[PAPER

 3:  LIAISON  –  GENERAL  HOSPITAL  PSYCHIATRY]   1

Gynaecological Liaison
Premenstrual Syndrome

PMS is a collection of psychological and somatic symptoms occurring during the

luteal phase of menstrual cycle. Most of the woman (95%) have symptoms are of
mild severity. However 5% suffer with severe symptoms. Severe PMS is classified
as premenstrual dysphoric disorder (PMDD) in DSM-IV – so the treatment for the
both eponyms is the same. The ICD includes “premenstrual tension syndrome”
under the heading “Diseases of the Genitourinary Tract”. PMDD is under
“depressive disorder not otherwise specified” in the DSM-IV, but appendix B
includes following criteria:

Clinical criteria for PMDD. (Adapted from DSM-IV)

In most menstrual cycles during the past year, at least five of the following symptoms should be
present for most of the week of the luteal phase, remitted within a few day after onset of
menses, and remained absent in the week after menses. At least one symptom must be 1, 2, 3,
or 4:

1. Depressed mood or dysphoria

2. Anxiety or tension
3. Irritability
4. Decreased interests in usual activates
5. Others symptoms- Concentration difficulties, marked lack of energy, marked changes in
appetite, overeating, or food craving, insomnia or hypersomnia, feeling overwhelmed ,breast
tenderness, bloating
 Symptoms markedly interfere with work, school, social activity or relationships
 Symptoms are not just an exacerbation of another disorder
 The first three criteria must be confirmed by prospective daily ratings for at least two
consecutive menstrual cycles

Pattern of symptom expression

1. Duration – Few days-2 weeks

2. Peak- 2 days before start of menses
3. Most severe symptoms- Anger and irritability, start earlier that other
symptoms
4. Women have same symptoms from one cycle to the next
5. Severe PMS affects 3-8% women in reproductive age.
6. Comorbidity with mood disorder- 30-70%
7. Risk of developing premenstrual depression and post natal depression
higher
Aetiology

1. Most accepted hypothesis- Increased sensitivity to normal, fluctuation of

gonadal harmones. PMS is not caused due to drop in progesterone
concentration.
2. Serotonin has a role in the pathogenesis. This is supported by following
evidence: serotonin enhancing treatments reduces PMS symptoms,
impairment in serotonin transmission provokes PMS symptoms and
serotonergic transmission is aberrant in women with PMS
3. Imaging studies suggest GABA's role in PMS due interaction between
Progesterone metabolites and GABA A receptors.

Treatment-

Mild symptoms- life style changes, CBT,, exercise or dietary regulation

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Severe PMS-

SRIs

 Response rate 60-90% compared to 30-40% for placebo

 Effective medications are
o Serotonergic tricyclic antidepressant- Clomipramine
o SSRI- Citalopram, Escitalopram, Fluoxetine, Paroxetine and
Sertraline
o SNRI- Venlafaxine
 Effect- Reduces both mood and somatic symptoms, improves quality of life
and social functioning
 First line treatment in PMS patients with severe mood symptoms
 Effect of SRIs in PMS is not just antidepressant effect
 Two most studied SSRI are fluoxetine and Sertraline
 Most effective- Fluoxetine
 Effective within one menstrual cycle – too rapid for antidepressant effect.
 Intermittent dosing during the luteal phase of the menstrual cycle is also
affective. This temporarily increases serotonin concentration during the
luteal phase. Intermittent dosing is effective only in luteal phase, 2 weeks
prior to menses.
 Insomnia, GIT disturbances and fatigue are most common side effect.
 A meta-analysis (Dimmock, 2000) showed an odds ratio of 6·91 (3·90 to
12·2) in favour of SSRIs compared to placebo. The placebo effect was
large too.
 There was no significant difference in symptom reduction between
continuous and intermittent dosing.
Advantages of intermittent dosing:-

 More affective than continues or semi-continues dosing ( Wikander et al.1998)

 Cheaper
 Fewer withdrawal rate due to side effects
 Less frequency and severity of side effects
Disadvantages of intermittent dosing:

 Less effective for somatic than for mood symptoms

 Less effective for somatic symptoms compared to continuous treatment
Note:SSRI does not act on ovarian steroid production and does not cause
ovulation disturbances.

 When SSRIs are used intermittently, discontinuation symptoms are rarely

present
SSRI in Depression SSRI in PMS
High frequency of sexual side effects Low frequency of sexual side effects
Continues dosing more effective Intermittent dosing more effective
Effective in three -four weeks Effective in few days
Receptor site difference than PMS Receptor site difference than PMS
Akathasia,increased suicidal ideation reported No reports of akathisia or increased suicidal ideation

 Other psychoactive drugs- Not effective, Alprazolam can used with caution
in premenstrual insomnia and overwhelming anxiety
 The use of evening primrose oil seems to be ineffective
 Calcium carbonate has been shown to decrease total symptom scores by
48% compared with a 30% reduction seen in the group on placebo.
 Vitamin B6 is about twice as likely as placebo to relieve symptoms of PMS.
But evidence is weak.
 Phototherapy has equivocal results.
 Hormonal- This treatment suppress the ovulation-Long acting GnRH
agonist, Oestrogen and certain new contraceptives; should be used only

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as a last resort because of the potential implications of introducing early

menopause in these women
Prognosis:-

1. Remission rates are low on cessation of treatment.

2. PMS can last until the menopause.
Note- Trials had large placebo effects; hence uncontrolled trials for PMS result
may not be valid

Yonkers et al. Prémenstrual syndrome. Lancet 2008;371;1200-10

Dimmock et al. Efficacy of selective serotonin- reuptake inhibitor in premenstrual

syndrome: a systemic review. The lancet 2000; 356: 1131-36

Wikander et al. Citalopram in premenstrual dysphoria: is intermittent treatment treatment

during luteal phases more effective than continuous medication throughout the menstrual
cycle J Clin psychopharmacology 1998;18: 390-98

Cardiology Liaison
Myocardial infarction and depression

 20% of patients with coronary heart disease have comorbid depression

 Patients who have persistent depression, despite treatment, may be at
increased cardiac risk.
 Some evidence that depression is a risk factor for cardiovascular morbidity
and mortality in patients with coronary heart disease
 So far, however, only two clinical trials have been conducted to determine
whether treating depression reduces the risk for cardiac events following a
recent acute myocardial infarction:
o the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study
o the Myocardial Infarction and Depression Intervention Trial (MIND-IT)
 In the primary analyses, both the ENRICHD and MIND-IT interventions
had only modest effects on depression and neither of them improved
survival.
 The Sertraline Antidepressant Heart Attack Randomized Trial (SADHART)
is to date the largest randomized trial evaluating use of an antidepressant
medication for depressed patients with heart disease.
o Sertraline vs placebo 16-week trial.
o no difference in safety (change in left ventricular ejection fraction, increase in
premature ventricular contractions, or prolongation of the QT interval) between the
treatment and placebo groups
o A nonsignificant reduction in the composite end point (MI or CHD death) in the
sertraline group (relative risk, 0.77; 95% confidence interval, 0.51-1.16).
o SSRIs may be directly cardioprotective by reducing platelet activation.
o But there was little difference in depression status between groups receiving
sertraline and placebo after 24 weeks of treatment. However, the effect of sertraline
was greater in the patients with severe and recurrent depression.
Heart failure and depression: The prevalence rates of clinically significant
depression among CHF patients is approximately 21.5%, determined using meta-analytic
tests. Thus the risk of clinical depression in CHF is 2 to 3 times the rate of the general
population. Substantially higher rates of clinically significant depression are present among
patients assessed with questionnaires (vs. diagnostic interviews) or with more severe CHF.
A higher prevalence is associated with higher NYHA functional class. Females have higher
prevalence of depression than males with CHF. This high rate is similar to the rate of
depression seen in CAD/Post MI patients. It appears that the relative risk of mortality in
patients with CHF who are depressed is about 2:1 when compared to the risk in non-
depressed CHF patients. Rates clinical events, rehospitalization, and general health care
use are markedly higher among CHF patients reporting more severe depression.

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Depression is nearly 3 times more common in patients after an acute myocardial infarction
(irrespective of the presence of CHF) than in the general community.

van Melle, J.P. et al (2007) Effects of antidepressant treatment on long-term depression

status and cardiac prognosis in depressed MI patients. British Journal of Psychiatry, 190,
460-466.

Rutledge, T., et al (2006). Depression in Heart Failure: A Meta-Analytic Review of

Prevalence, Intervention Effects, and Associations With Clinical Outcomes. J Am Coll
Cardiol, 48(8), 1527-1537

Endocrinology Liaison
(Levenson, JL. Psychiatric issues in endocrinology. Primary Psychiatry. 2006;13(4):27-30)

Hyperthyroidism:

 Symptoms: sweating, fatigue, heat intolerance, weight loss, weakness,

fine tremor, and tachycardia.
 Psychiatric symptoms – most commonly generalized anxiety;
depression, irritability, hypomania, and cognitive dysfunction are also
noted.
 If severe (thyrotoxicosis) – mania may occur.
Hypothyroidism:

 M:F ratio is 1:6 (source: Kumar & Clark Textbook of Medicine 6edn p
1077)
 Symptoms: weakness, fatigue, cold intolerance, weight gain,
constipation, and somnolence.
 Psychiatric symptoms - depression (often misdiagnosed as major
depressive disorder and hypothyroidism may be missed), also cognitive
dysfunction is noted.
 Psychosis may be seen in severe cases (myxedema madness).
 Subclinical hypothyroidism - a risk factor for depression and rapid
cycling in bipolar disorder.
Hyperparathyroidism:

 Symptoms directly proportional to serum calcium levels.

 At mild-moderate (10–14 mg/dL) - depression, apathy, irritability, lack
of initiative, and lack of spontaneity.
 If severe (>14 mg/dL) - delirious with psychosis, catatonia, or lethargy,
progressing to coma.
Hypoparathyroidism:

 Symptoms directly proportional to serum calcium levels.

 In mild hypocalcemia - patients have anxiety, paresthesias, irritability,
and emotional lability.
 If severe - mania, psychosis, tetany, and seizures may occur.
Cushing’s syndrome: (Cortisol excess)

 Most commonly results from exogenous corticosteroids

 ACTH secretion by a pituitary tumour is called Cushing’s disease
 Corticosteroid secretion by an adrenal adenoma is also a possible cause.
 Physical symptoms include diabetes, hypertension, muscle weakness,
obesity, and osteopenia
 Psychiatric symptoms may appear before physical signs. Depression is
most common, followed by anxiety, hypomania/mania, psychosis, and
cognitive dysfunction.
 Exogenous steroid produce more mania than endogenous steroids.

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 Psychiatric effects are often dose related.

Addison’s disease: (Cortisol depletion)

 Psychiatric symptoms - apathy, anhedonia, fatigue, and depressed

mood.
 May be misdiagnosed as major depressive disorder.
 Anorexia is common in both, but presence of nausea, vomiting and skin
changes (dark pigmentation in some) should suggest Addison’s disease.
Acromegaly:

 Due to growth hormone excess.

 Psychiatric symptoms include mood lability, personality change, and
depression.
 Psychosis may be due to treatment with dopamine agonists such as
bromocriptine.
Pheochromocytoma:

 Catecholamine-secreting tumour.
 Physically - tachycardia, labile hypertension, headache, sweating, and
palpitations - episodic.
 May mimic panic attacks.
 Screening by testing for urinary catecholamines (Vanillyl mandelic acid,
metanephrines)
 The best diagnostic test is a plasma metanephrine level which is more
specific.
Diabetes:

 Depression is 2–3 times more common in diabetics than in the general

population
 Depressed diabetics have poorer glycemic control and increased diabetic
complications
 An increased prevalence of diabetes type 2 is seen in patients with
bipolar disorder
 Diabetes is 2–4 times more common in patients with schizophrenia than
in the general population.
 Permanent cognitive dysfunction in diabetics rarely results from
recurrent hypoglycaemia; but frequent hyperglycemic episodes results in
cognitive dysfunction due to cerebral micro- and macrovascular damage.

Other consultations

Palliative liaison:

(from Dein, 2003)

 Prevalence of major depression in those with advanced cancer = 5–15%.

 10–15% present with less severe symptoms
 Somatic symptoms are not useful when diagnosing depression
 Pervasive global anhedonia, is more valid criterion for the diagnosis of
depression
 SSRIs (not much evidence) low dose amitriptyline (avoid in delirium risk;
useful if neuropathic pain) lofepramine and rapid-acting psychostimulant
such as dexamphetamine or methylphenidate (in a patient who has only
weeks of life) are useful.
 Delirium is common in palliative care settings. The prevalence is around

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44% in cancer in-patients, rising to 62% shortly before death.

 It may be either hypoactive – sedated subtype or hyperactive agitated
type.
 The aetiology is usually multi-factorial and a specific aetiology is
discovered in less than 50% of terminally ill patients with delirium
 Though small dose of haloperidol or lorazepam is frequently used, they are
not always successful in controlling the symptoms, especially in sedated
subtype.

Renal liaison:

(from Phipps & Turkington, 2001)

Psychotropics:

 Benzodiazepines should be used with caution

 The half-life of diazepam remains unchanged in end-stage renal disease
but its metabolite, desmethyldiazepam, may accumulate, causing
excessive sedation.
 The half-life of lorazepam is increased from 8–25 hours in normal adults to
32–72 hours in end-stage renal disease
 At a low level of renal function lorazepam dosage should be reduced by
50% to avoid excessive sedation.
 Imipramine and amitriptyline can be given at their usual dosage as renal
impairment does not increase their half-lives
 Half normal dose is used for citalopram in patients with renal impairment
or in elderly
 Half-life of paroxetine is considerably increased in severe renal
impairment, requiring dosage reduction.
 The dosage of fluoxetine and fluvoxamine does not have to be reduced in
the elderly or patients with renal impairment
 Sertraline manufacturers do not recommend it in renal impairment
 Haloperidol does not require dose reduction in renal impairment unless
excessive sedation or hypotension occurs.
 Amisulpride is renally excreted almost exclusively. Hence renal failure will
be a relative contraindication to use this drug. Product monograph suggest
alternate day dosing or dose reduction if no other alternatives are
possible.
 Risperidone and its active metabolite 9-hydroxy-risperidone are
substantially excreted in the urine, so that in renal impairment the
elimination half-life is prolonged
 Lithium is best avoided or given at low dosages.
Neuropsychiatric problems:

 Uraemic encephalopathy
o Occurs when the glomerular filtration rate (GFR) falls to 10% of
normal.
o The rate of onset is proportional to the rate at which the GFR falls
and
o The effects cause problems in cognition, psychomotor activity and
personality, with vomiting, restlessness, myoclonus and coma,
leading to death.
o This condition is reversible by treatment of the underlying disease,
dialysis or renal transplant
 Dialysis disequilibrium syndrome
o It is a temporary clinical disorder that may occur during or after the
first few dialysis treatments.

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o It is more common among younger patients

o High incidence among those with pre-existing neurological
problems such as cerebral trauma and recent stroke.
o Mild symptoms include headache and restlessness, which may be
followed by nausea, vomiting, hypertension, tremor, disorientation
and seizures
o The condition is now much less common with improved dialysis
technology.
o Most of the symptoms produced are secondary to cerebral oedema.

Dental liaison:

The term atypical facial pain was first introduced by Frazier and Russell in 1924.
The pain is atypical in its distribution, unilateral and poorly localised – not fitting
with any cranial neuralgia. It lasts most of the day and is described as a severe
ache, crushing or burning sensation. The Headache Classification Subcommittee
of the International Headache Society (2004) described persistent idiopathic
facial pain (PIFP) as

• Pain is in the face.

• Pain is present daily and persists for all or most of the day.
• Pain is confined at onset to a limited area on one side of the face, deep
ache, and poorly localized.
• In addition, the pain is not associated with sensory loss or other physical
signs, with no abnormalities in laboratory or imaging studies.
Psychiatric symptoms of depression and anxiety are prevalent in this population.
Treatment is very difficult and requires a multidisciplinary approach to address
the many facets of this pain syndrome. Pain disorder is one of several
somatoform disorders described in the revised DSM-IV-TR.

Lyme’s disease:

Lyme disease is caused by Borrelia burgdorferi, transmitted via wooden tick bite
which normally lives on deers. A red spot develops initially around the location
(crotch or armpit). This will develop a central clearing called erythema migrans
within 4 weeks. About 15% develop neuroborreliasis, where CNS is affected. Back
pain worse at night, facial numbness and facial palsy may dvelop.

Patients with late-stage Lyme disease may present with a variety of neurological
and psychiatric problems, ranging from mild to severe. These include:

• Cognitive deficits especially

Memory impairment or loss (“brain fog”)
Dyslexia and word-finding problems
Visual/spatial processing impairment
Slowed processing of information
• Psychosis
• Seizures
• Violent behavior, irritability
• Anxiety
• Depression
Neuroborreliosis can mimic virtually any type of encephalopathy or psychiatric
disorder and is often compared to neurosyphilis.
This is rare in UK; more common in North America.

SLE psychiatry:

(from gpnotebook)

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Systemic lupus erythematosus is the classic prototype of a multisystem disease of

autoimmune origin. It is non-organ specific and characterised by vasculitis and
anti-nuclear antibodies (ANA). Acute or insidious in its onset, it is a chronic,
remitting and relapsing, often febrile illness characterised principally by injury to
the skin (butterfly rash in middle aged woman), joints, kidney and serosal
membranes. CNS manifestations are:

1. peripheral neuropathy - including rarely, the Guillain Barre syndrome

2. seizures - grand mal most common; other types rare
3. movement disorders such as chorea and choreoathetosis
4. impaired memory, perception, orientation and intellectual function
5. severe headaches
6. stroke
7. B-cell lymphoma
8. limbic encephalitis-type picture
9. psychological disturbance:
a. particularly depression and anxiety
b. particularly in recently diagnosed patients and those with
disfiguring skin lesions
c. psychosis can also occur”
Ca Pancreas - insulinoma:

Insulinoma is one of the most common neuro-endocrine tumors of the pancreas.

Some cases with insulinoma present with neuropsychiatric symptoms and are
often misdiagnosed as psychosis / depression. Patients with insulinomas usually
have recurrent headache, lethargy, diplopia, and blurred vision, particularly with
exercise or fasting.

Neurosarcoidosis:

Idiopathic granulomas in various tissues – mainly lungs and mediastinal node.

May affect CNS especially cranial nerves producing bilateral facial palsy.
Depression is seen in 20%. Rarely psychosis can occur. Patients may have
erythema nodosum on their shin – a cutaneous sign. ACE levels in blood are
elevated due to macrophage activity. Treatment is with immunosuppression.

Metachromatic leucodystrophy:

http://www.ninds.nih.gov/disorders/metachromatic_leukodystrophy/metachroma
tic_leukodystrophy.htm

“Metachromatic leukodystrophy (MLD) impairs the growth or development of the

myelin sheath, and is caused by genetic defects of the enzyme arylsulfatase A.
MLD is one of several lipid storage diseases. There are three forms of MLD: late
infantile, juvenile, and adult. In the late infantile form, which is the most common
MLD, affected children have difficulty walking after the first year of life.
Symptoms include muscle wasting and weakness, muscle rigidity, developmental
delays, progressive loss of vision leading to blindness, convulsions, impaired
swallowing, paralysis, and dementia. Children may become comatose. Most
children with this form of MLD die by age 5. Children with the juvenile form of
MLD (between 3-10 years of age) usually begin with impaired school
performance, mental deterioration, and dementia and then develop symptoms
similar to the infantile form but with slower progression. The adult form
commonly begins after age 16 as a psychiatric disorder or progressive dementia.
Adult-onset MLD progresses more slowly than the infantile form”. Features of
adult form include:

 Mental deterioration

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 Impaired concentration
 Depression
 Psychiatric disturbances
 Ataxia
 Tremor
 Dementia

Nearly 60% of adolescent onset cases have schizophrenia like psychosis – this is
not seen in younger onset cases.

Neuroacanthocytosis:

Genetically heterogenous neurologic disorders characterized with acanthocytosis.

Neurologic problems usually consist of either movement disorders or ataxia,
personality changes, cognitive deterioration, axonal neuropathy, and seizures.
Acanthocytosis refers to a certain percentage of the patients' erythrocytes
(typically 10-30%) having an unusual starlike appearance with spiky- or thorny-
appearing projections. Personality changes include impulsivity, distractibility,
anxiety, depression, apathy, loss of introspection, and compulsivity.

A peculiar gait is characterized by lurching with long strides and quick,

involuntary knee flexion is seen. Seizures, generally tonic-clonic are noted. A
subcortical dementia may set in.

http://www.emedicine.com/neuro/topic246.htm

Phipps, A & Turkington, D. Psychiatry in the renal unit. Advances in Psychiatric Treatment
(2001) 7: 426-432

Dein, S. Psychiatric liaison in palliative care. Advances in Psychiatric Treatment (2003) 9:

241-248

Zahl, D., Hawton, K. (2004) Repetition of deliberate self-harm and subsequent suicide risk:
a long-term follow-up study in 11,583 patients. British Journal of Psychiatry, 185, 70-75

Safety first document; 2001. Dept of Health.

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