ROT

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ROT Dr Manoj Patel M.D. Asst. professor,
Department of psychiatry
A workshop on Case Receiving
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SAMUEL HAHNEMANN1755-1843
To him we owe our Art and our Science
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A Born Teacher
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CASE TAKING
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SCIENTIFIC ASPECT OF CASE TAKING COMPRISES OF
EVIDENCE
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CASE RECEIVING ARTISTIC ASPECT OF CASE TAKING
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APH. 83-103
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OBSERVER
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Hahnemann is sure
Observing is not an innate faculty it must be
acquired by Practice
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The Duties of an observer
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THE CASE IN HOMEOPATHIC PRACTCE

• A patient calls on the physician
• with
  complaints.
• A patient is brought to the physician
• with
  complaints.
• Does it make a difference to the physicians?
• To the outcome?

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• WE NEED TO EXAMINE.
• A Case well-taken, is half-cured.
• What is a case?
• WE NEED TO DEFINE.
• The patient poses a problem to whom?
• The problem belongs to whom
• is defined by whom?
• is resolved by whom?

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• WE NEED TOTAL CLARITY ON THESE
• FUNDAMENTAL ISSUES

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Our ExperienceAction Learning

• Patient centric study
• Guiding learning rather then teaching.
• Converting OPD experience in to assignments.
• Empowering P.G.Students to take responsibility of
  presenting experience through group learning.
• Teachers must prepare paper on homeopathic
  implication of assignments. Through integration
  of experience
• Educate through entertainment

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Directives

• Study the video case.
• Keep notes of proceedings.
• Create Assignments on various topics.
• Study man in health and diseases through case.

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CASE of Pot's spine Tics

• HISTORY She is a young female ref. by
  orthopaedic surgeon. She is suffering from Pot's
  spine since last 6 months with poor response on
  AKT. The disease is advancing? Due to lot of
  emotional disturbances that she is passing
  through she has further developed complication of
  a spiral abscess.
• Follow the first interaction with patient who
  is accompanied by mother.

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Learning in OPD setupthrough observing Pt.lt-gtPhy
Interaction
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video
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SPINE VERTEBRAL COLUMN
STRUCTURE
BONES VERTEBRA FIBROUS TISSUE IVD,
LIGAMENTS MUSCLES PARASPINAL MUSCE NERVE
SPINALCORD, NERVE ROOTS
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FUNCTION
Vertebra Support, maintenance of
posture. Weight bearing and transmission. Mi
nimal movements of the trunk. Protection of
delicate Spinal Cord, Nerve roots. Inter-verte
bral Discs Cushion / shock absorber for
spine. Allow minimal movements between
vertebras.
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VOLUNTARY MUSCLES NEURO-MUSCULAR JUNCTION MOTOR
NERVES

• VOLUNTARY CONTROL OVER MUSCLES
• WELL CO-ORDINATION OF MOVEMENTS

NORMAL CO-ORDINATED MOVEMENTS
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CONCEPT of POTTS SPINE

• AGENT
• 1.GERM THEORY-
• DISEASE AGENT?MAN?DISEASE
• AGENT Mycobacterium tuberculosis
• 2.EPIDEMIOLOGICAL TRAID-
• 
  

ENVIROMENT Poor quality of hygiene--Droplet
infection Poor housing
/ overcrowding
AGENT M. Tuberculosis

• Host factor
• Susceptibility
• Nutrition
• Mental- sensitivity
• Genetic factor

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POTTS SPINE

• DEFINATION
• A secondary mycobacterium tuberculosis
  infection typically affecting the vertebral
  body
• SPECTRUM OF THE DISEASE
• 1Pain in back
  
• 2Stiffness of the back
• 3Visible deformities
• 4Cold abscess and its spread
• 5Onset of paraplegia
• Potts paraplegia

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CLINICAL FEATURES

• Symptoms
• General features
• Fever- evening rise of temperature
• Fatigue
• Anorexia
• Weight loss
• Local
• Kyphus/ Gibbus- (is due to local abscess
  formation and sometimes may be too small to be
  evident)
• Mild Backache- it may be minimal in comparison to
  a potentially crippling disease
• Joint stiffness or spasm
• Signs
• Synovial thickening
• Muscle wasting
• Abscess- typically cold abscess (not red, and
  slightly warm)
• Range of movement is painfully restricted
• Spine tenderness
• Kyphus

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Investigations

• Haematology Raised total counts and lymphocyte
  counts haemoglobin may be low.
• ESR is raised
• Mantoux test- Positive
• Radiology
• Bone density is slightly reduced
• Soft tissue swelling
• Disc space is reduced
• Bone Destruction (Anteriorly of two adjacent
  vertebral bodies)
• X Ray Chest to rule out Pulmonary Tuberculosis
• Computerised Tomography
• Histology
• Bacteriology

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FACTORS OF BACTERIOLGY

• ? causative agent mycobacterium tuberculosis
• ? Acid-fast bacilli.
• ? Resistant to intracellular killing.
• ?Three types cause Koch's in men i.e.
• 1) Human type M. tuberculosis.
• 2) Bovine type M. bovis.
• 3) Atypical mycobacterium saprophytic
• i) photochromogens e.g. M. Kansasi.
• ii) scotochromogens e.g. M.scrofulaceum.
• iii) non-photochromogens e.g.
  M.intercellulare
• iv) rapid growers e.g. M. fortuitum.

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Natural history of disease

• a) Prepathogenic phase
• Mode of spread
• 1) Blood bornecommonest type
• 2) Lymph bornerare type
• Varieties
• Centraldisease start as diffuse osteomyelitis in
  middle body.
• Metaphysealdisease arises near epiphysis of bone
  and involves body of epiphysis. (Commonest)
• Anterior or posterior varietyfocus lies beneath
  anterior longitudinal ligament. (Rarely in
  adults)
• Appendiceal tuberculosistransverse process
  rarely vertebral arch affected

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Progress of Disease

• Related to reactivation of
  hematogenous foci or to spread
• from adjacent Para vertebral
  lymph nodes.
• Primary source of infection most
  often from the urinary
• tract, skin or lungs.
• Also considered as metastasis
  process resulting from
• hematogenous dissemination of
  tubercular bacilli.
• May begin in vertebra or inter
  vertebral disc involving
• adjacent structures.
• As tubercular process advances one
  or more vertebral
• bodies collapse causing an
  angular kyphsis (gibbus).

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Pathogenesis

• Tubercular bacilli after settling cause
  tubeculous endarteritis.
• In devitalized tissues tuberculous follicle is
  formed which grows slowly to form
  
  
  
  
  visible
  yellowish gray nodule.
• This nodule grows bony lamellae around it that
  gradually rarify and disappear.
• This leads to vertebral causing kyphosis,
  gibbus or hump back.
• Complication 1) abscess formation
• 2) Potts paraplegia

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Agent factor

• Low permeability of cell wall makes agent
  resistant to antibiotics.
• Liparabinomannan, a molecule in mycobacterial
  cell wall involved in pathogen-host interaction,
  facilitates survival of pathogen in macrophages.
• Virulence of bacilli is determined by its lipid
  rich cell wall and glycolipid capsule both of
  which confers resistance to compliment and free
  radicals of phagocytes.
• Few genetic factors and strains also determine
  virulence of bacteria.

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Host factors

• Age early childhood, majority between 3-5 years
  of age.
• Malnutrition and sever underweight.
• Individuals innate susceptibility to disease
  and level of function of cell mediated immunity.
• Few genetic factors determining hosts
  susceptibility to TB.
• Bactericidal activity of macrophages.
• Balance between hosts responses
• 1) Tissue damaging response
• 2) Macrophage activating response
• Interplay of various cytokines and their cross
  regulation determines hosis response.

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Environmental factors

• Prevalent in developing countries.
• Poverty
• Homelessness
• Overcrowding in poorly ventilated rooms.

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Psychological Factor

• Known to occur in individual with hyper
  sensitivity
• Kwon to occur during major psychological stress
• Historically it use to occur to painters,
  sculptures dramatist with artistic sensitivity.
• Premorbid Morbid personality

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Risk factors

• Immigration from countries with high prevalence
  of tuberculosis.
• HIV infection.
• Drug abuse.
• Dismantling of health services.

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3.MULTIFECTORIAL CAUSATION ?AGE FACTOR BELOW 5
YEAR ?SOCIAL FACTOR Poor quality of life /
Large family/ Lack of education
Lack of awareness of cause of
illness etc ?ECONOMIC FACTOR
MODEL Poor
housing factor 1
malnutrition factor 2 reaction
at cellular level

factor3 ?CULTURAL FACTOR
DISEASE
Overcrowding Population
explosion ?GENETIC FACTOR Not hereditary
disease but inherited susceptibility. ?
PSYCHOLOGICAL FACTORS Hypersensitive
individuals
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WEB
OF CAUSATION THIS THEORY SUITED FOR STUDY OF
CHRONIC DISEASE WHERTHE DISEASE AGENT IS OFTEN
NOT KNOWN BUT IS THE OUT COME OF INTERACTIONOF
MULTIPAL FECTOR CHENGE IN LIFE
STYLE ? STRESS /
AGE
SMOKE Poor
nutrition hard working
long time sitting
standing Lean,thin,debilited more stress on
vertebral body vital breathing
capacity of lung person
( T 10 L 2 ) Immunity
IV DISK softening or compressed
thickness of wall surface
area Decried affect
central tissue
destruction
primary infection in lung Part of vertebra
hyper sensitive to infection
childhood

secondary infection peripheral
pott's spine
Part of vertebra advanced age
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TICS HABIT/SPASM

• A sudden, rapid, coordinated and purposive
  intermittent and repetitive intermittent and
  repetitive in character and location increased by
  emotion and disappearing during sleep.

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MOTOR TICS

• May take many forms, such as the frequent
  blinking of an eye lids, rolling of eye balls,
  contortive twisting of the neck or a facial
  grimace. Tics are perhaps more common in people
  who are obsessional and compulsive may have their
  origin in past experience e.g. blepharospasm
  after an attack of conjunctivitis.

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VOCAL TICS

• They are seen in Gilles De La Tourette Syndrome
  which develops before the age of 21 years and is
  more common in boys, characterized by multiple
  motor and vocal tics including grunting,
  snuffing, coughing and other noises and in
  appropriate words. Compulsion (e.g. touching,
  self injury), obsess ional ruminations, attention
  deficit hyperactivity disorder, mimicking the
  utterances or acts of others ( Echolalia And
  Echopraxia) and making obscene remarks and
  gestures ( Copra Phenomenon) are variably
  associated.

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• CONCEPT AND SPECTRUM
  
  
  
• (A) Transient Motor Tics ------family history
  -- common in childhood --- boys.
• (B) CHRONIC MOTOR MOTOR TICS Childhood,
  persistent thought out adult life. Involvement of
  3 muscle group may occur thought life.
• (C) GILLES DE LA TOURRETT SYNDROME Evidence
  shows that called genes T.S
• Prevalence of approximately 12000. That has
  onset been 2 21 year of age inherited as
  Autonomic dominant.

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Tics Epidemiology Incidence 4-5/10000. Onset of
motor components-7yrs. Vocal
components-11 Boygirl ratio 31 Etiology Twin
studies indicate that concordances for the
disorder in monozygotic twins is significantly
greater than diazygomatic twins Evidence in some
families indicate it is transmitted in an
autosomal dominant fashion Inherited through an
autosomal pattern intermediate between dominant
and recessive. Neurochemical or neuroanatomical
factor Compelling evidence of dopamine system
involvement in Tics disorder includes observation
that pharmacological agents that antagonize
dopamine, suppress tics. Some evidence indicates
that pharmacological agents that antagonize
endogenous opiates reduce tics. Immunological
factors and post infection An auto immune
process sec to streptococcal infection. Post
streptococcal have also been asso with one
potential causative factor in development of ocd-
occurs upto 40 of people with tics disorder.
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FACTORS AFFECTING ABNORMAL PSYCHOLOGY

• 1.Tic disorders are not goal directed and become
  more frequent during anxiety and stress.
• for ex scratching head pulling nose, clearing
  throat so on. These actions which are initially
  goal directed become displaced in some time and
  this is known as DISPLACEMENT THEORY.

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• Tics are experienced as irresistible and are
  exacerbated by stress ,anxiety and period of
  frustration and are diminished in times of
  concentration.
• Some psychiatrists regard tics as psychogenically
  determined motor habits, but others believe that
  patient has a constitutional predisposition to
  tics and this is brought to light by emotional
  tensions.

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AETIOLOGY GeneticAutosomal(intermediate bet.
domonant recessive)
Neurochemical Neuroanat. Factors
Immunological factors Post-infection Sec. to
Streptococcal Infn.
Dopamine system Basal Ganglia
Adrenergic antagonists increse release of
norepinephrine
exacerbations
Remissions
STRUCTURE
At least 2yrs. of age. Mostly 7-18 yrs. Boys gt
Girls
Sudden, recurrent, many times/day, for gt1yr.
A/FX subst abuse, X gen. med condn
FORM
FUNCTION
Downward progression
Rapid, irresistible, non-rhythmic, stereo-typed
motor movement or vocalization (Behavioural)
prodrome/with irritability, attention
difficulties, poor frustration tolerance Accompani
ed with OCN, ADHD
Eyeblink
-Inc. central Dopaminergic activity -Abn.
Noradrenergic system Functn of MIND -Failure of
censorship- conscious subconscious -Mood low
First
Aggressive Sexual Component
ltstress gtoccupation, sleep, relaxation Can be
suppressed for varied periods(min-hrs)
LAB INVNil Abn nonspecific EEG
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Homeopathic Perspective

• Holistic concept
• Integrated concept of Health Disease
• Covers mind to miasam

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HOMOEOPATHIC VALUE

• Primary role of psychotherapy in Tics not
  effective psychotropic drugs lt tics. Thus, Hom.
  has an important role to play
• Spectrum of the disease
• -stage at which patient has come to us.
• -evaluate the remedy response.
• -decide follow up criteria.
• Gives a platform for case taking understanding
  patient as a person.

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HEALTH
A STATE OF DYNAMIC STABLE EQUILIBRIUM IN WHICH AN
INDIVIDUAL IS AT PEACE WITH HIMSELF AS WELL AS
WITH THE WORLD. HE HAS NO COMPLAINTS
STRUCTURAL INTEGRITY
IN PROPORTION TO TIME
EFFICIENT FUNCTIONING
BALANCED EXPRESSION
He live life for Higher purpose of his existence
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DISEASE
AN UNSTABLE STATE OF DISEQUILIBRIUM.IT REFLECTS
POOR ADAPTATION OF AN INDIVIDUAL TO HIS
ENVIRONMENT. PEACE IS DISTURBED AND WE HAVE
COMPLAINTS
STRUCTURAL ALTERATION
DISPROPORTION TO TIME
INEFFICIENT FUNCTIONING
SIGNS SYMPTOMS
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How do we apprehend Totality?
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Potts Disease (Spine Tuberculosis)
STRUCTURE
Spinal cord Nerve Roots
Compression
Immunity
Lungs
Easy Collapse of vertebrae on ant part
Haematogenous spread
Bone degeneration with cavitations
Abscess
Granulomas Caseous necrosis
(Dorsal Lumbar) Inter Vertebral Discs
Vertebral bodies (ant surface) adjacent to it.
Spine Of vertebrae
(Psoas abscess inguinal region)
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FUNCTION
1. Spine

• ?Capacity for Wt bearing of vertebrae
• Spine flexibility ?
• Spinal cord nerve compression
• ?
• neurological deficit
• Locomotion disability / deformity

2. Immunity

• Type IV hypersensitivity response
• Failure to contain infection.

3. Spinal Cord Nerves

• Impaired conduction
• Paresthesias
• Paralysis

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FORM
1. Spine

• Pain Stiffness in Back
• Visible deformity (Kyphosis)
• Localised swelling abscess.

2. Spinal Cord

• Spinal cord compression lower paralysis
  (Paraplegia)
• Radiculopathy at level of collapse

3. General constitutional symptoms of Koch's

• Low grade fever
• Weakness
• Wt loss

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Understanding Mind body Inter-dynamics

• Modern scientific study supporting homeopathic
  view of multi axial causation

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SECRETED BY MACROPHAGE
Interleukin (IL-1)
Liver - ? no. of circulating Neutrophils
Activate cells that participate in Immune response
Hypothalamus produce fever
ACT H
Cortisol provides Resistance to stress
inflammation
Suppresses further production of IL-1
Keeps immune response in check
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DEFICIENCY NUTRIENTS PHYSICAL EMOTIONAL
2
HOST SUSCEPTIBILITY
ENVIRONMENT
3
NOXIOUS FACTORS PHYSICAL
1
ENERGY - RELEASE
ABNORMAL
IMBALANCE
P N E MECH
4
DEFICIENCY SECONDARY
BIOCHEMIC ALTERATIONS HORMONAL INTRA EXTRA
CELLULAR
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P N E MECH
4
DISEASE
MANIFESTATIONS SIGNS SYMPTOMS
QUICK PERMANENT GENTLE
TOTAL REMOVAL

CURE
BALANCE HEALTH ABSENCE SIGNS
SYMPTOMS
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CONFLICT EXPRESSION
(1) Disturbed Imagination when the individual
indulges in Dreams day and night, Fancies and
Phantasies
(2) Altered Physiological Functions e.g.
Appetite, Digestion, Elimination, Sexual
functions and Sleep disturbances (including
dreams).
(3) Drop in Performance and Efficiency At
school college, play and work.
(4) Disturbed Intellectual Performance
Confusion and Aberrations of Perception and
Thinking. Impaired thinking, memory (Rote and
Logical or Associative), discrimination,
judgement and decision.
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(5) Emotional Disturbances Overt display of
Emotions with their inherent, complex, and
mutually reinforcing potential, the chief
amongst them being
Anger Sadness Love Hate
Envy, Jealousy, Suspicion Anxiety, Fear, Fright,
Guilt.
These give rise to various neurotic and psychotic
syndromes.
(6) Altered Psycho-Physiological Functioning
resulting from Suppressed / Repressed Emotions
Symbolization of Emotional Conflicts, as in
Organ Neurosis.
(7) Structural (Psycho-Physiological)
Alterations Resulting from Suppressed /
Repressed Emotions Somatization of Emotional
Conflicts, as in Psychosomatic Disorders.
(8) Altered Behaviour Speech, Gesturers and
Actions.
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ENVIRONS TO WHICH THE HUMAN ORGANISM IS
SUSCEPTIBLE ARE AS FOLLOWS
1. Physical Electrical, Magnetic, Lunar, Solar,
Planetary, Radiation.
Position and Balance in Space Time Periodicity
Epochs in Life. Extra-Sensory Perception,
Clairvoyance.
Sensory Inputs Pain Thermal
Meteriological Temperature weather,
Seasons, humidity.
Skin Touch, Pressure, Jar (Vibration),
Rubbing
Ears Noise, Music
Eyes Light, Vision
Tongues Taste, Desires and Aversions.
Nose Odours
Addictions Sex Reproduction.
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Emotional
Chemical Drugs, Heavy Metals, Fumes and
Gases. Occupational Hazards Odours
Biological Germs, Viruses, Parasites,
Fungi Prophylactic Vaccinations and
Inoculations and Sera, as well as
Therapeutic.
Socio-Cultural, Religious, Spiritual
Economico-Political Milieu
Sleep Dreams
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DEFINITIONS
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Phase 1 Mind Skin Mucous Membrane
----- Affections
SUPPRESSION of Manifestations
Phase 2 Controls Neuro-Endocrine and R.E.S.
affected
Phase 3 Functional Alterations Structural
Alterations (Internal)
Progressive Aberrations Vital Functions
and Structures
Phase 4 Destination
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DIRECTION OF TRAVEL OF DISEASE

• From the Periphery to the centre.
• From the superficial to the deeper areas.
• From the less vital to the more vital organs.
• From the characteristics to the common.
• From the subjective to the objective symptoms.

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PRIMARY PSORA
St

• RAPID
• ACUTE
• SHARP
• ALERT
• INTENSE
• SUDDEN
• SHARP SWINGS OSCILLATION
• CHANGEABLENESS

Fm
Fn
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SECONDARY PSORA
MIND
P.N.E. Axis
FUNCTIONAL DISTURBANCE WITH MINIMAL STRUCTURAL AL
TERATION
HYPERSENSITIVITY Imbalance of functional
nature

• GLAND
• R.E.S.
• CVS
• CNS
• Autonomous
• Nervous system

St

• RAPID
• SHARP
• SUDDEN

Fm
Fn
METABOLISM NUTRITION IMBALANCE
INCORDINATION ? SYMPATHETIC SYSTEM

• Heat / Burning
• Coldness
• Flushes
• Dryness

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OBSESSIVE COMPULSIVE NEUROSE
CONSTANT REPETATIVE THOUGHT
ACTION
FIXED IDEAS CANNOT REMOVED
SYCOTIC MIASM
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SYCOSIS

• Metastatic non suppurative Inflammn. Reaction
• - Nephritis
• - Rheum. Fever
• - Rheumatoid Arthritis
• - GOUT
• - Endocrinal Disorder
• 2. Ch. Inflammation

LOST CONTROL
R.E.S
St
MIND
SLOWNESS
? Actively Symptoms
Fm
Fn

• Parasympathetic
• Inappropriate
• Inefficient aberrant Immune
• Response
• Inefficient metabolic adjustment
• Recognition of self not self
• excessive / defective / absent

Anaemia Weakness Fatigue slowness /
dullness, indolence sluggishness.
SPASMODIC Acrid, thick, greenish yellow /
indelible offensive
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VERTEBRA
MSS
Tubercular Abscess ----
GRANUCOMATOUS ? CHRONIC INFLAMMATION
METASTSIS
DELAYED HYPERSENSITIVITY
POOR IMMUNITY
RES
ADRENAL
ENDOCRINES
PITUTARY
HYPOTHALAMUS
EMOTIONAL DISTURBANCE GRIEF
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Tubercular
MIND
Hypersensitivity - I - IV
Irritability Excitability Changeability
St
GLAND
P.N.E. R.E.S. - Sexual organ
Endocrine
Hypertrophy / Enlargement
Indurations
- Easy suppuration
slow healing
Fibrosis ? scarring

• TIME
• Acute
• Quick
• Tardy convalescences
• Protracted Recovery

MWD Poor
Fn
Fm
DEBILITY Changeable Emaciation
?Resistance to Infn Multiple Infection
?Activity Sympathetic Hyper dynamic ?E. S. R. -
Poor assimilation
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SYPHILIS
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DR. M. L. DHAWALE 1927-87
PHILOSOPHY
RESEARCH
HOMOEOPATHY
TRAINING
MODERN MEDICINE
EDUCATION
A CLINICIAN PAR EXCELLANCE who synthesized the
traditional and the modern
HOLISTIC APPROACH
CLINICO PATHOLOGICAL MIASMATIC CO-RELATION
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Come, let us all walk together
Satyam, Shivam, Sundaram
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GRATITUDE

• Respected President Dr. Bakshi, Vice President
  Dr.Ramjisingh,
• Respacted Dr.Arun Bhasme sir , Principals
  Beloved Teachers from
• 
  maharashtra goa Gujarat

• Respected sir Dr.Kishor Mehta

• Mitra , Hit-chintak Dr. Markandbhai Bhatt.

• Respected staff members of vyara college for
  organising event

• Students who have Tolerated our ignorance

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CREATION THE CREATOR
AUM PURNAH MADAH PURNAH MIDAM PURNATH PURNAH
MUDACHYATE PURNASHYA PURNAHMADAYA PURNA MEVAVA
SHISHYATE AUM SHANTI! SHANTI! SHANTI!