Objective 1:

• To list the important causative agents of meningitis.

TYPES OF MENINGITIS

• Acute Pyogenic Meningitis
• Aseptic Meningitis
• Chronic Meningitis
  • Tuberculous
  • Fungal
  • Syphillitic
  • Protozoal
  • Helminthe

Causative agents of acute pyogenic meningitis

• Neonates
– Escherichia coli
– Group B streptococci
– Listeria monocytogenes
– Streptococcus pneumoniae

• Children
– Neisseria meningitidis
– Streptococcus pneumoniae,
– Haemophilus influenzae

• Adults
– Streptococcus pneumoniae,
– Neisseria meningitidis

• Elderly
– Listeria species

Causative Agents of Aseptic meningitis

• Common:
- Enteroviruses
- Herpes simplex virus 2 (HSV 2)
- Arthropod borne viruses (Tickborne, West Nile, Murray Valley, Japanese B)
- HIV (Human Immunodeficiency Virus)

• Less common
- Varicella zoster virus (VZV)
- Epstein Barr virus (EBV)

Causative Agents of Chronic Meningitis

Tuberculous meningitis

• Mycobacterium tuberculosis

Syphillitic meningits

• Treponema pallidum

Fungal meningitis

• Cryptococcus neoformans (most common in HIV patients)
• Candida albicans
• Mucor species
• Aspergillus fumigatus
• Coccidioides immitis
• Histoplasma capsulatum
• Blastomyces dermatitidis

Protozoal

• Toxoplasma gondii
• Trypanosoma
• Acanthamoeba

Helminthes

• Taenia solium

Objective 2:

• To outline laboratory diagnosis of bacterial meningitis.

Specimens

• CSF
• Blood
• Sample
• Nasal swab
• Peticheal lesions
• Autopsy

A. Examination of CSF

Macroscopy
• CSF is cloudy under increased pressure and blood may be seen.

CSF is centrifuged and following methods are used:

• Microscopy
• Culture

Microscopy

Unstained preparations: wet mounts

Stained smears:

• Common stains: Gram stain, Ziehl-Neelsen stain
• Fluorescent dyes: Acridine orange, Auramine rhodamine

Gram stain (left) and ZN stain (right)

Culture

Culture Media

• Enriched solid media- blood agar, chocolate agar
• Selective solid medium- MacConkey agar
• Robertson Cooked meat broth (for anaerobes)

Steps:

• CSF inoculated in culture media
• incubation at 35-36°C under 5-10% CO2
• Colonies appear after 18-24 hours, identified by morphology and biochemical reactions.

B. Blood culture

• incubated for 4-7 days, with daily subcultures

C. Nasopharyngeal Swab

• Useful for detection of carriers
• Done without contamination with saliva

D. Petechial lesions

Menigococci may be demonstrated by microscopy and culture

E. Autopsy

• Specimen from meninges, lateral ventricles, or surface of brain and spinal cord
• Within 12 hours of death of patient
• Smear or culture

Biochemical tests

• Catalase test
• Oxidase test
• Indole test
• Urease test
• Coagulase test
• Citrate Utilization test
• Triple sugar iron agar

Agglutination test:

• Direct slide agglutination test with specific antisera
• Latex agglutination test
• Immunoflourescence test
• Other rapid identification methods
• Molecular diagnosis – PCR test

Various changes in Acute Pyogenic Meningitis:

References:

• Textbook of Microbiology
• Diagnostic Microbiology

Prepared and Presented for Correlation Seminar in Kist Medical College by:

Studying Online

Pathology is an interesting subject but it is as difficult as any other subjects in medical science like anatomy, physiology, pharmacology, etc. We all are made differently and we all have different way of learning or studying. The method that I use to study may or may not be suitable to you. Lectures, books, pictures and slides are the common sources of learning. Using online resources to learn may be very helpful to many of us.

It is a vast subject and its knowledge is always expanding. So, it is more important that the pathology learnt in the undergraduate curriculum (like MBBS Basic Science) is basic and relevant, emphasizing the understanding of mechanisms and principles rather than detailed facts. As students continue their medical education into PG trainee years, more detailed systemic pathology will become more relevant and more appropriately learnt at that time.

Site home: http://medicalschoolpathology.com

Medical School Pathology is a resourceful medical website designed to assist self learner medical students for learning pathology. It provides online access to lecture notes and videos of all 29 chapters based on Robbin’s Pathology. Besides, it also provides medics with online laboratory for learning histopathology. This site probably won’t be useful to lay person because the description are mostly medical and includes medical jargons.

Chapters

GENERAL PATHOLOGY

1. Cellular Adaptations, Cell Injury, and Cell Death
2. Acute and Chronic Inflammation
3. Tissue Repair: Cellular Growth, Fibrosis, and Wound Healing
4. Hemodynamic Disorders, Thrombosis, and Shock

Textbook for pathology

5. Genetic Disorders
6. Diseases of Immunity
7. Neoplasia
8. Infectious Diseases
9. Environmental and Nutritional Pathology
10. Diseases of Infancy and Childhood

DISEASES OF ORGAN SYSTEMS

11. Blood Vessels
12. The Heart
13. Red Cells and Bleeding Disorders
14. White Cells, Lymph Nodes, Spleen, and Thymus
15. The Lung
16. Head and Neck
17. The Gastrointestinal Tract
18. The Liver and Biliary Tract
19. The Pancreas
20. The Kidney
21. The Lower Urinary Tract and the Male Genital Tract
22. The Female Genital Tract
23. The Breast
24. The Endocrine System
25. The Skin
26. Bones, Joints, and Soft Tissue Tumors
27. Peripheral Nerve and Skeletal Muscle
28. The Central Nervous System
29. The Eye

Online Resources For Self-Learning

Download Lecture notes in Powerpoint
Watch and Download Lecture videos of General Pathology
Watch and Download Lecture videos of Systemic Pathology
Watch and Download Histopathology Videos
Online Access to Rock Lab for Independent Study
Shotgun Histology

Click on the picture to enlarge

Objective

• To highlight the present status of disease modifying anti-rheumatic drugs (DMARDs) in the treatment of rheumatoid arthritis

Introduction

• DMARDs (disease modifying antirheumatic drugs) are drugs which can suppress the rheumatoid process and bring about a remission, but do not have nonspecific anti-inflammatory or analgesic action.

Classification of Anti-rheumatic drugs

A. DMARDs:

• Immunosuppressants: Methotrexate, Cyclosporine, Azathioprine
• Sulfasalazine
• Chloroquine or hydroxychloroquine
• Leflunomide
• Gold salts
• d-Penicillamine

B. Biological response modifiers(BRMs):

• TNF-α inhibitors: Etanercept, Infliximab
• IL-1 antagonist: Anakinra

C. Adjuvant drugs

• Corticosteroids: Prednisolone

Immunosuppressants

Methotrexate:

• First choice and standard drug for rheumatoid arthritis.
• Acts by inhibiting an enzyme dihydrofolate reductase
• Also inhibits other enzyme involve in protein synthesis as well as anti-inflammatory and cytokines modulating effect.
• Initially low dose(7.5-15 mg/week)
• Best tolerated among other DMARDs

Adverse drug effects

1. Nausea and mouth ulcer
2. Pancytopenia (low blood cells)
3. Liver cirrhosis
4. Acute pneumonitis

Contraindications
• Pregnancy
• Lactating mother
• Liver disease
• Leucopenia
• Peptic ulcer

Sulfasalazine

• It is a compound of sulfapyridine and 5-amino salicyclic acid (5-ASA)
• Useful in both RA and ulcerative colitis
• Much more safer than gold salts
• Second line drugs for milder cases
• Mode of action is unknown

Adverse drug effects:

1. Neutropenia, hemolytic anemia
2. Thrombocytopenia

Gold Salts

• Water soluble gold preparation like sodium aurothiomalate
• Gets deposited in the synovial macrophages in actively inflammed joints and inhibits their function.

Adverse drug effects:

• Dermatitis, nephropathy, bone marrow depression and liver damage.

Etanercept

• It is a recombinant fusion protein of TNF-receptor and Fc portion of human IgG
• Reserved for the patients who have failed to respond to adequate trials of atleast two DMARDs

Adverse drug reaction:

1. Pain, redness, itching, swelling at the infection site
2. Chest infection may be increasedd-Penicillamine
3. Splits the rheumatoid factor and also selectively reduces the serum levels of calcium immunoglobin
4. Adverse drug reactions incidences are high so not commonly used

Gold salts and d-penicillamine should not be combined for the treatment of RA (because of severe ADRs). Gold salts and d-penicillamine are not used in the present context because of severe adverse reactions i.e.

• Bone marrow depression
• Kidney and liver damage
• Ulceration

Presented by Students of KistMCTH 1st year students

Reference

1. Text book of Pharmacology- K D Tripathi
2. Text book of Pharmacology- Bennett and Brown

Objectives

• To define Rheumatoid Factor .
• To explain briefly its significance in the diagnosis of rheumatoid arthritis.

Rheumatoid factor

• Rheumatoid factor (RF) is an autoantibody that is directed against organism’s own tissues, most relevant in rheumatoid arthritis.
• An antibody against the Fc portion of IgG, which is itself an antibody. RF and IgG join to form immune complexes which contribute to the disease process.

Diagnosis of RA

• Diagnosis is based on clinical test, signs and symptoms and imaging technique.
• The test for RF may be ordered when a person has signs of RA.
• Symptoms : pain, warmth, swelling, and morning stiffness in the joints, nodules under the skin
• X-rays of swollen joint capsules
• An RF test may be repeated when the first test is negative and symptoms persist.

Significant associations

• Rheumatoid disease including Rheumatoid Arthritis .
• Higher the level of RF, the worse the joint destruction and greater the chance of systemic involvement.

Associations
Rheumatoid arthritis (60-70%)
Sjögrens syndrome (≤100 %)
Felty’s syndrome (≤100 %)
Systemic sclerosis (30%)
Infective endocarditis (≤ 50%)
Systemic lupus erythematous (≤ 40%)
Infectious mononucleosis
Hepatitis
TB
Cancer

RF Test

• RF is commonly used as a blood test for the diagnosis of rheumatoid arthritis.
• A negative RF is seronegative , in about 15% of patients.
• During the first year of RA, RF is more likely to be negative but some individuals convert to seropositive later.

CRITERIA

• High levels of rheumatoid factor
• Generally above 20 IU/mL
• Upto dilution level 1:40 (of rheumatoid factor)
• In 80% cases

Other Serological Tests

• New test for the presence of anti-citrullinated protein antibodies (ACPAs).
• ANA (antinuclear antibody)
• CRP (C-reactive protein)
• ESR (erythrocyte sedimentation rate)
• CBC (Complete Blood Count)

SUMMARY

• Rheumatoid factor (RF) an antibody ( IgM )
• It is used for the diagnosis of Rheumatoid arthritis
• But it is not the confirmational test because it is observed in other related and unrelated diseases

Prepared by:
Samjhana Sharma (73)
Sashi Kumar Yadav (74)
Sat Prasad Nepal (75)
Sharmila Phellu (76)
Shraddha Shrestha (77)
Shuvechha Pandey (78)
Srijana Shakya (79)
Sulabh Shrestha (80)
Surakshya Rayamajhi (81)
Surendra Pariyar (82)
Sushil Dulal (83)
Sushmita Bajagain (84)
Tulsi Ram Shrestha (85)
Uday Chandra Prakash (86)

1. • To Define Antibiotic Resistance.
2. • To Discuss Various Factors Affecting Antibiotic Resistance

Antibiotic & Antibiotic Resistance

• Antibiotic: any of various chemical substances,produced by various microorganisms, esp. fungi, or made synthetically and capable of destroying or inhibiting the growth of microorganism.

• People may exhibit allergic reactions to antibiotics, but they are not resistant to them. It is the bacteria themselves, not the infected host, which become resistant.

Antibiotic Resistance

 Antibiotic Resistance: the ability of bacteria and other microorganisms to withstand an antibiotic to which they

were once sensitive

 Tolerance of micro-organisms to inhibitory action of antibiotics.

 Resistance to antibiotics is a biological phenomenon that can be accelerated by a variety of factors, including human practices.

 Resistance Can be: Drug Tolerance, Drug Destruction, Drug Impermeability, Cross resistance.

Antibiotic Resistance Is A Serious Worldwide Problem

• The monetary cost of treating antibiotic resistant infections worldwide is estimated to be many billions of dollars per year.

• According to the researchers : the resistance to antibiotics is increasing at a faster pace than it can be controlled.

• Since antibiotic resistance can pass from bacterium to bacterium and resistant bacterial infections can pass from

person to person. Thus, antibiotic use and antibiotic resistance can eventually affect an entire community.

Factors Affecting Antibiotic Resistance

• Patient’s incompliance to recommended treatment

– Forget to take medication

– Interrupt their treatment when they begin to feel better

– May be unable to afford full course

– May also be due to inadequate physician patient interaction

• Irrational use of antibiotics in humans

– Self-medication (Unnecessary, Inadequate dose )

– Misuse ( Easy availability in pharmacies without prescription )Factors Affecting Antibiotic

• Physicians:

– Over prescribing of broad spectrum drugs when narrow spectrum are appropriate

– Wrong prescription and guidelines from unskilled practitioners

– Unnecessary prescriptions common in private practitioners

• Hospitals :

– Nosocomial infections with highly resistant bacterial pathogens.

– Mainly due to poor infection control practices like handwashing, changing gloves, etc.

• Poor Quality Of Antibiotics:

– Expired and counterfeit antibiotics

– Due to lack of quality compliance and monitoring

• Irrational Use Of Antibiotics In Animals

– Used for growth and disease control in poultry, cattle, pigs, etc.

– We are indirectly taking these antibiotics when we are eating these animals.

• Inadequate Surveillance & Susceptibility Testing:

– Unknown susceptibility pattern of bacterial isolates encourages empirical selection of broad spectrum antibiotics.

– Due to lack of equipment and personnel.

• Crowding/Travel of People & Unhygienic Conditions:

– Residents of developing countries often carry antibiotic-resistant fecal commensal organisms . Visitors to developing countries passively acquire antibiotic-resistant E.coli, even if they are not taking prophylactic antibiotics, which suggests that they encounter a reservoir of antibiotic-resistant strains during travel.

Summary

• Developing prescription guidelines, Emphasizing on public awareness, emphasizing quality compliance and monitoring of antibiotics manufactured or dispensed, public sanitation, improved hospital infection control are some of the measures to be taken to combat the growing problem of Antibiotic Resistance.

Sources:

• • http://www.cdc.gov
• • http://www.who.int/en

• Prepared By:
• • Srijana Shakya (79)
• • Sulabh Shrestha (80)
• • Surakshya Rayamajhi (81)
• • Surendra Pariyar (82)
• • Sushil Dulal (83)
• • Sushmita Sharma (84)

Alcohol a social need or problem?

ALCOHOL  are hydroxy derivatives of aliphatic hydrocarbons.

MANUFACTURE:-

Zymase

C6H12 O6——> 2 CO2+ 2C 2 H 5 OH

(sugar)—-> (in yeast)

METABOLISM OF ALCOHOL

• Alcohol is metabolized in liver by alcohol dehydrogenase

90% – processed in liver.

10% – excreted (eliminated unchanged

from kidneys and lungs)

• Absorption 10% from stomach.

Mostly from small intestine.

Peak effect in 30 to 90 min (empty stomach 30 to 60 min)

Depends  upon:

• time of food intake.
• duration of consumption.
• type of drink consumed.

alc. DHASE —–                                                ald. DHASE

Alcohol————>acetaldehyde————————->acetic acid ——–>CO2+ H2O

CONCENTRATION OF ALCOHOL IN DIFFERENT LIQUORS

Beer :- 4 – 8%

Wine :- 12 %

Whisky and other liquors:- 40%

Illicit:- 20 – 40 %

1 unit = 30 ml of whisky or 360 ml of beer or 120 ml of wine

In 70 kg person 1 unit gives 15 – 20 mg/ dl of blood level

SAFE DRINKING:- MEN :- 21 unit/ week

WOMEN :- 14 unit / week

CALORIC VALUES OF ALCOHOL

1) Alcohol is full of calories

2) 2 – 3 gin and tonic/day for 4 wks will increase wt about 4 pounds.

3) 1 pint of beer = 1000- 2000 kcal

DETERMINANTS OF BAC

1. Quantity/ speed of drinking.
2. Concn of alcohol in the drink.
3. Body fat (W BAC 20 % > M)
4. Addition of soda carbonated beverage.
5. empty stomach.
6. Body wt:- higher the� body wt lower the BAC.
7. Carbohydrate food in stomach delays absorption.

BAC mg/dl—–Behavioral correlates

< 80— Euphoria, feeling of relaxation, talking freely, reduced alertness

>80— Noisy , moody , impaired judgment

100- 200— blurred vision , unsteady gate, gross motor incordination , slurred speech, aggressive

Quarrelsome and talking loudly.

200 – 300—Amnesia for experience( alcoholic blackout)

300 – 350— coma

350 – 600—– death

LEVELS OF ALCOHOL USE

SOCIAL USE:- without any apparent harm, exploration for curiosity, group activity, to relieve anxiety, dissolve inhibition, facilitate social interaction , dietary practice religious rituals.

HARMFUL USE/ ABUSE:- leads to impairment in one of more areas of daily life ( physical , social , occupational , family life, legal involvement)

ALCOHOL DEPENDANCE:-Feeling of compelled to drink,

A stereotyped pattern of drinking

Alcohol takes priority over anything else.

Development of tolerance

Psychological and physical withdrawal symp.

Relief after drinking

ICD’s 10 criteria for substance abuse

a pattern of psychoactive substance use that is causing damage to health; the damage may be to physical or mental health.

ICD’s 10 criteria for substance dependence

Three or more of the following must have been experienced or exhibited at some time during the previous year:

1. Difficulties in controlling substance-taking behavior in terms of its onset, termination, or levels of use

2. A strong desire or sense of compulsion to take the substance

3. Progressive neglect of alternative pleasures or interests because of psychoactive substance use, increased amount of time necessary to obtain or take the substance or to recover from its effects

4. Persisting with substance use despite clear evidence of overtly harmful consequences, depressive mood states consequent to heavy use, or drug related impairment of cognitive functioning

5. Evidence of tolerance, such that increased doses of the psychoactive substance are required in order to achieve effects originally produced by lower doses

6. A physiological withdrawal state when substance use has ceased or been reduced, as evidence by: the characteristic withdrawal syndrome for the substance; or use of the same (or a closely related) substance with the intention of relieving or avoiding withdrawal symptoms.

CAGE QUESTIONNAIRE FOR DIAGNOSIS OF ALCOHOLICS

C- Have you ever tried to Cut down on alcohol (amount)?

A- Have you ever been Annoyed by people’s criticism of alcoholism?

G- Have you ever felt Guilty about drinking?

E- Have you ever needed an Eye opener drink (early morning drink)?

A SCORE OF 2 OR > IDENTIFIES PROBLEM DRINKER.

CLINICAL FEATURES

Symptoms:-

1) Neglect of other activities.(social, occupational , recreational)

2) Excessive use:- consumed in large amount over a long period of time.

3) Impaired control of drinking habit.

4) Persistence of use inspite of physical or psychological problem created by it.

5) Large amount of time spent in alcohol related activities.

6) Withdrawal symptoms:- N/V, shaking, sweating, anxiety

7) Tolerance:- need of increasing amount of alcohol to feel its effect.

COMPLICATION

MEDICAL COMPLICATION

GI:- gastritis, reflux oesophagitis, esophageal avarices, peptic ulcer, ca stomach and stomach, malabsorption syndrome, pancreatitis.

HEPATO:- fatty liver, cirrhosis of liver, hepatitis, ca liver.

CNS:- peripheral neuropathy, delirium tremens , rum fits, alcoholic hallucinosis , wernicke- korsakoff psychosis, alcoholic dementia, cerebellar degeneration, alcoholic myopathy, suicide

CVS:- Cardiomyopathy, hypertension.

HEMATOLOGICAL:- anemia, leucopenia, decrease platelet and increase MCV

METABOLIC:- ketoacidosis, hypoglycemia, hypocalcaemia, hypomagnesaemia

MISCELLANEOUS:- Osteoporosis, psoriasis, fetal alcohol syndrome, impotence decrease immunity etc.

SOCIAL COMPLICATION:-

Accidents, marital disharmony, divorce, occupational problems,increase incidence of drug dependance, criminality, financial difficulties.

ACUTE ALCOHOL INTOXICATION

Brief period of excitement then generalized CNS depression.

Increased reaction time, slowed thinking, distractibility, and poor motor control.

Later , dysarthria , ataxia and in coordination, progressive loss of self control.

ALCOHOL WITHDRAWAL SYNDROM

Abrupt cessation or rapid decrease in amount of alcohol consumption causes:

1 MINOR WITHDRAWAL SYMPTOMS:- (12 – 18 hrs)

tremors, nausea/ vomiting, tachycardia, HTN, weakness, anxiety, insomnia.

2) MAJOR WITHDRAWAL SYMPTOMS:- (7 – 36 hrs)

a) Delirium tremens

b) Alcoholic seizure (rum fits)

c) Alcoholic hallucinosis.

DELIRIUM TREMENS

• Severe withdrawal syndrome, life threatening
• Starts 2- 3 days after cessation of alcohol intake and features last for 3 – 7 days.
• Acute organic brain syndrome with feature of :-
• Clouding of consciousness with Disorientation in time , place, person
• Poor attention span and distractibility.
• Visual , auditory hallucination, tactile hallucination, illusion , delirium.
• Autonomic disturbance:- tachycardia, sweating, fever, HTN, pupillary dilatation
• Psychomotor agitation, ataxia
• insomnia
• Dehydration with electrolyte imbalance

ALCOHOLIC SEIZURES ( RUM FITS)

• Generalized tonic clonic seizures occur in about 10% of alcohol dependence ptn. After 12- 48 hrs after cessation or decrease in amount of alcohol.
• Multiple seizures (2-6 at one time) common than single seizures.
• ALCOHOLIC HALLUCINOSIS
• Usually auditory hallucination during partial or complete abstinence following regular alcohol intake. In 2% ptn.
• Persists after the withdrawal syndrome is over and classically occurs in clear consciousness.
• Usually recovery occurs within one month and the duration is very rarely > 6 months.

WERNICKE�S ENCEPHALOPATHY

• This is an acute reaction to severe def of thiamin.
• Imp clinical signs:-
• Ocular signs:- nystagmus, ophthalmoplegia,b/l external rectus paralysis, pupilary irregularities, retinal hemorrhages and papiloedema
• HMF disturbances:- disorientation, confusion, recent memory disturbances, poor attention span and distractibility, apathy and ataxia.

KORSAKOFF�S PSYCHOSIS

• Follows wernicke’s encephalopathy
• Together refered as wernicke’s korsakoff’s psychosis.
• Cause:- severe, untreated thiamin deficiency secondary to chronic alcohol use.
• Clinically presents as organic amnestic syndrome characterized by gross memory impairement( anterograde amnesia )and confabulation.

TREAMENT

BEFORE TREATMENT:-

• Rule out physical disorder, psychiatric disorder,
• Assessment of motivation for treatment.
• Assessment of social support system
• Assessment of personality characteristics of the patient
• Assessment of the current and past social interpersonal and occupational functioning.

DETOXIFICATION in hospital for 7 to 14 days:-

BENZODIAZEPINES:-

CHLORDIAZEPOXIDE (80 – 200 Mg/day in divided dose).

DIAZEPAM( 40 – 80 Mg/day in divided dose)

CARBAMAZEPINE ( 600  -1600 Mg/ day)

IV THIAMIN 100 mg bid for 3 – 5 days followed by oral admin of B1 for at least 6 month.

GOOD NUTRITION with vitamin B,C, A supplements.

ALCOHOL DEPENDENCE:-

BEHAVIOURAL THERAPY:-

PSYCHOTHERAPY:-

DETERRENT AGENTS:-

DISULFIRAM 250- 500mg/day at bedtimes for 1 wk, then 250 mg/ day maintenance dose.

.

ANTI- CRAVING AGENT:-

• ACAMPROSATE
• NALTREXONE:-
• FLUOXETNE:-

OTHERS:- benzodiazepines, antidepressants, antipsychotics, lithium, carbamazepine, narcotics for special use.

PSYCHOSOCIAL REHABILITATION:-

TREATMENT OF WITHDRAWAL SYNDROMES:-

v� Minor withdrawal:-

T/T:- chlordiazepoxide or oxazepam.

v� Major withdrawal:-

Delirium Tremens:-

T/T:- iv benzodiazepines and

supportive care nutrition, electrolyte balance, vit B complex.

Alcoholic seizures:-

T/T:- iv benzodiazepines

Alcoholic hallucinosis:-

T/T:- neuroleptics ( haloperidol 2 – 5 mg bid)

Wernickes encephalopathy:-

T/T:- inj of thiamine( 100 mg IM)

Mind Games

Dissociative disorder:- (conversion disorder)

is a partial or complete loss of the normal integration between memories of the past, awareness of identity and immediate sensations, and control of bodily movements.

Previously known as conversion hysteria.

EPIDEMIOLOGY:-

According to DSM-IV-TR ( 11 to 500 cases per 100,000 population)

Women :men (adult ) 2-10:1 and among children there is higher predominance in girls.

Most common in rural populations, people with little education, those with low IQ, in low socio economic groups and military personnel exposed to combat situation. And commonly associated with major depressive disorder, anxiety disorder and schizophrenia.

ETIOLOGY:-

PSYCHOANALYTIC FACTOR:-repression of unconscious intrapsychic conflict and the conversion of anxiety into a physical symptom.

BEHAVIOURAL THEORY:-symptoms are learned response in the face of stress.

BIOLOGICAL THEORY:- hypofunction of the dominant hemisphere

CLINICAL FEATURE:-

MOTOR SYMPTOMS:- abnormal movements, gait disturbance(astasia abasia), weakness and paralysis. Gross rhythmical tremors, choreiform movements, tics and jerks may be present.

SENSORY SYMPTOMS:- anesthesia and paresthesia are common.

May involve the organs of special symptoms ( deafness, blindness, tunnel vision)

SEIZURE SYMPTOMS:- especially pseudo seizure, which can be differentiated by typical symptoms like non- stereotypical clinical pattern , occurs usually in indoor safe place, tongue bit/ incontinence rarely present, duration of episode longer, neurological sign is absent, EEG is normal, serum prolactin increased.

OTHER ASSOCAITED FEATURES:-

• PRIMARY GAIN:
• SECONDARY GAIN:
• LA BELLE INDIFFERENCE:-
• IDENTIFICATION:-

CLASSIFICATION:-ICD 10 (F44)

F44.0 DISSOCIATIVE AMNESIA

F44.1 DISSOCIATIVE FUGUE

F44.2 DISSOCIATIVE STUPOR

F44.3 TRANCE AND POSSESSION DISORDER

F44.4-44.7DISSOCIATIVE DISORDERS OF MOVEMENTS AND SENSATION

44.4 DISSOCIATIVE MOTOR DISORDERS

44.5 DISSOCIATIVE CONVULSIONS

44.6 DISSOCIATIVE ANAESTHESIA AND SENSORY LOSS

44.7 MIXED DISSOCIATIVE(CONVERSION ) DISORDER.

44.8 OTHERS DISSOCIATIVE(CONVERSION) DISORDER.

44.9 DISSOCIATIVE (CONVERSION) DISORDER, UNSPECIFIED

DIAGNOSTIC GUIDELINES OF DISSOCIATIVE DISORDER :-ICD-10

A) the clinical features as specified for the individual disorders in F44.

B) no evidence of a physical disorder that might explain the symptoms.

C) evidence for psychological causation, in the form of clear association in time with stressful events and problems or disturbed relationship (even if denied by the individual)

F44.0 DISSOCIATIVE AMNESIA

The main feature is loss of memory, usually of important recent events, which is not due to organic mental disorder and is too extensive to be explained by ordinary forgetfulness and fatigue. Usually due to traumatic events( accidents, unexpected bereavements ) and is usually partial and selective.

Several forms are present:-

Localized amnesia:-

Selective amnesia:-

Generalized amnesia:-

Continuous amnesia:-

Systematized amnesia:-

DIAGNOSTIC GUIDELINES (ICD 10)

A) amnesia , either partial or complete, for recent events that are of traumatic or stressful nature(these aspects may emerge only when other informants are available)

B) absence of organic brain disorders, intoxication, or excessive fatigue.

F44.1� DISSOCIATIVE FUGUE

All feature of dissociative amnesia + apparent purposeful journey away from home or place of work during which self care is maintained.

DIAGNOSTIC GUIDELINES( ICD-10)

A)the features of dissociative amnesia 44.0

B) purposeful travel beyond the usual everyday range.(differentiation between travel and wandering must be made by those with local knowledge)

C) maintenance of basic self care(eating ,washing) and simple social interaction with strangers( such as buying tickets or petrol, asking directions, ordering meals)

F44.2 DISSOCIATIVE STUPOR

Profound diminution or absence of voluntary movement and normal responsiveness to external stimuli such as light, noise, and touch. They are motionless and mute, but are aware of surroundings.

DIAGNOSTIC CRITERIA (ICD-10)

A) stupor, as described above.

B)Absence of a physical or other psychiatric disorder that might explain the stupor. And

C) evidence of recent stressful events or current problems.

F44.3 TRANCE AND POSSESSION DISORDER

Temporary loss of both the sense of personal identity and full awareness of the surrounding, sometime may even act as if taken over by another personality, spirit, deity, or a force.

F44.4-44.7 DISSOCIATIVE DISORDERS OF MOVEMENTS AND SENSATION

There is loss or interference of movements or loss of sensation.

DIAGNOSTIC GUIDELINES:-

A) there should be no evidence of physical disorder.

B) sufficient must be known about psychological and social setting and personal relationships of the patients to allow a convincing formulation to be made of the reasons for the appearance of the disorder.

44.4 DISSOCIATIVE MOTOR DISORDERS

Loss of ability to move whole or a part of limb or limbs.

Paralysis may be partial , with movements being weak or slow or complete.

Ataxia ,bizarre gait (astasia abasia), trembling of part or whole body.

44.5 DISSOCIATIVE CONVULSIONS

Pseudo seizures present.

44.6 DISSOCIATIVE ANAESTHESIA AND SENSORY LOSS

Presence of anesthetic areas of skin with boundaries.

Sensory loss may be accompanied by complaints of par aesthesia.

44.7 MIXED DISSOCIATIVE(CONVERSION )  DISORDER.

44.8 OTHERS DISSOCIATIVE(CONVERSION) DISORDER.

F44.80 Ganser’s syndrome: hysterical pseudo dementia (appromixate answer)

F44.81 Multiple personality disorder

F44.82 Transient dissociative disorder occurring in childhood and adolescence

F44.83 Other specified dissociative disorders.

44.9DISSOCIATIVE DISORDER ,UNSPECIFIED

D/D

NEUROLOGICAL DISORDER( DEMENTIA, DEGENERATIVE DISORDER)

BRAIN TUMORS, BASAL GANGLIA DISEASES

MYASTHENIA GRAVIS,POLIOMYOSITIS, MYOPATHIES, MULTIPLE SCLEROSIS, GB SYNDROMES.

SCHIZOPHRENIA, DEPRESSIVE DISORDER,AND ANXIETY DISORDER.

SOMATOFORM DISORDER.

MALINGERING AND FACTICIOUS DISORDER,

TREATMENT:-

Resolution is usually spontaneous.

1) BEHAVIOR THERAPY:-

Treat the patient normally, give enough care,actively encourage any improvement in symptomatology.

2)PSYCHOTHERAPY WITH ABREACTION Hypnosis , anxiolytics, and behavioral relaxation exercises .

3)PSYCHOANALYSIS: To find out conflict and resolve it.

4)DRUG THERAPY: iv,thiopentone , amytal or diazepam,

COURSE AND PROGNOSIS

INITIAL SYMPTOMS 90-100% Resolve within a few days or < a month, 75 %-may not experience another episode but 25% have additional episodes during period of stress.

Prognosis good- if sudden onset, easily identified stress factor, good premorbid adjustment, no comorbid medical or psychiatric disorder.

Prognosis bad- if symptoms persists for longer duration