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Important Mental Health Conditions –What You Need to Know
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.
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. PTSD following armed
combat has been known by a variety of names, including
“soldier’s heart” (Civil War), “shell shock” (WW1), “battle
fatigue” (WW2), and “Vietnam stress syndrome.”
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
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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
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.
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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.
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/pracGuideChapToc
_11.aspx (note: guideline is over 5 years old, but can
still be downloaded in PDF form); accessed 7-14-2011.
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. Brady KT, Sinha R. Co-occurring mental and substance
use disorders: the neurobiological effects of chronic
stress. Am J Psychiatry 2005; 162:1483-93.
iv. Brewin CR, Rose S, Andrews B et al. Brief screening
instrument for post-traumatic stress disorder. Br J Psych
2002; 181:159-62.
v. Garakani A, Mathew SJ, Charney DS. Neurobiology of
anxiety disorders and implications for treatment. Mt Sinai
J Med 2006; 73:941-9.
vi. Grinage BD. Diagnosis and management of posttraumatic stress disorder. Am Fam Phys 2003; 68:24018, 2409.
vii. Hoge CW, Castro CA, Messer SC et al. Combat duty in
Irag and Afghanistan, mental health problems, and
barriers to care. N Engl J Med 2004; 351:13-22.
viii. Kessler RC, Sonnega A, Bromet E et al. Posttraumatic
stress disorder in the National Comorbidity Survey. Arch
Gen Psych 1995; 52:1048-60.
ix. Marmar CR, Neylan TC, Schoenfeld FB. New directions in
the pharmacotherapy of posttraumatic stress disorder.
Psych Quarterly 2002; 73(4):259-70.
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x. 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.
xi. Thomas JL, Wilk JE, Riviere LA et al. Prevalence of
mental health problems and functional impairment among
active component and national guard soldiers 3 and 12
months following combat in Iraq. Arch Gen Psychiatry
2010; 67:614-23.
xii. Yehuda R. Post-traumatic stress disorder. New Engl J
Med 2002; 346:108-14.
III.
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 (major depressive disorder or MDD) =
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.
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
and/or psychotherapy, typically cognitive behavioral therapy or
CBT). Therapy for a major depressive episode needs to be
typically continued for months into the "maintenance period" as
the initial episode improves. Therapy of MDD very often
consists of trial-and-error with a variety of medications to find
the right fit, buttressed by careful listening and analysis of
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g.
h.
i.
j.
k.
l.
symptoms and patient progress, with modifications in the
medication regimen.
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.
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
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
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
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.
There is significant controversy about treatment of depression,
complicated by (A) proponents of drug therapy vs. “talk
therapy”; (B) variable and contradictory results of drug trials;
(C) appropriateness of drug therapy for mild depression (is it
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really depression or just ‘sadness’?); (D) lack of congruence
between drug trials and ‘real life’ management strategies. The
STAR*D Study attempted to provide practical guidelines for
treatment (see references below).
m. References
i. American Psychiatric Association. Work Group on Major
Depressive Disorder. Practice guidelines for the
Treatment of Patients with Major Depressive Disorder.
Third edition, November 2010. Available online at:
www.psychiatryonline.com/pracGuide/pracGuideChapToc
_7.aspx. Accessed 7-14-2011.
ii. Belmaker RH, Agam G. Major depressive disorder. N
Engl J Med 2008; 358:55-68.
iii. Bostwick JM. A generalist’s guide to treating patients
with depression with an emphasis on using side effects to
tailor antidepressant therapy. Mayo Clin Proc 2010;
85:538-50.
iv. Brent DA, Birmaher B. Clinical practice. Adolescent
depression. N Engl J Med 2002; 347:667-71.
v. 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.
vi. Dopheide JA. Recognizing and treating depression in
children and adolescents. Am J Health-Syst Pharm 2006;
63:233-43.
vii. Fournier JC, De Rubeis RJ, Hollon SD et al.
Antidepressant drug effects and depression severity.
JAMA 2010; 303:47-53.
viii. Gaynes BN, Rush AJ, Trivedi MH et al. The STAR*D
study: treating depression in the real world. Cleveland
Clin J Med 2008; 75:57-66.
ix. Jick H, Kaye JA, Jick SS. Antidepressants and the risk of
suicidal behaviors. JAMA 2004; 292:338-43.
x. Kirsch I, Deacon BJ, Huedo-Medina TB, et al. Initial
severity and antidepressant benefits: a meta-analysis of
data submitted to the Food and Drug Administration.
PLoS Medicine 2008; 5:e45.
xi. Kramer PD. In defense of antidepressants. New York
Times, July 10, 2011. Available at:
www.nytimes.com/2011/07/10/opinion/sunday/10antidep
ressants.html?scp=1&sq=in%20defense%20of%20antide
pressants&st=cse or at
www.nytimes.com/2011/07/10/opinion/sunday/10antidep
ressants.html?scp=2&sq=Peter%20D.%20Kramer&st=cs
e
xii. Mann JJ. The medical management of depression. N
Engl J Med 2005; 353:1819-34.
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xiii. Rush AJ, Warden D, Wisniewski SR, et al. STAR*D.
Revising conventional wisdom. CNS Drugs 2009;
23(8):627-47.
xiv. Whooley MA, Simon GE. Managing depression in
outpatients. N Engl J Med 2000; 343:1942-50.
xv. Williams JW Jr, Nöel PH, Cordes JA et al. Is this patient
clinically depressed? JAMA 2002; 287:1160-70.
IV.
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,
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.
b. 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.
c. 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.
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d. 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.
e. 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%).
f. 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
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).
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j.
k.
l.
V.
Atypical antipsychotic drugs are clozapine (Clozaril, 1991),
risperidone (Risperdal, 1993), olanzapine (Zyprexa, 1996),
quetiapine (Seroquel, 1998), ziprasidone (Geodon, 2001), and
aripiprazole (Abilify, 2002).
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)
References
i. Anonymous. Treatment of Patients with Schizophrenia,
Second Edition. April 2004. American Psychiatric
Association. Available online at:
www.psychiatryonline.com/pracGuide/pracGuideChapToc_6.a
spx. (Note: guideline is over 5 years old). Accessed 7-142011.
ii. Freedman R. Schizophrenia. N Engl J Med 2003; 349:173849.
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. Saks ER. The center cannot hold – my journey through
madness. New York: Hyperion, 2007.
Bipolar disorder
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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.
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.
c. 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
d. 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.
e. 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.
f. 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;
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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).
g. References
i. American Psychiatric Association. Treatment of patients
with bipolar disorder, second edition. April 2004.
http://www.psychiatryonline.com/pracGuide/pracGuideCh
apToc_8.aspx (note that the guideline is in the process of
being updated.) Accessed July 14, 2011.
ii. Anonymous. Bipolar disorder. National Institute of
Mental Health.
http://www.nimh.nih.gov/health/publications/bipolardisorder/complete-index.shtml Accessed July 14, 2011.
iii. Belmaker RH. Bipolar disorder. N Engl J Med 2004;
351:476-86.
iv. Benazzi F. Bipolar II disorder. Epidemiology, diagnosis
and management. CNS Drugs 2007; 21:727-40.
v. Frye MA. Bipolar disorder – a focus on depression. N
Engl J Med 2011; 364:51-9.
vi. 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 July 14, 2011.
vii. Jarema J. Atypical antipsychotics in the treatment of
mood disorders. Curr Opin Psychiatry 2007; 20:23-9.
viii. Loganathan M et al. When to suspect bipolar disorder. J
Family Practice 2010; 69:682-8.
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. Miklowitz DJ. Adjunctive psychotherapy for bipolar
disorder: state of the evidence. Am J Psychiatry 2008;
165:1408-19.
xii. Sachs GS et al. Effectiveness of adjunctive
antidepressant therapy for bipolar depression. N Engl J
Med 2007; 356:1711-22.
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xiii. Sherazi R et al. What’s new? The clinical epidemiology of
bipolar I disorder. Harv Rev Psychiatry 2006; 14:273-84.
xiv. 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.
VI.
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
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.
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