Professional Documents
Culture Documents
Investigations are carried out in clinical practice either to confirm a diagnosis or to sort out
differential diagnoses indicated by clinical history and examination. In psychiatric practice,
mostly, investigations are needed to exclude a medical condition or an organic aetiology
suspected to have caused behavioral symptoms simulating a functional psychiatric disorder.
Investigations are also carried out as “routine investigations” to assess comorbid general
medical conditions and to obtain baseline functions of certain organs or body systems to
monitor the side effects of the prescribed psychotropic medicines.
PURPOSES:
a. Clinical assessment
A psychiatric assessment is most commonly carried out for clinical and therapeutic purposes,
to establish a diagnosis and formulation of the individual's problems, and to plan their care
and treatment. This may be done in a hospital, in an out-patient setting, or as a home-based
assessment.
b. Forensic assessment
A forensic psychiatric assessment may have a number of purposes. A forensic assessment
may be required of an individual who has been charged with a crime, to establish whether the
person has the legal competence to stand trial. If a person with a mental illness is convicted of
an offense, a forensic report may be required to inform the Court's sentencing decision, as a
mental illness at the time of the offense may be a mitigating factor. A forensic assessment
may also take the form of a risk assessment, to comment on the relationship between the
person's mental illness and the risk of further violent offenses.
c. Medico legal assessment :
A medico-legal psychiatric assessment is required when a psychiatric report is used as
evidence in civil litigation, for example in relation to compensation for work-related stress or
after a traumatic event such as an accident. The psychiatric assessment may be requested in
order to establish a link between the trauma and the victim's psychological condition, or to
determine the extent of psychological harm and the amount of compensation to be awarded to
the victim.
Medico-legal psychiatric assessments are also utilized in the context of child safety and child
protection services. A child psychiatrist's assessment can provide information on the
psychological impact of abuse or neglect on a child. A child psychiatrist can carry out an
assessment of parenting capacity, taking into consideration the mental state of both the child
and the parents, and this may be used by child protective services to decide whether a child
should be placed in an alternative care arrangement such as foster care
I. LABORATORY INVESTIGATIONS IN
PSYCHIATRY :
Investigation are useful to detect alteration in biologic function & to screen for medical
disorders causing psychiatric symptoms. A logical and systematic approach to the use of
medical assessment and laboratory testing by the psychiatrist is vital to achieving the goals of
arriving at accurate diagnoses, identifying medical comorbidities, implementing appropriate
treatment, and delivering cost-effective care. With respect to the diagnosis or management of
medical disease, consultation with colleagues in other specialties is important. Good
clinicians recognize the limits of their expertise and the need for consultation with their non
psychiatric colleagues.
A. LABORATORY STUDIES :
a) TOXICOLOGY STUDIES
Testing to determine blood concentrations of certain psychotropic medications enables the
clinician to ascertain whether blood levels of medications are at therapeutic, sub therapeutic,
or toxic levels. Psychiatric symptoms are not uncommon when prescribed medications are at
toxic levels. In the debilitated and the elderly, pathological symptoms may occur at
therapeutic concentrations. The normal reference range varies between laboratories. It is
important to check with the laboratory performing the test to obtain the normal reference
range for that laboratory.
Testing for drugs of abuse is usually performed on urine specimens. It also may be performed
on specimens of blood, breath (alcohol), hair, saliva, and sweat. Urine screens provide
information about recent use of frequently abused drugs such as alcohol, amphetamines,
cocaine, marijuana, opioids, and phencyclidine along with 3,4-
methylenedioxymethamphetamine (MDMA) (ecstasy). Many substances may produce false
positives with urine drug screening tests. When a false positive is suspected, a confirmatory
test may be requested.
Tested Substances : Routine tests are available for phencyclidine (PCP), cocaine,
tetrahydrocannabinol (THC; also known as marijuana), benzodiazepines, methamphetamine
and its metabolite amphetamine, morphine (Duramorph), codeine, methadone (Dolophine ),
propoxyphene (Darvon), barbiturates, lysergic acid diethylamide (LSD), and MDMA. Drug
screening tests may have high false-positive rates. This is often due to the interaction of
prescribed medication with the test, resulting in false-positive results and lack of
confirmatory testing. False-negative tests are common as well. False-negative results may be
due to problems with specimen collection and storage.
Acetaminophen
Acetaminophen may produce hepatic necrosis, which in some cases may be fatal.
Acetaminophen is one of the most frequently used agents in intentional drug overdoses and is
a common cause of overdose related deaths. Toxicity is associated with levels greater than 5
mg/dL (>330 µmol/L) in patients without pre existing liver disease. Chronic abusers of
alcohol are particularly vulnerable to the effects of overdose. Acetylcysteine (Mucomyst)
treatment must occur promptly after overdose to prevent hepatotoxicity.
Salicylate Toxicity
Aspirin is frequently ingested in overdose. Consequently, serum salicylate levels often are
obtained in overdose cases. Some rheumatic patients may chronically ingest large amounts of
salicylate for therapeutic reasons. Ingestion of 10 to 30 g of aspirin may be fatal. Most
patients will develop symptoms of toxicity when salicylate levels are greater than 40 mg/dL
(2.9 mmol/L). Common symptoms of toxicity include acid-base abnormalities, tachypnea,
tinnitus, nausea, and vomiting. In cases of severe toxicity, symptoms may include
hyperthermia, altered mental status, pulmonary edema, and death.
Antipsychotic Agents
Clozapine (Clozaril) levels are trough levels determined in the morning before administration
of the morning dose of medication. A therapeutic range for clozapine has not been
established; however, a level of 100 mg/mL is widely considered to be the minimum
therapeutic threshold. At least 350 mg/mL of clozapine is considered to be necessary to
achieve therapeutic response in patients with refractory schizophrenia. The likelihood of
seizures and other side effects increases with clozapine levels greater than 1,200 mg/mL or
doses greater than 600 mg per day or both. Clozapine is a common cause of a leukopenia in
psychiatry. When moderate to severe leucopenia develops, clozapine treatment must be
interrupted, but patients may be retreated with clozapine in the future.
Mood Stabilizers
Carbamazepine (Tegretol) may produce changes in the levels of white blood cells,
platelets, and, under rare circumstances, red blood cells. Anemia, aplastic anemia,
leucopenia, and thrombocytopenia may all occur but are rare. Pretreatment
evaluations typically include CBC. Carbamazepine may produce hyponatremia. This
hyponatremia is usually mild and does not produce clinical symptoms. However,
carbamazepine may cause the syndrome of inappropriate secretion of antidiuretic
hormone (SIADH). Carbamazepine may produce a variety of congenital
abnormalities, including spina bifida and anomalies of the fingers. Manifestations of
toxicity may include nausea, vomiting, urinary retention, ataxia, confusion,
drowsiness, agitation, or nystagmus. At very high levels, symptoms may also include
cardiac dysrhythmias, seizures, and respiratory depression.
Lithium (Eskalith) has a narrow therapeutic index. Consequently, blood levels of
lithium must be monitored to achieve therapeutic dosing and avoid toxicity. Side
effects are dose dependent. Symptoms of toxicity include tremors, sedation, and
confusion. At higher levels delirium, seizures, and coma may occur. Symptoms of
toxicity may begin to manifest with serum levels of greater than 1.2 mEq/L and are
common with levels greater than 1.4 mEq/L. Elderly or debilitated patients may show
signs of toxicity with levels less than 1.2 mEq/L.
Valproate. Because of the risk of hepatotoxicity, ranging from mild dysfunction to
hepatic necrosis, pretreatment liver function tests are usually obtained. More
commonly valproate (valproic acid [Depakene] and divalproex [Depakote]) may
cause a sustained elevation in liver transaminase levels of as much as three times the
upper limit of normal. Valproate may increase the risk of birth defects. A pre
treatment urine pregnancy test is usually obtained in women of childbearing years.
Women should be cautioned to use adequate contraception.
Antidepressants
Monoamine Oxidase Inhibitors: Treatment with monamine oxidase inhibitors
(MAOis) can cause orthostasis and, rarely, hypertensive crisis. Baseline blood
pressure measurement should be obtained before the initiation of treatment, and blood
pressure should be monitored during treatment. There are no meaningful blood levels
for MAOis, and direct monitoring of MAOI blood levels is not clinically indicated.
Treatment with MAOis is occasionally associated with hepatotoxicity. For this reason,
liver function tests usually are obtained at the initiation of treatment and periodically
after.
Tricyclic and Tetracyclic Antidepressants: Routine laboratory studies obtained
before initiation of tricyclic or tetracyclic antidepressants (TC As) typically include
CBC, serum electrolytes, and liver function tests. Because TCAs affect cardiac
conduction, clinicians also may obtain an electrocardiogram (ECG) to assess for the
presence of abnormal cardiac rhythms and prolonged PR, QRS, and QTc complexes
before initiation of these medication.
c) ENDOCRINE EVALUATIONS
Endocrine disease is of great relevance to psychiatry. Management of psychiatric
illness is complicated by comorbid endocrine disease. Endocrine illness frequently
has psychiatric manifestations. For these reasons, screening for endocrine disease is
often of relevance to the psychiatrist.
Adrenal Disease
Adrenal disease may have psychiatric manifestations, including depression, anxiety,
mania, dementia, psychosis, and delirium. However, patients with adrenal disease
rarely come to the attention of psychiatrists.
Low plasma levels of cortisol are found in Addison's disease. These patients may
have symptoms that are also common in psychiatric conditions including fatigue,
anorexia, weight loss, and malaise. Patients may also have memory impairment,
confusion, or delirium. Depression or psychosis with hallucinations and delusions
may occur.
Elevated levels of cortisol are seen in Cushing's syndrome. About half of all patients
with Cushing's syndrome develop psychiatric symptoms. These symptoms may
include !ability, irritability, anxiety, panic attacks, depressed mood, euphoria, mania,
or paranoia.
Cognitive dysfunctions may include cognitive slowing and poor short-term memory.
Symptoms usually improve when cortisol normalizes. If not, or if symptoms are
severe, psychiatric treatment may be necessary. In particular, the dexamethasone-
suppression test (DST) remains a research tool in psychiatry that is not used in routine
clinical care.
Antidiuretic Hormone
Arginine vasopressin (AVP), also called antidiuretic hormone (ADH), is decreased in central
diabetes insipidus (DI). DI may be central (due to the pituitary or hypothalamus) or
nephrogenic. Nephrogenic DI may be acquired or due to an inherited X-linked condition.
Lithium induced DI is an example of an acquired form of DI. Lithium has been shown to
decrease the sensitivity of renal tubules to AVP. Patients with central DI respond to the
administration of vasopressin with a decrease in urine output. Secondary central DI may
develop in response to head trauma that produces damage in the pituitary or hypothalamus.
Excessive secretion of A VP results in increased retention of fluid in the body. This
condition is called SIADH. Water retention in SIADH causes hyponatremia. SIADH may
develop in response to injury to the brain or from medication administration (including
phenothiazines, butyrophenones, carbamazepine, and oxcarbazepine ). The hyponatremia
associated with this condition may produce delirium.
Para hormone
Para hormone (parathyroid hormone) modulates serum concentrations of calcium and
phosphorus. Deregulation in this hormone and the resulting production of abnormalities in
calcium and phosphorus may produce depression or delirium.
Prolactin
Prolactin levels may become elevated in response to the administration of antipsychotic
agents. Elevations in serum prolactin result from the blockade of dopamine receptors in the
pituitary. This blockade produces an increase in prolactin synthesis and release. Cerebral
MRI is not usually performed if the patient is taking an antipsychotic drug known to cause
hyperprolactinemia, and the magnitude of the prolactin elevation is consistent with drug-
induced causes. Prolactin levels may briefly rise after a seizure. For this reason, prompt
measurement of a prolactin level after possible seizure activity may assist in differentiating a
seizure from a pseudoseizure.
Thyroid Hormone
Disease of the thyroid is associated with many psychiatric manifestations. Thyroid disease is
most commonly associated with depression and anxiety but may also give rise to symptoms
of panic, dementia, and psychosis. Thyroid disease may mimic depression. It is difficult to
achieve euthymia if a patient is not euthyroid.
Pancreatic Function
Measurement of serum amylase is used to monitor pancreatic function. Elevations in amylase
levels may occur in alcohol-abusing patients who develop pancreatitis. Serum amylase levels
also may be fractionated into salivary and pancreatic components.
d) CLINICAL CHEMISTRY
Serum Electrolytes
Serum electrolyte levels may be useful in the initial evaluation of a psychiatric
patient. Levels of serum electrolytes often are abnormal in patients with delirium.
Abnormalities also may occur in response to the administration of psychotropic
medications.
Low serum chloride levels may occur in eating disorder patients who purge by self-
induced vomiting. Serum bicarbonate levels may be elevated in patients who purge or
who abuse laxatives. Bicarbonate levels are commonly low in patients who
hyperventilate in response to anxiety.
Hypokalaemia may be present in eating disorder patients who purge or abuse
laxatives and in psychogenic vomiting. Diuretic abuse by eating disorder patients also
may produce hypokalaemia.
Low levels of potassium are associated with weakness and fatigue. Characteristic
ECG changes occur with hypokalaemia and consist of cardiac arrhythmias, U waves,
flattened T waves, and ST-segment depression.
Eating disorder patients with anorexia nervosa or bulimia nervosa usually receive a
fairly standard set of laboratory studies, including serum electrolytes (particularly
potassium and phosphorus), blood glucose, thyroid function tests, liver enzymes, total
protein, serum albumin, BUN, Cr, CBC, and ECG. Serum amylase is often assessed
in bulimic patients.
Magnesium levels may be low in alcohol-abusing patients. Low magnesium levels are
associated with agitation, confusion, and delirium. If untreated, convulsions and coma
may follow.
Low levels of serum phosphorus may be present in eating disorder patients with
purging behavior. Phosphorus levels may also be low in anxiety patients who
hyperventilate. Hyperparathyroidism may produce low serum phosphorus levels.
Elevated serum phosphorus levels are seen in hypo para thyroidism.
Hyponatremia is seen in psychogenic polydipsia and SIADH and in response to
certain medications, such as carbamazepine.
Low sodium levels are associated with delirium. Serum calcium abnormalities are
associated with a variety of behavioral abnormalities. Low serum calcium levels are
associated with depression, delirium, and irritability.
Elevated levels are associated with depression, psychosis, and weakness. Laxative
abuse, common in eating disorder patients, can be associated with hypocalcemia.
Hypocalcemia secondary to hypoparathyroidism may occur in patients who have
undergone surgery for thyroid disease.
Serum copper levels are low in Wilson's disease, a rare abnormality in copper
metabolism. Copper is deposited in the brain and liver, resulting in decreased
intellectual functioning, personality changes, psychosis, and a movement disorder.
Symptoms are usually present in the second and third decades of life.
Laboratory assessment for Wilson's disease includes the measurement of serum
ceruloplasmin, the transport protein for copper, which is low, and urine copper,
measured in a 24-hour specimen, which is elevated.
Renal Function
Tests of renal function include BUN and Cr. Other relevant laboratory studies include
the routine urinalysis and Cr clearance. An elevated BUN often results in lethargy or
delirium. BUN commonly is elevated with dehydration. Elevations in BUN often are
associated with impaired clearance of lithium.
A less sensitive index of renal function is Cr. Elevations in Cr may indicate extensive
renal impairment. Elevated levels occur when approximately 50 percent of the
nephrons are damaged. Cr clearance is often assessed in patients taking lithium. It is a
sensitive measurement of renal function. The test is performed in a well-hydrated
patient by collecting all of the patient's urine for 24 hours.
During the midpoint of the 24-hour collection period, a serum Cr level also is
obtained. The resulting data are used to calculate the patient's Cr clearance. Usually,
the laboratory performs the calculation.
Elevated levels of porphobilinogen are found in the urine of symptomatic patients
with acute intermittent porphyria. Symptoms of this disease include psychosis,
apathy, or depression, along with intermittent abdominal pain, neuropathy, and
autonomic dysfunction.
If urine porphobilinogen levels are elevated when the patient is symptomatic,
collection of a 24-hour urine specimen for quantitative assessment of porphobilinogen
and aminolevulinic acid is indicated.
Liver Function
Liver function tests (LFTs) commonly include the serum aminotransferases, alkaline
phosphatase, y-glut amyl trans peptidase and tests of synthetic function, usually the
serum albumin concentration and prothrombin time, and the serum bilirubin, which
reflects hepatic transport capability.
Elevations in AST may occur with diseases of the liver, heart, lungs, kidneys, and
skeletal muscle. In patients with alcohol-induced liver disease, AST typically is more
elevated than ALT. In viral- and drug-induced liver disease, ALT is often elevated.
Serum GGT is elevated in hepato biliary disease, including alcohol-induced liver
disease and cirrhosis.
Alkaline phosphatase elevations occur in many diseases, including diseases of the
liver, bone, kidney, and thyroid. Levels of alkaline phosphatase may be elevated in
response to some psychiatric medications, most notably the phenothiazine's.
Serum ammonia levels are often elevated in patients with hepatic encephalopathy.
High levels are associated with the delirium of hepatic encephalopathy. Serum
ammonia levels also may be elevated in patients undergoing treatment with valproate.
Serum bilirubin is an index of hepatic and bile duct function.
Pre hepatic, unconjugated, or indirect bilirubin and post hepatic, conjugated, or direct
bilirubin are often assessed to help elucidate the origin of the elevation in bilirubin.
Lactate dehydrogenase (LDH) may be elevated in diseases of the liver, skeletal
muscle, heart, and kidney. It is also elevated in pernicious anaemia.
Vitamins Folate and B12
Folate and B12 deficiencies are common in patients who abuse alcohol. Folate and B12
deficiencies are associated with dementia; delirium; psychosis, including paranoia; fatigue;
and personality change. Folate and B12 can be directly measured. Low folate levels may be
found in patients who use contraceptive pills or other forms of oestrogen, who drink alcohol,
or who take phenytoin (Dilantin).
Syphilis
The fluorescent treponemal antibody absorption (FTA-ABS) test detects antibody against
Treponema pallidum spirochetes and is more sensitive and specific than nontreponemal tests
for syphilis. The test is used to confirm positive screening tests for syphilis, such as the rapid
plasma reagin (RPR) test and the VDRL test. The FTA-ABS test is also used when
neurosyphilis is suspected. Once positive, a patient usually remains so for life. False-positive
results may occur in patients with SLE.
Viral Hepatitis
Several types of viruses can cause viral hepatitis. Viral hepatitis produces abnormalities in
LFTs including elevation of liver enzymes, especially ALT. Symptoms range from mild flu-
like manifestations to rapidly progressive and fatal liver failure. Psychiatric manifestations
include depression, anxiety, weakness, and psychosis. Viral hepatitis can also impair the
metabolism of psychotropic medications that are metabolized by the liver. Impaired liver
metabolism requires an adjustment of the dose of medications metabolized by the liver or
consideration of agents that are less affected by alterations in liver metabolism. Viruses
causing hepatitis include: hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus
(HCV), and hepatitis D virus (HDV) (delta agent).
Chronic hepatitis, characterized by elevated aminotransferase levels for more than 6 months,
develops in 1 to 2 per cent of Immuno competent adults with acute hepatitis B. More than 80
per cent of all persons with acute hepatitis C develop chronic hepatitis, which, in many cases,
progresses slowly. Ultimately, cirrhosis develops in as many as 30 per cent of those with
chronic hepatitis C and 40 per cent of those with chronic hepatitis B; the risk of cirrhosis is
even higher in patients co infected with both viruses or with HIV. Patients with cirrhosis are
at risk, with a rate of 3 to 5 per cent per year, of hepatocellular carcinoma. Even in the
absence of cirrhosis, patients with chronic hepatitis B-particularly those with active viral
replication are at an increased risk.
Muscle Injury
Serum CK levels may rise in response to repeated intramuscular (IM) injections, prolonged or
agitated periods in restraint, or NMS. Dystonic reactions from neuroleptic administration may
also result in elevated levels of CK.
g) ELECTROCONVULSIVE THERAPY
Electroconvulsive therapy (ECT) is usually reserved for patients with the most treatment-
resistant depression. Typical laboratory tests obtained before the administration of ECT
include a CBC, serum electrolytes, urinalysis, and liver function tests. However, no specific
laboratory tests are required in the pre-ECT evaluation. Usually, an ECG is also obtained. A
spinal X-ray series is no longer considered routinely indicated because of the low risk of
spinal injury associated with modern administration techniques that use paralyzing agents. A
comprehensive medical history and physical examination are useful screening tools to
identify possible conditions that could complicate treatment.
h) ELECTROCARDIOGRAM
The ECG is a graphical representation of the electrical activity of the heart. Abnormalities in
this activity correlate with cardiac pathology. The ECG is most commonly used in psychiatry
to assess side effects of psychotropic medications.
Ziprasidone (Geodon) has been associated with a dose related prolongation of the
QTc interval. There is a known association of fatal arrhythmias (e.g., torsades de
pointes) with QTc prolongation from some other medications. For this reason,
clinicians usually obtain an ECG before initiation of treatment with ziprasidone.
Like ziprasidone, thioridazine (Mellaril) has been associated with prolongation of the
QTc interval in a dose-related manner. Prolongation of the QTc interval has been
associated with torsades de pointes arrhythmias and sudden death. An ECG should be
obtained before initiating treatment with thioridazine to rule out QTc prolongation.
TCAs are, at times, associated with ECG changes.
Anticholinergic effects may increase heart rate. Prolongation of the PR, QT, and QRS
intervals, along with ST-segment and T-wave abnormalities, may occur. The TCAs
can cause or increase pre existing atrio ventricular or bundle branch block. When the
QTc exceeds 0.440 second, a patient is at an increased risk for sudden death due to
cardiac arrhythmias. Many clinicians obtain an ECG before beginning a TCA in a
patient older than 40 years of age and in any patient with known cardiovascular
disease.
Lithium therapy can cause benign reversible T-wave changes, can impair sinoatrial
(SA) node function, and can cause heart block. ECGs are often obtained before
initiation of treatment with lithium and in cases of lithium toxicity or overdose.
Psychiatrists, when treating patients with certain psychiatric diagnoses, also use the
ECG. Eating disorder patients commonly have low potassium levels that may result in
abnormal ECG recordings. As the serum potassium drops below normal, T waves
become flat (or inverted), and U waves may appear.
Polysomnography
Polysomnography is used to assess disorders of sleep by concurrently assessing the EEG,
ECG, blood oxygen saturation, respirations, body temperature, electromyogram, and
electrooculogram. Polysomnography has demonstrated an increase in the overall amount
of rapid eye movement (REM) sleep and a shortened period before the onset of REM
sleep (decreased REM latency) in patients with major depression. These studies may
assist in differentiating depression from other conditions that mimic depression. For
example, patients who appear depressed from dementia do not have a decreased REM
latency or an increase in the amount of REM sleep.
Holter Monitoring
Holter monitoring is the continuous recording of a patient's ECG activity for a sustained
time period (e.g., 24 hours). Patients are ambulatory during this time. It is useful for the
evaluation of dizziness, palpitations, and syncope. It is commonly used in the evaluation
of patients with panic disorder who manifest cardiac symptoms.
Cardiac Ultrasound
Cardiac ultrasound is the visualization of cardiac anatomy by the use of computer-
transformed echoes of ultrasound. It is commonly used in the evaluation of mitral valve
prolapse. There is an unclear association between mitral valve prolapse and panic attacks
and anxiety disorders.
2. Screening for the presence of discrete abnormalities in patients at risk for the
development of neurological disorders.
This is appropriate for individuals who have no particular subjective symptoms suggestive of
a neurological problem, yet have systemic illnesses that might put them at risk for subtle
dysfunction. Diabetic patients, for example (particularly those with long standing poor
control), may develop peripheral nerve dysfunction. This may only be detected through
careful sensory testing (see below under Sensory Testing), which would have important
clinical implications.
In patients with neither signs nor risk factors for neurological disease, it's unlikely that the
detailed exam would uncover occult problems. Simply observing the patient during the
course of the usual H&P (i.e. watching them walk, get up and down from the exam table,
etc.) may well suffice. Many examiners incorporate some aspects of the neuro exam into their
standard evaluations. Cranial Nerve testing, for example, can be easily blended into the Head
and Neck evaluation. Deciding what other aspects to routinely include is based on judgment
and experience.
I. OLFACTORY NERVE :
Anatomy
Cranial nerve I is a special sensory nerve that provides the sense of smell. Inhaled scents are
detected by the olfactory epithelium lining the nasal cavity and transmitted to the olfactory
bulb, which lies adjacent to the cribriform plate of the ethmoid bone. Olfactory sensations are
relayed from the olfactory bulb to the brain via the olfactory tract.
Functions :
Smell, a function of the 1st (olfactory) cranial nerve, is usually evaluated only after head
trauma or when lesions of the anterior fossa (e.g., meningioma) are suspected or patients
report abnormal smell or taste.
Disorders
Damage to the olfactory nerve (I) can cause an inability to smell (anosmia), a distortion in
the sense of smell (parosmia), or a distortion or lack of taste. If there is suspicion of a
change in the sense of smell, each nostril is tested with substances of known odours such
as coffee or soap. Intensely smelling substances, for example ammonia, may lead to the
activation of pain receptors (nociceptors) of the trigeminal nerve that are located in the
nasal cavity and this can confound olfactory testing.
Test
1. Check to make sure that the patient is able to inhale and exhale through the open
nostril.
2. Have the patient close their eyes.
3. Present a small test tube filled with something that has a distinct, common odour (e.g.
ground coffee) to the open nostrils. The patient should be able to correctly identify the
odour at approximately 10 cm.
The optic nerve has only a special sensory component. Special sensory conveys visual
information from the retina (special afferent). Visual information enters the eye in the form of
photons of light which are converted to electrical signals in the retina. These signals are
carried via the optic nerves, chiasm, and tract to the lateral geniculate nucleus of each
thalamus and then to the visual centers of the brain for interpretation.
Functions
The optic nerve consists of sensory fibres conducting impulses from the retina. CN II is
responsible for vision including visual acuity, visual fields, colour vision, light and
accommodation reflexes.
Disorders
Visual field defects: Field defects start as small areas of visual loss (scotomas).
Monocular blindness: Lesions of one eye or optic nerve e.g. MS, giant cell arteritis.
Bilateral blindness: Methyl alcohol, tobacco amblyopia; neurosyphilis.
Bitemporal hemianopia: Optic chiasm compression eg internal carotid artery
aneurysm, pituitary adenoma or craniopharyngioma
Homonymous hemianopia: Affects half the visual field contralateral to the lesion in
each eye.
Lesions lie beyond the optic chiasm in the tracts, radiation or occipital cortex e.g. stroke,
abscess, tumour.
The somatic motor component of CN III plays a major role in controlling the muscles
responsible for the precise movement of the eyes for visual tracking or fixation on an
object.
The visceral motor component is involved in the pupillary light and accommodation
reflexes.
Disorders :
Damage to the Oculomotor nerve will result in the affected individual being unable to move
their eye normally, ptosis of the eyelid on the affected side, and the eye typically takes a
Down and Out appearance. Other signs and symptoms include strabismus and diplopia.
Test :
Ocular movements are tested by standing one meter in front of the patient and asking
the patient to follow a target with eyes only, and not the head. The target is moved in
an "H" shape and the patient is asked to report any diplopia. Then, the target is held at
the lateral ends of the patient's visual field. Nystagmus is tested for. One or two beats
is a normal finding. The accommodation reflex is tested by moving the target towards
the patient's nose. As the eyes converge, the pupils should constrict. The optokinetic
nystagmus test is optional and involves asking the patient to look at a moving strip of
horizontal lines. Nystagmus is normally observed.
The trochlear nerve has only a somatic motor component. The superior oblique muscle is one
of the six extra ocular muscles responsible for the precise movement of the eye for visual
tracking or fixation on an object.
Functions :
The superior oblique muscle controls the downward movement of the eyeball and, in part,
keeps the eyeball from rolling upward into the orbit (eye socket). The trochlear nerve runs
through the cavernous sinus and then enters the orbit through the supraorbital fissure.
Disorders:
Diplopia due to weakness of downward and outward eye movement. Commonest cause of a
pure vertical diplopia. Patient tends to compensate by tilting head towards the unaffected
side.
Test :
The visual pursuit test is performed by asking the patient to follow the practitioner’s finger or
the tip of a pen with their eyes whilst the patient’s head remains still. The examiner moves
the object in a vertical, horizontal and diagonal direction, asking the patient to follow the
movement with their eyes. This test is done under the assumption that the examiner’s visual
fields are intact. The trochlear nerve supplies the superior oblique ocular muscle, there for
particular attention should be paid as to whether the patient is capable of looking medially,
towards their nose.
An inability for the patient to look medially may be indicative of a lesion of the trochlear
nerve.
V. TRIGEMINAL NERVE :
The trigeminal nerve (the fifth cranial nerve, or simply CN V) is a nerve responsible for
sensation in the face and motor functions such as biting and chewing; it is the largest of the
cranial nerves. The trigeminal nerve has three different divisions. Each division has a slightly
different function.
Like the ophthalmic division, the maxillary division of your trigeminal nerve has a sensory
component. It transmits sensory information from the:
The mandibular division is the only part of the trigeminal nerve that has both sensory and
motor functions. It communicates sensory information from the:
It also stimulates movement of the muscles in the jaw and some of the muscles within the
inner ear.
Disorders :
The trigeminal nerve can also be a source of intense pain for some people. This is part of a
chronic condition called trigeminal neuralgia. It happens when the trigeminal nerve is under
pressure or irritated. This can happen when a vein or artery presses against the nerve.
Trigeminal neuralgia is more common in people over the age of 50.
o Stroke
o Facial injuries
o Brain tumor
o Neurological conditions, such as multiple sclerosis
The pain associated with trigeminal neuralgia can be very painful. People often describe it as
a shooting or jabbing pain that lasts anywhere from a few seconds to several hours.
Test :
The trigeminal nerve plays a role in many sensations that are felt in different parts of the face.
As a result, there are several ways to test the function of the trigeminal nerve.
Pin or cotton swab test. One or both sides of the face are touched with either a pin or
cotton swab. The person will then be asked whether they felt anything, and if so, where
they felt it. A doctor may also lightly touch the cornea of the eye with a cotton swab to test
the ophthalmic division. If the person doesn’t blink, the ophthalmic division of their
trigeminal nerve may be damaged.
Clenching test. A doctor will ask someone to clench their teeth or try to open their jaw
when resistance is applied. They’ll check muscle tone and movement for any signs of
trigeminal nerve damage.
The Abducens nerve is also known as the abducent or sixth cranial nerve (CN6). It
controls the eye's lateral rectus muscle, which moves the eye sideways, away from the
nose. Where the pons (a band of nerve fibers ) and the medulla (lower portion of the
brainstem) meet, CN6 departs from the brainstem and runs a course to the facial nerve. CN6
passes through the subarachnoid space (around the brain), cavernous sinus (a small, blood-
filled space behind the eyes) and, eventually, the superior orbital fissure (a groove in the
bones behind the eyes).
Disorders :
This nerve is susceptible to a number of clinical conditions. If the abducens nerve is injured,
double vision can result. The eye ends up pulled in toward the nose because the medial rectus
muscle works without opposition. Damage to the abducens nerve can result from anything
that stretches or compresses it, such as from the growth of tumors or blood vessels that bulge
into aneurysms. Meningitis infections (serious infection of the brain’s covering tissues) may
also develop and damage the nerve. Of all the possible conditions, diabetic neuropathy,
related to prolonged issues with blood sugar, is the most frequently occurring.
Test :
The visual pursuit test is performed by asking the patient to follow the practitioner’s finger or
the tip of a pen with their eyes whilst the patient’s head remains still. The examiner moves
the object in a vertical, horizontal and diagonal direction, asking the patient to follow the
movement with their eyes. This test is done under the assumption that the examiner’s visual
fields are intact. The Abducens nerve supplies motor innervation to the lateral rectus ocular
muscle, therefor particular attention should be paid as to whether the patient is able to look
laterally.
An inability for the patient to look medially may be indicative of a lesion of the trochlear
nerve.
The use and interpretation of medical examinations to determine the integrity and adequate
function of the facial nerve (seventh cranial nerve). This nerve provides the innervation for
one of the special senses: taste.
The facial nerve’s motor component innervates the muscles of facial expression as well as the
digastric, styloid and stapedius muscles. Its sensory component relays afferent information
relating to taste sensation from the anterior two-thirds of the tongue, and cutaneous sensation
from the skin in and around the auricle. The facial nerve also has a parasympathetic
component which sends fibres to the submandibular, sublingual and lacrimal glands.
Functions :
a. Motor function : Branches of the facial nerve are responsible for innervating many of the
muscles of the head and neck. All these muscles are derivatives of the second pharyngeal
arch. The first motor branch arises within the facial canal; the nerve to stapedius. The
nerve passes through the pyramidal eminence to supply the stapedius muscle in
the middle ear.
Between the stylomastoid foramen, and the parotid gland, three more motor branches are
given off:
Posterior auricular nerve – Ascends in front of the mastoid process, and innervates the
intrinsic and extrinsic muscles of the outer ear. It also supplies the occipital part of
the occipitofrontalis muscle.
Nerve to the posterior belly of the digastric muscle – Innervates the posterior belly of
the digastric muscle (a suprahyoid muscle of the neck). It is responsible for raising the
hyoid bone.
Nerve to the stylohyoid muscle – Innervates the stylohyoid muscle (a suprahyoid muscle
of the neck). It is responsible for raising the hyoid bone.
Within the parotid gland, the facial nerve terminates by bifurcating into five motor branches.
These innervate the muscles of facial expression:
Temporal branch – Innervates the frontalis, orbicularis oculi and corrugator supercilii
Zygomatic branch – Innervates the orbicularis oculi.
Buccal branch – Innervates the orbicularis oris, buccinator and zygomaticus muscles.
Marginal Mandibular branch – Innervates the mentalis muscle.
Cervical branch – Innervates the platysma.
b. Special sensory function :
The nerve arises in the facial canal, and travels across the bones of the middle ear, exiting via
the petrotympanic fissure, and entering the infratemporal fossa. Here, the chorda tympani
‘hitchhikes’ with the lingual nerve. The parasympathetic fibres of the chorda tympani stay
with the lingual nerve, but the main body of the nerve leaves to innervate the anterior 2/3 of
the tongue.
c. Parasympathetic function : The parasympathetic fibres of the facial nerve are carried by
the greater petrosal and chorda tympani branches.
d. Greater Petrosal Nerve: The greater petrosal nerve arises immediately distal to
the geniculate ganglion within the facial canal. It then moves in anteromedial direction,
exiting the temporal bone into the middle cranial fossa. From here, its travels across (but
not through) the foramen lacerum, combining with the deep petrosal nerve to form
the nerve of the pterygoid canal.
The nerve of pterygoid canal then passes through the pterygoid canal (Vidian canal) to enter
the pterygopalatine fossa, and synapses with the pterygopalatine ganglion. Branches from this
ganglion then go on to provide parasympathetic innervation to the mucous glands of the oral
cavity, nose and pharynx, and the lacrimal gland.
e. Chorda Tympani
The chorda tympani also carries some parasympathetic fibres. These combine with
the lingual nerve (a branch of the trigeminal nerve) in the infratemporal fossa and form the
submandibular ganglion. Branches from this ganglion travel to the submandibular and
sublingual salivary glands.
Disorders :
Bell’s palsy
This is the most common cause of facial paralysis - around 80% of all cases. It's also known
as idiopathic unilateral facial paralysis. 15% of patients have partial facial weakness. Most
people (85%) recover completely in six to nine months.
Lyme disease
This is a bacterial infection caught by being bitten by an infected tick. The target-shaped skin
rash before a range of other symptoms such as headache, fever or weakness. The neurological
symptoms, one of which is facial paralysis.
Trauma
A traumatic injury to head or face is one of the most common causes of severe permanent
facial paralysis. In particular, fractures through the temporal bone of your skull are
commonly associated with injury to the facial nerve, as well as injury to the labyrinth leading
to hearing loss and vertigo. We can use electrophysiological testing and imaging to find out
how severe injury is. We'll sometimes need to surgically decompress or graft the facial nerve.
Soft tissue injuries, such as lacerations, can also damage the facial nerve. It's important to
have these injuries seen and repaired correctly to give you the best chance of recovering.
Iatrogenic injury
Iatrogenic injury can occur during surgery on your head or face. The type of treatment
depend on the degree of injury to facial nerve. In severe cases, the need to repair the nerve.
Neurological conditions
Guillain-Barre syndrome or a peripheral neuropathy (damage to nerves in your extremities
such as hands, feet or arms) may present with weakness on both sides of your face. A stroke
may also cause you to lose movement in the lower part of your face.
Test :
Facing the patient, the practitioner instructs the patient to go through a series of facial
movements (grimaces). Instruct the patient to raise their eyebrows, frown, close their eyes
lightly and have the practitioner attempt to open them, move the their lips and show their
teeth, smile, and puff out their cheeks. The sensory component of the facial nerve can be
assessed by placing a small amount of salt or sugar on the anterior two-thirds of the patient’s
tongue and asking them to identify the taste. The efferent limb of the corneal reflex is under
the control of the facial nerve and can be assessed by lightly touching the patient’s cornea
with a clean piece of cotton wool.
Test findings ( Positive & Negative results):
The two limbs forming the corneal reflex are distinct nerves and therefor an absent or
weakened reflex may be indicative of a lesion or lesions either at the trigeminal nerve, facial
nerve, higher centres or a combination of the aforementioned.
A lower motor neuron lesion affecting the facial nerve can result in what is clinically referred
to as facial nerve palsy (referred to as Bell’s palsy when idiopathic). The clinical signs
include weakness in both the upper and lower muscles of facial expression on the same side
of the lesion.
In an upper motor neuron lesion, clinically referred to as central facial palsy, or central seven,
the clinical manifestations depict a weakness in only the muscles of the lower portion of the
face on the contralateral side of the lesion. This is due to the bilateral innervation of the upper
muscles of facial expression.
Taste sensation can be reduced and/or absent on the anterior two-thirds of the tongue.
Functions :
The vestibulocochlear nerve is responsible for both hearing and balance and brings
information from the inner ear to the brain. A human's sense of equilibrium is
determined by this nerve.
Two special organs help the nerve function properly: the cochlea and the vestibular
apparatus. The cochlea transforms sound waves into electrical signals that the brain
can interpret. The vestibular apparatus senses changes in the position of the head in
relation to gravity.
Disorders :
Unilateral sensorineural deafness, tinnitus. Slow growing lesions seldom present with
vestibular symptoms as compensation has time to occur.
Causes of a single VIII lesion loud noise; Paget's disease; Ménière's disease; Herpes
zoster; neurofibroma, acoustic neuroma, brainstem CVA; lead; aminoglycosides;
furosemide (frusemide); aspirin.
Test :
Hearing:
o mask the opposite ear and whisper numbers. The patient should not be able to read
your lips. Ask the patient to repeat the numbers. If they cannot do so, increase the
volume of your voice and repeat as needed. Note any asymmetry.
o compare air versus bone conduction using the Rinne test. Apply the vibrating fork
against the mastoid process. Utilize the 512 Hertz tuning fork. Ask the patient when
they can no longer hear it, then place it in front of the ear.
o test for lateralization using the Webertest. Apply the vibrating tuning fork to the
center of the forehead and ask the patient where they hear it.
2. Vestibular Function:
o the vestibular component of the auditory nerve is tested by observing for nystagmus
when extraocular movements are assessed.
Normal Response:
o Rinne – air conduction (perceiving the sound of the tuning fork in front of the ear) is
greater than bone conduction (with the tuning fork held against the mastoid process).
o Weber – normally, patients will either hear it equally from both ears or respond that
they are not sure.
Abnormal Response:
o Rinne: in conductive hearing loss, bone conduction is greater than air conduction. In
sensorineural deafness, air conduction is greater than bone conduction.
o the Weber is abnormal if the patient clearly lateralizes it to one ear. With a conductive
hearing loss, the patient lateralizes the sound to the affected ear. With sensorineural
deafness the sound is best heard by the non-involved ear.
IX. GLOSSOPHARYNGEAL :
3) Visceral sensory Carries visceral sensory information from the carotid sinus and
(general visceral body.
afferent)
4) General sensory Provides general sensory information from the skin of the
(general somatic external ear, internal surface of the tympanic membrane, upper
afferent) pharynx, and the posterior one-third of the tongue.
5) Special sensory Provides taste sensation from the posterior one-third of the
(special afferent) tongue.
Disorders :
Diseases of the ninth cranial (glossopharyngeal) nerve or its nuclei in the medulla. The nerve
may be injured by diseases affecting the lower brain stem, floor of the posterior fossa, jugular
foramen, or the nerve's extra cranial course. Clinical manifestations include loss of sensation
from the pharynx, decreased salivation, and syncope. Glossopharyngeal neuralgia refers to a
condition that features recurrent unilateral sharp pain in the tongue, angle of the jaw, external
auditory meatus and throat that may be associated with SYNCOPE. Episodes may be
triggered by cough, sneeze, swallowing, or pressure on the tragus of the ear.
X. VAGUS NERVE :
The Vagus nerve, "the wanderer", contains motor fibres (to the palate and vocal cords),
sensory components (posterior and floor of external acoustic meatus) and visceral afferent
and efferent fibres. It leaves the skull through the jugular foramen, passes within the
carotid sheath in the neck (giving off cardiac branches, and the recurrent laryngeal nerves
supplying the vocal cords), through the thorax supplying lungs, and continues on via the
oesophageal opening to supply the abdominal organs.
Functions :
4. General sensory Provides general sensory information from the skin of the back
(general somatic of the ear and external auditory meatus, parts of the external
afferent) surface of the tympanic membrane, and the pharynx.
Disorders :
a. Nerve damage: Damage to the Vagus nerve can have a range of symptoms
because the nerve is so long and affects many areas.
Potential symptoms of damage to the Vagus nerve include:
difficulty speaking or loss of voice
a voice that is hoarse or wheezy
trouble drinking liquids
loss of the gag reflex
pain in the ear
unusual heart rate
abnormal blood pressure
decreased production of stomach acid
nausea or vomiting
abdominal bloating or pain
The symptoms someone might have depend on what part of the nerve is damaged.
b. Gastro paresis: Experts believe that damage to the vagus nerve may also
cause a condition called gastroparesis. This condition affects the involuntary
contractions of the digestive system, which prevents the stomach from
properly emptying.
The 9th and 10th nerves are tested together. They are responsible for swallowing, phonation,
guttural and palatal articulation (the 7th nerve has a component for labial articulation). The
glossopharyngeal nerve also subserves taste to the posterior one-third of the tongue but this is
rarely tested.
Examination Technique:
o check palatial elevation by having the patient sustain an "ah." When observing palatal
movement, look at the palate rather than the uvula.
o assess the gag reflex by gentling stroking the soft palate on each side.
o swallowing can be assessed by giving the patient a sip of water and observing them
swallow.
o listen to the patient’s speech. Is there a nasal quality?
o assess palatal articulation with a "KA" sound, guttural with a "GO" sound and labial
with a "PA" sound.
Normal Response:
o the palate should elevate symmetrically, both when sustaining an "AH" and in
response to stimulation on either side. Some patients however do not have a gag
response and this can be normal if it is absent bilaterally. Patients should also be
asked if they feel the stimulus.
Abnormal Response:
o with unilateral palatal weakness, the palate fails to elevate on the weak side and the
gag reflex will be absent on that side.
XI. ACCESSORY NERVE :
The accessory nerve is the eleventh paired cranial nerve. It has a purely somatic motor
function, innervating the sternocleidomastoid and trapezius muscles.
Traditionally, the accessory nerve is divided into spinal and cranial parts.
a. Spinal part : The spinal portion arises from neurones of the upper spinal cord,
specifically C1-C5/C6 spinal nerve roots. These fibres coalesce to form the spinal part
of the accessory nerve, which then runs superiorly to enter the cranial cavity
via the foramen magnum.
The nerve traverses the posterior cranial fossa to reach the jugular foramen. It briefly meets
the cranial portion of the accessory nerve, before exiting the skull (along with the
glossopharyngeal and vagus nerves).
Outside the cranium, the spinal part descends along the internal carotid artery to reach the
sternocleidomastoid muscle, which it innervates. It then moves across the posterior triangle of
the neck to supply motor fibres to the trapezius.
b. Cranial Part
The cranial portion is much smaller, and arises from the lateral aspect of the medulla
oblongata. It leaves the cranium via the jugular foramen, where it briefly contacts the spinal
part of the accessory nerve.
Immediately after leaving the skull, cranial part combines with the vagus nerve (CN X) at
the inferior ganglion of vagus nerve (a ganglion is a collection of nerve cell bodies). The
fibres from the cranial part are then distributed through the vagus nerve. For this reason, the
cranial part of the accessory nerve is considered as part of the vagus nerve.
Function :
The spinal accessory nerve innervates two muscles – the sternocleidomastoid and trapezius.
Sternocleidomastoid
Attachments – Runs from the mastoid process of the temporal bone to the manubrium
(sternal head) and the medial third of the clavicle (clavicular head).
Actions – Lateral flexion and rotation of the neck when acting unilaterally, and extension
of the neck at the atlanto-occipital joints when acting bilaterally.
Trapezius
Attachments – Runs from the base of the skull and the spinous processes of the C7-T12
vertebrae to lateral third of the clavicle and the acromion of the scapula.
Actions – It is made up of upper, middle and lower fibres. The upper fibres of the
trapezius elevate the scapula and rotate it during abduction of the arm. The middle fibres
retract the scapula and the lower fibres pull the scapula inferiorly.
Disorders :
Palsy of accessory nerve :
The most common cause of accessory nerve damage is iatrogenic (i.e. due to a medical
procedure). In particular, operations such as cervical lymph node biopsy or cannulation of the
internal jugular vein can cause trauma to the nerve.
Clinical features include muscle wasting and partial paralysis of the sternocleidomastoid,
resulting in the inability to rotate the head or weakness in shrugging the shoulders. Damage to
the muscles may also result in an asymmetrical neckline.
Test : The spinal accessory supplies the trapezius and sternocleidomastoid muscles.
Examination Technique:
It passes briefly across the posterior fossa, leaves the skull through the hypoglossal canal and
supplies motor fibres to the tongue and most of the infrahyoid muscles. It has only a somatic
motor (general somatic efferent) component. Somatic motor Innervates all the intrinsic and
most of the extrinsic muscles of the tongue. CN XII supplies three of the four extrinsic
muscles of the tongue including genioglossus, styloglossus, and hyoglossus. The
palatoglossus muscle is supplied by CN X (vagus nerve).
These upper motor neuron fibres innervate predominantly the contralateral hypoglossal
nucleus. Signals for the voluntary control of the muscles of the tongue originate in the motor
cortex (in association with other cortical areas) and pass via the corticobulbar tract in the
posterior limb of the internal capsule to the hypoglossal nucleus in the medulla.
Functions :
o The hypoglossal nerve controls tongue movements of speech, food manipulation, and
swallowing. It supplies motor fibres to all of the muscles of the tongue, with the
exception of the palatoglossus muscle, which is innervated by the vagus nerve (cranial
nerve X) or, according to some classifications, by fibres from the glossopharyngeal
nerve (cranial nerve IX) that hitchhike within the vagus.
o While the hypoglossal nerve controls the tongue's involuntary activities of swallowing
to clear the mouth of saliva, most of the functions it controls are voluntary, meaning
that the execution of these activities requires conscious thought.
o Proper function of the hypoglossal nerve is important for executing the tongue
movements associated with speech. Many languages require specific and sometimes
unusual uses of the nerve to create unique speech sounds, which may contribute to the
difficulties some adults encounter when learning a new language. Several
corticonuclear-originating fibres supply innervation and aid in the unconscious
movements required upon engaging in speech and articulation.
Disorders :
The most common causes of injury in one case series were compression by tumours and
gunshot wounds. A wide variety of other causes can lead to damage of the nerve. These
include surgical damage, medullary stroke, multiple sclerosis, Guillain-Barre syndrome,
infection, sarcoidosis, and presence of an ectatic vessel in the hypoglossal canal. Damage can
be on one or both sides, which will affect symptoms that the damage causes. Because of the
close proximity of the nerve to other structures including nerves, arteries, and veins, it is rare
for the nerve to be damaged in isolation.
Progressive bulbar palsy, a form of motor neuron disease, is associated with combined
lesions of the hypoglossal nucleus and nucleus ambiguus with wasting (atrophy) of the motor
nerves of the pons and medulla. This may cause difficulty with tongue movements, speech,
chewing and swallowing caused by dysfunction of several cranial nerve nuclei. Motor neuron
disease is the most common disease affecting the hypoglossal nerve.
Test :
Examination Technique:
Normal Response:
o the tongue should be able to protrude relatively straight. Minimal degrees of deviation
(i.e. only millimeters) affecting only the tip are insignificant.
Abnormal Response:
o with tongue weakness, the tongue deviates towards the weak side.
7. CN VII: Facial Nerves Hemi facial paresis abnormal taste, sensory deficit
around ear, sensitivity to loud sound
8. CN VIII: Vestibular Vertigo, tinnitus, unilateral hearing loss
Nerve
9. CN IX: (RARE) Intermittent pain in the pharynx
Glossopharyngeal Nerve
10. CN X: Vagus Nerve Loss of palate rise, dysphagia, hoarse voice
11. CN XI: Spinal Accessory Shoulder drop and downward displacement of scapula
Nerve
12. CN XII: Hypoglossal Tongue deviations
Nerve
USES OF NEUROIMAGING
INDICATIONS FOR ORDERING NEUROIMAGING IN CLINICAL PRACTICE
a. Neurological Deficits.
In a neurological examination, any change that can be localized to the brain or spinal cord
requires neuroimaging. Neurological examination includes mental status, cranial nerves,
motor system, coordination, sensory system, and reflex components. Consultant psychiatrists
should consider a workup including neuroimaging for patients with new-onset psychosis and
acute changes in mental status. The clinical examination always assumes priority, and
neuroimaging is ordered on the basis of clinical suspicion of a central nervous system (CNS)
disorder.
b. Dementia:
Infarction of the cortical or subcortical areas, or stroke, can produce focal neurological
deficits, including cognitive and emotional changes. Strokes are easily seen on MRI scans.
In extensive atherosclerosis in brain , capillaries can cause countless tiny infarctions
of brain tissue; patients with this phenomenon may develop dementia as fewer and
fewer neural pathways participate in cognition. This state, called vascular dementia, is
characterized on MRI scans by patches of increased signal in the white matter.
The normal pressure hydrocephalus, a disorder of the drainage of cerebrospinal fluid
(CSF). This condition does not progress to the point of acutely increased intracranial
pressure but stabilizes at a pressure at the upper end of the normal range. The dilated
ventricles, which may be readily visualized with CT or MRI, exert pressure on the
frontal lobes.
Certain degenerative disorders of basal ganglia structures, associated with dementia,
may have a characteristic appearance on MRI scans. Huntington's disease typically
produces atrophy of the caudate nucleus; thalamic degeneration can interrupt the
neural links to the cortex.
Human immunodeficiency virus (HIV) infection can cause dementia directly, in
which case is seen a diffuse loss of brain volume, or it can allow proliferation of
Creutzfeldt-Jakob virus to yield progressive multifocal leukoencephalopathy, which
affects white matter tracts and appears as increased white matter signal on MRI scans.
Chronic demyelinating diseases, such as multiple sclerosis, can affect cognition
because of white matter disruption. Multiple sclerosis plaques are easily seen on MRI
scans as periventricular patches of increased signal intensity.
STRUCTURAL IMAGING :
Structural imaging of the brain deals with the structure of the brain and the diagnosis of gross
intracranial disease such as tumour, strokes and injury. The real progress in structural
imaging started with computed axial tomography (CAT or CT scanning), when more detailed
anatomical images of the brain became available for diagnostic and research purposes. In the
early 1980s magnetic resonance imaging (MRI )was introduced clinically, and during the last
30 years an explosion of technical refinements and diagnostic MR applications have
transformed imaging of the brain.
PRINCIPLES :
1. COMPUTERIZED TOMOGRAPHY (CT)
CT X-rays generate an image in a single plane. There is poorer grey–white tissue contrast
than with MRI, but CT is better for examining bony structures/tissue calcification. CT is still
clinically useful but increasingly being replaced by MRI
Recent developments
• Voxel-based quantitative morphometry, for more sophisticated volume measurements.
• Shape morphometrics, for examining shape rather than volume.
• Diffusion tensor imaging (DTI),which is MRI of myelin traits.
• Magneto encephalography (MEG) a very recent technique using measurement of alteration
in cerebral magnetic fields to provide detailed information on cortical activity. It may be
combined with MRI and is good for studying deeper brain structures.
MRI
Magnetic resonance imaging (MRI) is a type of scan that uses strong magnetic fields and
radio waves to produce detailed images of the inside of the body. MRI scanning entered
clinical practice in 1982 and soon became the test of choice for clinical psychiatrists and
neurologists. The technique does not rely on the absorption of X-rays but is based on nuclear
magnetic resonance (NMR). An MRI differs from a CAT scan (also called a CT scan or a
computed axial tomography scan) because it does not use radiation. An MRI of the brain
usually takes 30-45 minutes to perform.
Principle :
The principle of NMR is that the nuclei of all atoms are thought to spin about an axis, which
is randomly oriented in space. When atoms are placed in a magnetic field, the axes of all odd-
numbered nuclei align with the magnetic field. The axis of a nucleus deviates away from the
magnetic field when exposed to a pulse of radiofrequency electromagnetic radiation oriented
at 90 or 180 degrees to the magnetic field. When the pulse terminates, the axis of the spinning
nucleus realigns itself with the magnetic field, and during this realignment, it emits its own
radiofrequency signal. MRI scanners collect the emissions of individual, realigning nuclei
and use computer analysis to generate a series of two-dimensional images that represent the
brain. The images can be in the axial, coronal, or sagittal planes.
DEVELOPMENT OF MRI SCAN
The development of MRI technology, Paul Lauterbur was able to develop MRI during his
research of nuclear magnetic resonance (NMR). Lauterbur speculated that NMR could be
used to create an image of tissue inside the human body. That image could then be studied by
medical professionals in order to diagnose medical ailments.
Lauterbur speculated that NMR could be used to create an image of tissue inside the human
body. That image could then be studied by medical professionals in order to diagnose
medical ailments.
The demonstration, in 1976, that patients with schizophrenia had enlarged cerebral
ventricles , seemed to usher psychiatry into a new era where neuroimaging would help
identify mental disorders and ultimately clarify their mechanisms.
DEVELOPMENT OF CT SCAN :
CT was invented in 1972 by British engineer Godfrey Hounsfield of EMI Laboratories,
England and by South Africa-born physicist Allan Cormack of Tufts University,
Massachusetts. The first clinical CT scanners were installed between 1974 and 1976. In 1972,
CT scanning revolutionized diagnostic neuroradiology by allowing imaging of the brain
tissue in live patients. The original systems were dedicated to head imaging only, but "whole
body" systems with larger patient openings became available in 1976. CT became widely
available by about 1980.
The latest multi-slice CT systems can collect up to 4 slices of data in about 350 ms and
reconstruct a 512 x 512-matrix image from millions of data points in less than a second. An
entire chest (forty 8 mm slices) can be scanned in five to ten seconds using the most
advanced multi-slice CT system.
TYPES OF CT SCAN :
ADVANTAGES OF CT SCAN
CT offers excellent spatial resolution (<1 mm) and is effective at distinguishing
tissues with markedly different X-ray attenuation properties (e.g., bone vs. Soft tissue
vs. fluid vs. gas).
CT is an excellent modality for imaging bone.
Patient anxiety is usually less during a CT scan than during an MRI scan because the
scanning environment is traditionally more open, quieter, and scanning time is brief.
CT is best for patients with ferro-metallic implants (e.g., foreign bodies, some
aneurysm clips, pacemakers, etc.) as MRI is contraindicated in this patient
population.
CT is the imaging modality of choice for acute trauma or when an acute bleed or
ischemia is suspected.
LIMITATIONS OF CT SCAN
CT is not helpful in visualizing subtle white matter lesions due to CT’s poor ability to
distinguish between the X-ray attenuation properties of different soft tissue densities.
CT uses ionizing radiation and thus is strongly contraindicated in pregnancy.
RISKS
CT does involve exposure to radiation in the form of x-ray, but the benefit of an
accurate diagnosis far outweighs the risk.
Special care is taken during x-ray examinations to ensure maximum safety for the
patient by shielding the abdomen and pelvis with a lead apron, with the exception of
those examinations in which the abdomen and pelvis are being imaged. Women
should always inform their doctor or x-ray technologist if there is any possibility that
they are pregnant.
Nursing mothers should wait for 24 hours after contrast material injection before
resuming breast feeding.
There is a risk of an allergic reaction which may be serious whenever contrast
material containing iodine is injected. If you have a history of allergy to x-ray dye,
your radiologist may advise that you take special medication for 24 hours before the
exam to lessen the risk of allergic reaction. Another option is to undergo a different
exam that does not call for contrast injection.
Contrast injection should be avoided in patients with kidney disease or severe diabetes
because x-ray contrast material can further harm kidney function.
If a large amount of x-ray contrast leaks out under the skin where the IV is placed,
skin damage can result. If the patient feel any pain in this area during contrast
injection, they should immediately inform the technologist.
CT VERSUS MRI
1) CT is still the modality of choice for patients with suspected acute bleeds or acute
trauma.
2) MRI is superior to CT for the differentiation of white from grey matter and the
identification of white matter lesions.
3) MRI is superior to CT for the detection of posterior fossa and brainstem
pathology.
4) CT is recommended if MRI is contraindicated (i.e., paramagnetic protheses;
inability to tolerate scanner time, noise, or confinement).
5) MRI is recommended if radiation exposure is contraindicated (i.e., young
children or women of childbearing potential).
Epilepsy.
Sinus disease - mucosal thickening is a common incidental finding and not diagnostic.
Temporo mandibular joint dysfunction - will not show disc abnormality, which is the most
common cause of dysfunction.
RISKS
Generally, the benefit of the X-ray procedure is far more important than the small
estimated risk of the effects of radiation. At the radiation dose levels that are used in
diagnostic radiography, there is little or no evidence of health effects
The type of radiation used in X-rays is called ionising radiation. Medical research has
been unable to establish conclusively that there are significant effects for patients
exposed to ionising radiation at the doses used in diagnostic X-ray imaging.
Radiographers are trained to use the smallest possible amount of X-rays required to
produce a satisfactory image.
BENEFITS
X-ray imaging is useful to diagnose disease and injury, such as pneumonia, heart
failure, fractures, bone infections, arthritis, cancer, blockage of the bowel, collapsed
lung and so on. It is fast and easy, so it is particularly useful in emergency diagnosis
and treatment.
X-ray equipment is widely available in hospitals, X-ray clinics and other locations,
making it convenient for both patients and doctors, even in remote locations.
PNEUMOENCEPHALOGRAPHY
Pneumoencephalography, technique of diagnostic radiology that produces X-ray films of
the head after injection of air or gas between the membranes lining the brain and spinal
cord to sharpen the outlines of various brain structures. The air or gas is introduced, in small
increments, by exchange with cerebrospinal fluid, into the lower back, with the patient in the
sitting position. Pneumoencephalography reveals such conditions
as hydrocephalus (abnormal accumulation of fluid within the cranial cavity), mass lesions
that displace or deform the brain ventricles (cavities), and atrophic states of the brain tissues.
In ventriculography the air or gas is injected directly into the brain ventricles.
Pneumoencephalography, a painful and sometimes dangerous procedure, has been largely
displaced by the techniques of computerized axial tomography, magnetic resonance imaging,
and positron emission tomography. Today, the technique is used only in rare instances.
DEVELOPMENT :
The procedure was introduced in 1919 by the American neurosurgeon Walter Dandy and was
performed extensively until the late 1970s, when it was replaced by more-sophisticated and
less-invasive modern neuroimaging techniques.
INDICATIONS
Draining and monitoring of cerebrospinal fluid (CSF) flow from the lateral ventricles or
lumbar subarachnoid space is indicated in selected patients to:
Monitoring can also be used to evaluate the status pre- and postoperatively for space-
occupying lesions.
COMPLICATIONS
HISTORY :
The first SPECT measurements were performed in the 1960s (Kuhl and Edwards,
1964).
The concept of modern PET was developed during the 1970s
FUNCTIONAL MRI
This is an adaptation of MRI using exogenous contrast agents (e.g. GdPTA ) or the
endogenous contrast agent effect of deoxy haemoglobin in blood. It can achieve high spatial
and temporal resolution images of brain activity. It is now the major technology for
functional imaging available in clinical scanners. Overlay with structural images is possible.
fMRI is used in the study of perception (e.g. patients with schizophrenia hearing voices have
over activity in temporal lobes), emotions (sadness, anger) and treatment response (drugs
may alter and normalize blood flow in pre treatment /post-treatment comparisons).
1.The MRI and fMRI differ from each other in a way that the MRI views the anatomical
structure while the fMRI views the metabolic function.
2.An MRI studies the water molecule’s hydrogen nuclei whereas an fMRI calculates the
levels of oxygen.
3.An MRI’s structural imaging views at a high resolution the differences between tissue types
with respect to space. On the other hand, an fMRI’s functional imaging views the tissue
differences with respect to time.
4.The MRI has a high, spatial resolution while an fMRI has a long-distance, superior,
temporal resolution.
5.When talking about its technological advancements, the fMRI is still starting to build up its
name unlike the MRI wherein it is already at its peak as one of the widely used equipment
technologies in the medical world.
6.The fMRI is yet to be introduced for diagnostic purposes and is only used in experiments
unlike the revolutionary MRI.
7.The fMRI is considered to be more expensive than the MRI because of the additional
software and hardware required for it.
DEVELOPMENT :
The development of FMRI in the 1990s, generally credited to Seiji Ogawa and Ken Kwong,
is the latest in long line of innovations, including positron emission tomography (PET) and
near infrared spectroscopy (NIRS), which use blood flow and oxygen metabolism to infer
brain activity.
WORKING :
What fMRI detects is not brain activity per se, but blood flow. The volume of brain in which
blood flow increases exceeds the volume of activated neurons by about 1 to 2 cm and limits
the resolution of the technique. Sensitivity and resolution can be improved with the use of
nontoxic, ultra small iron oxide particles. Thus, two tasks that activate clusters of neurons 5
mm apart, such as recognizing two different faces, yield overlapping signals on fMRI and so
are usually indistinguishable by this technique. fMRI is useful to localize neuronal activity to
a particular lobe or subcortical nucleus and has even been able to localize activity to a single
gyrus. The method detects tissue perfusion, not neuronal metabolism. In contrast, PET
scanning may give information specifically about neuronal metabolism.
INDICATIONS
A. fMRI of Dementia.
fMRI methods provide information that can potentially be used in the study, diagnosis, and
prognosis of Alzheimer's disease and other forms of dementia as well as proving insights into
normal age-related changes in cognitive processing. Evidence that aging is associated with
weaker and more diffused activations as well as decreased hemispheric lateralization suggests
either a compensation for lost regional intensity or a dedifferentiation of processing. The
weaker activation, especially prefrontal, suggests potential encoding-stage dysfunctions
associated with aging.
fMRI studies have consistently demonstrated that patients with Alzheimer's disease have
decreased fMRI activation in the hippocampus and related structures within the MTL during
the encoding of new memories compared with cognitively intact older subjects. More
recently, fMRI studies of subjects at risk for Alzheimer's disease, by virtue of their genetics
or evidence of minimal cognitive impairment, have yielded variable results with some studies
suggesting there may be a phase of paradoxically increased activation early in the course of
prodromal Alzheimer's disease.
ELECTROENCEPHALOGRAPHY (EEG)
An EEG records regular and irregular oscillations of potentials between electrodes placed on
the scalp. Repetitive waves reflect summated synaptic potentials generated by cortical
pyramidal cells as response to rhythmic thalamic discharges. Amplitudes range from 5 to 150
microvolts. Frequencies (when regular) range from about 1 cycle/second (hertz) to 40Hz.
DEVELOPMENT
Infants have slower and usually higher-amplitude rhythms. They are asynchronous at first
and easily disturbed. Mature rhythms develop at between 2 and 6 years. Adults usually show
either alpha posteriorly and beta anteriorly but generalized low-amplitude beta may be
present – established by puberty. When the subject is drowsy, alpha becomes intermittent and
theta appears.
Alpha frequency tends to slow in old age, and delta activity is decreased; by 60 years,
Stage 4 represents 10 per cent of total sleep. There is decreased rapid eye movement (REM)
latency, with increased frequency and duration of nocturnal arousals.
NORMAL SLEEP
• Stage 1 (lightest) – low-voltage, desynchronized activity and sometimes low voltage-
regular activity at 4–6Hz. Undulating low-frequency deflections seen due to rolling eye
movements.
• Stage 2 – frequent spindle-shaped tracings at 13–15Hz (sleep spindles) and high voltage K
complexes (high-voltage slow waves plus short episode of fast activity over vertex,response
to sound).
• Stage 3 – high-voltage delta waves begin to appear.
• Stage 4 – delta waves occupy more than 60 per cent of record.
Features of normal sleep : Sleep is cyclical, with four or five periods of emergence from
stages 3 and 4 to a period lasting about 20 minutes – termed ‘paradoxical’ or
‘desynchronized’(REM) sleep:
• Low-voltage asynchronous fast waves on cortical EEG.
• Rapid eye movements, conjugate.
• Irregular respiration.
• Slight tachycardia with increased blood pressure.
• Increased gastric motility.
• Increased cerebral blood flow.
• Absent tendon reflexes.
• Penile erection.
• Vivid and bizarre dreams.
• 15–30 per cent of sleep time spent in REM.
Periodic complexes
• Herpes simplex encephalitis (look for localized temporal complexes).
• Creutzfeldt–Jakob disease (occurs in late stages).
• Sub acute sclerosing panencephalitis.
Triphasic waves : These indicate liver,renal,hypoxic or metabolic encephalopathies.
Frontal intermittent rhythmic delta activity (FIRDA)
• Metabolic encephalopathy.
• Brain stem dysfunction.
Alpha coma : There is widespread, non-reactive alpha-range activity. It occurs in generalized
encephalopathy.
Burst-suppression There are high-voltage bursts, followed by periods of extreme
suppression (flattening). It occurs with bihemispheric insult and deep anaesthesia.
C. STUPOR
Non-organic stupor due to depression, schizophrenia or hysteria shows a preservation of
alpha rhythm.
SPECT
Single-photon emission computed tomography (SPECT, or less commonly, SPET) is
a nuclear medicine tomographicimaging technique using gamma rays. It is very similar to
conventional nuclear medicine planar imaging using a gamma camera(that is, scintigraphy)
. but is able to provide true 3D information. This information is typically presented as cross-
sectional slices through the patient, but can be freely reformatted or manipulated as required.
PRINCIPLE :
SPECT uses compounds labelled with single photon-emitting isotopes: iodine-123,
technetium-99m, and xenon-133. Xenon133 is a noble gas that is inhaled directly. The xenon
quickly enters the blood and is distributed to areas of the brain as a function of regional blood
flow. Xenon-SPECT is thus referred to as the regional cerebral blood flow (rCBF) technique.
For technical reasons, xenon-SPECT can measure blood flow only on the surface of the brain,
which is an important limitation. Many mental tasks require communication between the
cortex and subcortical structures, and this activity is poorly measured by xenon-SPECT.
INTEGRATES : CT + RADIOACTIVE MATERIAL (TRACER)
Single photon emission (computerized) tomography (SPET; SPECT) uses single photon x-
ray) emitting isotopes – e.g. xenon 133,technetium 99 – to examine regional cerebral blood
flow (rCBF) or receptor pharmacology.
INDICATIONS
Spect And Schizophrenia
• A large number of studies have shown a pattern of functional underactivity, with reduced
rCBF predominantly in the frontal regions – the ‘hypofrontality hypothesis’.
• SPECT has also been used to examine neuroanatomical correlates of psychotic symptoms
and to determine the pattern of receptor binding of antipsychotics.
Xenon inhalation
• This is another index of rCBF. There is well-documented hypofrontality in schizophrenia,
with failure of activation during performance of the Wisconsin Card Sorting Test (WCST).
• There have been similar reports in affective disorder, but this may be a less consistent
finding.
Most people tolerate SPECT scans well, but there may be some instances where the test
would be ill-advised. The doctor may opt not to perform this test for the following reasons:
The tests use a low-dose of radiation, which is contraindicated for pregnant women. If
you’re nursing, you may be required to wait a certain amount of time before nursing
to allow your body time to excrete the radioactive tracer.
Though unusual, it’s possible to have an allergic reaction to the tracer. The healthcare
professionals is equipped to handle this situation should it arise.
Since the SPECT scan does use a low-dose of radiation, talk with the doctor if have any
concerns about risk of exposure. However, no long-term health risks have been associated
with using this method of imaging.
PET
Positron emission tomography (PET), with its array of radiopharmaceuticals, has been used
to study many physiologic and pathologic brain states. Its applications for brain imaging have
spanned both research and clinical uses. Specific psychiatric disorders in which PET studies
may influence the management of the patient include mood and anxiety disorders, attention
deficit disorder, schizophrenia, and obsessive compulsive disorder.
The isotopes used in PET decay by emitting positrons, antimatter particles that bind with and
annihilate electrons, thereby giving off photons that travel in 180-degree opposite directions.
Because detectors have twice as much signal from which to generate an image as SPECT
scanners have, the resolution of the PET image is higher. A wide range of compounds can be
used in PET studies, and the resolution of PET continues to be refined closer to its theoretical
minimum of 3 mm, which is the distance positrons move before colliding with an electron.
Relatively few PET scanners are available because they require an onsite cyclotron to make
the isotopes.
INDICATIONS
PET and schizophrenia
• Hypofrontality is studied in unmedicated and medicated states; related to negative
symptoms and treatment resistance.
• Activation studies to examine neuroanatomical specificity of psychotic symptoms, and
studies of dopamine receptor occupancy, have been carried out.
Affective Disorders
PET has made possible the study of the neuroanatomical pathways modulating mood. Pardo
and colleagues have reported the involvement of t he inferior frontal cortex in self-induced
dysphoria in normal subjects . In patients, depressive symptoms are associated with a hypo-
perfusion and hypo-metabolism in the prefrontal cortex
WORKING
MR spectroscopy is conducted on the same machine as conventional MRI. The MRI scan
uses a powerful magnet, radio waves, and a computer to create detailed images. Spectroscopy
is a series of tests that are added to the MRI scan of your brain or spine to measure the
chemical metabolism of a suspected tumor.
MR spectroscopy analyses molecules such as hydrogen ions or protons. Proton spectroscopy
is more commonly used. There are several different metabolites, or products of metabolism,
that can be measured to differentiate between tumor types:
Amino acids
Lipid
Lactate
Alanine
N-acetyl aspartate
Choline
Creatinine
Myoinositol
The frequency of these metabolites is measured in units called parts per million (ppm) and
plotted on a graph as peaks of varying height . By measuring each metabolite’s ppm and
comparing it to normal brain tissue, the neuro radiologist can determine the type of tissue
present.
MRS TECHNIQUE
MRS can be performed by two methods–single-voxel spectroscopy (SVS), where a single
sample volume is selected and a spectrum obtained from it, or multi-voxel spectroscopy
where spectra are obtained from multiple voxels in a single slab of tissue. SVS gives a better
signal-to-noise ratio and is a more robust technique. The disadvantage is that only a single
spectrum is obtained. The placement of the volume of interest (VOI) becomes critical and
may lead to errors of interpretation if not done correctly. With multi-voxel MRS, a much
larger area can be covered, eliminating the sampling error to an extent. This however is done
at the expense of a significant weakening in the signal-to-noise ratio and a longer scan time.
Both SVS and multi-voxel imaging utilize specialized MR pulse sequences. The two most
widely used are the Point Resolved Excitation Spin-echo Sequence (PRESS) and the
Stimulated Echo Acquisition Mode (STEAM) technique.
INDICATIONS :
a. MRS in Dementia.
MRS presents the opportunity to noninvasively obtain measures of several neurochemicals
related to neurotransmission, energy metabolism, and cellular function. Studies using MRS
have shown a trend for a general reduction in NAA measures with increasing age in MTL and
frontal cortical brain regions. The studies in MCI and Alzheimer's disease report patients with
these disorders have decreased levels of NAA and increased levels of myo-inositol (a form of
inositol normally found in the brain that contributes to osmotic regulation) compared with
those of age-matched comparison subjects.
b. MRS in Schizophrenia.
MRS has been applied widely in studies of cortical chemistry in schizophrenia. These studies
documented reductions in NAA levels in many cortical and limbic brain regions in
schizophrenic individuals and smaller reductions in family members of people diagnosed
with schizophrenia. Other metabolites have been measured in MRS studies of schizophrenic
patients. The most interesting finding may be the description of normal or low levels of
glutamate and increased levels of glutamine in medication-free patients with schizophrenia.
One preliminary study suggested that glutamine elevations were not present in medication-
free patients who were receiving benzodiazepines, drugs that would be predicted to suppress
excitatory neurotransmission.
c. MRS in Alcohol Dependence.
MRS studies evaluating NAA and choline have provided neurochemical evidence that
complements the MRI findings related to the emergence and recovery from alcohol-related
neurotoxicity. MRS studies of GABA have provided insights into alterations in cortical
inhibitory neurotransmissions associated with the recovery from alcohol dependence. During
acute withdrawal, cortical GABA levels appear to be normal. With recovery from alcohol
dependence, cortical GABA levels appear to decline and may be significantly below the level
seen in healthy subjects with extended sobriety.
APPLICATIONS
Conventional DWI (without DTI) directly visualizes the ischemic necrosis in cerebral
infarction in the form of a cytotoxic edema, appearing as a high DWI signal within minutes
of arterial occlusion. With perfusion MRI detecting both the infarcted core and the
salvageable penumbra, the latter can be quantified by DWI + perfusion MRI.
References :
1) http://www.ambonsall.com/pdf/Cranial%20Nerves.pdf
2) http://neuroexam.med.utoronto.ca/cranial_12.htm
3) www.slideshare.com
4) Peter Buckley, Del Prewette, Jonathan Bird and Glynn Harrison “
Examination notes in psychiatry”; Hodder Education publishers ; 2005
pp. 185-194
5) Alina Uzelac, Ryan Davis ; “Blueprints radiology” Lippincott
Williams and Wilkins ; 2006 pp. 1, 21, 31.
6) Benjamin James Sadock; Virginia Alcott Sadock; Pedro Ruiz;
“synopsis of psychiatry- Behavioral Sciences/Clinical Psychiatry”;
Wolters Kluwer- 11th ed. Pp.266-281
7) Sreevani R, “ A guide to mental health and psychiatric nursing”;
Jaypee publishers , second edition.