1

10 marks
1. Pyramidal tract
Origin :
• Primary motor Cortex (Area 4) - 30 %
• Premotor Cortex (area 6) - 30%
• Somatosensory cortex (Areas 3,1, 2, 5 & 7) - 40%
Course:
• Corona radiata: a radiating pattern in the subcortical areas
• Internal Capsule: through the genu and anterior 2/3rd of posterior limb of internal
capsule
• Mid brain: Fibers occupy middle 1/5th of cerebral peduncles
• Pons: The tract is split into a number of bundles by the presence of pontine nuclei
• Medulla:
Upper part:
forms a bulge called pyramid
Lower part:
80% of the fibers cross to the opposite side & 20% of the fibers descend on the same side
(The crossing of fibers is called motor decussaation)
• Spinal cord:
The crossed fibers form the lateral corticospinal tract
The uncrossed fibers form the anterior corticospinal tract
Termination:
lateral corticospinal tract – synapse with anterior horn cells directly and supply to
the distal limb muscles
anterior corticospinal tract – synapse with the anterior horn cells through internuncial neurons and
supply the axial and proximal limb muscles
Functions:
• Control of voluntary fine and skilled movements (lateral corticospinal tract)
• Control of gross voluntary movements (anterior corticospinal tract)
• Facilitates muscle tone
• Facilitates superficial reflexes
2
 3

2. CEREBELLUM

Functional divisions:
• Vestibulocerebellum (Flocculonodular lobe)
• Spinocerebellum (Vermis & intermediate zone)
• Neocerebellum (cerebrocerebellum)

Connections:

Peduncles Afferent fibers Efferent fibers

Superior Cerebellar Ventral spinocerebellar tract Dentato thalamocortical fibers
Peduncle Tectocerebellar Dentatorubral fibers
Trigemino cerebellar fibers

Middle Cerebellar Cerebro ponto cerebellar ----------------------

Peduncle

Inferior Cerebellar Dorsal spinocerebellar Cerebello reticular

Peduncle Cuneo cerebellar Cerebello vestibular
Reticulo cerebellar
Vestibulo cerebellar
Olivo cerebellar
 4

Functions:
1. Control of body posture & equilibrium (Vestibulocerebellum & Spinocerebellum)
• Influences antigravity muscles and maintains posture
• Maintains equilibrium during standing, walking etc.,
2. Control of Gaze (Movements of eyeballs) – Vestibulocerebellum
• Controls eye movements and coordinates with head
3. Control of muscle tone & Stretch reflex (Spinocerebellum)
• Facilitates γ motor neurons in the spinal cord
• Forms an important site of α – γ linkage
4. Control of voluntary movements (Neocerebellum)
• Planning and programming of voluntary movements
• Controls coordination of movements
• Correction of purposeful movements (comparator of a servo-mecanism)
• Regulates time, rate, range, force and direction of muscular activity
• Learning of motor skills
• Influences the activity of agonists, antagonists & synergistic muscles
• Smooth transition of movements
• Cognition
• Mental rehearsal of complex action
3. BASAL GANGLIA / BASAL NUCLEI-

Components:
1. Caudate nucleus Corpus striatum
2. Putamen
3. Globus pallidus
- Externa
- Interna
4. Substantia nigra
5. Subthalamic Body
Connections:
Direct pathway:
+ Cortex

+ Glutamine

Striatum Dopamine Substantia nigra

D1

- GABA
Globus pallidus Interna

+
Thalamus
 5

- Excitatory pathway
- Facilitates the intended movement

Indirect pathway:
-
Cortex

+ Glutamine

Globus pallidus Externa Striatum Dopamine Substantia nigra

D2
- GABA
Subthalamic nucleus + Globus pallidus Interna

PPN -
Brain stem & Spinal cord Thalamus

- Inhibitory pathway
- Inhibits the unwanted movement

Basal Ganglia functions

• Control of motor activity
• Initiation of voluntary movements
• Suppression of unwanted movements
• Planning and Programming of a voluntary movement
• Execution of automatic associated movement
- Swinging of arms during walking
- Gestures during speech
• Cognitive control of motor activity
• Inhibits muscle tone – inhibits γ motor neuron discharge
• ---------------------------------------------------------------------------------------------------------------------
 6

5 marks
1. PAIN PATHWAY
Pain is carried by two pathways:
i) Neospinothalamic pathway
ii) Paleospinothalamic pathway
Neospinothalamic tract: (carries fast pain)
1st order neuron: Aδ fibers from receptors to spinal cord
2nd order neuron: From dorsal horn of spinal cord → cross to opposite side → ascend in the lateral
white column → end in the ventral postero lateral (VPL) & ventral postero
medial (VPM) nuclei of thalamus.
3rd order neuron: From thalamus to somatosensory cortex (areas 3, 2 &1)
Paleospinothalamic tract: (carries slow pain)
1st order neuron: ‘C’fibers from receptors to spinal cord
2nd order neuron: From dorsal horn of spinal cord → cross to opposite side → ascend in the lateral
white column → end in intralaminar & midline nuclei of thalamus
3rd order neuron: From thalamus to entire cerebral Cortex
Special features:
Neospinothalamic tract: concerned with localization and interpretation of quality of pain
Paleospinothalamic tract: concerned with perception of pain, arousal and alertness
 7

2. Modulation of Pain/ Endogenous Pain Relief System

Gate control theory of pain
- Large myelinated A fibers interact with small unmyelinated C fibers via inhibitory cells of the
Substatia gelatinosa of the spinal cord
- Stimulation of C fibers inhibits SG cells & favours passage of pain
- Stimulation of large ‘A’ fibers increases SG activity & block pain transmission by presynaptic
inhibition
Endogenous pain relief from PAG/central pain suppressing mechanism
- Descending pathways arise from Periaqueductal gray matter →release Encephalin → Descend &
connect with Nucleus raphe magnus of medulla →release of Serotonin → posterior horn cells of
spinal cord → inhibits the release of substance “P” from the pain fibers
Opioid peptides:
Enkephalins & Endorphins-
Two sites of action:
-Block the pain receptors
-At spinal level – binds to opioid receptors & decreases the pain transmission
---------------------------------------------------------------------------------------------------- --
3. REFERRED PAIN
Visceral pain felt at the somatic structures is called referred pain
Eg: Appendicitis pain at the umbilicus
Cardiac pain at the inner aspect of left arm
Theories of referred pain: (mechanism of referred pain)
1. Convergence theory: Fibers carrying pain from the viscera & the corresponding dermatome
(somatic structures) converge on the same pathway to the cortex
2. Facilitation theory: The visceral pain facilitates Substantia Gelatinosa Rolando [SGR] cells
which receive somatic pain nerves

CONVERGENCE THEORY

-------------------------------------------------------------------------------------------------------------------------------

4.Withdrawl reflex
Refers to the withdrawal of body parts by flexion of limbs when a painful (noxious) stimulus is applied.
-It is a polysynaptic reflex
Receptors: Nociceptors
Afferent Limb: Type III & IV somatic afferents
Center: Spinal Cord
 8

Efferent fibers: Somatomotor neuron supplying the flexor muscles of same side and
extensor muscles of opposite side.
Response:
Mild stimulus- flexion of limb of same side and extension of limb of opposite side.
Stronger stimulus - response in all four limbs.
(Reason: a) Irradiation of impulse, b) Recruitment of more motor units)
Special features:
Withdrawl reflex is a protective reflex (protects the tissue from damage)
Pre potent (stops all other spinal reflexes temporarily)
Shows local sign ie., response depends upon the location of the stimulus
Stronger stimulus causes wide spread and prolonged response

3 MARKS
Functions of Hypothalamus
a) Regulation of food intake

Ventromedial Nucleus Lateral Nucleus

(Satiety center) (Feeding Center)

Inhibits feeding center Hunger

↑Food intake ↓food intake

b) Regulation of water intake
Tonicity of body fluid ECF volume

Osmoreceptors Baroreceptors

Thirst center Thirst center Angiotensin II

 9

↑Water intake ↑Water intake Subfornical organ

Thirst center
c) Regulation of body Temperature
Pre optic nucleus of anterior hypothalamus (heat loss center) → Sweating and vasodilatation
Posterior hypothalamus (heat gain center) → Shivering & vasoconstriction

APPLIED

1. Differentiate UMN & LMN lesion

UMN Lesion LMN lesion

1. Damage to the motor tracts above the anterior 1. Damage to the anterior horn cell and
horn cell below
2. Spastic paralysis 2. Flaccid paralysis
3. Exaggeration of deep reflexes & loss of 3. Loss of both superficial and deep
superficial reflexes reflexes
4. Babinski Sign positive 4. Babinski sign negative
5. No muscular atrophy 5. Atrophy of paralysis
(E.g) Hemiplegia (E.g) Poliomyelitis

2. Hemisection of spinal cord (Brown – sequard syndrome)

Refers to lesion in one lateral half of the spinal cord

Level of spinal cord Same side Opposite side

Below the level of section Sensory: Sensory:
Damage of dorsal column -Loss of pain
tracts Temperature and crude touch
-Loss of fine touch, tactile
discrimination, pressure, Motor : Normal
vibration, kinaesthetics and
stereognosis Vasomotor: Normal
Motor: UMN paralysis
Vasomotor: Temporary loss
of vasomotor tone
(vasodilatation)
At the level of lesion Sensory Sensory: Not affected
-Anaesthesia (complete loss
of sensation) Motor: Not affected
Motor: LMN paralysis
Vasomotor: Loss of Vasomotor: Not affected
vasomotor tone

3. PARKINSONISM/ PARKINSON’S DISEASE

-a disease caused by lesion in basal ganglia
Causes
Degeneration of nigrostriatal fibers
 10

Clinical Features
Akinesia / Bradykinesia
-Lack of initiation of movements
-retardation of movements
- loss of automatic, associated movements (statue like appearance, mask like face)
-Defect in speech
-loss of timing & scaling of movements (micrographia)
Rigidity
• Hypertonia in the agonistic and antagonistic muscle
• Caused by increased discharge of gamma motor neuron
• 2 types of rigidity
Cog wheel – intermittent resistance in passive movement
Lead pipe – continuous resistance to passive movement
Tremor
• Occurs at rest
• Pill rolling tremor
o Alternate contraction & relaxation of agonists and antagonist of hands and fingers at a
frequency of 6-8 hertz/second
• Absent in sleep
Festinant gait
• body is bent forward
• moves forward with short quick shuffling steps as if to catch center of gravity
TREATMENT
Levo Dopa --- can cross the blood brain barrier, but dopamine cannot cross

4. CEREBELLAR LESION
Features: (4 A, 4 D & SIN)

Ataxia Dysmetria Scanning speech

Atonia Decomposition Intention tremor
Asynergia Dysdiadochokinesia Nystagmus
Asthenia Drunken gait

Physiological Basis:
Ataxia - In co-ordination of movements
Atonia/ Hypotonia - Cerebellum has got a excitatory influence over muscle tone. So lesion of
cerebellum leads to loss of this excitation and there by hypotonia occurs
Asynergia – Lack of coordination
Asthenia – Slow movements (muscles get tired easily)

Dysmetria - errors in the rate, range, force and direction of movements (This leads to
decomposition of movement, overshooting & undershooting the targets (intention
tremor), Rebound phenomenon etc.,)
Dysdiadochokinesia - Inability to perform rapid, alternate movements(supination & pronation of
hands)
Decomposition of movement – movement occurring in stages
 11

Drunken gait – Walking in a clumsy manner with a wide base (walks in a zig zag line)

Scanning speech – Slow and lalling (Like a baby)

Intention tremors - Oscillatory movements of hands during movements/ tremor that develops during
movement
Nystagmus - Jerky movements of eyes when trying to fix the eyes on a subject
Other Features:
Posture – Head rotated to normal side. The trunk is bent with the concavity towards the
affected side.
Equilibrium – Loss of equilibrium
Rebound phenomenon – failure of termination of movement
5. Effect of lesion of pyramidal tract At Various Levels
Motor cortex – monoplegia
Corona radiata – monoplegia
Internal capsule – contralateral hemiplegia
Brain stem – contralateral hemiplegia.
Above C5 – both upper & lower limbs (Quadriplegia)
Below T1 – only lower limbs (Paraplegia)
APPLIED QUESTIONS
1. A 65 year old patient complains to the doctor that his muscles are stiff and can initiate
movements with difficulty. On examination it is found that there is rigidity, rest tremor, absence
of automatic associated movements
a) What is your diagnosis? a) Parkinsonism
b) How will you treat? b) With L-Dopa
2. A patient was admitted to the hospital with the following complaints:
inability to perform alternate movements rapidly and oscillatory movements of hand during a
voluntary movement but not at rest.
a) What is medical terminology used for the above symptoms?
b) Where is the probable site of lesion?
a) Inability to perform alternate movements – Adiadocokinesia
Oscillatory movements of hands during movements – intention tremors
b) Cerebellar lesion
3. A patient was admitted to hospital with involuntary rhythmic movements of his hands which
disappear on voluntary movements. On examination he showed rigidity throughout passive
movement
a) What is the lesion? Where is it located?
b) What is the possible cause of this disease?
a) Lesion of nigrostriatal fibres in the basal ganglia
b) Deficiency of dopamine
4. A sixty year old man has expressionless face and tremor of hands even at rest. Name the condition
and the physiological basis for the use of L- Dopa in his treatment
The condition is called Parkinsonism. As L- Dopa can cross the blood brain barrier, it is used for
treatment.
5. A 65 years old man came to the doctor with the complaint that his movements were slow with no
appreciated swinging of arms while walking, difficulty in standing up, tremors in the hand at rest.
O/E, there was muscular rigidity, mask- like face, “ pill- rolling” movements in the fingers and the
speech was slurred and monotonous. No sensory loss was seen and the stretch reflexes were
 12

normal.
a) What is your diagnosis? a) Parkinsonism
b) Which part of the CNS is affected? b) Basal ganglia
c) What is the treatment? c) L- Dopa (a derivative of dopamine)
6. A patient complaints of incordination of movement and instability in maintaining posture. O/E, he
Was found to have intention tremor and inability to perform rapid alternate movement. Which
structure of the CNS is most likely involved in this dysfunction? What will be the state of muscle
tone in this disease and what is the physiological basis of change of the muscle tone?
Structure involved – Cerebellum
Muscle tone status – Hypotonia
7.Name the disease that results after destruction of the dopamine secreting fibers of thesubstantia
nigra. Mention two important clinical features of the condition
Parkinsonism. Clinical features – Rigidity & tremor at rest
8. A 5 year old boy complains of pain in the back & neck. He had a body temperature of 102®F. The
following morning, there was complete paralysis of the right leg. On examination, the muscle tone
was greatly reduced, tendon reflexes were abolished in affected limb. After a month, the muscles of
the affected limb showed marked atrophy. There was no sensory loss.
1. What is your diagnosis? Poliomyelitis
2. What is the type of lesion? LMN lesion
 1

CNS Notes 2nd Part

1.Synaptic inhibitions & facilitation

1. Direct postsynaptic inhibition:
Stimulation of an afferent neuron inhibits an efferent neuron. The inhibition is direct and is
usually through an internuncial neuron. The neurotransmitter released is inhibitory in nature
Example: Golgi bottle neuron inhibition in reciprocal innervation and crossed extensor reflex
Mechanism : Stimulation of an afferent neuron from muscle spindle activates a golgi bottle
neuron that releases glycine which causes hyperpolarisation of the motor neuron
that supply to the antagonistic muscles.
2. Indirect postsynaptic inhibition:
Inhibition that occurs due to the effects of previous discharge from the postsynaptic neuron.
Mechanism: 2 ways:
i) Postsynaptic neuron remains refractory to the incoming stimuli because it has just fired and is
in the refractory period
ii) Neurons which initiate an excitatory impulse may inhibit themselves in a negative feedback
fashion.
Example: Renshaw cell inhibition:
The spinal motor neuron regularly gives recurrent collateral which synapses with an inhibitory
interneuron that terminates on the cell body of the same neuron. This inhibitory interneuron is
called Renshaw cell . This prevents excess discharge from the anterior horn cell
3. Presynaptic inhibition:
Inhibition occurs usually at the presynaptic terminals before the signal reaches the synapse.
Mostly modulatory in nature and usually axo-axonic type.
Example: Pain modulation in the spinal cord
Mechanism: A reflex response to stimulation of an afferent nerve is either abolished or
decreased by stimulating another afferent nerve .The second afferent nerve ending
synapses with presynaptic nerve terminal through an inhibitory interneuron. The
inhibitory neurotransmitter (Eg . GABA) released by this interneuron decreases
the depolarization of the presynaptic nerve terminals. Calcium entry into the
nerve terminals is decreased causing a decreased release of excitatory
neurotransmitter. This leads to a reduced response
4. Feedforward inhibition:
The afferent fibers first stimulate the efferent fibers and then inhibit the same fibers through
interneurons
Example: In cerebellum , the afferent fibers first stimulate the deep nuclei and then inhibit
them through purkinjee cells.
PRESYNAPTIC FACILITATION
A reflex response to stimulation of an afferent nerve is increased by stimulating another afferent
nerve.The second afferent nerve ending synapses with presynaptic nerve terminal through an
interneuron. The excitatory neurotransmitter (mostly serotonin) released by this interneuron
decreases the K+ current at presynaptic nerve terminals and increases the duration of
depolarization of the presynaptic nerve terminals. Calcium entry into the nerve terminals is
increased causing a increased release of excitatory neurotransmitter. This leads to an increased
response
-----------------------------------------------------------------------------------------------------------------------------
 2

2. Properties of Receptors
a. Specificity:
Each type of receptor is highly specific for a particular stimulus for which it is designed and is
non responsive to normal intensities of other type of stimuli (e.g) Rods and cones respond to
normal intensities of light, but respond to only high intensity of touch.
b. Adequate stimulus:
The stimulus which can easily stimulate a receptor is the adequate stimulus for that receptor.
(e.g) Light is the adequate stimulus for rods & cones.
c. Labelled Line Principle:
The specificity of nerve fibers for transmitting only one modality of sensation is called labeled
line principle.
d. Doctrine of specific nerve energies:
Also called as Muller’s law. The sensation evoked by impulses generated in a receptor depends
in part upon the specific part of the brain they ultimately activate.
e. Law of projection:
When a stimulus is applied anywhere in the pathway of a sensation, the sensation is projected to
the receptors. (e.g) Phantom limb & Phantom pain
Phantom Limb: The non existing limb in an amputated person gives the sensation of pain &
proprioception as if it is existing.
Phantom pain: The pain sensation from the non existing limb of an amputated person can be
explained by law of projection ie., the stimulus applied anywhere in the pathway causes
projection of sensation to receptors)
Mechanism
Amputation → formation of neuromas → discharge of impulses by pressure or
Spontaneously→ sensation produced is projected to the place where the receptors were
presented.
f. Adaptation:
Reduction in sensitivity of receptors in the presence of a constant stimulus
• Phasic receptors: Fast adapting receptors (e.g) receptors for smell & pacinian corpuscles.
• Tonic receptors: Slow – adapting receptors (e.g) proprioceptors
• Receptors that do not adapt at all - Pain receptors (Nociceptors)
g. Intensity discrimination:
Weber Fechner Law: The magnitude of sensation felt is proportionate to the log of intensity of
stimulus
R=KSA
(R = Magnitude of sensation felt, S=intensity of stimulus, K & A = constants)
Intensity discrimination depends upon
• Number of receptors stimulated (spatial summation)
• Frequency of action potential reaching the cortex (Temporal summation)
------------------------------------------------------------------------------------------------------------------------------
 3

3. Sensory Tracts
1.Dorsal column pathway
Origin: From the dorsal column of spinal cord
Course:
I order neuron
• In the posterior nerve root
• After entering into spinal cord, ascend in the dorsal column of spinal cord
• Terminate in the nucleus gracilis & nucleus cuneatus of medulla
II order neuron
• From nucleus gracilis & nucleus cuneatus
• Cross to the opposite side (sensory decussation)
• Crossed fibers (called as inter nal arcuate fibers) upward in the medial lemniscus through pons &
mid brain.
• Terminate in the ventral postero lateral nucleus of thalamus (VPLN)
III order Neuron
• From VPLN of thalamus
• Pass through posterior limb of internal capsule
• Terminates in the SI & SII areas of cortex
• Sensations carried:
Fine touch, tactile localization, tactile discrimination, vibration, pressure, pain, conscious
proprioception & stereognosis.

2. Antero – lateral pathway

Origin: From the dorsal horn of spinal cord
Course:
I order neuron
• In the posterior nerve root
• After entering into spinal cord ascend up 1-3 segments or immediately end in nuclei of dorsal
horn.
II. Order neuron
• Starts from dorsal horn spinal cord
• Cross to opposite side in the anterior commissure
• Form 2 pathways
- Anterior spinothalamic tract
- Lateral spinothalamic tract
• Anterior spinothalamic tract runs in the anterior white column
• Lateral spinothalamic tract runs in the lateral white column of spinal cord
• Pass through medulla, pons, & mid brain
• Terminate in the VPLN of thalamus
III. Order neuron:
• from VPLN of thalamus
• pass through internal capsule
• terminate in the somatosensory cortex
Sensations carried:
Anterior spinothalamic tract – crude touch & pressure
Lateral spinothalamic tract – pain & temperature
 4

4. Regulation of Muscle Tone

Resistance of the muscle to stretch due to continuous state of tension in the muscle is called
muscle tone
Control of muscle tone:
• Muscle tone is purely a spinal segmental reflex.
• Produced by continuous, asynchronous, low frequency discharge from anterior horn motor
neurons
• This depends up on the activation of muscle spindle & stretch reflex.
Role of muscle Spindle
• Receptor organ present in the muscle
• Consists of infrafusal fibers (nuclear bag and nuclear chain fibers)
Sensory supply
▪ Group-Ia (annulospiral ending) – supply both fibers
▪ Group-II (Flower spray endings) – supply only nuclear chain fibers
Motor nerve supply
Gamma motor neuron
Muscle spindle participate in stretch reflex which play an important role in regulation of muscle tone
and posture
Role of stretch reflex
Reflex arc:
• Receptor - Muscle spindle
• Stimulus – Stretch
• Afferent – Group Ia & II fibers
• Center – Spinal Cord
• Efferent limb – motor nerve fiber ( α motor neuron)
• Response: Contraction of extra fusal fibers
Two types of reflexes
Dynamic stretch reflex: (phasic stretch reflex)
Activation of Group Ia fibers - contraction of agonist muscle and relaxation of antagonistic
muscle (helps is movement)
Tonic stretch reflex:
Activation of Group Ia & II fibers - continuous steady contraction of the antigravity muscles due
to asynchoronous discharge of motor units supplying the muscle
(necessary for maintaining muscle tone and posture)
Role of γ motor neurons on muscle tone
• γ motor neuron increases the sensitivity of muscle spindle to stretch
• increase inγ motor (gamma motor) neuron discharge increases muscle tone
• γ motor neuron discharge is increased in following conditions
noxious (painful) stimulation of skin
anxiety
Jendrassik phenomenon
Role of higher centers in regulation of muscle tone
Brainstem:
Brain stem reticular formation
Facilitatory reticulospinal tract(Pons) Inhibitory reticulospinal tract(Medulla)

Facilitates motor neuron discharge Inhibits motor neuron discharge

↑muscle tone ↓muscle tone

 5

Cerebellum: Increases muscle tone by

Facilitating motor cortex
Facilitating descending pathways
Cerebral cortex

Cerebral cortex Indirect pathway

Pyramidal tract Brain stem nuclei

Facilitates muscle tone Inhibits muscle tone

Applied
Hypotonia: ↓in muscle tone (lower motor neuron lesion & cerebellar lesion)
Hypertonia: ↑ in muscle tone (UMN lesion)
Spasticity – hypertonia only in antagonistic muscles (clasp knife rigidity)
(e.g) Hemiplegia due to pyramidal lesion
Rigidity: Hypertonia in both agonistic & antagonistic muscle
e.g Basal ganglia lesion – Parkinsonism
-------------------------------------------------------------------------------------------------------------------------------
5. VESTIBULAR APPARATUS
Components:
Vestibule (Utricle & Saccule)
Semicircular canals
Receptors:
Vestibule (otolithic organ) – Macula
Semicircular canals – Crista ampullaris
Stimulus
Vestibule - Linear acceleration
Semicircular canals – angular rotation
Activation of semi circular canals
Angular rotation

Movement of fluid in the semi circular canals

Bending of stereocilia towards the kinocilium

Entry of K+ into the hair cell

Depolarization

Calcium influx

Release of excitatory neurotransmitter (Glutamate)

On the opposite side:
Stereocilia move away from kinociliun

Hyperpolarization

Inhibition of Semicircular canals on opposite side

-Both of these cause relaxation of muscles on same side & contraction of muscles on opposite side
 6

Functions of Semicircular canals:

-helps to maintain equilibrium during rotational movements
-helps in visual fixation during angular rotation of head (vestibule-ocular reflex)

Otolith organ (vestibule) activation

Utricle responds to horizontal acceleration & Saccule responds to vertical acceleration
Functions of otolithic organ:
-gives information about static position of head
-respond to linear acceleration in different directions
Vestibular pathway

Vestibular apparatus

Vestibular division of VIII cranial nerve

Vestibular nucleus (Brain stem)

Vestibulo – cerebellar tract

Vermis of cerebellum

Cerebellar cortex Vestibular nucleus Vestibulospinal tract Spinal cord

6. Nuclei & Functions of Hypothalamus (important - regulation of water
balance, regulation of food intake & body temperature)
Nuclei of hypothalamus
1. Supra optic area: Includes supra optic, Suprachiasmatic, paraventricular & anterior nuclei
2. Preoptic area: Medial & lateral preoptic nuclei
3. Tuberal area: Ventromedial, dorsomedial, arcuate, lateral & posterior nucleus
4. Mammillary area: Medial & lateral mamillary, pre & supramamillary nuclei.
Functions of Hypothalamus
a) Regulation of food intake

Ventromedial Nucleus Lateral Nucleus

(Satiety center) (Feeding Center)

Inhibits feeding center Hunger

↑Food intake ↓food intake

b) Regulation of water intake

Tonicity of body fluid ECF volume

Osmoreceptors Baroreceptors

Thirst center Thirst center Angiotensin II

↑Water intake ↑Water intake Subfornical organ

Thirst center
 7

c) Regulation of body Temperature

Pre optic nucleus of anterior hypothalamus (heat loss center) → Sweating and vasodilatation
Posterior hypothalamus (heat gain center) → Shivering & vasoconstriction
d) Control of ANS
(Acts as a head ganglion of ANS)

Stimulation of anterior Stimulation of posterior

Hypothalamus Hypothalamus

↑HR, BP & HCL secretion ↓HR & BP, Pupillary dilatation,

Micturition, erection of penis sweating & piloerection
(Parasympathetic effects) (sympathetic effects)
e) Control of Pituitary
Hypothalamus Supra optic & paraventricular nuclei of hypothalamus

Releasing &
inhibitory
Hormones

Anterior pituitary Posterior pituitary

Trophic hormones ADH Oxytocin

Target endocrine gland Water re-absorption Milk secretion

In kidney in mammary glands
&
contraction of uterus
f) Role in circadian rhythm
-Hypothalamus play a role in influencing the changes in body functions tuned to the day and night
cycle (circadian rhythm)

Retina

Optic tract

Suprachiasmatic nucleus of hypothalamus

Pineal gland

Melatonin

Day & night variations

g) Role in emotions:
Hypothalamus is a part of papez circuit which is responsible for emotional behavior.
 8

h) Role in stress
Hypothalamus helps to protect the body from damaging effects of stress
Stress

Cerebral cortex & Limbic system

Sympathetic
Nervous system Hypothalamus Adrenal cortex Adrenal medulla

Glucocorticoids Catecholamines
i) Role in sleep wakeful cycle
Hypothalmus has 2 sleep centers
- diencephalic sleep zone
- basal fore brain sleep zone
j) Role in sexual behavior
Hypothalamic areas (Preoptic & anterior hypothalamus) are responsible for sexual behavior like
mating, attracting the opposite sex etc.
k) Reward & punishment
Ventromedial nucleus – Reward center
Posterior & lateral nucleus - Punishment center
Important Functions:
a) Role of Hypothalamus in food intake
Food intake is controlled by 2 nuclei. They are
i) Ventromedial nucleus (VMN) – Satiety center
Inhibits the feedings center
Produces satiety (satisfaction) after taking food
Destruction of VMN - Hyperphagia & obesity
Stimulation of VMN - Hypophagia (↓food intake)
ii) Lateral nucleus (LN) – Feeding center
Stimulaters appetite
Produces hunger
Destruction of LN – aphagia & starvation
Stimulation of LN – Hyperphagia (↑ food intake)
Hypothesis about food intake
1. Glucostatic Hypothesis
Hyperglycemia in blood → ↓VMN activity → ↓ food intake
Hypoglycemia in blood →↑VMN activity →↑ food intake
2. Lipostatic Hypothesis:
Adipose tissue secretes “leptin” → inhibits hypothalaminus →↓ food intake
3. Gut peptide Hypothesis
Presence of food in GI tract → release of intestinal peptides (GRP, glucagon, somatostatin &
CCK) → acts on brain → satiety
4. Thermostatic Hypothesis
↓Body temperature →↑ food intake
↑Body temperature →↓ food intake
b) Role of Hypothalamus in regulation of water intake
• Mainly involves ‘thirst center
• Dorsal or lateral hypothalamus acts as thirst center
• Water intake mainly depends upon the stimulation of thirst center
• Thirst center is stimulated in 2 conditions
 9

a) in the increased tonicity of the body fluid

b) in the decreased ECF volume
a) Increase in the tonicity of body fluid

Stimulation of osmoreceptors

Stimulation of thirst center

Water intake
b) Decrease in ECF volume

Baroreceptors

Stimulation of Thirst center Angiotensi II

↑Water intake Subfornical organ

Thirst center
C. Regulation of Body Temperature
• Hypothalamus is called as ‘biological thermostat as it controls the body temperature constant
• Involves preoptic region of the anterior hypothalamus & posterior hypothalamus
Preoptic nucleus of anterior hypothalamus -- heat loss center
Posterior hypothalamus -- heat gain center
Stimulation of the centers occurs through 2 mechanisms
a) Cutaneous thermoreceptors
b) Blood flowing through hypothalamus
(-mediated through serotonergic pathway)
Stimulation of anterior hypothalamus Stimulation of posterior hypothalamus

Vasodilatation, sweating Vasoconstriction

& panting Shivering & Piloerection
-------------------------------------------------------------------------------------------------------------------------------
7. THALAMUS
Specific sensory nuclei
• ventrobasal group (VPLN & VPMN)
• medial & lateral geniculate bodies
Non specific sensory nuclei
• midline & intralaminar nuclei
Nuclei concerned with efferent control
• ventrolateral & ventro Anterior Nuclei
Nuclei concerned with higher functions
• dorsomedial, dorsolateral, pulvinar, posterolateral & Anterior nucleus
Functions
a) Sensory Relay Center:
sensory relay center for the following sensations:
• Tactile sensation
• vibration
• pressure
• conscious proprioception
 10

• stereognosis
• sexual sensation
• visual sensation (LGB)
b) Centre for crude sensations:
• Perceives the crude touch, pain & Temperature Sensation
c) Integrator of motor signals
• controls the smooth, slow and coordinated movements by its connections with cerebellum basal
ganglia & cerebral cortex.
d) Role in memory & emotions
• Being a part of Papez circuit, it influences recent memory & emotions.
Papez circuit
Mammillary body of Hypothalamus

Anterior Nucleus Hippocampus

Of thalamus

Cingulate gyrus
e) Role in sleep wakefulness cycle
• influences sleep wakefulness cycle.
• stimulation causes alertness of animal which facilitates learning process
• produces the B-rhythm of EEG
• Non-specific Nuclei are responsible for them
• Connections involved. (Reticulo thalamo cortical & Cortico thalamo reticular)
--------------------------------------------------------------------------------------------------------------------
8. Withdrawl reflex
•Refers to the withdrawal of body parts by flexion of limbs when a painful (noxious)
stimulus is applied.
• -It is a polysynaptic reflex
Receptors: Nociceptors
Afferent Limb: Type III & IV somatic afferents
Center: Spinal Cord
Efferent fibers: Somatomotor neuron supplying the flexor muscles of same side and
extensor muscles of opposite side.
Response:
Mild stimulus- flexion of limb of same side and extension of limb of opposite side.
Stronger stimulus - response in all four limbs.
(Reason: a) Irradiation of impulse, b) Recruitment of more motor units)
Special features:
• Withdrawl reflex is a protective reflex (protects the tissue from damage)
• Pre potent (stops all other spinal reflexes temporarily)
• Shows local sign ie., response depends upon the location of the stimulus
• Stronger stimulus causes wide spread and prolonged response
(Causes: After discharge due to involvement of many interneuronal pathways
& reverberatory circuits in the spinal cord)
 11

----------------------------------------------------------------------------------------------------
9. Modulation of Pain/ Endogenous Pain Relief System
Analgesia [inhibition of pain]:
1. Gate control theory
2. Endogenous pain relief from PAG(Peri Aqueductal Grey matter) & NRM / Central Pain
suppressing Mechanisms
3. By release of Endogenous opioid peptides (Enkephalins & Endorphins)
Gate control theory of pain
- the posterior or dorsal horn acts as a Gate for pain
- pain impulses in the spinal cord can be modified or gated by other afferent impulses [touch
,pressure vibration] that enter the spinal cord
- Large myelinated A fibers interact with small unmyelinated C fibers via
inhibitory cells of the Substatia gelatinosa of the spinal cord
- Stimulation of C fibers inhibits SG cells & favours passage of impulses along
the pathway of pain in the spinal cord.
- Stimulation of large ‘A’ fibers increases SG activity & block impulse
transmission to nerve cells concerned with pain-
(inhibit transmission of pain from the ‘C’ fibers to Spinothalamic tract.-
presynaptic inhibition)
- pain inhibiting opioids also act at the level of gate
Endogenous pain relief from PAG/central pain suppressing mechanism
- Descending pathways arise from Periaqueductal gray matter [surrounding aqueduct of Sylvius]
[release Encephalin] → Descend & connect with Nucleus raphe magnus of medulla →release
of Serotonin → posterior horn cells of spinal cord → inhibits the release of substance “P” from
the pain fibers
 12

Opioid peptides:
oEnkephalins—
▪ Met enkephalins ,Leu enkephalins
o Endorphins-
▪ Beta endorphins, & Dynorphins
o Similar in action to Morphine
o Present in PAG (peri aqueductal gray matter),NRM( nucleus raphae
magnus),periventricular
o areas, posterior horn cells, GITract & Hypothalamus
o Endogenous morphine - ENDORPHINE
◼ Two sites of action:
-Terminals of pain fibers (receptors) & decrease the response of the receptors
to nociceptive stimuli
-At spinal level – binds to opioid receptors & decreases the release of
substance - P
---------------------------------------------------------------------------------------------------- --

10. REFERRED PAIN

Visceral pain instead of being felt at the site of the viscera is frequently felt at some
distance,on somatic structures. This is called referred pain
Eg: Appendicitis pain at the umbilicus
Cardiac pain at the inner aspect of left arm
Cholecystitis at the tip of the shoulder.
Theories of referred pain: (mechanism of referred pain)
1. Convergence theory: Fibers carrying pain- both from the viscus & the
corresponding dermatome (somatic structures) converge on the same pathway to
the cortex
2. Facilitation theory: The visceral pain produces a subliminal fringe effect on the
Substantia Gelatinosa Rolando [SGR] cells which receive somatic pain nerves

CONVERGENCE THEORY
 13

11. Inverse Stretch Reflex

Refers to relaxation of muscle in response to a strong stretch.
Also called as lengthening reaction or clasp knife reflex.
Receptors: Golgi tendon organ
Afferent fibers: Group Ib fibers
Center: Corresponding spinal segment
Efferent fibers: α motor neuron to the corresponding muscle
Response: Inhibition of α motor neuron by the inhibitory interneuron and relaxation of the
corresponding muscle.
Functions:
-Monitors the force generated in the muscle
-reflex is called autogenic inhibition
-monitors muscle tension and prevents rupture of muscle
-along with stretch reflex maintains optimal motor responses for postural adjustments
----------------------------------------------------------------------------------------------------------------------------- ------
12. Reciprocal innervations
-refers to the contraction of agonist muscles and relaxations of the antagonistic muscles in response to
the stimulation of an afferent nerve
Circuit:
Afferent fibers: Group Ia & II fibers
Center: spinal card
Efferent fibers: motor neurons supplying agonist and antagonistic muscle
Response: contraction of agonist muscle and relaxation of antagonistic muscle
(relaxation is due to stimulation of an inhibitory interneuron)
Importance:
-essential for normal physiological movements like walking
-useful in eliciting crossed extensor reflex between two upper limbs

13. Crossed extensor reflex

- stimulation of a limb causes flexion of limb on same side and extension of opposite limb.
- Mediated through interneurons
-Take part in withdrawal reflex
 1

CONDITIONED REFLEXES
Learning refers to a neural mechanism by which the individual changes his or her behavior on the
basis of past experience or acquisition of new information by the individual

Learning

Reflex Learning Incidental Learning

Non Associative Associative

Associate learning can be studied by conditioned reflexes
Conditioned Reflexes

Classical conditioning Operant conditioning

Classical conditioning
-refers to a reflex response to a stimulus that is acquired by repeatedly pairing the stimulus with
another stimulus that does not normally produce the response.

The stimulus which normally produce the response-- unconditioned stimulus

The stimulus that normally does not produce the response – conditioned stimulus

Pavlov’s experiment
Meat placed in the mouth of a dog --- salivation
(unconditioned stimulus)

Bell ringing alone --- no salivation

(conditioned stimulus)

UCS + CS --- salivation

After repetition of UCS + CS for many times

Conditioned stimulus alone ---salivation

(bell ringing)

Operant conditioning

The animal has to operate first to learn the process

(e.g) the animal presses a bar to get a food pellet.

Features of conditioned reflexes

If the CS is presented repeatedly without UCS, the conditioned reflex eventually disappears. This
is called extinction or internal inhibition.

It the CS is presented repeatedly with UCS, the conditioned reflex is reinforced. This is a must
for maintaining a conditioned reflex.

Physiological basis of conditioned reflex

The development of a conditioned reflex is due to formation of a new functional connection
between the neurons of CNS

HABITUATION & SENSITIZATION

Habituation
Refers to decrease in response to a benign stimulus when the stimulus is presented repeatedly.
When the stimulus is applied for the first time. It is novel & evokes reaction. This response is
called “orientation reflex” or “what is it” response.
Eventually the subject totally ignores the stimulus and gets habituated to it.
 2

Physiological basis of Habituation

Gradual inactivation of Calcium channels and consequent reduction in the release of a
neurotransmitter.
Example for Habituation
Riding a bicycle for the first time may be exciting. After repeating it, it becomes a habit.
Sensitization
When a habituated stimulus is coupled with a distinctly pleasant or unpleasant stimulus, a greater
response is produced.
Physiological basis of Sensitization
-due to increased levels of cAMP via an increase in Ca2+ levels in the post synaptic neuron
-the response in transient but can be prolonged
Example for sensitization
-the mother who sleeps through many kinds of noise but wakes promptly when her baby cries.
Importance of / significance of Habituation and sensitization
-Habituation & sensitization take part in learning & memory
-Habituation takes part in negative memory which prevents over burdening of memory storage.
-Sensitization takes part in positive memory
---------------------------------------------------------------------------------------------------------------------
Papez Circuit
Mammillary body of Hypothalamus
Mammillo thalamic
tract

Anterior Nucleus of thalamus Hippocampus

Cingulate gyrus
Significance of this circuit
-Hippocampus connections to diencephalon (thalamus & hypothalamus) takes part in recent
memory
-Hippocampal connections to amygdala is involved in emotions related to memory
-Hippocampus is a part of limbic system which is concerned with emotional behavior like anger,
fear, etc.,
-Anterior Nucleus of thalamus forms a part of diencephalic sleep zone – stimulation of which
produces slow waves in EEG –
---------------------------------------------------------------------------------------------------------------------
Memory
-Refers to the ability to recall past events at a conscious or a subconscious level.
Types of memory
On the basis of recall of stored information
a) Non declarative (implicit) memory
-Subconscious recall of skills, habits & classical conditioned reflexes
-Also called as reflexive memory
(e.g) cycling, driving etc.,)
b) Declarative (Explicity) memory
-conscious recollection of stored information
2 types
i) short term memory
-recalling within a few minutes or few days
(e.g) recalling a phone number to dial immediately after memorizing it.
ii) Long term memory: (remote memory)
-recalling the stored information even after few days or few years
(e.g) remembering about the picnic enjoyed
Mechanism of short term memory
1. Post titanic potentiation or facilitation
When an excitatory presynaptic neuron is stimulated for a brief period by a tetanizing current,
the synapse becomes more excitable after stoppage of stimulus.This is due to accumulation of
Calcium in presynaptic nerve endings.
 3

2. Reverberatory circuit theory

Reverberation of impulses between cerebral cortex brainstem and subcortical nuclei
through reverberating circuits.
3. Presynaptic facilitation
The presynaptic neuron is facilitated for a long time by neurons that lie on presynaptic
Terminals. Neurotransmitter involved is serotonin
Mechanism of long term memory
Long term potentiation
Physiological changes
-changes in the gene expression in postsynaption neuron
- in the synthesis and release of excitatory neurotransmitter
-changes in the response of receptors in the post synaptic membrance
Anatomical changes
-changes in the member & shapes of dendritic spines
-changes in number & size of synapses
-thickening of cortex
-formation of new synaptic connections
Chemical changes
-increase in RNA, protein & neurotransmitter synthesis
Consolidation of recent memory into permanent (long term memory)
-refers to the transfer of information from short term memory to long term memory
-recent memory initiates chemical, physical and structural changes in the synapses that
are responsible for permanent memory
-Hippocampus is the area mainly responsible for recent memory and its consolidation in
permanent memory
-consolidation will be lost in case of
-brain injury
-electric shock
Neural connections involved in memory (Learn from book)
Applied
Amnesia – loss of memory
Korsakoff’s syndrome – loss of memory in alcoholics
Reterograde amnesia – inability to remember the events that occurs before the
impairment of brain function
Anterograde amnesia – failure to learn new things, but long term memory is intact
CEREBROSPINAL FLUID
Cerebrospinal fluid is the fluid present in te ventricular system of the brain, subarachnoid space &
central spinal canal
Formation of CSF

CSF is mainly formed by choroidal plexus, which are covered by specialized ependymal cells.
The choroidal plexus are located in the cerebral ventricles (lateral, third and fourth). About 500
ml of CSF is secreted per day.

Normal CSF pressure – 60 – 100mm Hg of water

Amount of CSF - 160 Mgml

Circulation:
Lateral ventricles
Foramen of Manroe
III Ventricle
Aqueduct of sylvius
IV ventricle

Foramina of magendie Foramina of luschka

Subarachnoid space Subarachanoid space

80% dural sinus 20% spinal veins

 4

Absorption
Arachnoid villi play an important role in absorption of CSF
The CSF is removed through arachnoid villi into dural venous sinuses in the cranium

Functions:
1) Protective function:
-forms a liquid cushion surrounding brain and spinal cord. The brain simply floats in the fluid.
This prevents any mechanical injury
-gives buoyancy to brain. This reduces brain weight by 97% and thus prevents the brain from
crushing under its own weight

2) Medium of exchange
-nutritive substances are provided to the cells of CNS by CSF only. CSF is in direct contact with
neurons.
-CSFacts as a lymph and removes proteins and waste products of metabolism from the cells.

3. Reservoir function / regulation of cranial content volume

Monro Kellie Doctrine – The volume of blood, CSF & brain in the cranium at any time must be
relatively constant.
CSF regulates the contents of cranium
-increase in blood volume of brain → drainage of CSF
-decrease in blood volume of brain → retention of CSF
Thus the total volume of cranial content is kept constant.
4.Other functions
- Provides a proper chemical environment for the optimal activity of the neurons
-Useful for the diagnosis of brain disorder as it reflects the brain function
Applied
1. Lumbar puncture:- CSF is drawn from subarachnoid space by inserting needle between the L3
& L4
CSF can also be drained by cisternal and ventricular puncture
2. Hydrocephalus: Accumulation of CSF
Causes: increase in production of CSF, obstruction to CSF circulation
If CSF accumulates in ventricles --- internal hydrocephalus
If CSF accumulates in subarachnoid space --- external hydrocephalus
3.Counter – coup injury: When the head receives a severe blow, the brain gets injured on the
opposite side of blow
-----------------------------------------------------------------------------------------------------------------
APHASIA
Definition
Speech disorders in the comprehension or production of spoken or written language. The
disorders are not due to defects of vision or hearing or due to motor paralysis, but caused by
lesions in the association areas which are responsible for integrating activity.
Types
Sensory or wernicke’s or Fluent aphasia
Motor or Broca’s or Non-fluent aphasia
Global Aphasia
Anomic Aphasia
Causes:
1. Cerebral thrombosis
2. Cerebral infarction
3. Injury to the brain during accidents
4. Inadequate blood flow to the parts of the brain due to vascular changes
5. Tumours of the brain
 5

Type of Site of lesion Characteristic features Characteristic

Name errors (e.g)
aphasia Chair
Fluent Wernicke’s area Excessive talk with full of Stool or choss
a) Wernicke’s (Area 22) Jargon & Neologisms (Neologisms)
aphasia
(sensory
aphasia)
b) Conduction
Aphasia

1) Pure word Angular gyrus/ Trouble in understanding the I know.. I have

blindness Visuopsychic area written language or pictures. lots of them
Can not name the colors or
objects
(Pure word blindness)
2) Pure word Areas 40, 41 & 42 Trouble in comprehending the Flair……. no
deafness (in and around spoken word. Unable to repeat swair……..fair
auditory cortex) or write on dictation
Non fluent Broca’s area (AreaSlow speech, words are hard to “Tssair”
c) motor/ Broca’s 44) come by, limited to two or
aphasia three words to express the
whole range of meaning &
emotion
d) Global Both wernicke’s & Scanty non fluent speech.
Aphasia Broca’s area All aspects of speech and
language are impaired

-----------------------------------------------------------------------------------------------------------------
Reticular Formation
Reticular formation – Functions
1. Role in muscle tone regulation:
- Descending extrapyramidal tracts from reticular formation (Reticulo spinal tract) -
regulate muscle tone, posture & equilibrium
- mainly modulates the tone of antigravity muscles.
Two tracts:
Lateral Facititatory reticulo spinal tract from pons
Medial Inhibitory reticulo spinal tract from medulla
2. Role in sleep & wakefulness cycle
The ascending reticular activating system of reticular formation has a role in this process
ARAS:
RF of midbrain

Intralaminar Nuclei of Thalamus (Non specific nucles)

Cerebral cortex (all parts)

Activation of ARAS →Wakefulness, alertness & consciousness

Inactivation of ARAS → Sleep
Other functions of ARAS
- Influences learning and memory
- Keeps the person in alert state
- Responsible for the genesis of EEG waves
3) Modulation of pain:
Raphae magnus nucleus of retircular formation

Descending serotonergic fibers

Excites SGR (substantia gelatinosa of Rolando) cells of spinal cord

Modulation of pain
 6

4) Control of visceral / vegetative functions:-

VM (Vaso Motor Center), Cardia Center, Respiratory center
Vomiting Center, Salivary Centers, etc., in descending Reticular formation of brain stem

Through Autonomic Nervous system

Control visceral functions (Gastric Secretion, GI mofility, BP, heart rate, respiratory rate,
salivation, vomiting etc.,

5) Control of neuroendocrine systems in the hypothalamus

6) Influences biological clocks (circadian rhythm) by its connections with hypothalamus
--------------------------------------------------------------------------------------------------------------
ELECTROENCEPHALOGRAM(EEG)
Definition:
Electroencephalogram is a record of summated potentials of the cerebral cortex recorded from the
surface of the scalp
Hans Berger is called the father of modern electroencephalography

Normal EEG pattern: (the waves of normal EEG)

Alpha rhythm
Beta rhythm
Theta rhythm
Delta rhythm

α Rhythm : (alpha rhythm)

-prominent component of EEG
-obtained from adult humans who are awake but with closed eyes.
-recorded from parieto – occipital area
-also called as Berger rhythm
Frenquency: 8-13 Hz
Voltage: 50uv

β(beta) rhythm:
-obtained when the eyes are opened
-indicates an alert state
-recorded from parietal and frontal regions
Frequency: 18-30 Hz (Faster rhythm)
Voltage: 5-10 uv
Theta rhythm:
-recorded from the parietal and temporal regions of children.
-do not occur in normal waking adult
But obtained from adults in emotional stress and many brain disorders
Frequency: 4-7 hz
Amplitude: (10uv)
Delta waves:
-present during sleep
-absent in wakeful adults, but present in wakeful infants
-presence of these waves in wakeful adults indicates some lesion of the brain
-recorded from occipital and other regions.
Frequency: 1-4 Hz
Amplitude: 200 uv
Applied – alpha block
-refers to a phenomenon in which alpha waves are replaced by B-rhythm (fast, irregular
waves of low amplitude)
Occurs in
-when the eyes are opened
-in conscious mental activity
-application of a stimulus
 7

USES OF EEG

Useful in:

Diagnosis of epilepsy
Localization of lesions in brain
Neurophysiological investigation
Studying of sleep pattern
Finding out the prognosis of head injuries and vascular lesions
Differentiating organic and functional disorders of brain

--------------------------------------------------------------------------------------------------------------------
SLEEP
What are the types of sleep? Differetniate them
Types of sleep:
Rapid eye movement sleep (REM)
Slow wave sleep or NREM
Differences

NREM Sleep REM Sleep(Parodoxical sleep)

1. Rapid Eye movement Absent Present
2. Brain activity Less More
3. Muscle tone Hypotonia More hypotonia
4. EEG δ( Delta) waves) β (beta) rhythm
5. Dreams Can not be recalled can be recalled
6. PGO (ponto
Geniculo occipital
Spikes No PGO spikes Present

7. Pulse, BP &
Respiratory rate Low & regular increased & irregular

8. Hormonal level Decrease in serotonin Decrease in nor adrenaline

content of raphae content in locus cerulus
Nucleus Increase in Acetylcholine
Of cortex
9. Threshold for arousal Elevated Further elevated

10. % of total sleep

Duration 75% 25%

11. O2 consumption Less More

-------------------------------------------------------------------------------------------------------------------

LIMBIC SYSTEM
Components
Amygdala
Hippocampus
Cingulate gyrus
Septal Nuclei
Medial Forebrain Bundle
Pre pyriform cortex
Entorhinal cortex
Diagonal brand of Broca
 8

Functions
a) Emotional behavior
Seat of emotions
mainly due to papez circuit involvement
Physical changes during emotions.
a) Somatic changes – Grinding of teeth, shouting, crying etc.,
b) Visceral changes -↑HR,↑RR,↑BP, Sweating etc.,
Mental changes
Awareness of sensation (cognition)
Feeling (Affect)
Urge to take action (conation)
- Amygdala stimulates emotions
- Lesion of amygdala → placidity
b) Feeding behavior
- Limbic system is responsible for discriminative feeding
- Amygdala is mainly involved
- Lesion in amygdala → hyperphagia with indiscriminative ingestion of all kinds
of food.
c) Maternal behavior
- refers to the nursing (breastfeeding) and protection of the off spring by the mother.
- Cingulate gyrus & retrosplenial portion of the limbic cortex are involved in this
- Lesion in these areas depress mater nal behavior
d) Sexual behavior
- refers to the basic sex drive (urge to copulate)
- Limbic system suppress the sexual behaviour
- Piriform cortex of limbic lobe is involved
- Bilateral lesion in this area →↑ in sexual activity
- (attempt to copulate even the animals of other species & inanimate things)
e) Motivational behavior
- refers to the motivation of learning and behavior
- reward & punishment centers in the limbic system are responsible for motivation
- septal nuclei (Reward center) & entorhinal cortex (punishment center) are parts of
limbic system
f) Autonomic functions
- Stimulation of many parts of the limbic system specially that of amygdala produces
autonomic responses such as
- changes in cardiovascular system
- changes in respiratory system
- changes in GI system
- changes are mediated through hypothalamus
 1

Special senses

10 marks
Describe the visual pathway & the effect of lesions at various levels with the suitable
diagram
The visual pathway consists of
1. Retina
2. Optic nerve
3. Optic chiasma
4. Optic tract
5. Lateral geniculate nucleus
6. Optic radiation(geniculo-calcarine tract)
7. Visual cortex
 2

1. Retina:
- rods & cones in the retina convert light in to electrical impulses.
2. Optic nerve:
- formed by the fibers of ganglion cells.
- the fibers in the lateral (temporal ) half of the nerve carry the impulses from the nasal field of the
same eye.
- the fibers in the medial half of the nerve carry impulses from the temporal field of the same eye.
3. Optic chiasma:
- formed by the crossing of medial fibres of both the optic nerves.
4. Optic tract:
- consists of nasal fibres from the opposite optic nerve and temporal fibers from the optic nerve of the
same side.
- fibres run backwards and relay in lateral geniculate nucleus of thalamus.
5. Lateral geniculate nucleus(LGN):
- The LGN is divided into six layers of cells.
- The crossed fibers of the optic tract terminate in layers 1, 4 and 6 while the uncrossed fibers terminate
in layers 2, 3 and 5.
6. Optic radiation:
- arise from the LGN
- is also referred as geniculo-calcarine tract
- the fibers are arranged supero medially & infero laterally
- terminates in primary visual area(17)
- also projected to visual association areas 18 and 19.
7. Visual cortex:
- The primary visual cortex is Brodmann area 17
- also known as V1
- located on the medial surface of the occipital lobe along the walls and lips of calcarine fissure.
Other connections
1. to suprachiasmatic nucleus of hypothalamus - concerned with circadian rhythm.
2. to pretectal nucleus which inturn sends fibres to 3rd cranial nerve nucleus = mediates the light
reflex.
3. From the occipital cortex to the frontal eye field (area 8) - concerned with the movement of
eyeball (convergence) & accommodation reflex
4. From occipital cortex to superior colliculi and from there to III, IV, VI cranial nuclei and to the
spinal cord - mediate tone, posture, equilibrium and visuospinal reflexes.

Effect of lesion of visual pathway at different levels

• The loss of vision in one entire visual field is referred as anopia.

• Loss of vision in one half of the visual field is called hemianopia. It is of two types:
– Homonymous hemianopia
– Heteronymous hemianopia
 3

Site of lesion Condition Diagram

1 Right optic Right eye anopia
nerve
2 Optic Bitemporal
chiasma hemianopia
3 Lateral Binasal
Fibers hemianopia
4 Right optic Left homonymous
Tract Hemianopia

5 Rjght optic Left homonymous

radiation Hemianopia
1 Inferolateral Left homonymous
2 6
3 fibers of Superior
optic Quadranopia
radiation
4
7 Superomedial Left homonymous
Fibers of Inferior
5 Optic Quadranopia
radiation
6
8 Inferolateral Left homonymous
fibers of Superior
7 optic Quadranopia
radiation in With macular
calcarine Sparing
fissure
8 9 Superomedial Left homonymous
9 fibers of Inferior
optic Quadranopia
radiation in With macular
10 calcarine Sparing
fissure
10 Visual cortex Left homonymous
Hemianopia
With macular
Sparing
 4

5 marks
1. Describe the circulation & functions of aqueous humour.
Aqueous humour
❖ Homogenous fluid that fills the anterior & Posterior chambers
❖ pH 7.1-7.3
❖ Refractive index 1.33
❖ Composition – Less glucose & more Lactic Acid than plasma with high ascorbic acid
Formation of Aqueous Humour:
❖ Formed by the ciliary processes-
❖ Mechanism:
1. Active secretion
2. Ultra-filtration
❖ Rate of formation: 2-3 cu.mm per minute
Circulation of Aqueous Humour:
❖ Aqueous humor circulates within the eye
❖ Formed by the ciliary processes
❖ Secreted into posterior chamber
❖ Passes between ligaments of lens
❖ Passes through pupil into Anterior chamber
❖ Flows into angle between cornea & iris
❖ Flows through trabeculae
❖ Flows into canal of Schelmn & extra ocular veins
❖ Re-enters blood circulation

Functions Of Aqueous humour:

 Provides nutrition to cornea & lens (avascular structures)
 Maintains IOP (Intra ocular pressure)
 Maintains shape of eyeball
 Acts as refractive medium
------------------------------------------------------------------------------------------------------------------------------
2. Describe the mechanism of accommodation for near vision
• It is the ability of the eye to see distant and near objects clearly. This involves the process of
adjusting the shape of the lens so that the external image falls exactly on the retina.
Accommodation of the Lens for near vision
• Ciliary muscles contract
• Ciliary body pulls forward and inward
• Tension on suspensory ligaments of lens is decreased
• Lens becomes thicker (rounder) due to its elasticity
• Pupils constricts
Near point:
• It is the nearest point to the eyes at which an object can be brought into clear focus by
accommodation.
– At age 10: Near point – 9 cm
– At age 60: Near point – 83 cm
• The near point recedes with age.
Near response
1. Convergence of eye ball
2. Constriction of pupil
3. Curvature (anterior) change in lens
 5

Accommodation of the Lens for far vision

• Ciliary muscle is relaxed
• Ciliary body is pulled backward and outward
• Tension on suspensory ligaments of lens is increased
• Lens becomes thinner (flatter) due to its elasticity
• Pupils dilate
Accommodation Reflex
Changes in the eye in response to changing the gaze from long distant to short distant
Responses:
Constriction of pupil
Convergence of eyes (medial )
Curvature of lens (increase in anterior)
Pathway of the Accommodation reflex

Near vision
.
Retina

Optic nerve

LGN

Visual cortex

Frontal eye field

Superior colliculus

III cranial nerve nucleus

Ciliary ganglion

Short ciliary nerve

Sphincter papillae Ciliary muscle Medial rectus

Constriction of pupil Curvature of lens Convergence of eye balls

(increase in anterior)
 6

-------------------------------------------------------------------------------------------------------------------------------
3. Briefly describe the mechanism of dark adaptation
Adaptation to dark (Scotopic vision)
On entering dark room from bright area, initially the vision is poor, later it improves.This decline
in visual threshold is called dark adaptation.
Time duration for dark adaptation depends
1. Intensity of light
2. Duration of exposure
3. Vit A Content
Two phases
1. Adaptation of the cones (5min)
2. Adaptation of rods (20min)

Changes in the eye during dark adaptation

1. Pupils dilate
2. Sensitivity of the photoreceptors to light increases
3. Resynthesis of photo pigments
4. Decrease in visual acuity
5. Vision changes from cone to rods (photopic to scotopic). This is called PURKINJE SHIFT.
Visual Purple//Rhodopsin Cycle

Rhodopsin (11 cis retinal+ opsin ) Pre-lumi rhodopsin

Light
Dark Lumi rhodopsin

Meta rhodopsin I
Opsin
Meta rhodopsin II
+
Retinal isomerase
11 cis retinal All transretinal
Isomerase
11 cis retinol All transretinol (Vitamin A)
 7

---------------------------------------------------------------------------------------------------------------------------
4. Write short notes on colour vision
• A sensation evoked by different wavelengths of light.
• Function of cones.
Physiological Basis of colour vision
• Three different types of cones
• Three types of pigments (the opsin protein part differs from rhodopsin),
• Each pigment has maximum absorption at different wavelengths
• blue-absorbing cones – cyanopsin pigment (max absorption at 445nm)
• green-absorbing cones – Iodopsin pigment (max absorption at 535 nm)
• red-absorbing cones – porphyropsin pigment (max absorption at 570 nm)
Primary colours
• Red
• Green
• Blue
Theories of colour vision
• Young – Helmholtz theory
• Granit modulator & dominator theory
• Hering opponent colour theory
• Land’s retinex theory
Young – Helmholtz theory
• Trichromatic theory
• Red , green , blue – 3 primary colours
• The 3 types of cones have 3 different pigments
• Each pigment is maximally sensitive to one primary colour
- But also responds to other 2 primary colours
• Sensations of various colours are due to stimulation of different receptors at
different intensities.
Processing of colour perception
• Analysis of colour occurs in the retina
• Information is then passed on to the brain for interpretation.
• Centre of fovea is blue blind.
• Blue cones are absent here.
• Retina , lateral geniculate nucleus , visual cortex all have a combined role in
perception of colour.
Colored light strikes the retina
↓
Depending on the color mixture cone will respond
↓
Response is in the form of local potentials
↓
LP transmitted in bipolar cells
↓
Ganglion cells activated
↓
Signals from the 3 cones are processed in the ganglion cell
↓
Reach the layers of LGN
↓
Processed in LGN
 8

↓
Transmitted to cortex V1
↓
Impulses reach V4

COLOUR BLOBS

• Primary visual area 17 contains color blobs – clusters of colour sensitive peg shaped neurons.
------------------------------------------------------------------------------------------------------------------------------

5. What are the errors of refraction? How will you correct it?
• In a normal human eye light rays are focused on retina.
• If not focused on retina-called Refractive errors.
• Due to abnormality in cornea or lens.
• Normal eye is called Emmetropic Eye
• Abnormal focus is called Ametropic Eye
Refractive Errors
1. Myopia (short sight)
2. Hypermetropia (Long sight)
3. Presbyopia
4. Astigmatism
5. Anisometropia
6. Aphakia
7. Cataract
 9

Error Defect Cause Feature Correction

Myopia Long distant objects Longer eye ball / high Light rays are Biconcave
not clear refractive power of lens focused in front of lens
retina

Hypermetropia Short distant objects Shorter eye ball / Low Light rays are Biconvex
not clear refractive power of lens focused behind the lens
retina

Presbyopia Short distant objects Loss of elasticity & Decrease in the Biconvex
not clear plasticity of lens and power of lens
also decrease in power accommodation of
of ciliary muscle due to eye
aging

Astigmatism Blurring of vision Ununiform curvature of Light is focussed Cylindrical

the cornea at multiple points lens
on retina

Aniso Difference in the Congenital Eye with high Correction

metria refractive power refractive power – of each eye
between the two Dominant eye separately
eyes Eye with less with
refractive power – appropriate
Suppressed eye lenses
 10

Aphakia Diplopia & Removal of lens Complete loss of Wearing

Astigmatism due to following cataract accommodation spectacles
absence of lens surgery / dislocation of (hypermetropic) with power
lens of + 11
diopters/IOL
implantation

-------------------------------------------------------------------------------------------------------------------------------
6. Describe the functions of middle ear.
Components of middle ear:
1. Three small bones (ossicles):
1)Malleus
2)Incus
3)Stapes
2. Two small muscles:
1)Tensor tympani
2)Stapedius muscle
Functions of middle ear
1. Tympanic Reflex:
• When loud sounds are transmitted through the ossicular system (Malleus, Incus, stapes) into
the CNS, a reflex occurs to cause contraction of both Stapedius and tensor tympani muscles.
This is called tympanic reflex or attenuation reflex
• The contraction of tensor tympani muscles pulls the handle of the malleus inward, while the
stapedius muscle contraction pulls the stapes outward
• These two forces oppose each other and this causes rigidity of the entire ossicular system
which greatly reduces the transmission of low frequency sounds.
Significance of tympanic reflex
to protect the cochlea from damaging vibrations caused by excessive loud sound i.e. low
frequency sounds.
2. Impedance Matching:-
• Whenever sound wave travels from a thinner medium to denser medium, some
amount of sound energy is lost at the interphase of two medium.
• This happens in ear also. When sound travels from air filled middle ear into
denser fluid medium of inner ear, there is a loss of sound energy at oval window
• Middle ear compensates this by increasing the sound energy level by several times at oval
window.
• Middle ear achieves this by three mechanism which are combinely referred as impedance
matching.
The mechanism are:-
1. Area difference
• As the area of the tympanic membrane is large than the area of the oval window,
the forces collected over the tympanic membrane are concentrated on a smaller
area of oval window.
• This increases the pressure at the oval window by 17 times.
2. Lever action of the middle ear bones.
• The arm of incus is shorter than that of malleus and this produces a lever action.
• This increases the force by 1.32 times and decreases the velocity at the stapes.
 11

3. Buckling factor:-
• The tympanic membrance is conical in shape. As the membrane moves in and out
it buckles so that the arm of the malleus moves less than the surface of the
membrane.
• This also increase the force and decreases the velocity
3. Function of Eustachian tube:
Equalizes the pressure on both sides of tympanic membrane
-------------------------------------------------------------------------------------------------------------------------------
7. Describe organ of corti
Organ of Corti
• Receptor organ of hearing
• Situated on the basilar membrane
• Extends from the base to apex of cochlea
Main components of Organ of Corti

1. Inner hair cells

2. Outer hair cells
3. Rods of corti
4. Tunnel of Corti
5. Lamina reticularis
6. Basilar membrane
7. Tectorial membrane
8. Deiters' cells
9. Hensen's cells

2 7

1 5

3 9

8
6
4

• INNER HAIR CELLS

- one row ( 3500 in number)
- flask shaped
- connected to lamina reticularis
- Stereocilia of hair cells float freely
• OUTER HAIR CELLS
- three or four rows ( 20000 in number)
- test tube shaped
- stereocilia –embedded in the tectorial membrane
 12

8. Trace the pathway for hearing

I order neuron :
From the bases of the hair cells → cell bodies form the spiral ganglion around the modiolus
→ axons form the cochlear nerve →joins with the vestibular nerve to form the
vestibulocochlear nerve → end in cochlear nuclei
II order neuron :
From cochlear nuclei → ascend to the nearby superior olivary nucleus (of both sides) → then
ascend in the lateral lemniscus → end in inferior colliculi of midbrain
III order neuron:
From inferior colliculi to medial geniculate bodies of thalamus
IV order neurons: complete the pathway from thalamus to primary auditory complex
 13

9. Trace the olfactory pathway

receptor cell axon

↓
pierce the cribriform plate of ethmoid
↓
enters olfactory bulb
↓
synapse with dendrites of mitral cells to form olfactory glomeruli
↓
axons of mitral cells pass posteriorly through olfactory stria
↓
olfactory cortex
(anterior olfactory nucleus, olfactory tubercle, prepyriform cortex, amygdala, entorhinal cortex
↓
From the olfactory cortex signals reach
↓
– Orbito frontal cortex
– Hypothalamus
– Hippocampus
Thus olfactory impulses are projected both to
– Neocortex
Perception & discrimination of odours
– Limbic system
Emotional, motivational, behavioral & physiological effects of odours

Olfactory
Cribriform plate of ethmoid bone Glomerulus
straie
bone

Olfactory bulb

Olfactory
neuron

Olfactory receptors
 14

10. High light the special features of olfactory pathway

Pathway involves only two sets of neurons

No relay in thalamus
Olfactory signals do not reach somatosensory cortex but reach orbitofrontal cortex
Impulses reach limbic system
Pathway involves only two sets of neurons
No relay in thalamus
Olfactory signals do not reach somatosensory cortex but reach orbitofrontal cortex
Impulses reach limbic system
-------------------------------------------------------------------------------------------------------------------
11. Trace the taste pathway
Taste buds

Taste fibres in vii, ix & x nerves (I order neuron)

Tractus solitarius (in medulla)

Nucleus tractus solitarius (II order neuron)
 Cross over
Joins medial leminiscus

VPM (Ventral Postero Medial Nucleus of thalamus (III order neuron)

Brodman’s area 43

Gustatory Pathway from Taste

Buds

Figure 16.2
 15

12. Name the primary taste sensation. How are they distributed on the tongue?
Outline the basic taste modalities & explain the mechanism of taste sensation

Primary taste sensations

1. Sweet
2. Salt
3. Sour
4. Bitter
5. Umami

BASIC TASTE PRODUCED BY MECHANISM OF PART OF TONGUE MOST

SENSATIONS STIMULATION SENSITIVE

Sweet Sugars, glycols & ↑ cAMP→↓K+ Tip

aldehydes. conductance

Bitter Alkaloids ↑ IP3→ ↑Ca++ release Back

Sour H+ ions Blocking K+ channels Posterior ½ of lateral

Salt Anions of ionised salts Na+ ion permeability Anterior ½ of lateral

Umami Monosodium -------- ---------

Glutamate
 1

Integrated Physiology ( Skin, Temperature regulation , Exercise & Yoga)

1. Explain the physiological basis of bradycardia in athelets.
Due to increased vagal tone caused by regular physical activity, athletes have bradycardia
2. Briefly describe how blood supply in skeletal muscle increases during exercise
Two mechanisms cause vasodilation:.
-The neural mechanism is the activation of the sympathetic vasodilator system.
-The local mechanisms are accumulation of metabolites and rise in temperature
in the active muscles.
-Vasodilation opens up many closed capillaries by opening up precapillary sphincters
3. Describe the effect of exercise on heart rate, cardiac output & blood pressure
Heart rate increases due to decreased vagal tone & also due to sympathetic stimulation
Cardiac output increases as the heart rate and stroke volume increase
Systolic BP rises moderately and diastolic BP usually remains unchanged or falls in heavy exercise
4. Explain briefly the respiratory changes during muscular exercise
Ventilation is increased & increase in the O2 extraction from blood in exercising muscles
5. What are the types of yogic exercise? What are the health benefits of yoga?
Types of yogic exercises:
a) Asanas or body postures
b) Pranayama or breathing exercises
c) Purification practices or kiryas
d) Music and sound therapy
e) Deep relaxation
Health benefits of yoga:
On CNS :
Stability of ANS
Predominance of alpha waves ( more mental relaxation)
Improvement of higher intellectual activities
Higher cerebral blood flow
On CVS:
Decrease in heart rate & systolic BP
Increased cardio vascular efficiency
On Respiration:
Decrease in rate
Increase in tidal volume, Vital capacity & respiratory efficiency
On digestion
Relax GIT → effective elimination
Stimulate peristalsis → Proper digestion and absorption
On musculo skeletal system:
Increase in flexibility, range of movement, strength, endurance & energy level
6. What are the different ways of heat loss from the body?
Radiation, Conduction, convection, sweating & vasodilation
7. What is the pathogenesis of fever?
Endotoxin, Inflammation & other pyrogenic stimuli
↓
Monocytes, macrophages & Kupffer cells
↓ cytokines
Preoptic area of hypothalamus
↓ Prostaglandins
Raise temperature set point
↓
Fever
 2

8. Explain briefly how shivering is a protective mechanism.

- It is one of the important mechanisms of thermogenesis (heat production)
- It helps to prevent the fall in body temperature in cold environment
9. What are the different ways of heat production in the body?
a) Hypothalamic stimulation of shivering
b) Sympathetic excitation of chemical thermogenesis)
c) Increased thyroxine output → increased BMR
10. List out the effects of fever
- Increase in phagocytic activities
- Increase in blood flow to the injured tissues → large numbers of the leucocytes reach the site
- increase in antibody production & “T” cell proliferation
- increase in metabolic reactions → faster repair of tissues
- decrease in bacterial multiplication
 1

REPRODUCTIVE SYSTEM
10 marks

1. MENSTRUAL CYCLE
- Refers to cyclical changes that takes place in the women
- Preparatory step for fertilization and Pregnancy
Duration - 25 – 35 Days
Average – 28 Days
Changes include:
Ovarian Cycle
Uterine Cycle
Cervical Cycle
Vaginal Cycle
Ovarian Cycle
Follicular Phase
Ovulation
Luteal Phase
1. Follicular Phase
-Involves the development of a follicle
- One follicle matures each month
- During the lifetime of a female only 400 follicles mature
Stages of follicular development:
Primordial follicle → Primary Follicle → Secondary follicle → Tertiary follicle
(Involves addition of granulosa cells surrounding the oocyte & also formation
of theca cells)→Antral follicle(Having fluid filled space) → Matured
Graafian follicle
2. Ovulatory Phase
The process of expulsion of secondary oocyte from ovary into peritonial cavity
following rupture of mature graffian follicle
Timing:
14th day of sexual cycle
Events of Ovulation
- Rapid swelling of follicle
- Formation of stigma
- Release of proteolytic enzymes
- Dissolution of capsular wall
- Rupture of graffian follicle
3. Luteal Phase ( 15th - 28th Day)
Events :
- Formation of corpus hemorrhagicum (ruptured follicle filled with blood)
- Formation of corpus luteum (clotted blood replaced with yellow colored
lipid rich luteal cells)
- Formation of corpus albicans ( regression of corpus luteum)
 2

Uterine (Endometrial) Cycle

Menstrual (Bleeding) Phase
Proliferative phase
Secretory phase
1.Menstrual Phase
The lining of the uterus (endometrium) breaks down and is lost from the body. This is
called menstruation or a period
Duration - Days 1-5
Components:
- 30 – 50 ml blood (75% Arterial)
- Ovum - unfertilized
- Mucus
- Endometrial debris – damaged endometrial tissue, serous fluid, a large amount
of prostaglandins & fibrinolysin
Mechanism of menstruation
1. steroid production declines.
2. shrinking of endometrial tissue
3. reduction in blood flow to superficial layers – ischemic hypoxia & damage to
the epithelial and stroma cells & constriction of spiral arteries
4. Individual arteries re-open → tearing and rupturing the ischemic tissues.
5. Bleeding into the cavity
- About 50% of degenerating tissues is resorbed and 50% is lost as 'menstrual
bleeding'.
2. Proliferative Phase
- Days 6-13
- increase in estrogen causing the endometrium to thicken (from 1mm to 4 mm)
- angiogenesis
- stimulation of endometrial glands to grow
3. Secretory Phase
Days 15-28 :
increase in progesterone causes
- endometrial thickness
- increased vascularity
- secretion of endometrial glands
(in preparation for the developing embryo)
Cervical Cycle
1. Preovulatory Phase - Estrogen is predominant hormone
- Cervical mucus - Thin, Watery & Alkaline
2. Postovulatory Phase - Progesterone
- Cervical mucus - Thick & Tenacious
Vaginal Cycle
1. Preovulatory Phase - Estrogen predominance
Thick & Cornified Epithelium
2. Postovulatory Phase - Progesterone predominance
Thick & viscid secretion
Infiltrated with Leucocytes
 3

Hormonal Control of Sexual Cycle

Gonadotropins from Anterior pituitary
FSH - development of follicles (follicular phase)
LH - triggers ovulation
Ovarian Hormones
Estrogen – influences proliferative phase of endometrial cycle
Progesterone – influences secretory phase of endometrial cycle

Menstrual Disorders
Premenstrual Syndrome
Amenorrhoea - Absent
- Primary
- Secondary – Pregnancy
Menorrhagia – Excess bleeeding
Metorrhagia – intermenstrual bleeding
Oligomenorrhoea – decreased frequency
Dysmenorrhoea – painful menstruation
 4

2. CONTRACEPTION
- Refers to prevention of Conception
Methods of Contraception
Temporary Permanent
1. Barrier Methods 1. Vasectomy
2. Natural Methods 2. Tubectomy
3. Intrauterine Devices
4. Hormonal Contraception (Oral pills)
1. Barrier Methods
- Prevention of deposition of sperms in vagina
Mechanical Methods
Males - Nirodh (Condoms)
Females - Pouch (Female condom)
Diaphragm
Cervical Cap
Chemical Methods
Spermicides - Kill the Sperms
Jelly
Cream
Sponge
Combined (Mechanical & Chemical) - More Effective
2. Natural Methods
Rhythm Method – Following safe period
Coitus Interruptus
Complete abstinence
SafePeriod
Definition – the period of least fertility during menstrual cycle
Duration - 5-6 days after menstruation & 5-6 days before next cycle
Significance – rhythm method of contraception
3. Intrauterine Devices
Lippe’s Loop
Cu T 200
Multiload Cu T-250
Progestasert
Mechanism of Action
Increase tubal motility
Prevent implantation
Spermicidal activity
4.Hormonal /Oral Contraceptives
Sex Hormones - Oral Pills
Mechanism of Action
Negative feedback mechanism
Suppress FSH & LH secretion
Pills
Combined Pill - Progesterone & Oestrogen
21 Days - From the day bleeding stops
 5

Withdrawal bleeding occurs

Sequential Pill - 15 days Oestrogen + Combination
Mini pill - Low dose estrogen
Postcoital pill – within 72 hours after sexual intercourse
Complications of oral contraceptives
Thromboembolic phenomenon
Increase in weight
Jaundice
Avoid in Diabetics
Fibroid Uterus
Permanent Contraceptive Methods
Vasectomy
Tubectomy
Medical Termination of Pregnancy (MTP) or Abortion
Dilatation & curettage (D&C)
Vacuum aspiration
Administration of prostaglandins
---------------------------------------------------------------------------------------------------------

5 MARKS
1. SERTOLI CELLS
Sertoli cells are the supportive cells found in the seminiferous tubules of testis.
Functions:
1. Play a role in the maturation of sperms
2. Provide nutrition to the developing spermatozoa
3. Play a part in the mechanism of blood testis barrier
4. Phagocytize damaged germ cells.
5. Takes part in aromatization of testosterone into estrogen
6. Secretes the following substances:
- MIS (Mullerian Inhibiting substance)
- Inhibins
- Androgen binding protein
7. Influence Leydig cell secretion through activins & inhibins
2. SPERMATOGENESIS
Definition: The development and maturation of spermatozoa (male gametes) is called
spermatogenesis.
Stages:
I.Spermatocytogenesis: Development of spermatogonia into spermatids
1. Spermatogonium A: Primitive germ cells which are diploid (44+XY) and
divide by mitosis to spermatogonium B cells
2.Spermatogonium B: These are also Primitive germ cells which are
diploid (44+XY) and divide by mitosis. These cells
give rise to primary spermatocyte
3. Primary spermatocyte: Diploid cells which divide by meiosis to form
secondary spermatocyte.
 6

4. Secondary spermatocyte: These are haploid cells (22+X or Y). They

undergo second meiotic division to form spermatids
5. Spermatids: Haploid cells which transform into motile spermatozoa.
II.Spermiogenesis: Transformation of spermatids into tailed, motile spermatozoa
(sperms)
Spermatozoa: Matured male gamates, haploid and posses a head, middle
piece and a tail. About 512 spermatozoa develop from a single
spermatogonium

Spermatocytogenesis

Spermiogenesis
 7

Regulation of Spermatogenesis:
A.Hormones:
1. Testosterone: Secreted from Leydig cells of testis. Acts on seminiferous
tubules and stimulates the proliferation of spermatogonia into
primary spermatocyte
2. FSH: Stimulates proliferation as well as maturation of spermatozoa. Trophic to
Sertoli cells which play an important role in maturation.
3.LH: Stimulates the Leydig cells to produce testosterone which is required for
Spermatogenesis
4. Other hormones which are required for spermatogenesis: Thyroxine, Growth
hormone & Insulin
B.General factors:
1. Temperature: Speramatogenesis requires 2 to 3oc less than the core temperature
of the body
2. Irradiation: Exposure to harmful radiation causes degeneration of seminiferous
tubules and leads to sterility
3. Toxins: Bacterial and viral toxins may cause selective destruction of
seminiferous ubules. E.g. Mumps
4. Vitamins: Vitamins A, C & E are required for spermatogenesis

3. TESTOSTERONE.
Secreted from Leydig cells of testis. About 4-9 mg is secreted per day.
Mechanism of Action:
It combines with cytoplasmic receptor and reaches DNA. It acts on DNA and
stimulates mRNA and protein synthesis
Functions:
1. In Fetus:
a) Sex differentiation: Stimulates the development of Wolffian duct into
male accessory sex organs. Development of male external genitalia
requires dihydrotestosterone which is derived from testosterone
b) Descent of testes: Along with MIS, testosterone stimulates the descent of
testes from abdominal cavity into scrotum through inguinal canal
2.During Puberty:
a) On accessory sex organs: Stimulates the development and growth of the
male accessory organs like vas deference, seminal vesicles,
prostate, scrotum & penis
b) On distribution of body hair: General body hair increases. Moustache &
beard appear.Pubic hair appear & attains male pattern
c) On voice: Becomes deeper and low pitched due to growth of vocal cords &
larynx
d) On skin: Thick with more sebaceous secretion. Acne appears on face
e) Mental behavior: More aggressive
3. Spermatogenesis: Stimulates the proliferation of spermatogonia into primary
spermatocyte in seminiferous tubules.

4. On growth: Stimulates skeletal growth. But finally it causes fusion of

 8

epiphyseal plates and arrest growth

5. On muscle mass: Testosterone is a protein anabolic hormone. It increases
protein synthesis.This increases the muscle mass and muscle power in
males.
6. On erythropoiesis: Stimulates the production of erytropoietin there by
increases RBC count. Hence males have higher RBC count than females

4. PLACENTA
Nutritive Function
-Transport of Glucose, Amino acids , Fatty acids & Vitamins from maternal blood
to foetal blood
- Storage of Glycogen, Lipids, Fructose
Respiratory Function
-Diffusion of O2 from maternal blood to foetal blood
-Diffusion of CO2 from foetal blood to maternal blood
Double Bohr effect
- Increased affinity of Foetal Hb (Hb F) shifts the ODC of foetal blood to left
- Increased Level of CO2 shifts the ODC of maternal blood to right
(Both the effects increase the O2 content of foetal blood)
Excretory function: Transport of metabolic waste products like urea, uric acid,
creatinine from foetal blood to maternal blood
Endocrine function
Placental Hormones
-Human Chorionic Gonadotrophin (HCG)
- Human Placental Lactogen (HPL, HCS - Human Chorionic
Somatomammotrophin)
-Human Chorionic Thyrotrophin (HCT)
-Oestrogen , Progesterone
-Relaxin
Human Chorionic Gonadotrophin (HCG)
Growth of Corpus Luteum
Presence in Serum & Urine - Diagnostic of Pregnancy
Growth of Testis / Ovarian Follicles in Fetus
Human Placental Lactogen
- Maternal Growth Hormone of Pregnancy
- Growth of Breast glands
- Retention of Nitrogen, Calcium , Sodium
- Makes Glucose & Fats available to the Fetus
Oestrogen
- Growth of ducts of Breast glands
- Increases the sensitivity of uterus to Oxytocin
Progesterone
- Growth of alveoli of Breast glands
- Maintenance of Pregnancy
-
Relaxin - Relaxes Pelvic joints & Pubic symphysis
 9

Softens and dilates the uterine cervix Facilitates delivery

6. INDICATORS OF OVULATION
1. Basal Body Temperature- A rise of 0.50C after ovulation
2. Billings Method -
Cervical Mucus :
Before ovulation- Elastic, Stretchable upto 10 cms (Spinnbarkeit effect)
After ovulation – Thick and can not be stretched
3. Fern Test
Before Ovulation –cervical mucus produce a fern pattern when dried on a glass
slide
After Ovulation – Fern pattern disappears
4. Biopsy of the endometrium – checking for the secretory phase
5. Endoscopy
6. Blood Gonadotrophins Level
7. Ultrasound Abdomen
7. NEUROENDOCRINE REFLEXES
Partiturition/Ferguson Reflex
Uterine contraction
 10

Milk let down or suckling reflex

Suckling of breast by the baby
↓
Stimulation of mechanoreceptors on nipple & areola
↓
Afferents (somatic nerve)

spinal cord
↓
Hypothalamus

Anterior pituitary Posterior pituitary

(Lactotrops) (Paraventricular nucleus)
↓ ↓
Prolactin Oxytocin

8. FETO_PLACENTAL UNIT
- Fetus & Placenta function as a unit in synthesising estrogen & progesterone
- Helps to maintain the level of steroids which inturn maintain the pregnancy
Maternal blood Placenta Foetal Adrenal
Progesterone Progesterone Cortisol, Corticosterone

Acetate

Pregnenolone DHEAS

16 – OH DHEAS 16 – OH DHEAS

Estrogen Estrogen

9. HCG
-Secreted by syncytiotrophoblast of placenta
-Reaches its maximum level at 60th -70th day of pregnancy
Functions:
- Growth of corpus luteum
- Secretion of progesterone & estrogen from Corpus Luteum
- Growth of testes & testosterone secretion in male foetus
- Androgen production from fetal adrenal cortex
- Formation of primordial follicle in fetal ovary
- Growth of breast
- High level in urine – diagnosis of pregnancy