Introduction :

In recent years, mental health professionals have become increasingly aware of the importance of
genetic factors in the etiology (causes) of mental disorders. Since the Human Genome Project
began its mapping of the entire sequence of human DNA in 1990, the implications of its findings
for psychiatric diagnosis and treatment have accumulated rapidly. A new subspecialty known as
biological psychiatry (also called physiological psychology or psychiatric genetics) has emerged
from the discoveries of the last two decades. Biological psychiatry got its start in the late 1980s,
when several research groups identified genes associated with manic depression and
schizophrenia respectively. These studies ran into difficulties fairly quickly, however, because of
the complexity of the relationship between genetic factors and mental illness.(3)

At present, an increased risk of psychiatric disorders can be identified through a detailed family
history. The empirical risk of developing a disorder has been determined for many psychiatric
disorders and can be used as a general guide. In this case, Genetic counseling can extend and
enhance patient care by providing information to patients about the complexities of inheriting
psychiatric disorders and the associated risks of recurrence.

Spontaneous panic attacks with chlomipramine

Recurrent spontaneous panic attacks are psychophysiological symptoms present in panic disorder and
agoraphobia with panic attacks. Effective pharmacological treatment for panic attacks is essential to any
treatment plan for these conditions. The authors administered chlomipramine to 20 patients who had
panic disorder or agoraphobia with panic attacks, and after 8 weeks of treatment 75% of the patients
with each diagnosis were asymptomatic. These results support the claim that chlomipramine is highly
effective in preventing recurrence of panic attacks. (Gloger et all.,1981) .

Panic attacks. A review of treatments and pathogenesis

In the psychiatric literature, panic attacks have been considered as part of the clinical manifestations of
anxiety neurosis, agoraphobia, functional cardiovascular disturbances, and the phobic depersonalization

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syndrome. Even though recurrent spontaneous panic attacks are described in these entities, the
importance ascribed to them has been minor one. Therefore, panic attacks are poorly understood from
a psycho-physio pathological point of view. In the past years, new trends in the nosology of psychiatric
disorders have grouped the recurrent spontaneous panic attacks under the heading "panic disorder and
agoraphobia with panic attacks." In this view, we present the results of the controlled pharmacological
trials on patients complaining of panic attacks. Some relationships between panic attacks, panic
disorder, and agoraphobia are discussed. (Grunhaus et all.,1981) .

Emotion in Bipolar Disorder

Bipolar disorder is a disorder of emotion regulation. Less is known, however, about the specific
processes that foster the maintenance of such prolonged and intense emotions-particularly positive-
over time in this disorder. We investigated group-related differences in the ability to maintain positive
and negative emotion representations over time using a previously validated emotion working memory
task (Mikels et al., 2005, 2008) among individuals with bipolar I disorder (BD; n = 29) compared with
both major depressive disorder (MDD; n = 29) and healthy control (n = 30) groups. Results revealed that
the BD group exhibited a selective deficit in maintaining negative-but not positive-emotions compared
to both the MDD and the control groups. The MDD and control groups did not differ significantly. These
findings suggest that the heightened magnitude and duration of positive emotion observed in BD may,
in part, be accounted for by difficulties maintaining negative emotions. (PsycINFO Database Record (c)
2012 APA, all rights reserved). (Gruber et all.,2012).

Pathological panic states with propranolol

The authors report on the effects of propranolol, a beta-adrenergic blocking agent, on 10 patients with
pathological panic states. Propranolol was effective in treating acute pathological panic, but modest
doses of the drug administered for brief periods of time did not alleviate chronic panic attacks
associated with agoraphobia. The drug suppressed panic associated with depressive syndromes but did
not affect the depression and had no clear effect on anticipatory anxiety. The authors suggest that
further study of these findings may clarify other clinical problems. (Heiser and Defrancisco,1976).

Morbid risk of anxiety and mood disorders in the United States

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Estimates of 12-month and lifetime prevalence and of lifetime morbid risk (LMR) of the Diagnostic and
Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) anxiety and mood
disorders are presented based on US epidemiological surveys among people aged 13+. The presentation
is designed for use in the upcoming DSM-5 manual to provide more coherent estimates than would
otherwise be available. Prevalence estimates are presented for the age groups proposed by DSM-5
workgroups as the most useful to consider for policy planning purposes. The LMR/12-month prevalence
estimates ranked by frequency are as follows: major depressive episode: 29.9%/8.6%; specific phobia:
18.4/12.1%; social phobia: 13.0/7.4%; post-traumatic stress disorder: 10.1/3.7%; generalized anxiety
disorder: 9.0/2.0%; separation anxiety disorder: 8.7/1.2%; panic disorder: 6.8%/2.4%; bipolar disorder:
4.1/1.8%; agoraphobia: 3.7/1.7%; obsessive-compulsive disorder: 2.7/1.2. Four broad patterns of results
are most noteworthy: first, that the most common (lifetime prevalence/morbid risk) lifetime anxiety-
mood disorders in the United States are major depression (16.6/29.9%), specific phobia (15.6/18.4%),
and social phobia (10.7/13.0%) and the least common are agoraphobia (2.5/3.7%) and obsessive-
compulsive disorder (2.3/2.7%); second, that the anxiety-mood disorders with the earlier median ages-
of-onset are phobias and separation anxiety disorder (ages 15-17) and those with the latest are panic
disorder, major depression, and generalized anxiety disorder (ages 23-30); third, that LMR is
considerably higher than lifetime prevalence for most anxiety-mood disorders, although the magnitude
of this difference is much higher for disorders with later than earlier ages-of-onset; and fourth, that the
ratio of 12-month to lifetime prevalence, roughly characterizing persistence, varies meaningfully in ways
consistent with independent evidence about differential persistence of these disorders.(Kessler et
all.,2012).

Distribution of ancestral secondary cases in anxiety neurosis

The Slater computational model for use in distinguishing between polygenic inheritance and the effects
of a single dominant gene with incomplete penetrance was applied to 15 kindreds of anxiety neurosis
(panic disorder). The number of observed unilateral pairs (two ancestral cases from one side of the
kindred) was significantly greater than the number expected. Therefore, these results suggest a
dominant mode of transmission for anxiety neurosis. (Pauls et all.,1979).

Evidence and place in patient management

Asenapine is a new second-generation antipsychotic approved in September 2010 by the European
Medicines Agency for the treatment of bipolar disorder. It demonstrated significant efficacy compared

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with placebo in acute mania or mixed episodes as monotherapy or adjunctive therapy to mood
stabilizers (lithium or valproate). Early improvement was noted at day 2 and was strongly associated
with response and remission at week 3. Asenapine also appeared effective in treating acute mania in
older patients with bipolar disorder. Post hoc analyses of asenapine showed efficacy in treating
depressive symptoms during manic or mixed episodes compared with placebo. The efficacy of asenapine
in patients with acute mania appeared to remain constant during maintenance treatment. Asenapine
was reasonably well tolerated, especially with regard to metabolic effects. There were minimal signs of
glucose elevation or lipid changes and the risk of weight gain appeared limited. The prolactin elevation
was smaller than other antipsychotic comparators. Only oral hypoesthesia occurred as a new adverse
event compared with other second-generation antipsychotics. Asenapine presents several advantages
over other second-generation antipsychotics, such as sublingual formulation, early efficacy and good
metabolic tolerability. This tolerability profile confirms the heterogeneity of the second-generation
antipsychotic class and supports the view of some authors for the need to re-evaluate the boundaries of
this group. (Samalin et all.,2013).

Mitral valve prolapse in anxiety neurosis

Our purpose was to determine the incidence of mitral valve prolapse in patients with anxiety neurosis or
panic disorder, with symptoms including recurrent anxiety attacks, dyspnea, palpitations, chest pain,
dizziness, and paresthesias. Twenty-one patients and 20 age- and sex-matched normal controls were
studied. Objective cardiac abnormalities were significantly (p < 0.05) more frequent in the patient group
as compared to the control group; these comprised echocardiographic prolapse, ST-T abnormalities on
resting ECG, premature ventricular contractions on exercise ECG, and the combination of echo prolapse
with clicks/murmurs of exercise-induced PVC. We conclude that patients with anxiety neurosis or panic
disorder may also have evidence of an organic abnormality--the mitral prolapse syndrome. (Venkatesh
et all., 1980).

Further evidence for slow binocular rivalry rate as a trait

marker for bipolar disorder

Binocular rivalry refers to a situation where contradictory information is presented simultaneously to

the same location of each eye. This leads to the alternation of images every few seconds. The rate of

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alternation between images has been shown to be slower in euthymic participants with bipolar disorder
than in healthy controls. The alternation rate is not uniformly slowed in bipolar disorder patients and
may be influenced by clinical variables. The present study examined whether bipolar disorder patients
have slower alternation rates, examined the influence of depression and explored the role of clinical
variables and cognitive functions on alternation rate.Method:Ninety-six patients with bipolar disorder
and 24 control participants took part in the study. Current mood status and binocular rivalry
performance were analysed with nonparametric tests. A slow and a normal alternation group were
created by median split. We subsequently explored the distribution of several clinical variables across
these groups. Further, we investigated associations between alternation rate and various cognitive
functions, such as visual processing, memory, attention and general motor speed.Results:The median
alternation rate was significantly slower for participants with bipolar disorder type I (0.39 Hz) and for
participants with bipolar spectrum disorder (0.43 Hz) than for control participants (0.47 Hz). Depression
had no effect on alternation rate. There were no differences between participants with bipolar disorder
type I and type II and in regard to medication regime and predominance of one rivalry image. There
were also no differences in regard to the clinical variables and no significant associations between
alternation rate and the cognitive functions explored.Conclusion:We replicated a slowing in alternation
rate in some bipolar disorder participants. The alternation rate was not affected by depressed mood or
any of the other factors explored, which supports views of binocular rivalry rates as a trait marker in
bipolar disorder.( Vierck et all.,2013)

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Reference:

Gloger S., Grunhaus L., Birmacher B. and Troudart T., 1981. Spontaneous panic attacks with
chlomipramine. Am J Psychiatry. 9:1215-1307.

Grunhaus L., Gloger S. and Weisstub E., 1981. Panic attacks. A review of treatments and
pathogenesis. J Nerv Ment Dis. 10:608-620.

Gruber J., Purcell A.L., Perna M.J. and Mikels J.A.,2012. Emotion in Bipolar Disorder. Ther
Emotion. 3:201-303.

Heiser J.F. and Defrancisco D., 1976. Pathological panic states with propranolol. Am J
Psychiatry. 12:1389-1394.

Kessler R.C., Petukhova M., Sampson N.A., Zaslavsky A.M. and Wittchen H.U., 2012. Morbid
risk of anxiety and mood disorders in the United States. Int J Methods Psychiatr Res. 3:169-84.

Pauls D.L., Crowe R.R. and Noyes R.Jr., 1997 . Distribution of ancestral secondary cases in
anxiety neurosis. J Affect Disord. 4:387-90.

Samalin L., Charpeaud T. and Llorca P.M., 2013. Evidence and place in patient management.
Ther Adv Chronic Dis. 4:5-14.

Venkatesh A., Pauls D.L., Crowe R., Noyes R.Jr., Valkenburg C., Martins J.B. and Kerber
R.E.,1980. Mitral valve prolapse in anxiety neurosis. Am Heart J. 3:302-305.

Vierck E., Porter R.J., Luty S.E., Moor S., Crowe M.T., Carter J.D. and Inder M.L., 2013.
Further evidence for slow binocular rivalry rate as a trait marker for bipolar disorder. Aust N Z J
Psychiatry. available in pubmed.

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