INVESTIGATIONS IN PSYCHIATRY

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.

SR.NO. TEST PURPOSE

1) Basic laboratory tests (e.g., complete Used to screen for general medical conditions or
blood count; blood chemistries, provide baseline measures prior to treatment.
including lipid profile, B12, folate; Recommended frequency of screening may vary
urinalysis) with health status and with specific on going
treatments (e.g., second-generation
antipsychotics, lithium).
2) Medication levels Used to monitor therapeutic levels of
medications.
3) Pregnancy test Some psychiatric conditions and treatments may
entail risks to a pregnant woman or her fetus.
4) Fasting blood glucose or haemoglobin Used to diagnose diabetes or help determine risk.
A1c Patients prescribed second-generation
antipsychotics may be at increased risk of
developing diabetes.
5) Lyme serology, syphilis serology, HIV May assist in evaluation of cognitive and
test behavioral changes. Individuals with behavioral
problems such as impulsivity or drug use may be
at increased risk for HIV infection.
6) Thyroid function tests May be important for patients with suspected
mood disorder, anxiety disorder, or dementia.
Used to monitor lithium effects.
7) Toxicology screen, blood alcohol level Used to screen for substance use or abuse.
Individuals with a mental disorder are at
increased risk for substance abuse.
8) Electrocardiogram Used to assess effects of medications that may
influence cardiac conduction (e.g., tricyclic
antidepressants, some antipsychotics). May also
be indicated depending on age and health status.
9) Chest X ray Used to diagnose cardiopulmonary disorders
(e.g., pneumonia, tuberculosis) that may
contribute to delirium. May also be part of a pre-
ECT evaluation depending on age and health
status
10) Lumbar puncture Used to diagnose central nervous system
infection (e.g., meningitis, herpes,
toxoplasmosis, syphilis, Lyme disease). May be
important for differential diagnosis of delirium

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.

Drugs of Abuse that Can Be Detected in Urine

Sr.no. Drug Length of time detected in urine

1) Alcohol 7-12hrs
2) Amphetamine 48-72 hrs.
3) Barbiturate 24 hrs. (short acting); 3 wks. (long acting)
4) Benzodiazepine 3 days
5) Cocaine 6-8 hrs. (metabolites 2-4 days)
6) Codeine 48 hrs.
7) Heroin 36-72 hrs.
8) Marijuana 2-7 days
9) Methadone 3 days
10) Methaqualone 7 days
11) Morphine 48-72 hrs.
i) Alcohol:
There is no single test or finding on physical examination that is diagnostic for
alcohol abuse. The history of the pattern of alcohol ingestion is most important in
making the diagnosis.
Laboratory studies in patients who abuse alcohol may reveal macrocytosis. This
occurs in most patients who consume four or more drinks per day. Alcoholic liver
disease is characterized by elevations in AST and ALT, typically in a ratio of AST
to ALT of 2: 1 or greater. The y-glutamyl transpeptidase (GGT) level may be
elevated. Carbohydrate-deficient transferrin (CDT) may be helpful in the
identification of chronic heavy alcohol use. It has a sensitivity of 60 to 70 percent
and a specificity of 80 to 90 percent.
ii) Environmental Toxins
Specific toxins are associated with a variety of behavioral abnormalities. Exposure
to toxins commonly occurs through occupation or hobbies.
  Aluminium intoxication can cause a dementia-like condition. Aluminium
can be detected in the urine or blood.
 Arsenic intoxication may cause fatigue, loss of consciousness, anaemia,
and hair loss. Arsenic can be detected in urine, blood, and hair.
 Manganese intoxication may present with delirium, confusion, and a
parkinsonian syndrome. Manganese may be detected in urine, blood, and
hair.
 Symptoms of mercury intoxication include apathy, poor memory, lability,
headache, and fatigue. Mercury can be detected in urine, blood, and hair.
Manifestations of lead intoxication include encephalopathy, irritability,
apathy, and anorexia.
 Lead can be detected in blood or urine. Lead levels typically are assessed
by collecting a 24-hour urine sample.
 The free erythrocyte protoporphyrin test is a screening test for chronic lead
intoxication. This test is commonly coupled with a blood lead level.
Significant exposure to organic compounds, such as insecticides, may produce
behavioral abnormalities. Many insecticides have strong anticholinergic effects.
There are no readily available laboratory tests to detect these compounds. Poison
control centers may assist in the identification of appropriate testing facilities
iii) Volatile Solvent Inhalation:
Chronic abuse of volatile solvents is associated with damage to the brain, liver,
kidneys, lung, heart, bone marrow, and blood. Abuse may produce hypoxia or
anoxia.
Signs of abuse include short-term memory loss, cognitive impairment, slurred and
"scanning" speech, and tremor. Cardiac arrhythmias may occur. Exposure to
toluene, which is present in many cleaning solutions, paints, and glues, has been
associated with loss of clear gray-white matter differentiation and with brain
atrophy on MRI scans.
Methemoglobinemia has occurred with butyl nitrite abuse. Chronic use of volatile
solvents is associated with the production of panic attacks and an organic
personality disorder. Chronic use may also produce impairment in working
memory and executive cognitive function.
b) SERUM MEDICATION CONCENTRATIONS
Serum concentrations of psychotropic medications are assessed to minimize the risk of
toxicity to patients receiving these medications and to ensure the administration of amounts
sufficient to produce therapeutic response. This is particularly true for medications with
therapeutic blood levels. Medication levels are often influenced by hepatic metabolism. This
metabolism occurs via the action of enzymes in the liver.

 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.

Sr.no. Hormone Location and Target organ Function Possible

signification of behavioural
release coorelation to
altered secretion
a) ADH Posterior Kidney (causes Conservation Polydipsia; altered
pituitary; release increased of body water pain response;
stimulated by reabsorption) and modified sleep
dehydration, maintenance of pattern
pain, stress blood pressure
b) Oxytocin Posterior Uterus; breasts Contraction of May play role in
pituitary; release the uterus for stress response by
stimulated by labour; release stimulation of
end of of breast milk ACTH
pregnancy;
 stress; during
sexual arousal
c) Growth hormone Anterior Bones and Growth in Anorexia nervosa
(GH) pituitary; release tissues children;
stimulated by protein
growth synthesis in
hormone- adults
releasing
hormone from
hypothalamus
d) Thyroid-stimulating Anterior Thyroid gland Stimulation of Increased levels:
hormone (TSH) pituitary; release secretion of insomnia, anxiety,
stimulated by needed thyroid emotional lability
thyrotropin- hormones for Decreased levels:
releasing metabolism of fatigue, depression
hormone from food and
hypothalamus regulation of
temperature
e) Adrenocorticotropic Anterior Adrenal cortex Stimulation of Increased levels:
hormone (ACTH) pituitary; release secretion of mood disorders,
stimulated by cortisol, which psychosis
corticotropin- plays a role in Decreased levels:
releasing response to depression, apathy,
hormone from stress fatigue
hypothalamus
f) Prolactin Anterior Breasts Stimulation of Increased levels:
pituitary; release milk depression,
stimulated by production anxiety, decreased
prolactin libido, irritability
releasing
hormone from
hypothalamus
g) Gonadotropic Anterior Ovaries and Stimulation of Decreased levels:
hormones pituitary; release testes secretion of depression and
stimulated by oestrogen, anorexia nervosa
gonadotropin- progesterone, Increased
releasing and testosterone:
hormone from testosterone; increased sexual
hypothalamus role in behavior and
ovulation and aggressiveness
sperm
production
h) Melanocyte Anterior Pineal gland Stimulation of Increased levels:
stimulating pituitary; release secretion of depression
hormone (MSH) stimulated by melatonin
onset of
darkness

 Anabolic Steroid Use

Use of anabolic steroids has been associated with irritability, aggression, depression, and
psychosis. Athletes and bodybuilders are common abusers of anabolic steroids. Urine
specimens can be used to screen for these agents. Because so many compounds have been
synthesized, a variety of tests may be required to confirm the diagnosis, depending on the
compound that has been used. Consultation with a specialist is advised. Generally, androgens
other than testosterone can be detected by gas chromatography and mass spectroscopy.

 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.

 Human Chorionic Gonadotropin

Human chorionic gonadotropin (hCG) can be assessed in the urine and blood. The urine test
for hCG is the basis for the commonly used urine pregnancy test. This immunometric test is
able to detect pregnancy approximately 2 weeks after an expected menstrual period has
passed. Routine tests are most accurate when performed 1 to 2 weeks after a missed period
and are not reliably accurate until the 2-week period has passed. However, there are
ultrasensitive urine hCG tests that can accurately detect pregnancy 7 days after fertilization.
Pregnancy tests often are obtained before initiating certain psychotropic medications, such as
lithium, carbamazepine, and valproate, which are associated with congenital anomalies.

 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.

 Systemic Lupus Erythematosus :

SLE is an autoimmune disorder. Tests for SLE are based on the detection of antibodies
formed as part of the disease. Antinuclear antibodies are found in virtually all patients with
SLE. Antibody levels also are used to monitor the severity of the illness. A fluorescent test is
used to detect the antinuclear antibodies. This test can be positive in a variety of rheumatic
diseases. For this reason, a positive result usually is followed by additional tests, including a
test to detect anti-deoxyribonucleic acid (DNA) antibodies. Anti-DNA antibodies, when
associated with antinuclear antibodies, are strongly suggestive of a diagnosis of lupus. Anti-
DNA antibodies are followed to monitor the response to treatment. Psychiatric manifestations
of lupus include depression, dementia, delirium, mania, and psychosis. About 5 percent of
patients with lupus present with symptoms of psychosis including hallucinations and
delusions.

 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).

e) INFECTIOUS DISEASE TESTING

Testing for sexually transmitted diseases (STDs) has become common, given the current
frequency of these diseases. Some psychiatric illnesses, such as mania and substance abuse,
are associated with a higher risk of contracting STDs. STDs include herpes simplex virus
types 1 and 2, chlamydia, hepatitis viruses, gonorrhoea, syphilis, and human Immuno
deficiency virus (HIV). Risk factors for STD include contact with sex workers, drug abuse,
prior history of STDs, meeting partners on the Internet, multiple sex partners, a new sex
partner, and being young or unmarried. Other diseases to think about are Epstein-Barr virus
and gonorrhoea.

 Intravenous Drug Use

The IV route is used for many substances of abuse. Most commonly, heroin, amphetamines,
and cocaine are used alone or in combination via the IV route. Because needles often are
contaminated, IV drug users are at risk for bacterial endocarditis, hepatitis B and C, HIV
infection, and acquired immunodeficiency syndrome (AIDS) from HIV infection. It has been
estimated that over 60 per cent of new cases of hepatitis C occur in individuals with a history
of injecting illicit drugs.
CBC and Serum Blood Cultures. The use of contaminated needles or non sterile injection
sites places IV drug users at risk for bacterial infections, including abscesses, bacteraemia,
and bacterial endocarditis. Findings on physical examination suggestive of endocarditis,
possible bacteraemia, or abscess necessitate obtaining a CBC to rule out an elevated WBC
count. Blood cultures should be obtained from at least two different sites if the patient is
febrile or if findings are suggestive of bacteraemia or endocarditis, and internal medicine
consultation should be obtained.

 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.

f) NEUROLEPTIC MALIGNANT SYNDROME

Neuroleptic malignant syndrome (NMS) is a rare, potentially fatal, consequence of
neuroleptic administration. The syndrome consists of autonomic instability, hyperpyrexia,
severe extrapyramidal symptoms (i.e., rigidity), and delirium.
Liver enzymes become elevated with liver failure. Patients may die from hyperpyrexia,
aspiration pneumonia, renal failure, hepatic failure, respiratory arrest, or cardiovascular
collapse.
A typical laboratory workup for NMS includes a CBC, serum electrolytes, BUN, Cr, and CK.
A urinalysis, including an assessment of urine myoglobin, is also usually performed. As part
of the differential diagnosis, blood and urine cultures are performed as part of a fever
workup. Pronounced elevations in the white blood cell (WBC) count may occur in NMS.
White blood cell counts are typically in the range from 10,000 to 40,000 per mm3 .

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.

II. CRANIAL STUDIES

Cranial nerves are the nerves that emerge directly from the brain (including the brainstem),
in contrast to spinal nerves (which emerge from segments of the spinal cord). 10 of the
cranial nerves originate in the brainstem. Cranial nerves relay information between the brain
and parts of the body, primarily to and from regions of the head and neck .
Most typically, humans are considered to have twelve pairs of cranial nerves (I–XII), with
the terminal nerve (0) more recently canonized. They are: the olfactory nerve (I), the optic
nerve (II), oculomotor nerve (III), trochlear nerve (IV), trigeminal nerve (V), Abducens
nerve (VI), facial nerve (VII), Vestibulo cochlear nerve (VIII), glossopharyngeal
nerve (IX), Vagus (X), accessory nerve (XI), and hypoglossal nerve (XII).

The goals of the cranial examination are several:

1. For patients presenting with symptoms suggestive of a neurological problem, the

examination should:
a. Determine, on the basis of an organized and thorough examination, whether in
fact neurological dysfunction exists.
b. Identify which component(s) of the neurological system are affected (e.g.
motor, sensory, cranial nerves, or possibly several systems simultaneously).
c. If possible, determine the precise location of the problem (e.g. peripheral v
central nervous system; region and side of the brain affected etc.).
d. On the basis of these findings, generate a list of possible etiologies. Unlikely
diagnoses can be excluded and appropriate testing (e.g. brain and spinal cord
imaging) then applied in an orderly and logical fashion.

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.

3. Cursory screening/documentation of baseline function for those who are

otherwise healthy.

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.

II. OPTIC NERVE

Anatomy :

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.

 Pupillary Abnormalities see pupillary abnormalities article.

 Optic neuritis (pain on moving eye, loss of central vision, afferent pupillary defect,
papilloedema).
Causes: demyelination; rarely sinusitis, syphilis, collagen vascular disorders.
 Optic atrophy (pale optic discs and reduced acuity): MS; frontal tumours; Friedreich's
ataxia; retinitis pigmentosa; syphilis; glaucoma; Leber's optic atrophy; optic nerve
compression.
 Papilloedema (swollen discs):
 Raised ICP (tumour, abscess, encephalitis, hydrocephalus, benign intracranial
hypertension);
 Retro-orbital lesion (e.g. cavernous sinus thrombosis);
 Inflammation (e.g. optic neuritis);
 Ischaemia (e.g. accelerated hypertension).
Test
 Visual acuity can be tested using a Snellen chart after correcting for any refraction
errors
 Visual fields should be tested using a red pin that is held equidistant from yourself
and the patient. The pin is gradually moved into the centre of vision until it is visible
to both yourself and the patient.
 Pupillary reflexes (direct and consensual reflexes) should be tested using a pen torch .
Shining a light into the patient’s eyes should make their pupils constrict. Both pupils
should constrict at the same time, independent of which eye the light is actually
focused on
 The accommodation reflex can be tested by asking the patient to focus on a distant
object; then placing your finger near the tip of the patient’s nose, ask them to focus on
your finger, whilst you continue observing their eyes, which should converge and the
pupils should constrict
 Colour vision can be examined using standardised tests such as Ishihara plates.
 Fundoscopy enables examination of the red reflex, optic disc and surrounding media.
Look for any papilloedema, macular changes or retinal abnormalities such as diabetic
retinopathy (haemorrhages, cotton wool spots and neovascularisation) and
hypertensive retinopathy (silver wiring, A-V nipping, haemorrhages, cotton wool
spots and rarely papilloedema) .
 III. OCULOMOTOR NERVE

It consists of two components with distinct functions:

 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.

 Extraocular movements is tested by inspecting for ptosis, eye position

and nystagmus. The pupil size is measured, its shape and any asymmetry is tested. A
commonly used abbreviation to describe normal pupils is PERRLA (pupils equal,
round and reactive to light and accommodation).
 Pupillary light reflex is tested by having the patient stare into the distance as the
examiner shines the penlight obliquely into each pupil. Pupillary constriction is tested
for on the eye examined (direct response) and on the opposite eye (consensual
response). The swinging flashlight test involves moving the light between the two
pupils. Normally both direct and consensual responses are elicited when the light
shines on an eye, and some dilation will occur during the swing between.
 IV. TROCHLEAR NERVE

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.

Test findings (Positive & Negative results):

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.

a. Ophthalmic division : The ophthalmic division conveys sensory information from

the:
o Scalp
o Forehead
o Upper parts of the sinuses
o Upper eyelid and associated mucous membranes
o Cornea of the eye
o Bridge of the nose
b. Maxillary division

Like the ophthalmic division, the maxillary division of your trigeminal nerve has a sensory
component. It transmits sensory information from the:

o Lower eyelid and associated mucous membranes

o Middle part of the sinuses
o Nasal cavity and middle part of the nose
o Cheeks
o Upper lip
o Some of the teeth of the upper jaw and associated mucous membranes
o Roof of the mouth
c. Mandibular

The mandibular division is the only part of the trigeminal nerve that has both sensory and
motor functions. It communicates sensory information from the:

o Outer part of the ear

o Lower part of the mouth and the associated mucous membranes
o Front and middle parts of the tongue
o Teeth of the lower jaw and the associated mucous membranes
o Lower lip
o Chin

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.

Several things can cause irritation of the trigeminal nerve, including:

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.

Common methods include:

 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.

VI. ABDUCENS NERVE:

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.

Test findings ( Positive & Negative results):

An inability for the patient to look medially may be indicative of a lesion of the trochlear
nerve.

VII. FACIAL 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.

 Ramsay Hunt syndrome

Ramsay Hunt syndrome is caused by a virus in the facial nerve, and is a more severe cause of
facial paralysis. Less than half of patients will recover completely..

 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.

 Skull base tumours

Tumours within the facial nerve, benign tumours close to and compressing the facial nerve,
or malignant tumours invading the facial nerve may cause facial weakness. The tumours most
commonly involved are acoustic neuroma, facial neuroma and tumours in the region of the
parotid gland. These tumours may be accompanied with progressive or recurrent facial
weakness and other symptoms such as hearing loss or a mass in your neck.

 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.

VIII. VESTIBULOCOCHLEAR NERVE :

The vestibulocochlear nerve (sometimes referred to as the auditory nerve) is the eighth of
twelve cranial nerves. This group includes all the nerves that emerge from the cranium
(skull), as opposed to those that emerge from the vertebral column (spinal cord). It is a paired
set of nerves (one from each ear) and the nerve is located in the internal auditory canal, a part
of the skull's temporal bone.

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 :

It contains sensory, motor (stylopharyngeus only) and parasympathetic fibres (salivary

glands). It passes across the posterior fossa, through the jugular foramen and into the neck
supplying tonsil, palate and posterior third of tongue. The glossopharyngeal nerve consists of
five components with distinct functions:
SR. NO. FUNCTION DESCRIPTION
1) Brachial motor Supplies the stylopharyngeus muscle.
(special visceral
efferent)

2) Visceral motor Parasympathetic innervation of the smooth muscle and glands of

(general visceral the pharynx, larynx, and viscera of the thorax and abdomen.
efferent)

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 :

SR.NO. FUNCTION DESCRIPTION

1. Branchial motor Supplies the voluntary muscles of the pharynx and most of the
(special visceral larynx, as well as one extrinsic muscle of the tongue.
efferent)

2. Visceral motor Parasympathetic innervation of the smooth muscle and glands

(general visceral
 efferent) of the pharynx, larynx, and viscera of the thorax and abdomen.

3. Visceral sensory Provides visceral sensory information from the larynx,

(general visceral oesophagus, trachea, and abdominal and thoracic viscera, as
afferent) well as the stretch receptors of the aortic arch and
chemoreceptors of the aortic bodies.

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.

5. Special sensory A very minor component of CN X. Provides taste sensation

(special afferent) from the epiglottis region.

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.

Symptoms of gastroparesis include:

 nausea or vomiting, especially vomiting undigested food hours after eating
 loss of appetite or feeling full shortly after starting a meal
 acid reflux
 abdominal pain or bloating
 unexplained weight loss
 fluctuations in blood sugar
d. Vasovagal syncope
The vagus nerve stimulates certain muscles in the heart that help to slow heart rate.
When it overreacts, it can cause a sudden drop in heart rate and blood pressure,
 resulting in fainting. This is known as vasovagal syncope. Sometimes the vagus nerve
overreacts to certain stress triggers, such as:
 exposure to extreme heat
 fear of bodily harm

 the sight of blood or having blood drawn

 straining, including trying to having a bowel movement

 standing for a long time

Test :

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:

o observe for atrophy or asymmetry of the muscles.

o observe for quickness of shoulder shrug and ask the patient to shrug their shoulders
against resistance.
o ask the patient to turn their head to the opposite side against resistance, both watch
and palpate the sternocleidomastoid muscle.
o ask the patient to flex their head forward against resistance, placing your opposite
hand against the back of the head gently to support the patient’s neck should there be
any weakness.

XII. HYPOGLOSSAL NERVE :

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 :

The hypoglossal nerve is motor to the tongue.

Examination Technique:

o observe for tongue atrophy or enlargement.

o do not overcall tongue fasciculations. It is very difficult to relax the tongue.
o ask the patient to protrude the tongue.
o ask the patient to push the tongue into each cheek or alternatively to protrude the
tongue and push it laterally against a tongue depressor.
o ask the patient to move the tongue quickly from side to side.
o if there is facial weakness, correct this by supporting the upper lip on the side of
weakness, otherwise there may appear to be deviation of the tongue but once the
facial weakness is corrected for, the tongue will no longer appear to deviate.

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.

Pathologic features of cranial nerves

Sr.no. Cranial nerve Pathologic features

1. CN I: Olfactory Nerve Unilateral anosmia

2. CN II: Optic Nerve Sight Unilateral vision loss

3. CN III: Oculomotor Ptosis , eye deviated laterally and downward,

Nerve diplopia, dilated and nonreactive pupil, loss of
accommodation
4. CN IV: Trochlear Nerve Inability to move eye downward and laterally,
diplopia, head tilt toward unaffected eye
5. CN V: Trigeminal Nerve Partial facial; anaesthesia periodic lancinating facial
pain
6. CN VI: Abducens nerves Diplopia, inability to move affected eye laterally

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

XIII. RADIOLOGICAL EXAMINATION

The specialty of radiology includes conventional techniques that use ionizing radiation,
such as radiography (plain film), fluoroscopy, computed tomography (CT), and nuclear
medicine. It also includes the techniques of magnetic resonance imaging (MRI) and
ultrasound, which produce images with magnetic fields and sound waves, respectively,
thereby avoiding the risks of radiation.
Imaging of the central nervous system (CNS) can be broadly divided into two domains:
structural and functional.
Neuroimaging methodologies allow measurement of the structure, function, and
chemistry of the living human brain. Computer tomographic (CT) scanners, the first
widely used neuroimaging devices, allowed assessment of structural brain lesions such as
tumours or strokes. Magnetic resonance imaging (MRI) scans, developed next,
distinguish grey and white matter better than CT scans do and allow visualizations of
smaller brain lesions as well as white matter.
HISTORY OF NEUROIMAGING
 The first chapter of the history of neuroimaging traces back to the Italian
neuroscientist Angelo Mosso who invented the 'human circulation balance', which
could non-invasively measure the redistribution of blood during emotional and
intellectual activity.
 In 1918 , The American neurosurgeon Walter dandy introduced the technique of
ventriculography. x-ray images of the ventricular system within the brain were
obtained by injection of filtered air directly into one or both lateral ventricles of
the brain.
 In 1927 Egas Moniz introduced cerebral angiography, whereby both normal and
abnormal blood vessels in and around the brain could be visualized with great
precision.
 1946 – MR phenomenon explained by Bloch & Purcell
 1952 – Nobel prize
 1950 – 1970 – NMR developed as an analytical tool
 1963 – 1st instance of SPECT using anger camera – Kuhn & Edwards
 1972 – computerized tomography Godfrey Hounsfield, Alan Mcleod
Cormack
 1979 – Nobel prize
 1973 – Back projection MRI – Lauterbar
 1983 – Compton camera for SPECT – Manbir Singh & David Doria
 1985 – DTI – Le Bihan D & Breton E
 1986 – Gradient echo imaging, NMR microscope
 MR angiography – Dumoulin
 1992 – functional MRI by Richard .R. Ernst

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.

INDICATIONS FOR NEUROIMAGING IN CLINICAL RESEARCH

a. Analysis of clinically defined groups of patients.
Psychiatric research aims to categorize patients with psychiatric disorders to facilitate the
discovery of neuroanatomical and neurochemical bases of mental illness. Researchers have
used functional neuroimaging to study groups of patients with such psychiatric conditions as
schizophrenia, affective disorders, and anxiety disorders, among others.
 In schizophrenia, for example, neuro pathological volumetric analyses have suggested
a loss of brain weight, specifically of grey matter. A paucity of axons and dendrites
appears present in the cortex, and CT and MRI may show compensatory enlargement
of the lateral and third ventricles. Specifically, the temporal lobes of persons with
schizophrenia appear to lose the most volume relative to healthy persons.
 Disorders of mood and affect can also be associated with loss of brain volume and
decreased metabolic activity in the frontal lobes. Inactivation of the left prefrontal
cortex appears to depress mood; inactivation of the right prefrontal cortex elevates it.
  Among anxiety disorders, studies of obsessive-compulsive disorder with conventional
CT and MRI have shown either no specific abnormalities or a smaller caudate
nucleus.
 Functional PET and SPECT studies suggest abnormalities in the corticolimbic, basal
ganglia, and thalamic structures in the disorder. When patients are experiencing
obsessive-compulsive disorder symptoms, the orbital prefrontal cortex shows
abnormal activity.
 A partial normalization of caudate glucose metabolism appears in patients taking
medications such as fluoxetine (Prozac) or clomipramine (Anafranil) or undergoing
behavior modification.
b. Analysis of brain activity during performance of specific tasks.
Many original conceptions of different brain region functions emerged from observing
deficits caused by local injuries, tumours, or strokes. Functional neuroimaging allows
researchers to review and reassess classic teachings in the intact brain. Most work, to date,
has been aimed at language and vision. Although many technical peculiarities and limitations
of SPECT, PET, and functional MRI (fMRI) have been overcome, none of these techniques
has demonstrated clear superiority.
Studies have been designed to reveal the functional neuro anatomy of all sensory modalities,
gross and fine motor skills, language, memory, calculations, learning, and disorders of
thought, mood, and anxiety. Unconscious sensations transmitted by the autonomic nervous
system have been localized to specific brain regions. These analyses provide a basis for
comparison with results of studies of clinically defined patient groups and may lead to
improved therapies for mental illnesses.

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

2. MAGNETIC RESONANCE IMAGING (MRI)

MRI images are generated from motion of tissue protons when excited within a magnetic
field. MRI possesses superior anatomical resolution and multiplanar scanning capacity than
CT. It allows for three-dimensional reconstruction and volumetric quantification. MRI tissue-
relaxation parameters (T1 and T2) may also give information on tissue hydration status and
iron or lipid metabolism.

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.

GENERAL GUIDELINES FOR STRUCTURAL RADIOLOGY

 Criteria for appropriate structural brain imaging (Dougherty and Rauch 2001):
1. Patients with acute changes in mental status (including changes in affect, behavior, or
personality) plus at least one of three additional criteria:
 Age greater than 50 years
  Abnormal neurological exam (especially focal abnormalities)
 History of significant head trauma
2. New onset psychosis.
3. New onset delirium or dementia of unknown cause.
4. Possibly for treatment refractory patients.
5. Possibly prior to an initial course of electroconvulsive therapy
6. Adherence to the criteria listed above yield positive findings in 10–45% of cases.
7. However, only 1–5% will produce findings that lead to specific medical intervention.
8. Lastly, if structural neuroimaging is indicated, one should use MRI unless the
problem is an acute trauma or an acute bleed is suspected

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.

USES OF MRI IN PSYCHIATRIC DISORDERS:

 MRI AND SCHIZOPHRENIA
• Confirmed ventricular enlargement (lateral ventricles, 4th ventricle) and
cortical tissue loss or hypoplasia, as seen in CT studies or longitudinal studies,
generally suggests a non-progressive nature, favouring a neurodevelopmental
basis . but some patients show neuro progression.
• There is an association with subtle anomalies (e.g. agenesis of corpus
callosum, cavum septum pellucidum) of neurodevelopmental origin.
Reduction in size of mesial temporal lobe and superior temporal gyrus
(especially on the left) is correlated with positive symptoms. Other findings
include smaller frontal lobes, and larger basal ganglia structures (probably
medication-related).
 •Improved (tissue segmentation) methodology has suggested more widespread
grey matter cortical loss and findings consistent with generalized subtle tissue
loss.
• T1 and T2 findings are inconsistent.
• There are associations of brain abnormalities with many clinical indices:
poorer premorbid function, negative symptoms, obstetric complications,
family history of schizophrenia, treatment resistance.
 MRI AND AFFECTIVE DISORDERS
o There is a high prevalence of white matter/hyper intensity lesions in bipolar
patients, particularly in elderly depressives.
o Some studies report reductions in size of caudate and putamen nuclei in
depression; others find only temporal lobe (right hippocampus) reduction.
o Neuroimaging findings are less pronounced than in schizophrenia. Late-onset
depression has more brain changes than early-onset. Brain abnormalities on
neuroimaging generally are associated with cognitive impairment, poorer
outcome and higher mortality.
 MRI AND ALZHEIMER’S DISEASE (AD)
o Selective loss of hippocampal tissue may occur early in AD, and in mild
cognitive impairment (MCI). Presence of apolipoprotein E gene is associated
with more (and earlier) neuroimaging abnormalities.
o Both ventricular enlargement and cortical tissue loss show high prevalence in
the ‘normal’ population after age 60.
o In Alzheimer’s disease, ventricular enlargement is marked and progressive and
is of both diagnostic and prognostic significance. Cortical tissue loss is less
clearly related.
o MRI or CT is useful to distinguish aetiology and type of dementia: ‘patchy’
atrophy and multiple lucencies in multi-infarct dementia; atrophy of caudate
and fronto temporal region in Huntington’s chorea; hypodensities in basal
ganglia in Wilson’s disease.
o There is severe, bilateral atrophy of anterior frontal ( temporal) lobes in Pick’s
disease; cortical and subcortical atrophy in Parkinson’s disease.
o Ventricular enlargement and cerebral atrophy is seen in chronic alcoholics.
Cerebral atrophy is related to the extent of cognitive impairment.
o In some patients, abstinence is associated with reversibility of CT findings.
 MRI AND SUBSTANCE ABUSE
o Reduction in cortical grey matter and T1 changes correlate with cognitive
impairments in alcoholics.
o MRI detects neuro pathological changes in Wernicke–Korsakoff’ s syndrome
(WKS).
o Gadolinium-enhanced MRI indicates blood–brain barrier impermeability in
WKS reduces after 1 week of thiamine treatment.
o Some report white matter hyper intensities in opiate addicts.
 MRI AND AUTISM
o Generally larger brains are reported.
o Reports of hypoplasia of the 4th ventricle, cerebellar vermis and parietal tissue
loss.
 MRI AND GILLES DE LA TOURETTE’S SYNDROME (GTS)
There are some reports of asymmetry and/or reduction in basal ganglia structures in GTS.
RISKS OF MRI :
 MR images are made without using any ionizing radiation, so patients are not exposed to
the harmful effects of ionizing radiation. But while there are no known health hazards from
temporary exposure to the MR environment, the MR environment involves a strong, static
magnetic field, a magnetic field that changes with time (pulsed gradient field), and
radiofrequency energy, each of which carry specific safety concerns:
 The strong, static magnetic field will attract magnetic objects (from small items such as
keys and cell phones, to large, heavy items such as oxygen tanks and floor buffers) and
may cause damage to the scanner or injury to the patient or medical professionals if those
objects become projectiles. Careful screening of people and objects entering the MR
environment is critical to ensure nothing enters the magnet area that may become a
projectile.
 The magnetic fields that change with time create loud knocking noises which may harm
hearing if adequate ear protection is not used. They may also cause peripheral muscle or
nerve stimulation that may feel like a twitching sensation.
 The radiofrequency energy used during the MRI scan could lead to heating of the body.
The potential for heating is greater during long MRI examinations.
CT SCAN
Computed tomography (CT) is a method of using x-rays in multiple projections to produce
axial images of the body. The image production differs from conventional radiography in that
the x-rays pass through the patient to highly sensitive detectors instead of film. These
detectors then send the information to a computer that reconstructs the images. It uses a
combination of X-rays and a computer to create pictures of your organs, bones, and other tissues.
It shows more detail than a regular X-ray.
CT is a method of using x-rays to produce axial images of the body; these images are viewed
as if looking from the feet up toward the head. CT is more sensitive than conventional plain
film in distinguishing differences of tissue density. CT scanners effectively take a series of
head X-ray pictures from all vantage points, 360 degrees around a patient's head.
Principle :
The CT scanner uses a motorized x-ray source that rotates around the circular opening of a
donut-shaped structure called a gantry. During a CT scan, the patient lies on a bed that slowly
moves through the gantry while the x-ray tube rotates around the patient, shooting narrow
beams of x-rays through the body. CT scanners use special digital x-ray detectors, which are
located directly opposite the x-ray source. As the x-rays leave the patient, they are picked up
by the detectors and transmitted to a computer.

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 :

a. CT Scans That Do Not Require Preparation

The following CT scans are never done with contrast and require no preparation on the part
of the patient:

 CT Temporal Bones / CT IAC (Internal Auditory Canal)/ CT Mandible/CT

Facial Bones/ CT Orbits – used to detect fractures, tumors, trauma, infections and
other anomalies in the mastoids, middle and inner ear and the jaw bone/face.
 CT Sinuses – most commonly done to check for a deviated septum or sinusitis or
polyps.
 CT Ankle/CT Foot/ CT Elbow/ CT Clavicle & Sternoclavicular (S/C) Joints/ CT
Hand/ CT Hip/ CT Knee/ CT Sacrum & Coccyx/ CT Wrist – most often done to
diagnose fractures, injury to the ligament and dislocations.

b. CT Scans That May Require IV Contrast

The contrast material is iodine based and is used to enhance the detail in blood vessels and
soft tissue. It is particularly helpful in isolating pathologies such as cancer.

 CT Head – usually done to detect infarction, the source of headaches, seizures,

dizziness, tumors, stroke, TIA, hemorrhage and trauma to the bones
 CT Neck Soft Tissue – done to detect mass, tumor, foreign object, gland lesion,
infection or abscess.
 CT Extremities – most often done to diagnose mass, fractures, injury to the ligament
and dislocations.
 CT Spine – done to assess injury or abnormalities in the cervical, thoracic or lumbar
spine
 CT Chest – usually performed to detect acute and chronic changes in the lungs, such
as fibrosis, emphysema, and tumors
 CT Urogram – evaluates the kidneys, ureters, and bladder for stones, blockages and
cancers or stenosis.

INDICATIONS OF CT SCAN IN PSYCHIATRY

 Confusion &/or dementias of unknown cause
 First episode of psychosis
 First episode of major affective disorder after 50 years of age
 Personality changes after 50 years of age
  Psychiatric symptoms following head injury
 To rule out complications due to possible head trauma
 Prolonged catatonia
 Co existence of seizure with psychiatric symptoms
 Movement disorders of unknown aetiology
 Focal neurological signs accompanying psychiatric symptoms

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).

PLAIN SKULL RADIOGRAPHY :

Skull radiography is the radiological investigation of the skull vault and associated bony
structures. Seldom requested in modern medicine, plain radiography of the skull is often a
last resort in trauma imaging in the absence of a CT. However, it is still utilised in the setting
of skeletal surveys.

Major Indications of Skull radiographs

 Headache.

 Possible pituitary problems - (CT/MRI preferred).

 Possible space-occupying lesion.

 Epilepsy.

 Dementia or memory loss.

 Middle or inner ear problems.

 Nasal trauma - coned views may be requested by the appropriate specialist.

 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:

 Reduce intracranial pressure (ICP), e.g., pre-, intra-, or postoperative.

 Monitor CSF chemistry, cytology, and physiology.
 Provide temporary CSF drainage in patients with infected cerebrospinal fluid shunts.

Monitoring of intracranial pressure (ICP) is indicated in selected patients with:

 Severe head injury

 Subarachnoid hemorrhage graded III, IV, or V preoperatively
 Reyes syndrome or similar encephalopathy’s
 Hydrocephalus
 Intracranial hemorrhage
 Miscellaneous problems when drainage is to be used as a therapeutic maneuver.

Monitoring can also be used to evaluate the status pre- and postoperatively for space-
occupying lesions.

COMPLICATIONS

 Infections, particularly meningitis, ventriculitis, and wound infections

 Over drainage, leading to:
 Intracranial hemorrhage
 Permanent neurological deficit
 Frequent punctures of the brain to insert the ventricular catheter can predispose to
intracerebral hemorrhage and edema leading to a further rise in Intracranial Pressure
(ICP).
 Poor recording of ICP will result if the catheter, patient line or other components of
the monitoring system become clogged with blood clots, brain tissue fragments, or
fibrinous debris.
 Ventricular wall collapse, in small patients, resulting in obstruction of the catheter and
predisposing to tentorial herniation. It is therefore important to avoid excessive
release of CSF before the system catheter is attached to the patient line.
 Limiting the duration of monitoring from a single site to less than five days will
reduce the infection rate.

FUNCTIONAL BRAIN IMAGING

Functional neuroimaging is the use of neuroimaging technology to measure an aspect of
brain function, often with a view to understanding the relationship between activity in
certain brain areas and specific mental functions. It is primarily used as a research tool
in cognitive neuroscience, cognitive psychology, neuropsychology, and social neuroscience.
Functional imaging is the study of human brain function based on analysis of data acquired
using brain imaging modalities such as Electroencephalography (EEG) , Magneto
encephalography (MEG) , functional Magnetic Resonance Imaging (fMRI) , Positron
Emission Tomography (PET) or Optical Imaging.
Modern functional imaging has two main advantages over the multi/single-unit recordings
used to study the electrophysiology of neurons.
 The first is that it is generally non-invasive, and is therefore applicable routinely in
humans. This allows for the study of unique human attributes such as language.
 The second is that it can provide a wide field of view. Rather than recording
information about a single or small number of neuronal cells, an image may be
gathered summarizing simultaneous activity across the whole brain. This provides a
different yet complementary perspective on neural coding
A disadvantage, however, is that functional imaging provides only an indirect measure of the
quantities of primary interest to neuroscientists e.g., firing rates and membrane potentials.
Current research is aimed at bridging this gap using a combination of experimental and
mathematical modelling approaches.

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).

DIFFRENCE B/W MRI AND fMRI

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.

B. fMRI of Alcohol Dependence.

fMRI studies have provided insights into the functional consequences of alcoholism-related
neurotoxicity. Studies suggest that recovering alcohol-dependent patients show abnormal
activation patterns in frontal cortex, thalamus, striatum, cerebellum, and hippocampus related
to impairments in attention, learning and memory, motor coordination, and inhibitory control
of behavior. Studies have begun to explore pharmacological modulation of resting circuit
activity to probe mechanisms underlying circuit dysfunction in alcoholism, illustrated by
blunted responses to benzodiazepines.
ADVANTAGES
• Possible to study both cerebral anatomy & functional neurophysiology using a single
technique (Bullmore & Fletcher 2003)
• No radio active exposure
• Used in criminal psychiatry or federal investigations as a lie detector
LIMITATIONS OF FMRI
• FMRI assess neuronal activity indirectly by measuring blood flow (or tissue perfusion). this
limits its resolution.
• Two tasks that activates clusters of neurons 5 mm apart will yield overlapping signals on
FMRI & thus are indistinguishable by this technique.
• Sensitivity & resolution can be improved by using ultra-small non toxic iron oxide particles.
• Acquisition of sufficient images for study can require 20 minutes to 3 hours, during which
the subject’s head must remain in exactly the same position.

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.

THE NORMAL EEG

Frequency ranges
• Delta – less than 4Hz.May occur as regular waves or irregularly. Diffusely distributed over
scalp in sleeping adults and in children but invariably abnormal in non sleeping adults.
• Theta – 4–7Hz. Transient are components found in 15 per cent of the normal population.
• Alpha – 8–13Hz. Prominent over occipital region, accentuated by eye closure and
attenuated by attention. A consistent difference of 1Hz or more between hemispheres is
pathological. Slowing seen in early phenytoin toxicity.
• Beta – 14Hz and above. Principally front central. May be enhanced by anxiety, alcohol and
some drugs (barbiturates, benzodiazepines).
• Mu – Arch-like 7–11Hz waves over precentral areas, attenuated by contralateral limb
movements.
• Lambda – Single sharp waves in occipital region, usually associated with visual ‘scanning’.
• Vertex waves – Electronegative sharp waves over vertex, evoked by auditory stimulus.

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.

NEUROTRANSMITTERS AND SLEEP EEG

• Histamine – active wakefulness, neurones in hypothalamus.
• Cholinergic – wakefulness, REM sleep.
• Adrenergic – decreased REM sleep (MAOIs, clonidine, propranolol ).
• Serotonergic – increased non-REM sleep.
• Dopamine – increased REM sleep.

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.

ABNORMAL EEG PATTERNS

Abnormalities include:
• Reduced amount and amplitude of normal frequencies (generalized or localized).
• Increased slow frequencies (generalized or localized).
• Abnormal waveforms – spikes (duration less than 80ms), sharp waves (duration 80–
200ms),spike and wave complexes.
Abnormal forms may occur spontaneously or may be provoked by photic stimulation,
sleeping, or hyper stimulation.
b. Diffuse abnormalities
• Rhythmic slowing.
• Occasionally periodic discharges.
c. Focal abnormalities
• Polymorphic, arrhythmic unreactive delta.
• Periodic lateralized epileptiform discharges.
d. Epilepsy
• Initial interictal EEG is abnormal in 75 per cent of suffers.
• With repeated recordings,90–95 per cent will show abnormalities.
 • 2 per cent of normal population have abnormalities considered to be
epileptiform.
• Absence seizures:
– 3/second spike and wave in infancy.
– 4/second spike and wave in a juvenile.
• Primary generalized tonic–clonic seizures:
– Interictal – bursts of spike and wave.
– Ictal – 10-Hz fast activity during tonic phase, followed by lower-
frequency spike and wave complexes during clonic phase.
– Postictal – generalized slowing range.
• Myoclonic epilepsy:
– Polyspike and wave.
• Partial (focal) epilepsy:
– Interictal
– focal spikes or sharp waves.
– Ictal
– focal rhythmic discharge.

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.

USES OF THE EEG IN PSYCHIATRY

A. DETECTION OF ORGANIC PSYCHOSIS
In general, there is first a decrease in frequency and responsiveness of rhythm, progressing to
increased amounts of activity at slower frequencies in both and ranges. Changes are usually
diffuse and symmetrical, especially where there are extra cerebral causes. Focal lesions
usually produce localized abnormality.

B. DIAGNOSIS OF SEIZURE AND SLEEP DISORDERS

This is especially important to help identify atypical forms of epilepsy associated with
psychotic experiences, sudden affective disturbance or behavioural change. Notes 1 The EEG
showing ictal activity during a major or focal seizure is diagnostic of epilepsy. Absence of
simultaneous EEG changes during the episodes therefore almost excludes a genuine fit. 2 An
abnormal interictal EEG does not clinch a diagnosis of epilepsy. Taken together with a full
and careful history, interictal spike and wave disturbances give support to a diagnosis of
liability to epilepsy. 3 A normal interictal EEG does not exclude a diagnosis of epilepsy,
which must be based on eyewitness accounts and history. 4 In temporal lobe epilepsy, a
routine and a sleep EEG will reveal spike foci in about 90 per cent of patients.

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.

 Spect and affective disorders

• Some studies report hypofrontality less pronounced than that in schizophrenia, with reversal
during antidepressant therapy.
• Studies also show different pattern of sadness in normal subjects compared with depressed
patients.

 Spect and Alzheimer’s disease

• Decreased rCBF in posterior parietal and temporal regions correlates with
neuropsychological deficits.
• Primary motor, sensory, and visual cortices are relatively unaffected until late in illness.

 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.

RISK AND CONTRAINDICATIONS

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.

 PET and other disorders

• PET studies in affective disorder and Alzheimer’s have shown similar findings to their
respective SPECT research.
• Decreased activity in the right para hippocampus has been demonstrated in panic disorder.
Hyper metabolism in orbitofrontal cortex and caudate nucleus has been reported in OCD; it
normalizes with treatment

 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

Neurochemical Findings from Positron Emission Tomography Radiotracer Scans

Sr. No. Neurotransmitter Work

1) Dopamine o Decreased uptake of dopamine in striatum in parkinsonian
patients
o Dopamine release higher in patients with schizophrenia than in
controls
 o High dopamine release associated with positive symptoms in
schizophrenia
2) Receptors
o D1 receptor o Lower D1 receptor binding in prefrontal cortex of patients with
schizophrenia compared with controls; correlates with negative
symptoms
o D2 receptor o Schizophrenia associated with small elevations of binding at
D2 receptor
o Serotonin o Reduction in receptor binding in patients with unipolar major
type 1 A (5- depression
HT1A)
3) Transporters
o Dopamine o Amphetamine and cocaine cause an increase in dopamine
o Tourette disorder shows increase in dopamine transporter
system (may account for success of dopamine blocking
therapies)
o Serotonin o Serotonin binding is low in depression, alcoholism, cocainism,
binge eating, and impulse control
4) Metabolism
o Nicotine o Cigarette smoking inhibits monamine oxidase activity in brain
o Amyloid-β o Can be visualized in vivo with positron emission tomography
deposits

MAGNETIC RESONANCE SPECTROSCOPY

Magnetic Resonance (MR) spectroscopy is a non invasive diagnostic test for measuring
biochemical changes in the brain, especially the presence of tumors. While magnetic
resonance imaging (MRI) identifies the anatomical location of a tumor, MR spectroscopy
compares the chemical composition of normal brain tissue with abnormal tumor tissue. This
test can also be used to detect tissue changes in stroke and epilepsy.

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.

BRAIN ELECTRICAL ACTIVITY MAPPING

BEAM involves computer-assisted imaging and statistical analysis of electrical brain activity.
The idea behind this technique is that significant abnormalities in the electrical activity of the
brain relate to psychiatric disorders, therefore making detection of aberrant electrical activity
potentially useful for diagnosis. BEAM is relatively inexpensive, non-invasive, and produces
vivid images of electrical activity.
USES:
(1) localizes tumors in patients with normal or nondiagnostic EEGs,
(2) adds additional information to that visible on computerized axial tomography, and
(3) demonstrates electrophysiological abnormalities in patients with functional lesions but
normal CT scans.

DIFFUSION TENSOR IMAGING

Diffusion-weighted magnetic resonance imaging (DWI or DW-MRI) is the use of
specific MRI sequences as well as software that generates images from the resulting data, that
uses the diffusion of water molecules to generate contrast in MR images. It allows the
mapping of the diffusion process of molecules, mainly water, in biological tissues, in
vivo and non-invasively. Molecular diffusion in tissues is not free, but reflects interactions
with many obstacles, such as macromolecules, fibers, and membranes. Water molecule
diffusion patterns can therefore reveal microscopic details about tissue architecture, either
normal or in a diseased state. A special kind of DWI, diffusion tensor imaging (DTI), has
been used extensively to map white matter tractography in the brain.

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.