicating the cross cultural validity of the construct of alexithymia. In the present study, no significant difference was found between males and females on alexithymia. Same results were found when gender differences were studied across each factor separately. In a study on 417 normal adults using TAS-26, Pasini et. al. had found no significant gender differences in total TAS scores24. Cox et. al. had studied 55 somatoform patients using TAS20 and found alexithymia unrelated to age and gender. 11 However, the significant effect of gender is consistent with the literature on the design and validation of the TAS-20.25 A study by Parker et. al. reported that men tended to have significantly higher TAS-20 scores than did women.23 This contrasts with three earlier studies that had used the original TAS, and demonstrated no significant gender difference.26-28 Thus, no consistent pattern in gender differences has been reported in literature on alexithymia.22,29-31 The present study adds weight to the lack of gender difference in alexithymia. We present a case for equal distribution of the alexithymic characteristics in young normal adults pursuing post graduation, irrespective of their gender. Alexithymia has been related to social origin and degree of psychological sophistication of the clients.32,33 In the urban area, due to proactive role of women and equal parenting, both males and females are provided with homogenous social environment that facilitate similar psychological sophistication among them. It may be due to this equality that no significance gender differences are found in present study. Less emotionally mature individuals scored more on alexithymia as a whole as compared to high emotionally mature individuals i.e. persons who are emotionally mature tend to be less alexithymic. In other words, persons who are emotionally mature experience less difficulty in identifying and communicating feelings as compared to low emotionally mature individuals. A significant inverse relationship was also found between alexithymia and emotional maturity that means more a person is alexithymic, less is his emotional maturity. Emotional maturity is a mental state in which a person is able to make effective adjustment with himself/herself, members of his/her family, his/her peers in school, work place, society and culture. When a person reaches high level of emotional maturity, he realizes that he can no longer view his emotional states as the responsibility of external forces such as people, places, things, forces, fate and spirits. He learns to drop ex-pressions from his speech that show disownership of feelings, and a helplessness or 84 Journal of Mental Health & Human Behavior, 2007 Kaur et al : Emotional maturity victimization of feelings. Emotional maturity consists of emotional responsibility, emotional honesty, emotional openness, emotional assertiveness, emotional understandings and emotional detachment. Emotional Openness is the person’s willingness and skill in sharing his/ her feelings in an appropriate manner and at appropriate times. Such individuals experience and learn the value of ventilating feelings and also the dangers involved in hiding feelings from self and others. Emotional assertiveness is concerned with positive self-ex-pression. This is the ability to ask for and receive the nurturing that one needs and wants- first from self and then from others, and to express all feelings appropriate to any situation without aggressive overtones. These two characteristics i.e. emotional openness and emotional assertiveness are two important parts of emotional maturity and emotional maturity is a necessary step to self-understanding and acceptance, which leads to optimum psychological functioning. But alexithymics must be low on these two characteristics because if one is unable to identify one’s feelings; selfunderstanding and acceptance would not be feasible for him/her. Alexithymics tend to be less emotionally mature because they can’t identify & communicate their feelings which inhibit selfunderstanding and acceptance that is essential part of emotional maturity. So if we want our clients to be emotionally mature, which is the ultimate goal of counselling and psychotherapy, we must take into account the alexithymic level of the client. Persons who are emotionally mature are stable and realistic about life, possessing good ego-strength. They can tolerate frustration for unsatisfactory conditions which is very important part of successful life. They don’t get annoyed easily. Everybody faces problems in life but those who are emotionally mature possess the ability to deal with them and they accept all the problems and solve them without getting too emotionally involved in them.All these are qualities that are essential for psychological well-being and mental health. According to the World Health Organization (WHO), “Mental health is the emotional and spiritual resilience which allows us to enjoy life and to survive pain, disappointment and sadness. It is a positive sense of well being and an underlying belief in our own, and others’ dignity and worth” and to help the clients in achieving these qualities alexithymia must be conquered. Alexithymia has also been associated with hypertension,8 inflammatory bowel disease,9 functional gastrointestinal disorders,10 somatoform disorders, 11 panic disorder 12 and eating disorders.13 It has been noted that in these psychosomatic and somatoform disorders wherein alexithymia presence is well established, the therapist tends to develop strong negative counter-transference during therapeutic interactions. Hence focused attention to alexithymia would be significant for any effective psychological intervention through good therapeutic alliance. If we can reduce or modify the alexithymic characteristics then we can proceed further towards symptom management and enhancement of overall well being of the clients. It is suggested that for handling alexithymia, the following four stages must be included in therapy sessions with clients. 1. Make the client an observer of his inner states and non-verbal cues. 2. Develop affect tolerance and hence decrease the perceived frightening nature of affect. 3. Recognize the emotions as signals that are self-limited in duration and controllability. 4. Begin to verbalize the emotional states with the counsellor/therapist as teacher or guide, providing feedback and enhancing selfesteem and consequently self-reliance and independence in thought and action. 85 Journal of Mental Health & Human Behavior, 2007 Kaur et al : Emotional maturity To conclude, emotional maturity which is a known component of psychological well-being and mental health is an essential condition for successful life. Those who are emotionally mature are more contend or satisfied with life and live “fully”27. Further, handling alexithymia as an integral part of therapy would enhance the management of any dysfunction, particularly because if a person is unable to express his/her emotions, a healthy relationship is near to impossible to make, without which rapport building and therapeutic relationship would be incomplete; and personal growth towards psychological health & well-being would be stunted. REFERENCES 1. 2. Taylor GJ, Bagby RM. Measurement of Alexithymia. Psychiatr Clin N Am. 1988;11(3), 351-366. Taylor GJ, Bagby RM. An overview of the Alexithymia construct. In R. Bar-On & J. D. A. Parker (Eds.), The handbook of emotional intelligence. San Francisco: Jossey-Bass. 2000; pp. 40–67. Taylor GJ, Bagby RM, Parker JDA. Disorders of affect regulation Alexithymia in medical and psychiatric illness. Cambridge: Cambridge University Press. 1997. Sifneos PE. Clinical Observations on some patients suffering from a variety of psychosomatic diseases. Acta Medicina Psychosomatica 1967; 7, 1-10. Bar-On R, Parker JDA. The Handbook of Emotional Intelligence: Theory, Development, Assessment, and Application at Home, School, and in the Workplace. San Francisco, California: Jossey-Bass. 2000. Krystal H. Integration and self-healing: Affect, trauma, Alexithymia. Hillsdale, NJ: Analytic Press. 1988. Taylor GJ. Recent developments in Alexithymia theory and research. Can J Psychiatry- Revue Canadienne de Psychiatrie. 2000; 45, 134–142. Todarello O, Taylor GJ, Parker JDA, et al. Alexithymia in essential hypertensive and psychiatric outpatients: a comparative study. J Psychosom Res 1995;39, 987 - 994. Porcelli P, Zaka S, Leoci C, et al. Alexithymia in inflammatory bowel disease. Psychother Psychosom. 1995; 64, 49-53. comparison with inflammatory bowel disease. Psychother Psychosom 1999; 68, 283 – 269. 11. Cox BJ, Kuch K, Parker JDA, et al. Alexithymia in somatoform disorder patients with chronic pain. J Psychosom Res 1994; 38, 523 - 527. 12. Zeitlin SB, McNally RJ. Alexithymia and anxiety sensitivity in panic disorder and obsessivecompulsive disorder. Am J Psychiatry 1993; 150, 658 - 660. 13. De Groot JM, Rodin G, Olmstead MP. Alexithymia, depression and treatment outcome in bulimia nervosa, Compr Psychiatry 1995; 34, 53 - 60. 14. Mayer JD, Salovey P. What is emotional intelligence? In P. Salovey & D. J. Slutyer (Eds.), Emotional development and emotional intelligence: Educational implications. New York: Basic Books. 1997; pp. 3–34. 15. Austin EJ, Saklofske DH, Egan V. Personality, wellbeing and health correlates of trait emotional intelligence. Pers Individ Dif 2005; 38, 547–558. 16. Parker JDA, Taylor GJ, Bagby RM. The relationship between emotional intelligence and Alexithymia. Pers Individ Dif 2001; 30, 107–115. 17. Maslow, A.H. Lessons from the peak experiences. In R.E. Farson (Ed.). Science and human affairs. Palo Alto, Calif.: Science and Behavior Books. 1965. 18. Rogers CR. Towards a science of the person. Journal of Humanistic Psychology 1963;3, 72-93. 19. Covey SR. Author of the seven habits of highly effective people. Principle-Centered leadership. A Philosophy for life and for Suiccess in Business. Great Britain: Simon Schuster Ltd. 1997. 20. Arrizza N. What Is Your “Emotional Maturity Quotient” Or EMQ? 2006; Online available http:// ezinearticles.com/?expert=Nick_Arrizza,_M.D. 21. Panday R, Mandal KM, Taylor JG et al. Cross-cultural Alexithymia: Development and validation of hindi translation of 20 item Toranto Alexithymia Scale. J Clin Psychol 1996; 52(2). 22. Bagby RM, Parker JD, Taylor GJ. The twenty-item Toronto Alexithymia Scale-I: Item selection and crossvalidation of the factor structure. J Psychosom Res 1994; 38, 23-32. 23. Parker JDA, Taylor GJ, Bagby RM. Alexithymia and the processing of emotional stimuli: An experimental study. Journal of New Trends in Experimental and Clinical Psychiatry 1993; 9, 9-14. 24. Pasini A, Delle Chiaie R, Serpia S et al. Alexithymia as 3. 4. 5. 6. 7. 8. 9. 10. Porcelli P, Taylor GJ, Parker JDA, et al. Alexithymia and functional gastrointestinal disorders: a Journal of Mental Health & Human Behavior, 2007 86 Kaur et al : Emotional maturity related to sex, age and educational level: Results of the toronto alexithymia scale in 417 normal subjects. Compr Psychiatry 1992; Vol.33, No.1: 42-46. 25. Bagby RM, Taylor GJ, Parker JDA. The 20-Item TorontoAlexithymia-Scale .2. Convergent, Discriminant, and Concurrent Validity. J Psychosom Res 1994b; 38, 33–40. 26. Bagby RM, Taylor GJ, Atkinson L Alexithymia: A comparative study of three self-report measures. J Psychosom Res 1988; 32, 107-16. 27. Parker JDA, Taylor GJ, Bagby RM. The alexithymia construct: Relationship with sociodemographic variables and intelligence. Compr Psychiatry 1989; 30, 434-41. 28. Taylor GJ, Parker JDA, Bagby RM, et al. Alexithymia and somatic complaints in psychiatric out-patients. J Psychosom Res 1992;36, 417-24. 29. Fischer PC, Smith RJ, Leonard E, et al. Sex differences on affective dimensions: Continuing examination. J Couns Dev 1993; 71, 440-443. 30. Roger D, Najarian B. The construction and validation of a new scale for measuring emotion control. Pers Individ Dif 1989; 10, 845-853. 31. Thayer JF, Rossy LA, Ruiz-Padial, et al. Gender differences in the relationship between emotional regulation and depressive symptoms. Cognitive Ther Res 2003; 27, 349-364. 32. Lesser IM, Ford CV, Friedman CTH. Alexithymia in somatizing patients. Gen Hosp Psychiatry 1979; 1, 256-262. 33. Pierloot R, Vinck J. A pragmatic approach to the concept of alexithymia. Psychother Psychosom 1977; 28, 156166. Harprit Kaur, Lecturer Parwinder Singh, Research Fellow Varinderjeet Singh Research Scholar Department of Psychology, Punjabi University, Patiala. Corresponding Address : Harprit Kaur, Lecturer Department of Psychology Punjabi University, Patiala. Journal of Mental Health & Human Behavior, 2007 87 ORIGINAL ARTICLE Journal of Mental Health & Human Behavior, 2007 88 Arun et al : Effect of maternal employment Journal of Mental Health & Human Behavior, 2007 89 Arun et al : Effect of maternal employment Journal of Mental Health & Human Behavior, 2007 90 Arun et al : Effect of maternal employment Table 2 Scores on Childhood Psychopathology Measurement Scale CPMS Working mothers N=50 Low intelligence with behavior problems Conduct Disorder Anxiety Depression Psychotic Symptoms Special Symptoms Physical Illness Somatisation Total CPMS Mean SD Mean SD Mean SD Mean SD Mean SD Mean SD Mean SD Mean SD Mean SD 0.8 0.903 1.54 1.567 0.5 0.735 0.84 1.037 0.24 0.555 0.22 0.464 0.46 0.542 5.969 0.69 5 3.464 Non- working mothers N=50 0.5 1.11 0.94 1.42 0.22 0.506 0.18 0.66 0.02 0.141 0.12 0.385 0.24 0.431 9.49 0.626 2.56 2.449 t test p values 0.142 0.047* 0.029* 0.0002*** 0.008*** 0.244 0.027* 0.644 0.0002*** Journal of Mental Health & Human Behavior, 2007 91 Arun et al : Effect of maternal employment Journal of Mental Health & Human Behavior, 2007 92 Arun et al : Effect of maternal employment Journal of Mental Health & Human Behavior, 2007 93 Arun et al : Effect of maternal employment Priti Arun, Professor Jaspreet Kaur, Psychologist Sophia Tinku, Formerly Social Worker Lok Raj, Formerly Senior Lecturer Department of Psychiatry Government Medical College and Hospital Sector 32, Chandigarh. Corresponding Address : Priti Arun, Professor Department of Psychiatry Government Medical College and Hospital Sector 32, Chandigarh. drpritiarun@gmail.com Journal of Mental Health & Human Behavior, 2007 94 ORIGINAL ARTICLE Study of Psychiatric Patients in Pingla Ashram Rahul Jindal, Kuldip C Sharma, Jagjeet Singh Abstract : Out of 170 inmates admitted in a non-government asylum, 62.3% were found to be burdened with physical and psychiatric morbidity. Out of them 42.8% had psychiatric morbidity. 64% were admitted by the police and 56% had been staying in Pingla Ashram for more than 3 years. 42% were admitted to Pingla Ashram as the family could not cope with their violent behaviour at home. Before the study, main method to control violent inmates was chaining (64%) and restraining (28%). Out of the 50 psychiatric patients admitted to the Psychiatry Ward of Medical College Hospital 64% were diagnosed as having schizophrenia, 20% having mood disorders and 16% having mental retardation with behavioural problems. After treatment in the Psychiatry ward, they were sent back to Pingla Ashram, where they were followed up. At the time of discharge from Psychiatry ward, 70% showed improvement. At 3 months, 50% and at 6 months 42% maintained improvement achieved with treatment. 10% of the inmates were sent home after treatment, while 20% of the inmates could not be sent as no relatives came nobody came to take the inmates home in spite of repeated reminders. 4% inmates ran out of Ashram back to their home after getting well. No inmate was chained after the treatment in the ward. Key Words: Pingla Ashram, Pingalwara INTRODUCTION At the time of India’s Independence, there were about 10,000 beds in mental hospitals for a population of 400 millions. Over the years, population has increased by nearly two and half times, but the number of beds have increased to only about 21,000. Thus, the population to bed ratio has remained more or less constant at 1 bed for 5,000 population. The prevalence of severe mental morbidity in India ranges from 3-10 per 1000, which is more than 5 times the bed strength available.1 The 35 mental hospitals of varying sizes spread all over the country provide care to chronic mentally ill patients, but a number of problems like over crowding, long stay patients, poor funding, inadequate facilities for rehabilitation etc. plague the mental hospitals contributing to the poor quality of care and services. Keeping in mind such a situation, WHO in 2000 gave the slogan “Stop exclusion-Dare to care”, meaning that there is a need to look for uncared patients, caring them in community rather than excluding them in mental hospitals or ignoring them. Bhagat Puran Singh Ji is renowned for the service of the destitute, homeless, handicapped and mentally ill patients. At the time of partition, he came in contact with a four year old crippled abandoned child in Lahore, whom he carried to India. He started a shelter home and named it Pingalwara, for the care of discarded and handicapped persons. He served inmates with great devotion and soon it became the main stay for the uncared in the northern states of India. In one of the study it was reported that there were 736 inmates in Pingalwara at Amritsar.2 Out of them 300 (40%) were patients of mental disorder, 300 (40%) were disabled or suffering from chronic physical disorders and 20% had curable diseases. Following the example of Bhagat Puran Singh Ji Journal of Mental Health & Human Behavior, 2007 95 Jindal et al : Patients in a Pingla Ashram Pingalwara like shelter homes came up in other parts of Punjab, including the one at Patiala. The Erawadi tragedy highlighted the mismanagement in asylums and similar shelter homes, as a result Mental hospitals came under public scrutiny. Government of India ordered every state to dechain the mentally ill patients in asylums. 2,3 Hence, the present study was undertaken in order to study the condition of mental patients in an asylum of this area. METHODOLOGY The study was carried out in the Pingla Ashram situated in a village Sanour 3.5 km away from Patiala. The incharge of the Pingla Ashram was contacted for the permission to conduct the study. All the inmates of the Pingla Ashram were screened. Inmates showing odd behaviour or reported to be mentally ill by the attendants staying in Pingla Ashram were taken up for detail assessment by admitting them in the Psychiatry ward. 50 inmates were admitted. The sociodemographic variables, mode of admission to Pingla Ashram, history of mental illness in the past, if available were recorded from the varied sources i.e records, relatives and patients. The attendants were also interviewed for assessment of behavioral pattern of inmates. Detailed MSE was carried out in order to make the diagnosis according to ICD-10. After the treatment in Psychiatry Ward, which varied from two weeks to one month, the inmates were discharged and sent back to Pingalwara. They were advised to take treatment under supervision. They were followed up in the Ashram at 3 months and 6 months after the discharge from the ward. After treatment in the ward some of the inmates expressed their desire to go back to their families or home. The relatives of all the inmates, where address or phone numbers were available, were contacted and some of them were sent home. Journal of Mental Health & Human Behavior, 2007 RESULTS At the time of study the Pingalwara had 175 inmates. Out of them, majority (62.3%) had physical and psychiatric morbidity. The morbidity due to psychiatric disorders was 42.9% (Table 1). Among the inmates admitted to Psychiatry ward for detailed study, males (70%) outnumbered the females (30%). They were from all the age groups i.e. 12% in 16-25 age group, 20% in 2635 age group, 24% in 35-45 age group, 20% in 46-55 age group, 16% in 56-65 age group. Only 4% were below 15 years and a 4% above 65 years of age. The education status was not known in 80%, while 2% were matriculate, 2% were middle, and 4% were primary educated, 12% were illiterate. Marital status in 20% was not known, while 28% were married, 48% were unmarried, 4% were divorced. Occupation was known in 84%. Among the males, 12% were in Govt. Job, 8% were Table 1 Details of Morbidity among inmates of Pingla Ashram N A. B. C. Total No. of Inmates Inmates without morbidity Inmates with morbidity Details of morbidity Psychiatric Morbidity Schizophrenia Mood Disorder Mental Retardation Others Physicial Morbidity Handicapped (N=12) Orthopeadically Visual Hearing Medical (N=20) Epilepsy Hemiplegia Cancer (N=2) 175 66 109 75 32 10 25 8 34 10 1 1 17 3 2 %age 37.7% 62.3% 42.9% 19.4% 96 Jindal et al : Patients in a Pingla Ashram Table 2 Details of Admission to Pingla Ashram 1. Mode of Admission A. Admitted by relatives Parents Sibs Spouse B. Admitted by others Police Panchayat etc Other Unrelated people 2. A. N 14 5 8 1 36 32 2 2 %age 28% 10% 16% 2% 72% 64% 4% 4% 52 6% 4% 20% 22% 48% 10% 18% 16% 8% 24% 24% labourers, while 36% were employed somewhere and among females 28% were housewives. Domicile was known in 80% only, with 56% being from urban area. Regarding the diagnosis of the psychiatric patients, 64% had schizophrenia – 20% disorganized (F 20.1); 30% undifferentiated (F20.3), 10% simple (F20.6), 2% catatonia (F. 20.2), 2% paranoid (F 20.0). 20% had mood disorder – 16%, Depression (F-32), 4% Bipolar affective disorder (F31). 16% had mental retardation with behavioral problem - 12% had severe degree of mental retardation (F72) and 4% had profound mental retardation. Duration of mental illness was known in 70% of the inmates. Inmates were chronic patients as 90% had been ill for more than 5 years. Majority of these patients had been admitted by police (Table 2) and 64% had been chained at Pingla Ashram. Nature of treatment in the past was known in 70%. 30% were treated with drugs, 20% were treated with drugs and ECT, and 20% were never treated. At the time of discharge, 70% had improved. (Table 3) B. 3. Reasons for Admission Known 26 a. Loss of parents 3 b. Lack of social support 2 c. Unable to cope with behaviour (N=21) Treated 10 Untreated 11 Not Known 24 Duration of stay 1year 2 years 3 years 4 years 5 years More than 5 years 5 9 8 4 12 12 4. Mode of the management prior to start of study Medication 1 2% Chaining 32 64% Restraining 14 28% Isolation 3 6% Table 3 : Outcome after Treatment in Psychiatry Ward N At the time of discharge from ward At 3 months At 6 months 50 42 42 N 35 25 21 Improved %age 70% 50% 42% Not Improved N %age 15 30% 17 34% 21 42% Table 4 : Intervention Efforts To Settle Treated Inmates in their Families or Homes A. Without Any Available Contact B. Contact Available 1. Inmates were sent back to home 2. Relatives were contacted, but nobody came to take them 3. Inmates did not want to go home because a) Husband got remarried b) Patient had eloped from home, now not able to face family. c) Nobody to look after in the family 4. After staying in the ward and getting better, left Pingla Ashram at their own as nobody came to take inspite of repeated letters. 5. Died N 29 21 5 10 3 1 1 1 2 1 %age 58% 42% 10% 20% 6% 4% 2% Journal of Mental Health & Human Behavior, 2007 97 Jindal et al : Patients in a Pingla Ashram DISCUSSION The National Survey of Mental Health carried by Government of India (2002) shows that there is a marked gap between the patient load and hospital beds for psychiatric patients. As compared to the number of patients reported to be suffering with various mental disorders(n=3645206), the number of beds available in government and private sector in the states of Punjab and Haryana, Himachal Pradesh, Chandigarh and Jammu and Kashmir are very few(n=1251). Hence there is a great demand for resources or means, that can take care of psychiatric patients in the society. Hence, the contribution of private institutions cannot be undermined. Out of 175 inmates in the Pingalwara, 109 (62.3%) had some type of morbidity. Maximum morbidity was due to psychiatric disorders. Out of 75 psychiatric patients, 25 had mental retardation, while 50 had various psychiatric disorders, who were admitted to Psychiatry ward for detailed study. In the Pingalwara of Amritsar, 40% inmates had mental disorder 2. 72% of the inmates were admitted by persons other than relatives and out of them 64% were admitted by the police. In a study,4 63% were admitted by police to Agra Mental Hospital, while in another study,5 50% were admitted by police among 1439 Mental Hospital patients. The relatives of 42% inmates found it difficult to cope with erratic behaviour of the patients and they tend to dispose them off. Most of these patients had chronic schizophrenis. In a study,6 68% had schizophrenia among the long stay patients at Mental Hospital,Ranchi. In single day census on 1307 patients at NIMHANS, 66% had schizophrenia7. In another study,8 70% patients were rejected by their families. Further, the inmates have a long stay in Pingla Ashram, 56% had been staying for more than 4 years indicating that these are the persons who are either not accepted by the families or can’t stay with them. In the study 4 carried out at Agra 33% had been staying in Mental Hospitals for more than 15 years, 18% were staying between 10-15 years while the rest stay for less than 10 years. In another study,9 8% of the patients were staying in the Mental Hospital for 26-35 years, 15% for 16-25 years and 29% for 6-15 years. Another recent study,7 25% were staying at Mental Hospital for more than 15 years and 38% between 5-15 years. In the Pingalwara, the inmates were chained (64%) or restrained (28%) as they were not administered any treatment. Subsequent to commencement of study, inmates were treated in psychiatry ward and were then sent back to Pingalwara. At time of discharge from the ward, 70% had shown improvement of varying degree i.e. they had started taking care of their personal hygiene, violent behaviour decreased and psychiatric symptoms got controlled. After three months, when these inmates were contacted in Pingalwara 50% of them had been maintaining improvement. However at 6 months follow-up 42% maintained improvement. One of the reason for decline in improvement could be due to the fact that drugs were not always available for the patients. In a study conducted at Agra it was reported that 32% patients improved during their stay in Hospital, while 33% worsened.4 After treatment from the Psychiatry ward, relatives of the improved cases were contacted. In 58%, no contact could be traced, only in 42% contact could be traced. After treatment, 10% could be sent home. Surprisingly, the relatives of 20% of inmates did not cooperate and did not agree to take the patients home inspite of repeated contact. They were putting up unreasonable excuses indicating gross apathy on their part for the patients. Thus after psychiatric treatment, 26% of inmates were fit to be kept at home if relatives so desired, but they were unfortunate to Journal of Mental Health & Human Behavior, 2007 98 Jindal et al : Patients in a Pingla Ashram have unacceptable relatives and were compelled to pass time in compromised living conditions of the Pingalwara. There are a large number of psychiatric patients who can’t or are not looked after by their families. Thus there is a great need to create additional psychiatric beds/ facilities and efforts of social organizations and NGOs should be lauded and encouraged. However, these organizations need to be assisted and supervised as there are no psychiatric facilities resulting in Human Right violation of mentally ill persons. There is also a need to educate families about psychiatric disorders and treatment so that there is increased acceptance of these patients by their families. REFERENCES 1. Murthy K, Venugopal D, Alimchandani AK. Mental Hospitals in India. Indian J Psychiatry 2000; 42(2): 125-132. 2. 3. 4. Singh RP. The beginning In: Pingalwara. Singh RP (ed.) Print Well, Amritsar, 1st edition. 2001: 4-7. Ali FI. Insane care. The Week 2001; 8(3): 1-4. Gupta SP, Yadav BS, Bhardwaj RC et al. Psychosocial problems of long stay Mental Patients. Indian J Psychiatry 1980; 22:251-255. Somasundram O, Kumar M. Behaviour characteristic of the Mentally Retarded in State Mental Hospital. Indian J Psychiatry 1984; 26(2): 115-120. Bhaskaran K, Dhawan, Mohan Y. A study of the affects of prolonged hospitlization on schizophrenia. Indian J Psychiatry 1972; 14: 106-113. Reddy V. Long stay patients in Government Mental Hospital in India. Indian J Psychiatry 2001; 43(1): 25-31. Raghuram R, Shaila Pai, Channabasavanna M et al: Home Care for chronic Mental illness in Bangalore: An Experiment in the prevention of repeated hospitalization. Br J Psychiatry 1985; 147: 175-179. Somasundram O, Kumar M. Changing pattern of admission in a State Mental Hospital. Indian J Psychiatry 1984; 26(4): 317-321. 5. 6. 7. 8. 9. Rahul Jindal, Consultant Psychiatrist, Jindal Hospital, Malout, Punjab Kuldip C Sharma, Professor and Head Department of Psychiatry Jagjeet Singh, Professor, Department of Social and Preventive Medicine, Govt. Medical College, Patiala Corresponding Address : Dr. Kuldip C. Sharma, Professor & Head, Department of Psychiatry, Govt. Medical College & Rajindra Hospital, Patiala, Punjab. sharmakc@rediffmail.com Journal of Mental Health & Human Behavior, 2007 99 CASE CONFERENCE Narcolepsy: Clinical Presentation, Differential Diagnosis and Management Sandeep Grover, Swapnil Gupta Abstract: Narcolepsy is a neuropsychiatric condition which usually begins in adolescence and early adulthood, and is characterized by the classic tetrad of sleep attacks, cataplexy, hypnagogic hallucinations and sleep paralysis. Despite typical clinical features it is often undiagnosed or misdiagnosed. We present a case of a thirty-one year old housewife who presented with 3 year history of excessive day time sleepiness, cataplexy, poor night time sleep, hypnagogic hallucinations. Her symptoms led marked dysfunction socio-occupational dysfunction. She was diagnosed as a case of Narcolepsy and managed with methylphenidate. Key Words : Narcolepsy, Management INTRODUCTION Narcolepsy is a neuropsychiatric condition described as a disorder of sleep-state boundary control. It is a relatively uncommon disorder with a prevalence of 1 in 2000.1 Narcolepsy usually has its onset in adolescence and early adulthood, although it may begin even in early childhood and late adulthood. It is characterized by the classic tetrad of sleep attacks, cataplexy, hypnagogic hallucinations and sleep paralysis.2 Most patients also suffer from marked disturbances in nocturnal sleep. Despite typical clinical features, a central problem in the management of patients with narcolepsy is the long duration for which such patients go undiagnosed or misdiagnosed.3 The disorder also takes a significant toll on the psychological, social and occupational functioning of the patient. The patients may suffer from embarrassment, poor self-esteem, anxiety and depression due to their condition. The pharmacological management of narcolepsy typically consists of stimulant medications. We present a case of a thirty-one year old housewife who was diagnosed as a case of Narcolepsy and discuss the diagnostic and management issues. THE CASE KD a 31year old illiterate housewife belonging to an urban joint family of lower socio-economic status, who was premorbidly well adjusted and had no abnormality in birth and early developmental history presented with the chief complaint of excessive daytime sleepiness since 3 years. Further exploration of her history revealed that since last 3 years patients was having frequent day time naps, disturbed night time sleep, and weakness of hands and dropping of things from hands. The episodes of day time naps would begin at any time during the day, irrespective of the activity she was performing. Characteristically, the episode would begin without any warning and the onset was characterized by intense sleepiness, nodding of the head and inability to stand erect. Thus the patient had to interrupt whatever task she would be doing and lie down. She would make efforts to control her sleepiness by focusing on the task at hand or talking to someone but would not be able to resist it beyond five to ten minutes and would go to sleep. She would remain asleep for 15-20 minutes at a stretch, during which she would not be disturbed Journal of Mental Health & Human Behavior, 2007 100 Grover & Gupta : Narcolepsy by minor noises in the house or surroundings and after waking up would feel fresh. After waking up, she would resume her unfinished work and never had any difficulty in recalling what she been doing before going to sleep. During the 3 years, the frequency of the sleep episodes increased gradually from a frequency of 3 to about 5-6 episodes per day and led to problems in completing the day today activities like cooking, washing clothes and conversations with other people. Along with the above symptom, the patient also complained of poor night time sleep. She would go to sleep at a particular fixed time (usually 11 PM), and would be seen sleeping within 10 15 minutes of going to bed. As per the patient, within few minutes of going to bed, she would have vivid and intense dream like phenomenon in which she could see and hear the things. The content of such phenomenon mainly consisted of events that had occurred during the daytime, for example, she would see her family members and she engaged in various activities. Such phenomenon was however not associated with seeing or hearing frightening things or waking up from the sleep. In addition she would also frequently wake up at night. These awakenings would occur 2-3 hours after falling asleep without any specific reason like nightmares and occurred 3-4 times every night. During these awakenings she would either drink water or use the toilet and then try to sleep again and usually would fall asleep in next 15-30 minutes. However, despite the above problems, she would wake up by herself at her usual time (6 AM) without any difficulty, but wouldn’t be satisfied with her night time sleep and would not feel fresh. After a year of the onset of the above symptoms, the patient developed a new symptom in the form of an experience of sudden weakness in the body whenever she laughed. The weakness would last for a fraction of a second to few seconds and would often lead to dropping of things from her hand. As per the patient, “whenever she would have a bout of laughter, she would feel that her body was going weak and that she would fall down. She could feel that her knees were buckling and that she could not hold her back erect. She also felt that she was losing grip on any object that she was holding at that time and that it would fall down and break”. Over the years due to the above phenomenon, patient often avoided laughing. However, such phenomenon did not occur during other emotional arousal states like crying or during sexual arousal. The above symptoms had been gradually progressing over the 2 years before her presentation to the psychiatry out-patient’s department. In addition to the above, patient had decreased libido. The patient’s medical history was insignificant except for a recent increase in weight without any change in her appetite. She had gained approximately 25% of her body weight over the past two years. Over the years all the above symptoms led to significant interference in her day to day functioning, interpersonal relationship problems with husband and mother in law, poor socialization with others, avoidance of social gathering and poor up keep of household things. There was no history suggestive of obstructive sleep apnea, restless leg syndrome, sleep walking, sleep talking, bruxism, night mares, snoring, persistent sadness of mood, anhedonia, decreased energy, depressive cognitions, cold intolerance, constipation, skin changes, menstrual disturbances, acne, hirsuitism and alcohol, nicotine, caffeine or sedative-hypnotics use. There was no family history of any psychiatric disorder. Her physical examination was normal except for being mildly obese. Her mental state examination revealed marked distress and preoccupation with the symptoms. Journal of Mental Health & Human Behavior, 2007 101 Grover & Gupta : Narcolepsy With the above history and examination findings a diagnosis of narcolepsy was considered. On investigation, results of hemoglobin, total and differential count, fasting blood sugar, erythrocyte sedimentation rate, liver and renal function tests and thyroid function tests were in the normal range. Polysomnography was advised, but patient and family refused the same because of financial constraints. On the basis of clinical manifestations, patient was started on Tab. methylphenidate in a dose of 5 mg per day which was gradually increased to 10 mg per day. In addition to methylphenidate patient was asked to maintain a sleep dairy, follow sleep hygiene and have regular daytime naps. Patient and husband were psychoeducated about the nature of the illness and it was emphasized that patient was not indulging in daytime naps deliberately, but was forced to do so due to the nature of the illness. The interpersonal problems between the patient and the husband were also addressed. Patient showed remarkable improvement in all her symptoms in a month with the above management. Later patient was asked to take drug holidays during the weekends, during which husband would assist her in doing household work. After the initial workup, patient has been under follow up treatment for last 5 years and had 7 relapses. Each relapse would follow discontinuation of medication by 4-5 weeks. After which methylphenidate would be reinstituted and patient would improve in all the symptoms. DISCUSSION Narcolepsy is a neuropsychiatric condition, which was first described by Gelineau in 1880.4 It is characterized by classical tetrad of excessive daytime sleepiness, cataplexy, hypnagogic hallucinations and sleep paralysis. However, only 11% to 14% of patients report all 4 symptoms. The excessive daytime sleepiness is usually the first, most common and most troublesome Journal of Mental Health & Human Behavior, 2007 symptom to appear and it is described as overwhelming drowsiness and an uncontrollable need to sleep during the day5-7. These episodes occur not only in monotonous situations but also in situations where the patient is engaged in activity. The sleep episodes last for few minutes to up to a half-hour and on awakening patient reports feeling refreshed. However due to repeated episodes of sleepiness, patients usually report decreased alertness, poor attention and concentration throughout the day. Cataplexy, i.e., sudden loss of muscle tone is seen in up to 60% of all cases of narcolepsy,8 manifests as complete weakness of most muscles, in the form of head drooping or slurring of speech to a fall due to total body paralysis lasting for a few seconds to a few minutes. Cataplexy is uncontrollable and is often triggered by intense emotions, usually positive ones such as such as laughter or excitement, but sometimes fear, surprise or anger. Sleep paralysis manifests as a temporary inability (usually lasting for only seconds to minutes) to move or speak while falling asleep or upon waking. This sleep paralysis mimics the type of temporary paralysis that normally occurs during rapid eye movement (REM) sleep. Hypnagogic hallucinations occur at the onset of the sleep and are experienced as real, and they may be particularly vivid and frightening. They may take the form of visual, tactile, auditory or multi-sensory phenomena lasting for up to a few minutes. Our index case had symptoms of excessive day time sleepiness, cataplexy, hypnagogic hallucinations and disturbed night time sleep. Differential diagnosis of Narcolepsy Narcolepsy is often misdiagnosed. The differential diagnosis depends on the predominant symptom and clinical diagnosis of narcolepsy is based on presence of symptoms from the classic tetrad in various combinations. The differential diagnosis of excessive day time sleep includes sleep 102 Grover & Gupta : Narcolepsy apnea, sleep deprivation, restless leg syndrome, substance use or dependence, depression, Kleine-Levin syndrome, idiopathic hypersomnia, side effects of medications, poor sleep hygiene and severe infections etc. A good history from both patient and bed partner, can help in distinguishing most of these disorders. Sleep apnea is usually seen in obese males with history of loud snoring and evidence of pauses in breathing. Idiopathic hypersomnia is distinguished from narcolepsy by the presence of unrefreshing naps, more persistent daytime sleepiness, longer and less disrupted nocturnal sleep, and absence of sleep-onset REM period. Patients with restless leg syndrome will give history of compulsion to move legs; different unpleasant sensations in the legs precipitated by rest and relieved by activity, worsening of symptoms during early evening or later at night, and will be found to have accompanying iron deficiency anemia and metabolic disturbances. In addition to excessive daytime sleepiness, patients with Kleine-Levin syndrome will report overeating, hallucinations and hypersexuality. Proper evaluation can provide evidence for presence of depression, substance use or dependence, sleep deprivation and poor sleep hygiene.9 The differential diagnosis of cataplexy also includes partial complex seizures, syncope, and events related to psychological factors similar to pseudoseizures10. The preserved consciousness that is invariably associated with cataplexy aids in discriminating these episodes from those with different pathophysiologic mechanisms. Our index case didn’t have history suggestive of snoring, compulsive movements of legs, hypersexuality, increased appetite, substance abuse. Her excessive daytime sleepiness episodes were also refreshing. All this excluded the absence of other possible diagnosis. How to diagnose Narcolepsy An exhaustive medical history and clinical Journal of Mental Health & Human Behavior, 2007 examination are essential for proper diagnosis. However, it is important to remember that none of the 4 symptoms described above are exclusive to narcolepsy. Specialized tests, which can be performed in a sleep disorders clinic, to establish the diagnosis of narcolepsy are: polysomnogram (PSG) and the multiple sleep latency test (MSLT). The PSG is an overnight test that takes continuous multiple measurements while a patient is asleep to document abnormalities in the sleep cycle. It can help to demonstrate as to whether REM sleep occurs at abnormal times in the sleep cycle and mainly helps to exclude other causes of nocturnal sleep disruption like obstructive sleep apnoea, periodic limb movement disorder and rapid eye movement sleep behaviour disorder. The MSLT is performed during the daytime to measure a person’s tendency to fall asleep and to determine whether isolated elements of REM sleep intrude at inappropriate times during the waking hours. As part of the test, an individual is asked to take four or five short naps usually scheduled two hours apart. Of late, orexin levels in cerebrospinal fluid and HLA testing are also done. Low CSF orexin levels are found in narcolepsy and rarely in other neurological conditions. A correlation exists between narcolepsy and histocompatability human leukocyte antigen (HLA) subtype DQB1*0602. In patients of narcolepsy without cataplexy, a combination of HLA subtyping and CSF orexin levels is highly specific2. The diagnosis of narcolepsy is based on the revised criteria given by the international classification of sleep disorders (ICSD).2 ICDS gives 8 criteria for diagnosis of narcolepsy and the minimal requirement for diagnosis includes presence of recurrent daytime naps or lapses into sleep, occurring almost daily for at least 3 months (Criteria B) along with sudden bilateral loss of postural muscle tone occurs in association with intense emotion (Criteria C). Alternatively narcolepsy can also be diagnosed if the patient 103 Grover & Gupta : Narcolepsy has excessive sleepiness or sudden muscle weakness (Criteria A); Associated features, which includes sleep paralysis, hypnagogic hallucinations, automatic behaviors and disrupted major sleep episode (Criteria D), polysomnography showing (one or more of the findings) sleep latency less than 10 minutes, REM sleep latency less than 20 minutes, MSLT showing a mean sleep latency of less than 5 minutes and 2 or more sleep-onset REM periods (Criteria E) and absence of any medical or mental disorder accounting for the above symptoms (Criteria G). Other criterias for narcolepsy as per ICDS are HLA typing showing DQB1*0602 or DR2 positivity (Criteria F) and presence of other sleep disorders (e.g., periodic limb movement disorder or central sleep apnea syndrome) but are not the primary cause of the symptoms (Criteria H). However these criterias are not essential for diagnosis2. Our index case had excessive daytime naps (criteria B) along with catalepsy (criteria C) and hypnagogic hallucinations and fulfilled the diagnosis of narcolepsy as per ICDS.2 Psychosocial aspects of narcolepsy Patients with narcolepsy face challenges at school, work and at home. Public awareness regarding this disorder is poor resulting in these patients being labeled as “lazy” or unwilling to work. Narcolepsy also leads to disruption of family life and interpersonal relationships5, 11,12 and reduced enjoyment of certain recreational activities.13 Students with narcolepsy report that their illness was the cause of poor grades, problems with peers and teachers and caused embarrassment.14 Children with narcolepsy and other disorders of excessive daytime sleepiness were found to have more peer problems, conduct problems and depression.15 In our case also narcolepsy led to psychosocial problems in the form of interpersonal problems with husband and mother in law, difficulty in doing household work and poor Journal of Mental Health & Human Behavior, 2007 socialization. MANAGEMENT Because of its diverse symptomatology, the treatment of narcolepsy is complex and involves use of both pharmacological and nonpharmacological measures. The non-pharmacological treatment includes maintenance of optimal sleep hygiene, including a consistent sleep-wake schedule to facilitate adequate sleep.16 Other measures include scheduled naps during the day and avoidance of high risk work. Besides these special academic needs, family conflict, other psychosocial problems needs to be addressed. The pharmacological treatment options include use of central nervous system stimulants (like methylphenidate, dextroamphetamine, methamphetamine, and amphetamine) and modafinil. Of the stimulants, methylphenidate is the most frequently used stimulant which improves sleep tendency in a dose-related fashion and also reduces cataplexy. The mechanism of action of modafinil is not understood, but it has been evaluated in a multicenter, double-blind, placebo-controlled trial and have been reported to improve sleepiness.17 Unlike traditional medications, modafinil does not appear to affect total sleep time or suppress REM sleep. The most common adverse effect is headache. Its safety in children has not been established. For patients with cataplexy severe enough to warrant targeted treatment, the antidepressant medications have been the mainstay of treatment for years.18 The noradrenergic compounds, such as imipramine and venlafaxine, are viewed as the most effective treatments for cataplexy. One published report of a small study indicated that the selective noradrenergic reuptake inhibitor reboxetine is efficacious.19 Selective serotonin reuptake inhibitors have also been prescribed for cataplexy.2 104 Grover & Gupta : Narcolepsy 10. Krahn L, Hansen M, Shepard J: Pseudocataplexy. Psychosomatics 2001; 42:356–358. 11. Roth T, Roehrs TA, Rosenthal L. Normative and pathological aspects of daytime sleepiness. In: Oldham JM, Riba MB, eds. Review of Psychiatry. Vol 13. Washington, DC: American Psychiatric Press Inc; 1994:707-728. 12. Kales A, Soldatos CR, Bixler EO. Narcolepsy-cataplexy II: Psychosocial consequences and associated psychopathology. Arch Neurol 1982; 39:169-71. 13. Parsons M. Fits and other causes of loss of consciousness while driving. Q J Med 1986; 58: 295-303. 14. Broughton R, Ghanem Q, Hishikawa Y, et al. Life effects of narcolepsy in 180 patients from North America, Asia and Europe compared to normal controls. Can J Neurol Sci 1981; 8:299-304. 15. Stores G, Montgomery P, Wiggs L. The psychosocial problems of children with narcolepsy and those with excessive daytime sleepiness of uncertain origin. Pediatrics 2006; 118:1116-23. 16. Garma L, Marchand F. Non-pharmacological approaches to the treatment of narcolepsy. Sleep 1994; 17 (8 suppl) : S97–S102. 17. Mitler M, Harsh J, Hirshkowitz M, Guilleminault C. Long-term efficacy and safety of modafinil (Provigil) for the treatment of excessive daytime sleepiness associated with narcolepsy. Sleep Med 2000; 1: 231–243. 18. Mitler M, Hayduk R: Benefits and risks of pharmacotherapy for narcolepsy. Drug Safety 2002; 25: 790–809 19. Larrosa O, de la Llave Y, Bario S, Granizo JJ, Garcia-Borreguero D. Stimulant and anticataplectic effects of reboxetine in patients with narcolepsy: a pilot study. Sleep 2001; 24:282–85. Index case was treated with both pharmacological and nonpharmacological treatment and exemplify that patients with narcolepsy should be followed up regularly and major focus of management should be ensuring medication compliance and addressing the psychosocial issues. REFERENCES 1. Hublin C, Kaprio J, Partinme M. The prevalence of narcolepsy: An epidemiological study of the Finnish twin cohort. Ann Neurol 1994; 35:709-16. American Academy of Sleep Medicine. International Classification of Sleep Disorders (ICSD), Revised: Diagnostic and coding manual. Chicago, Illinois: American Academy of Sleep Medicine 2001. Morrish E, King MA, Smith IE, Shneerson JM. Factors associated with a delay in the diagnosis of narcolepsy. Sleep Medicine 2004; 5:37-41. Gelineau JB. De la narcolepsie. Gaz des Hopitaux 1880; 54, 635–637. Alaia SL. Life effects of narcolepsy: measures of negative impact, social support and psychological well-being. Loss Grief Care 1992; 5:1-22. Aldrich MS. The neurobiology of narcolepsy. Trends Neurosci 1991; 14:235-239. Parkes D. Introduction to the mechanism of action of different treatments of narcolepsy. Sleep 1994; 17:S93-S96. Silber MH, Krahn LE, Olson EJ, et al. The epidemiology of narcolepsy in Olmsted County, Minnesota: a population based study. Sleep 2002; 25:197–202. Green PM, Stillman MJ. Narcolepsy – signs, symptoms, differential diagnosis and management. Arch Fam Med 1998; 7: 472-478. 2. 3. 4. 5. 6. 7. 8. 9. Sandeep Grover, Assistant Professor Swapnil Gupta, Formerly Junior Resident Department of Psychiatry Postgraduate Institute of Medical Education & Research, Chandigarh 160012 Corresponding Address : Dr Sandeep Grover, Assistant Professor Department of Psychiatry, Postgraduate Institute of Medical Education & Research, Chandigarh 160012 Email:drsandeepg2002@yahoo.com Journal of Mental Health & Human Behavior, 2007 105 CASE REPORT Alcohol Dependence With Seasonal Bipolarity And SelfMedication For Psychotic Symptoms: A Case Report Anindya Banerjee, Surendra Kumar Mattoo, Munish Aggarwal Abstract : Affective and psychotic symptoms are often found in patients with alcohol dependence, and may present with significant diagnostic difficulties. Self-medication with alcohol for such symptoms has been described for affective but not psychotic symptoms. We present a case with alcohol dependence with seasonal bipolarity who self-medicated for psychotic symptoms. Key Words: Alcohol dependence, seasonal bipolar, self-medication INTRODUCTION The comorbidity of alcohol with psychiatric symptoms is widely documented. Up to 80% of alcohol dependent patients complain of depressive symptoms and 30% or more fulfill criteria for a major depressive episode.1-2 Alcohol dependent cases also have at least a three times higher risk for bipolar disorder, compared to the general population.3 However, some authors have questioned this high rate, asserting that substance-induced hypomanic or mania-like clinical condition could be misdiagnosed as an independent bipolar disorder during acute or protracted withdrawal from alcohol.4 We present the case of an alcohol dependent male who had seasonal affective symptoms during some of his alcohol withdrawal episodes and who self-medicated with alcohol to ameliorate his auditory hallucinations. THE CASE A 40 year old married male electrician pre-morbidly well adjusted and with family history of alcohol dependence in father, presented with history of alcohol use for 23 years, including 17 years in a dependent pattern with tolerance, craving, impaired control over use, neglect of work and family, and characteristic withdrawal symptoms like irritability, restlessness, mild tremors and insomnia. In the first 11 years of alcohol use even though he did not make any serious attempt to quit alcohol, he tried to cover his withdrawal symptoms with gradually escalating doses of up to 135 mg of dextropropoxyphene capsule or up to 60-80 mg of nitrazepam or 30-40 mg of diazepam tablet on each occasion up to twice a month; he stopped these for the fear of unspecified harm to health. His drinking continued to increase further and for the last 4 years he was drinking heavily, even in daytime, with associated severe socio-occupational dysfunction. During these four years under family pressure he stopped alcohol 9 times spread over all seasons. On each occasion, he experienced withdrawal symptoms (anxiety, irritability, tremors and insomnia) for the initial 4–5 days of abstinence. On four out of nine times (between April and July every year) withdrawal symptoms were followed by sadness of mood, easy fatigability, slowness in the activities, absenteeism, low confidence, and pessimistic ideation about having wasted his life and the future of his family being bleak. There were associated decreased appetite, sleep, and self-care, and constipation. There was no history suggestive of decreased attention and concentration, ideas of hopelessness, or suicidal ideas. Journal of Mental Health & Human Behavior, 2007 106 Banerjee et al : Alcohol Dependence, Seasonal Bipolarity & Self-Medication The above ‘depressive’ symptoms would last for 4–5 days and would be followed by 1–2 days of hearing of voices in the evening for 4–5 minutes on 5–6 occasions in clear consciousness. The voices would be of 2–3 men of a neighboring family, be abusive and derogatory, and he would act on them indulging in verbal altercation with neighbors. There was no sadness, altered sensorium or disorientation associated with the period of hearing voices. Ascribing the hearing of voices to loss of sleep due to stoppage of alcohol and to prevent himself from ‘going crazy’ he would resume alcohol intake. The psychotic symptoms would promptly terminate and he would continue drinking in a dependent manner with no affective or psychotic symptoms till his next abstinence attempt after 4-5 months. About 2 months before admission he stopped alcohol, had withdrawal symptoms as described above for 4–5 days and after remaining well for 10 days, started becoming irritable, overactive, over talkative and unduly generous in his dealings. He also had decreased need for sleep and increased libido. After 2 weeks in this state, he restarted taking alcohol, due to craving. All the above symptoms subsided soon thereafter. The review of the course of symptoms led to a conclusion that during the last four years his affective and hallucinatory episodes were secondary to alcohol withdrawal in summer months (5 out of 9 non-summer alcohol withdrawals had not been associated with affective and hallucinatory episodes). Hence, the management focused on alcohol dependence, emphasizing on relapse prevention strategies. Disulfiram was started with informed consent. It was decided to withhold psychotropics at present and institute them later if the affective or psychotic symptoms reappear in the absence of alcohol use. DISCUSSION The case had several points of interest. To start with, there was a diagnostic dilemma whether the mood symptoms were due to an independent disorder or secondary to alcohol use. The short lasting nature of depressive and psychotic symptoms, absence of family history for affective/ psychotic illness and the temporal association with an alcohol withdrawal state support the diagnosis of an alcohol-induced disorder. However, not all episodes of alcohol withdrawal were associated with behavioral symptoms. The seasonal pattern was another key feature, which has been described in independent affective disorder, but not in association with alcohol induced mood states. The other unique point in the case was the recurrent use of alcohol by the patient to terminate hallucinations. Khantzian has proposed a model of substance abuse that asserts that some drugdependent individuals select a drug of choice to provide relief from specific painful affective states, particularly depression and anxiety. This model is popularly known as the self-medication hypothesis.5 However, we could find no reports of self-medication of alcohol to terminate psychotic symptoms. On the contrary, available literature suggests that alcohol use exacerbates, rather than improves, psychotic symptoms and is associated with increased hallucinations and decreased treatment response.6,7 This case illustrates diagnostic difficulties encountered in relation to comorbid substance use and psychiatric symptoms. The diagnosis in such cases will usually be clarified in the longterm follow up. The goal should be to maintain abstinence from alcohol and follow up closely for any psychiatric symptoms; emergence of symptoms during abstinence will clinch the diagnosis of an independent psychiatric disorder. Journal of Mental Health & Human Behavior, 2007 107 Banerjee et al : Alcohol Dependence, Seasonal Bipolarity & Self-Medication REFERENCES 1. Kessler RC, Nelson CB, McGonagle KA et al. The epidemiology of co-occurring addictive and mental disorders. Am J Orthopsychiatry 1996; 66: 17-31. Regier DA, Farmer ME, Rao DS et al. Comorbidity of mental disorders with alcohol and other drug use. JAMA 1990; 264: 2511-2518. Schuckit MA, Tipp JE, Bucholz KK et al. The life-time rates of three major mood disorders and four major anxiety disorders in alcoholics and controls. Addiction 1997; 92: 1289-1304. 4. 5. Raimo EB, Schuckit MA. Alcohol dependence and mood disorders. Addict Behav 1998; 23: 933-946. Khantzian EJ. The self-medication hypothesis of substance use disorders: reconsideration and recent applications. Harv Rev Psychiatry 1997; 4: 231-244. Tsuang JW, Lohr JB. Effects of alcohol on symptoms in alcoholic and nonalcoholic patients with schizophrenia. Hosp Comm Psychiatry 1994; 45: 1229-1230. Sokolski KN, Cummings JL, Abrams BI et al. Effects of substance abuse on hallucination rates and treatment response in chronic psychiatric patients. J Clin Psychiatry 1994; 55: 380-387. 2. 6. 3. 7. Anindya Banerjee, Senior Resident Surendra Kumar Mattoo, Additional Professor Munish Aggarwal, Junior Resident Drug De-addiction & Treatment Centre, Department of Psychiatry, Postgraduate Institute of Medical Education & Research, Chandigarh Corresponding Address : Dr SK Mattoo, Department of Psychiatry, PGIMER, Chandigarh 160012. skm_ddtc@glide.net.in ACKNOWLEDGEMENT The help provided by the following colleagues for reviewing the articles submitted to the journal during 2006-07 is acknowledged. Ajeet Kumar Sidana, Chandigarh B.S. Chavan, Chandigarh R.K. Chaddha, New Delhi Rachna Bhargva, Chandigarh Suresh Kumar, Chandigarh Uday Sinha, New Delhi Journal of Mental Health & Human Behavior, 2007 108 Journal of Mental Health & Human Behavior, 2007 109 Instruction for Contributors The Journal of Mental Health & Human Behavior is the official journal of the Indian Psychiatric Society – North Zone. The journal aims to provide an update on current research work in Northern India in the field of mental health. Submission should be sent to: Dr.Priti Arun Editor Journal of Mental Health & Human Behavior Department of Psychiatry, GMCH-32, Chandigarh - 160 047 E.mail : editornz@yahoo.co.in General Advice to Authors Articles are unlikely to be accepted for publication if they do not conform substantially to the Journal style. In addition to original articles the journal also publishes editorials, review articles, brief reports, letters and case conferences. 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