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Important Mental Health Conditions –What You Need to Know Course SD-11 David C. Bright, O.D. VHA Greater Los Angeles Healthcare System Southern California College of Optometry I. Introduction a. Our patients often have multiple medical problems, some of which have a significant impact on eye health, others which have virtually no impact on the eyes but can profoundly affect daily activities and quality of life. b. This course will cover common and important mental health conditions, what interactions (if any) they have on the visual system and ocular health, their current management strategies, in an attempt to give the optometric practitioner a view of the patient ‘beyond the eyeballs.’ II. Anxiety a. Generalized anxiety disorder (GAD) is a common psychiatric condition, probably second only to depression. Described as 6 months of symptom duration (prominent worrying and impairment) plus 3 or more of the following features occurring on most days: fatigue, restlessness, poor concentration, irritability, muscle tension, and unsatisfying sleep (but not anhedonia, which is seen in depression). GAD is characterized by unrealistic or excessive worry and is disproportionate to the severity of the stress. It is often described as uncontrollable and is diffused over many life events and activities ("generalized" as opposed to more focused worry with other anxiety disorders). Physical (somatic) symptoms include tachycardia, dyspnea, urinary frequency, tremor, or excessive sweating. In contrast to GAD, mild anxiety sharpens the senses and probably improves performance. b. Other anxiety disorders are panic disorder, obsessive compulsive disorder, social anxiety disorder, and PTSD. Generalized anxiety disorder is more common with the aging process (increasing exponentially with age) and more common in women (about twice as frequent as in men). GAD has frequent co-morbidities and major depression may co-exist in up to 2/3's of patients. c. Symptoms are physical (tachycardia, chest pain), cognitive (confusion, poor concentration, difficulty making decisions), behavioral (restlessness, agitation), affective (crying, hostility), and uncontrollable worry (apprehension, dread). Symptoms are long-lasting, with a much greater duration than a panic attack. 1 d. Benzodiazepines (BZDs) are the cornerstone of therapy for anxiety. They act quickly, are dependable, and have a long history of trusted performance. They act by binding to the GABA receptor, thus potentiating its affinity for GABA, which is the predominant inhibitor neurotransmitter of the brain. Leadings BZDs are alprazolam/Xanax, clonazepam/Klonopin, diazepam/Valium, and lorazepam/Ativan. e. Physical dependence and withdrawal symptoms can occur with long-term BZD therapy but these drugs provide rapid relief. Other BZD side effects include sedation, incoordination, confusion, and anterograde amnesia. f. Buspirone (BuSpar) is a non-BZD anxiety drug, taking about 2 weeks to have its effects noted, but has no sedating or muscle relaxant effects. It cannot be used on an as-needed basis. g. Antidepressants (not all) are as effective as BZDs for anxiety and lack problems with dependence/abuse and adverse effects on memory and coordination. h. SSRI antidepressants (specifically paroxetine/Paxil and escitalopram/Lexapro) are now considered to be as effective as BZDs, but take longer to have their benefits felt; they are safer since there is no interaction with alcohol and no dependence. Venlafaxine/Effexor is an SNRI and is as effective as the SSRIs listed above. Tricyclics are as beneficial but anticholinergic side effects are often intolerable. i. References i. Anonymous. Principles of diagnosis and management of anxiety disorders. Can J Psychiatry 2006; 51, Suppl 2:9S-21S. ii. Anxiety Disorders. National Institute of Mental Health. U.S. Department of Health and Human Services. Available online at: www.nimh.nih.gov/health/publications/anxietydisorders/nimhanxiety.pdf Accessed 8-11-09. iii. Bourin M, Lambert O. Pharmacotherapy of anxious disorders. Hum Psychopharmacol Clin Exp 2002; 17:383400. iv. Flint AJ. Generalized anxiety disorder in elderly patients. Epidemiology, diagnosis and treatment options. Drugs Aging 2005; 22:101-14. v. Fricchione G. Clinical Practice. Generalized anxiety disorder. N Engl J Med 2004; 351:675-82. vi. Gale C, Oakley-Browne M. Anxiety disorder. BMJ 2000; 321:1204-7. vii. Hale AS. ABC of Mental Health. Anxiety. BMJ 1997; 341:886-9. viii. Kapczinski FFD, Silva de Lima M, dos Santos Souza JJSS, et al. Antidepressants for generalized anxiety disorder (review). The Cochrane Collaboration, 2009, Issue 3. 2 ix. Pary R, Matuschka PR, Lewis S, et al. Generalized anxiety disorder. Southern J Med 2003; 96:581-6. x. Sramek JJ, Zarotsky V, Cutler NR. Generalized anxiety disorder. Treatment options. Drugs 2002; 62(11):163548. xi. Tyrer P, Baldwin D. Generalized anxiety disorder. Lancet 2006; 368:2156-66. III. Post-traumatic stress disorder (PTSD) a. PTSD demographics: following sexual assault, witnessing mass casualties in war or natural disasters, physical assault, motor vehicle accident, disease epidemics. PTSD diagnostic criteria were established in 1980 in the Diagnostic and Statistical Manual of Mental Disorders (DSM III), resulting from increased awareness due to the Viet Nam conflict. b. Exposed to a traumatic event i. Witnessed/involved with events of actual or threatened death or serious injury to self/others ii. Response of intense fear, helplessness, horror c. Characterized by three "symptom clusters" i. Re-experiencing ii. Avoidance/numbing iii. Hyperarousal d. Cluster 1 = re-experiencing, characterized by: i. Recurrent recollections (thoughts, images) of the event ii. Event is repeated (reliving it, flashbacks, "dissociative flashbacks" occurring upon awakening) iii. Recurrent distressing dreams (nightmares) iv. Psychological distress or "physiological reactivity" at events/entities that symbolize or resemble the trauma e. Cluster 2 = avoidance/numbing, characterized by: i. Avoiding thoughts, feelings, activities, places, people relating to or connected with the traumatic event(s) ii. Diminished interest/participation, reduced range of affect, detached or estranged from family and society f. Cluster 3 = hyperarousal, characterized by; i. Persistent symptoms of increased arousal ii. Difficulty falling or staying asleep iii. Difficulty concentrating iv. Hypervigilance, exaggerated startle response g. Duration of above symptoms is longer than 1 month h. Symptoms cause marked distress and poor functioning in social and occupational situations. PTSD is a chronic disease, with frequent psychiatric and medical co-morbidities, marked functional impairment, and economic costs. i. PTSD is not a simple diagnosis to make, since the great majority of patients with lifetime PTSD have co-morbidities (typically 3 major depressive episodes, alcohol dependence, or drug dependence.) Up to 88% of men and 79% of women with PTSD have co-morbidities. j. The criteria for PTSD diagnosis are complicated. (N Engl J Med 2002 reference below has the most detailed criteria listing.) A short questionnaire is able to suggest PTSD. Questions relate to a patient's reactions to a stressful event, those reactions happening 2 or more times in the past week: i. Upsetting thoughts of memories about the event that enter your mind against your will ii. Upsetting dreams about the event iii. Acting or feeling if the event is happening again iv. Feeling upset by reminders of the event v. Bodily reactions (racing heart beat, upset stomach, sweating, dizziness) when reminded of the event vi. Difficulty falling or staying asleep vii. Irritability or outbursts of anger viii. Difficulty concentrating ix. Heightened awareness of danger to yourself or others x. Being jumpy or being startled at something unexpected k. First line treatment = SSRIs i. Able to ameliorate the 3 core symptom complexes ii. Able to ameliorate depression or other anxiety disorders than may accompany PTSD, such as panic, social phobia, or obsessive compulsive disorder iii. Primary drugs are sertraline/Zoloft, paroxetine/Paxil l. Other antidepressants: venlafaxine/Effexor (SNRI) is second line; third line drugs are tricyclics (amitriptyline, imipramine), and some MAO inhibitors (but little data on these groups, and their side effect profiles are more severe than the SSRIs). m. Benzodiazepines: good for anxiety and sleep issues, but unable to ameliorate the 3 core symptom complexes; significant concerns for dependence/abuse with comorbid substance abuse so their use is typically avoided. n. Atypical antipsychotics – for comorbid psychoses accompanying PTSD; not first or second line drugs, but used as needed (Seroquel, Risperdal, etc.). o. Anticonvulsants – help with reexperiencing symptoms, but uncertain benefits for numbing or hyperarousal symptoms p. Alpha-1 antagonist (prazosin) – benefit for relief of nightmares. Proposed increased CNS adrenergic activity at night, with overstimulation of alpha-1 receptors in hippocampus and amygdala. q. Beta blockers – specifically propranolol. Proposed mechanism of consolidation of short-term, labile memories into long-term memories occurs in the aymgdala; propranolol is proposed to interfere with neurotransmitters participating in the consolidation of memories. 4 r. References i. American Psychiatric Association. Working Group on ASD and PTSD. Practice Guideline for the Treatment of Patients with Acute Stress Disorder and Posttraumatic Stress Disorder. Available online at: www.psychiatryonline.com/pracGuide/loadGuidelinePDF.a spx?file=ASD_PTSD_05-15-06. Accessed 11-11-09. ii. Asnis GM, Kohn SR, Henderson M, Brown NL. SSRIs versus non-SSRIs in post-traumatic stress disorder. An update with recommendations. Drugs 2004; 64:383-404. iii. Brewin CR, Rose S, Andrews B et al. Brief screening instrument for post-traumatic stress disorder. Br J Psych 2002; 181:159-62. iv. Garakani A, Mathew SJ, Charney DS. Neurobiology of anxiety disorders and implications for treatment. Mt Sinai J Med 2006; 73:941-9. v. Grinage BD. Diagnosis and management of posttraumatic stress disorder. Am Fam Phys 2003; 68:24018, 2409. vi. Kessler RC, Sonnega A, Bromet E et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psych 1995; 52:1048-60. vii. Marmar CR, Neylan TC, Schoenfeld FB. New directions in the pharmacotherapy of posttraumatic stress disorder. Psych Quarterly 2002; 73(4):259-70. viii. Taylor HR, Freeman MK, Cates ME. Prazosin for treatment of nightmares related to posttraumatic stress disorder. Am J Health-Syst Pharm 2008; 65:716-22. ix. Yehuda R. Post-traumatic stress disorder. New Engl J Med 2002; 346:108-14. IV. Depression a. Very common – 2nd only to hypertension as the most commonly seen condition in primary care practice b. Lifetime prevalence of depression is 17%; 1 in 10 patients has a major depressive episode. Depression has a prevalence as high as 25% in nursing homes. Frequencies for men and women differ: 12% in men, versus 20% in women. The risk of suicide is 30-fold higher than in the community at large. c. Major depressive episode = depressed mood or anhedonia for 2+ weeks, plus 3+ of the following: insomnia, feeling worthless or guilty, fatigue, diminished concentration, changes in appetite, psychomotor retardation, recurrent suicidal thoughts. The episode is characterized by a change in affect, behavior, and quality of life. Single depressive episodes raise risks of subsequent episodes: there is a 28% chance of a second episode in 1 year, with a 62% chance of a second episode in 5 years. 5 d. Generally felt not to be related to a prior, predisposing stressful event. Somatic symptoms (anorexia, weight loss, constipation, poor sleep, lost libido, vague aches, or poor concentration) may be part of depression but can obscure the classic "low mood." e. Major depressive episodes need to be contrasted with dysthymia and bipolar disorder i. Dysthymia is depression for > 2 years; symptoms are less severe than in a major depressive episode ii. Bipolar disorder is diagnosed by a single manic episode. Bipolar type I is alternation between fully manic and depressive episodes; bipolar type II is alternation between "hypomanic" and depressive episodes. f. 50-70% of patients respond to initial therapy (either meds or psychotherapy). Therapy for a major depressive episode needs to be typically continued for months into the "maintenance period" as the initial episode improves. g. Serotonin- and/or norepinephrine-reuptake inhibitors i. Tertiary amine tricyclics (Elavil, Sinequan, Tofranil) – older drugs, known as "tricyclics" ii. Secondary amine tricyclics (Norpramin, Pamelor) – also older drugs iii. Bicyclic = combined serotonin and norepinephrine reuptake inhibitors or SNRIs (venlafaxine/Effexor and duloxetine/Cymbalta) – newer drugs without as many adverse effects iv. Older tricyclic drugs were called "dirty drugs" due to their profound side effects that included sedation; orthostatic hypotension; cardiac side effects including ventricular arrhythmias and conduction defects; and anticholinergic problems including dry mouth, constipation, and urinary retention. h. SSRIs are fluoxetine/Prozac, paroxetine/Paxil, sertraline/Zoloft, citalopram/Celexa, escitalopram/Lexapro, fluvoxamine/Luvox i. Minimal/variable sedation and few anticholinergic effects, also minimal/no cardiac effects ii. However, notorious for causing sexual dysfunction (delayed ejaculation and anorgasmia, with incidences up to 60% of patients) and GI upset (nausea, vomiting, diarrhea); also likely to cause anxiety and insomnia at start of therapy iii. Much preferred to the older tricyclic antidepressants due to side effect profiles i. Mirtazapine/Remeron has a complex and unduplicated mechanism making it quite unique; effects are to enhance both norepinephrine and serotonin effects; no anticholinergic effects, less sexual dysfunction, but likely to cause somnolence and weight gain 6 j. Norepinephrine- and dopamine-reuptake inhibitor is bupropion/Wellbutrin; considered to be the least likely to cause adverse drug events (ADEs) - less nausea, diarrhea, somnolence or sexual dysfunction vs. SSRIs k. Clinical trials have indicated that some drugs work better for certain types of depression if there are comorbid features or other characteristics. Although the SSRIs revolutionized the treatment of depression in the 90's, the older SSRI drugs are often used more for anxiety and the even-newer antidepressants are increasingly popular for depression treatment. l. References i. American Psychiatric Association. Work Group on Major Depressive Disorder. Practice guidelines for the Treatment of Patients with Major Depressive Disorder. Second edition. Available online at www.psychiatryonline.com/pracGuide/loadguidelinePdf.as px?file=MDD2e_05-15-06. Accessed 11-10-09. ii. Belmaker RH, Agam G. Major depressive disorder. N Engl J Med 2008; 358:55-68. iii. Brent DA, Birmaher B. Clinical practice. Adolescent depression. N Engl J Med 2002; 347:667-71. iv. DeJesus RS, Vickers KS, Melin GJ, Williams MD. A system-based approach to depression management in primary care using the Patient Health Questionnaire-9. Mayo Clin Proc 2007; 82:1395-1402. v. Dopheide JA. Recognizing and treating depression in children and adolescents. Am J Health-Syst Pharm 2006; 63:233-43. vi. Jick H, Kaye JA, Jick SS. Antidepressants and the risk of suicidal behaviors. JAMA 2004; 292:338-43. vii. Mann JJ. The medical management of depression. N Engl J Med 2005; 353:1819-34. viii. Whooley MA, Simon GE. Managing depression in outpatients. N Engl J Med 2000; 343:1942-50. ix. Williams JW Jr, Nöel PH, Cordes JA et al. Is this patient clinically depressed? JAMA 2002; 287:1160-70. V. Schizophrenia a. Affects about 1% of the population, but the greatest risk factor is a positive family history, being 6.5% in first-degree relatives of patients. Typically presents in late adolescence or early adulthood (70% of incident cases occur between 15-35 years of age). Men may have an earlier age of onset, often have a more serious form of the disease, with more negative symptoms (see below) and worse outcome. It is also more frequent in individuals born in cities, the larger the city and the longer the duration of residence, 7 b. c. d. e. f. the greater the risk. Overall, the heritable component accounts for about 70% of the risk for schizophrenia, and 30% of the risk results from perinatal (prematurity) and childhood brain injury, plus psychosocial stress over life events. Life expectancy is 20% shorter than usual, with the most common cause of death being suicide (10% of patients), this risk for suicide being 20-fold higher than in the general population. Named as such by the observation of the “disconnection or splitting of psychic functions” but does not mean a “split personality.” A more apt description would be “shattered,” analogous to a waking nightmare – in which the often terrifying bizarre images and impossible occurrences of a typical nightmare (which would dissipate upon awakening) won’t go away. Positive symptoms (overt psychotic features); these are characterized by a lack of insight and failure to appreciate that these symptoms are not real or caused by the illness. i. Hallucinations – disturbed perceptions without stimuli; auditory hallucinations (‘hearing voices’) are most common – speaking about or to the patient; hallucinations are also less specific auditory (machinery or repetitious noises), or involve touch, taste, smell, or vision. ii. Delusions – these are falsely held beliefs that are not shared by others in the community or family; persecution (victims of some threat), passivity (their thoughts or actions are controlled by an external force), and delusions along themes (grandiosity, sexual, or religious foci). iii. Thought disorders – distorted, disorganized, or illogical speech; “knight’s move” thinking characterized by a chesslike, sudden right-angle veering off. Negative symptoms, which include withdrawal, self-neglect, loss of motivation and initiative, emotional blunting (flat affect), social withdrawal, poor mental creativity, anhedonia, and paucity of speech. Schizophrenic patients have trouble with memory, paying attention, and executive function. Many individuals have a history of behavioral dysfunction (primarily social difficulties and learning difficulties.) Negative features wreak havoc with family, friends, and co-workers. Most common positive symptoms are lack of insight (97%), auditory hallucinations (74%), ideas of reference (70%), delusions of reference (67%), suspiciousness or flatness of affect (both 66%), delusional mood or delusions of persecution (both 64%), thought alienation (52%), and thoughts spoken aloud (50%). An acute psychotic episode results from a combination of multiple factors (increased dopamine, neuronal inhibitory transmitters, loss of neurons, etc.) so that the patient is hypersensitive to stimuli and unable to regulate his/her responses through normal inhibitory mechanisms – the patient cannot sort through what is known and 8 what is unknown, the world becoming overwhelming and threatening or controlling them. g. Treatments started with the advent of “neuroleptic” drugs from the 1950’s, the first being chlorpromazine (Thorazine), found to have benefit in schizophrenic patients being tested for the drug’s use as a new antihistamine. The “classic antipsychotic” drugs (see below) decrease dopamine-mediated neurotransmission, which diminishes the distractibility and improves perceptual abilities of schizophrenic patients. Dopamine is not the sole factor, however. Inhibitory interneurons are decreased in number, the enzymes that synthesize the inhibitor neurotransmitter GABA are less active, plus brain matter itself is less developed in several regions, including the hippocampus and superior temporal cortex. h. “Typical” antipsychotic drugs date from the 1950’s; “atypical” antipsychotic drugs date from 1991, beginning with clozapine. Atypical drugs have less extrapyramidal side effects (movement disorders), but cause more weight gain. Globally, antipsychotic drugs act as dopamine antagonists: “typical” drugs have D2 receptor antagonism, while “atypical” drugs have D2, plus D1, D4, and serotonin antagonism. In carefully structured, nose-to-nose comparisons, neither group of drugs is superior for control of psychosis, but atypical drugs are better tolerated (due to movement disorders, mainly tardive dyskinesia) and may better relieve “negative” symptoms. However, clozapine is the most effective last-ditch drug when others have failed. i. Typical antipsychotic drugs are chlorpromazine (Thorazine, 1953), perphenazine (Trilafon, 1957), trifluoperazine (Stelazine, 1958), fluphenazine (Prolixin, 1959), thioridazine (Mellaril, 1961), haloperidol (Haldol, 1966), thiothixine (Navane, 1968), and loxapine (Loxitane, 1978). j. Atypical antipsychotic drugs are clozapine (Clozaril, 1991), risperidone (Risperdal, 1993), olanzapine (Zyprexa, 1996), quetiapine (Seroquel, 1998), ziprasidone (Geodon, 2001), and aripiprazole (Abilify, 2002). k. Typical antipsychotic drugs are famous for causing ocular side effects: i. Chlorpromazine/Thorazine – anterior subscapsular cataracts ii. Thioridazine/Mellaril – pigmentary retinopathy iii. Fluphenazine/Prolixin – accommodative paresis (premature presbyopia) l. References i. Anonymous. Treating Schizophrenia. A quick reference guide. American Psychiatric Association. Available online at: www.psychiatryonline.com/pracGuide/loadPracQuickRefPdf.a spx?file=Schizophrenia_QRG Accessed 8-11-09. ii. Freedman R. Schizophrenia. N Engl J Med 2003; 349:173849. 9 iii. Gardner DM, Baldessarini RJ, Waraich P. Modern antipsychotic drugs: a critical overview. CMAJ 2005; 172:1703-11. iv. Geddes J, Freemantle N, Harrison P et al. Atypical antipsychotics in the treatment of schizophrenia: systematic overview and meta-regression analysis. BMJ 2000; 321:1371-6. v. Keefe RSE, Bilder RM, Davis SM, et al. Neurocognitive effects of antipsychotic medications in patients with chronic schizophrenia in the CATIE Trial. Arch Gen Psychiatry 2007; 64:633-47. vi. Leucht S, Komossa K, Rummel-Kluge C, et al. A metaanalysis of head-to-head comparisons of second-generation antipsychotics in the treatment of schizophrenia. Am J Psychiatry2009; 166:152-63. vii. Lieberman JA, Stroup TS, McEvoy JP et al. Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. N Engl J Med 2005; 353:1209-23. viii. Mortensen PB, Pedersen CB, Westergaard T et al. Effects of family history and place and season of birth on the risk of schizophrenia. N Engl J Med 1999; 340:603-8. ix. Picchioni MM, Murray RM. Schizophrenia. BMJ 2007; 335:91-5. x. Work Group on Schizophrenia. Practice Guideline for the Treatment of Patients with Schizophrenia. Second edition, April 2004. American Psychiatric Association. Available online at: www.psychiatryonline.com/pracGuide/loadGuidelinePdf.aspx? file=Schizophrenia2e_Inactivated_04-16-09 [note: Guideline inactivated 4-09, awaiting revision.] Accessed 811-09. xi. Saks ER. The center cannot hold – my journey through madness. New York: Hyperion, 2007. VI. Bipolar disorder a. Previously known as “manic-depressive disorder” which inaccurately implied a regular cycling between a manic episode and a depressive episode (additionally inaccurately implying equal durations of these episodes). Actually, depressive episodes last longer and may occur repeatedly before there is a manic episode. Presently, bipolar disorder is now defined as ‘bipolar I disorder’ and ‘bipolar II disorder.’ b. Bipolar I disorder has at least one episode of mania, while bipolar II disorder has at least one episode of hypomania. The major difference between them is the greater severity of the elevated mood and the associated functional disability (which is characterized by psychosis, the need for urgent care or hospitalization, or marked impairment) seen with bipolar I. 10 c. d. e. f. g. Both types have manic features and the symptoms are the same; the dividing point is the degree of disability associated with the mania in type I. Mania or hypomania requires an elevated (euphoric) and/or irritable mood, plus at least 3 of the following symptoms (or 4 of the following if the mood is only irritable): i. Grandiosity or inflated self-esteem ii. Decreased need for sleep iii. Increased talking or pressured speech iv. Racing thoughts v. Distractibility vi. Overactivity (an increase in goal-directed activity) vii. Psychomotor agitation viii. Excessive involvement in pleasurable activities with a high potential for painful consequences Bipolar I is characterized by a behavioral disturbance “sufficiently severe to cause marked impairment in social or occupational functioning or to require hospitalization, or is characterized by the presence of psychotic features.” Bipolar II has a hypomanic episode (in contrast to a manic episode) that is not severe enough to cause marked impairment in social or occupational functioning; there are no psychotic features. The diagnosis of bipolar disorder is typically based on mania or hypomania, although the depressive phase confers the greatest burden and impact on quality of life. Similarly to schizophrenia, the age of onset is in adolescence and early adulthood. The cornerstone of pharmacologic management of bipolar disorders is mood stabilizers. The use of antidepressants is considerably less established at this time. There are a number of FDA-approved drugs for either acute mania or acute mania and maintenance therapy: i. Atypical antipsychotic agents: aripiprazole (Abilify), both mania and maintenance; asenapine (Saphris) for mania; olanzapine (Zyprexa) for mania and maintenance; quetiapine (Seroquel) for mania or maintenance; risperidone (Risperdal) for mania; ziprasidone (Geodon) for mania or maintenance ii. Antiepileptic drugs: carbamazepine (Tegretol) for mania; divalproex sodium (Depakote) or mania; lamotrigene (Lamictal) for maintenance. iii. Lithium for mania iv. Medications for bipolar depression: quetiapine (Seroquel), and the combination of olanzapine with fluoxetine (Zyprexa and Prozac). References i. Frye MA. Bipolar disorder – a focus on depression. N Engl J med 2011; 364:51-9. 11 ii. Sherazi R et al. What’s new? The clinical epidemiology of bipolar I disorder. Harv Rev Psychiatry 2006; 14:273-84. iii. Benazzi F. Bipolar II disorder. Epidemiology, diagnosis and management. CNS Drugs 2007; 21:727-40. iv. Sachs GS et al. Effectiveness of adjunctive antidepressant therapy for bipolar depression. N Engl J Med 2007; 356:1711-22. v. Loganathan M et al. When to suspect bipolar disorder. J Family Practice 2010; 69:682-8. vi. Smith LA et al. Effectiveness of mood stabilizers and antipsychotics in the maintenance phase of bipolar disorder: a systematic review of randomized controlled trials. Bipolar Disorders 2007;9:394-412. vii. Miklowitz DJ. Adjunctive psychotherapy for bipolar disorder: state of the evidence. Am J Psychiatry 2008; 165:1408-19. viii. Belmaker RH. Bipolar disorder. N Engl J Med 2004; 351:476-86. ix. Malhi GS et al. The management of individuals with bipolar disorder. Drugs 2009; 69:2063-101. x. Michalak EE et al. Burden of bipolar depression. Impact of disorder and medications on quality of life. CNS Drugs 2008; 22:389-406. xi. Anonymous. Bipolar disorder. National Institute of Mental Health. http://www.nimh.nih.gov/health/publications/bipolardisorder/complete-index.shtml Accessed February 1, 2011. xii. American Psychiatric Association. Treatment of patients with bipolar disorder, second edition. April 2002. http://www.psychiatryonline.com/pracGuide/pracGuideCh apToc_8.aspx (note that the guideline is in the process of being updated.) Accessed February 1, 2011. xiii. Hirschfield RM. Guideline watch: practice guideline for the treatment of patients with bipolar disorder, second edition, American Psychiatric Association Guidelines for the treatment of psychiatric disorders 2004. November 2005. http://www.psychiatryonline.com/content.aspx?aid=1484 30. Accessed February 1, 2011. VII. Conclusions – Some of these commonly encountered conditions have little impact on eye health or the visual system, and the drugs used for their treatment are claimed to have similarly little ocular impact. Ocular side effects are generally more common with older 12 medications (particularly the typical antipsychotic medications), although light sensitivity has been attributed to a number of newer drugs; additionally, we need to recall that many of the above conditions are rarely managed with monotherapy alone. Mental illness can be a subject which we avoid or stigmatize, to the detriment of those dealing with it. Greater awareness and understanding of the challenging nature of these conditions is warranted, as is increased advocacy for its management. 13