Unit 10 The Nervous System

Unit
The Nervous System

10
Organization of the nervous system (Fig. 10.1)
Structural and Functional unit: NEURON
i n
Central Nervous System Peripheral Nervous System
a
Brain Spinal Cord Somatic nervous system Autonomic nervous
system (ANS)
J
Fore brain Mid brain Hind brain Spinal nerves Cranial nerves
.
(31 pairs) (12 pairs)
Pons Medulla Cerebellum

oblongata Sympathetic nervous Parasympathetic
K
system (Thoraco lumbar nervous system
outflow: T1–L2) (cranio sacral
.
outflow–
Cerebral Subcortical nuclei CN: III, VII, IX, X
hemisphere (i) Basal ganglia Ventral part Dorsal part and S2, 3, 4)
(ii) Thalamus, and ‘Cerebral peduncle’ (Tectum)
A
(iii) Hypothalamus with (connecting pons (superior and
pituitary complex with thalamus) inferior colliculi)
Olfactory bulb Septum

Telencephalon
Amygdala Striatum
Thalamus Globus pallidus

Diencephalon Hypothalamus
Cerebral Hemisphere
Pituitary complex
Hippocampus
Mesencephalon (mid brain)
Tectum
Superior colliculus
Inferior colliculus
Rhombencephalon (hind brain)
Cerebellum
Ventral Spinal cord Dorsal
Fig. 10.1 Organization of the nervous system
1
2
Important points
1. Brain stem i.e. mid brain, pons and medulla (absolutely essential for life), because:
(i) All cranial nerves take origin from here
(ii) contains neurons in reticular formation that are concerned with regulation of BP, HR, respiration,
vomiting, swallowing, sneezing and coughing.
The Synapse
Definition
Types (Fig. 10.2)

1. Axo-dendritic: (most common)
n
2. Axo-somatic.
i
3. Axo-axonal.
4. Dendro-dendritic (rare). Location-smell pathway
a
Axo-dendritic synapse
Axo-axonal synapse
J
Dendrite
.
Myelin
K
Axon
.
Dendro-dendritic Axo-somatic synapse
synapse
A
Fig. 10.2 Type of synapses
Structure (Fig. 10.3)

Synaptic vesicle
Axon (contain chemical
transmitter)
Mitochondrion
(provide ATP) Presynaptic
membrane
Postsynaptic
Subsynaptic membrane membrane
(contain receptors)
Receptor Synaptic cleft
(20–30 nm)
Fig. 10.3 Structure of a synapse
Functional classification of synapses

Chemical synapses Electrical synapses
1. Transmission of impulse: chemical mediator. 1. Via gap junction
2. Seen at most of the synaptic junctions in 2. Seen at some of the synaptic junctions. (Sp. limbic
nervous system; transfer signals in one system); transfer signal in either direction
direction only.
3. Synaptic cleft: present. 3. replaced by low resistance bridges.
10: The Nervous System ❑ 3
4. Synaptic delay: 0.5 msec. 4. absent

5. Sensitive to hypoxia. 5. Relatively insensitive to hypoxia.
6. Convergence of neurons with large variety 6. There are not too many synapses on the same
of neurotransmitters → infinite process of neuron; transmission across it is rapid and efficient.
informations; transmission of impulse across
it is slow.
Electrical events at synapses

A single stimulus to presynaptic neuron → potential change in postsynaptic neuron of <15 mV which
is either depolarizing or hyperpolarizing depending on type of neurotransmitter whether excitatory or
inhibitory.
n
EPSP (Excitatory post synaptic potentials) IPSP (Inhibitory post synaptic potentials)
i
1. Initial response is depolarizing 1. Initial response is hyperpolarizing.
2. Response: Latency 0·5 msec; peak 1–1·5 msec, 2. Latency 1–1·5 msec; peak: 1·5–2 msec, then
a
then ↓s slowly in another 4 msec. declines slowly in another 3 msec.
3. Excitability to other stimuli: ↑s 3. ↓s
J
4. Shows summation (spatial and temporal). 4. Same as with EPSP.
(Fig. 10.11 & 10.12)
.
5. Ionic basis: (Fig. 10.4) 5. (i) ↑ Cl– influx (mainly) or ↑ K+ efflux; or
(i) ↑ Na+ (mainly) or ↑ Ca2+ influx; or (ii) ↓ Na+ influx. (Fig. 10.5)
(ii) ↓ K+ efflux.
K
Presynaptic
.
membrane
(E)
A
(+) (+)
(–) (–)
Na+
Postsynaptic membrane Subsynaptic membrane
Fig. 10.4 Ionic basis of EPSPs (Excitatory transmitter (E) increases

permeability of subsynaptic membrane to Na+)
(I)
(+) (+)
(–) (–)
Cl–
Fig. 10.5 Ionic basis of IPSPs ((Inhibitory transmitter (I) increases

permeability of postsynaptic membrane to Cl–.)
Genesis (how action potential is produced in postsynaptic neuron?)

Cause: It is due to initial segment (IS) spike.
(i) lowest threshold
(ii) Voltage gated Na+ channels are highly concentrated in this region.
4
Inhibition at Synapses: Presynaptic and Postsynaptic inhibition

1. Presynaptic Inhibition (Fig. 10.6)
(i) Occurs at the presynaptic terminals before the signals ever reaches the synapse.
(ii) Induced by axo-axonal synapse.
(iii) Example: Ascending tracts showing lateral inhibition → precise localisation of sensations.
(iv) Inhibitory transmitter: GABA (acting via GABAA → ↑ Cl– influx, whereas via GABAB → ↑ K+
efflux).
n
Inhibitory interneuron
i
Flexor muscle
Axo-axonal synapse
afferent (Ia) releases GABA
(presynaptic inhibition)
a
Extensor muscle
afferent (Ia)
Extensor motor neuron
. J
K
Fig. 10.6 Pathways for presynaptic inhibition (Convergence of flexor Ia fibers on to inhibitory interneuron which in turn makes contacts on
the terminals of an afferent Ia fiber from extensor muscle.)
.
Important Note: Conversely, presynaptic facilitation is produced. It is mediated by serotonin → ↑ Ca2+ influx
→ depolarization to continue.
A
2. Postsynaptic inhibition: Direct and Indirect inhibition
(i) Direct (or Afferent) inhibition (Fig. 10.7)
(a) Definition: Post synaptic inhibition during the course of an IPSP
(b) Caused by stimulation of an inhibitory interneuron which passes directly to inhibit the
postsynaptic neuron.
Dorsal root ganglion
EPSP
Motor neuron
of protagonist
muscle
Ventral Golgi bottle neuron
root (an interneuron
releasing glycine)
IPSP
Motor neuron of
Protagonist muscle antagonist muscle
(extensor)
Antagonist muscle (flexor)
Fig. 10.7 Postsynaptic inhibition in the spinal cord an example of “direct inhibition”
(c) Examples: Inhibition of stretch reflexes

• Reciprocal inhibition: Stretching of an agonist muscle → (+) Golgi bottle neuron (an inhibitory
interneuron) → glycine → IPSP in motor neurons supplying the antagonist muscle → its
relaxation (thus ensures smooth contraction of the agonist muscle).
• Golgi tendon organ inhibition: Strong stretch to an agonist muscle → (+) golgi tendon organs
at musculotendon junction → (+) inhibitory interneuron → (–) motor neuron supplying
the same muscle (also called autogenic inhibition). Response is called inverse stretch reflex
significance: Protective reflex prevent muscle from rupturing. (Fig. 10.8)
Dorsal root
i n
Interneuron releasing
inhibitory mediator
IPSP
a
lb fiber from Motor neuron
Golgi tendon
la fiber
organ
from
J
muscle
Ventral root
K . Motor end-plate on
.
extrafusal fiber
Fig. 10.8 Pathway responsible for the stretch reflex ( ) and
A
inverse stretch reflex ( )
(ii) Indirect inhibition

(a) Definition: Inhibition due to the effects of previous postsynaptic neuron discharge.
(b) Examples
• The postsynaptic cell can be refractory to excitation because it has just fired & is in
refractory period.
• During after hyperpolarization.
• Renshaw cell inhibition (a negative feedback fashion). Mechanism: Motor neuron axons →
via a collateral → release A-ch → (+) Renshaw cell → (–) same motor neuron from which
collateral has originated. (Fig. 10.9)
(–)
Motor
neuron
(+)
Renshaw cell A-ch Ventral horn

body (inhibitory
interneuron)
direction of impulse
Fig. 10.9 Renshaw cell inhibition or negative feedback inhibition

6
Properties of Synapses
1. Convergence and divergence (Fig. 10.10)
[A] [B]
i n
Convergence Divergence
Fig. 10.10 ‘Convergence’ of neural input from many neurons onto
a
a single neuron (A); and ‘divergence’ of output from a single
neuron onto many others (B)
J
2. Law of forward (or one way) conduction:
3. Susceptible to hypoxia.
.
4. Fatigue
5. Synaptic delay
(i) Normal: 0·5 msec.
K
(ii) Significance: Significance: Mono or polysynaptic reflex.
.
6. Summation:
(i) Spatial summation (Fig. 10.11)
(ii) Temporal summation (Fig. 10.12)
A
Postsynaptic neuron fires
EPSPs spread from several

synapses to axon hillock
Simultaneous stimulation by
several presynaptic neurons
15
mV
0 5 10 0 5 10 0 5 10
msec msec msec
(a) EPSP = 7 mV (b) EPSP = 9 mV (c) a+b = 16 mV
thus an action
potential is
generated
Fig. 10.11 Spatial summation
Postsynaptic neuron fires 15 EPSP EPSP

8 mV 8 mV 8 mV 12 mV
}
mV
0
S1 S2 S1 S2 S1 S2
0 5 10 0 5 10 0 5 10
EPSPs spread from one msec msec msec
synapse to axon hillock (a) S2 applied after the decay (b) S2 applied just before (c) Time interval between
of S1 response the decay of S1 response S1 and S2 shortened and an
action potential is generated
High frequency stimulation by
one presynaptic neuron
Fig. 10.12 Temporal summation
n
7. Occlusion (Fig. 10.13A)
i
8. Subliminal fringe (Fig. 10.13B)
Physiological significance e.g. phenomenon of referred pain.
a
: motor neurons influenced by the afferent fibres a or b
: motor neurons common to both a and b
.
b = 10
J a = 3
b = 3
b = 3
K
a = 10
a+b = 14 a+b = 12
.
Fig. 10.13 (A) Occlusion Fig. 10.13 (B) Subliminal fringe
9. Synaptic plasticity
A
(i) Synaptic conduction can be ↑ or ↓ on the basis of past experience.
(ii) Significance: important role in learning, memory and genesis of emotion.
(iii) Forms (Fig. 10.14)
(a) Post-tetanic potentiation: important to acquire short term memory
Mechanism: due to ↑ Ca2+ influx in the presynaptic neuron.
(b) Long term potentiation important to acquire long term memory.
Mechanism: due to ↑ in intracellular Ca2+ in the postsynaptic neuron.
(c) Long term depression: Associated with ↓ in synaptic conduction following ↓ Ca2+ influx (help
learning of motor skills).
(iv) Sensitization Example: a deep asleep mother wakes up with cry of her child.
Axo-axonal ending mediating

presynaptic facilitation
Presynaptic
axonal
ending
(i) Post-tetanic potentiation Postsynaptic

(ii) Fatigue or habituation neuron
Long-term
potentiation
Fig. 10.14 Synaptic plasticity: Presynaptic and postsynaptic sites

producing changes in the strength of synaptic transmission
8
Sensory Receptors
Definition
Function
Functional classification
Receptor type Stimulus receptor energy
1. Mechanoreceptors Mechanical, e.g. touch, pressure, baroreceptors; vibration.
2. Chemoreceptors Chemical (i.e. change in chemical composition of the environment in which receptors
are located) e.g. receptors for taste, smell, osmoreceptors, glucoreceptors.
n
3. Thermoreceptors Thermal (degree of warmth i.e. temperature).
4. Nociceptors Noxious i.e. stimuli which are damaging or injurious to the body tissues, e.g.
i
pain.
5. Photoreceptors Electromagnetic: Light e.g. rods and cones in retina.
a
Skin/Cutaneous Receptors (Fig. 10.15)
J
1. Mechanoreceptors: Touch and pressure receptors.
Sensory nerve Location: Maximum
.
Receptor Function Adaptation
endings density
A. M
erkel’s discs and • Touch (Tactile Aβ and Aδ Finger tips, lips, nipples, Rapid
Meissner’s corpuscle receptors) base of hair, orifices
K
• Pressure (openings).
• Vibration
.
B. Pacinian corpuscles Pressure i.e. Aβ Skin, S/C tissue, mesentery, Rapid
sustained touch tendons, joints.
C. Ruffini’s end organs Warmth, touch Aδ or ‘C’ group Dermis Slow
A
pressure of fibers
D. Krause’s end bulbs Mechanoreceptors Aδ Conjunctiva, lips, tongue, Rapid
genitalia, nerve sheaths.
E. Naked nerve endings Mechanoreceptors, Aδ and C Dermis Slow
pain, temperature
Deep pressure
Touch pain
Heat
Cold
Epidermis
(B) Dermis
(E) (D)
(A)
(C) (C)
Hypodermis
Fig. 10.15 Cutaneous receptors: sensory receptors in the skin

A: Tactile (Meissner’s) corpuscle (light touch); B: Tactile
(Merkle’s) corpuscles (touch); C: Free terminal (pain)
D: Lamellated (Pacinian) corpuscle (deep pressure);
E: Ruffini corpuscle (warmth)
Important Note: ‘Joint receptors’ are mainly the Pacinian corpuscles, Golgi tendon organs and Ruffini’s end
organs which are situated in the ligaments of the joint. They are quickly adapting receptors and form the
endings of group I fibers.
2. Thermoreceptors or temperature receptors: (cold and warm). (Fig. 10.16)

Cold receptors Warm receptors
1. Endings of thin myelinated Aδ fibers. 1. Endings of unmyelinated ‘C’ fibers.
2. Density: 4–10 times more than warm receptors. 2. Less
3. Fire steadily at tissue temperature between 10 3. Fire steadily at tissue temperature between 35°
and 35°C; peak discharge at 25–30°C. and 45°C; peak discharge at 38°–43°C.
n
Important Note:
i
1. Metal objects feel colder than wooden objects of the same temperature.
2. Paradoxical cold fiber discharge. (Fig. 10.16)
a
(A) (B)
10 Cold fiber
9
Paradoxical cold
J
8 fiber discharge
7
.
Impulse/sec
4 Warm fiber
K
3
.
2
A
15 20 25 30 35 40 45 50
Static skin temperature (°C)
Fig. 10.16 Steady discharge of a typical single cold and warm fiber (A)
and paradoxical cold fiber discharge (B) as a function of the temperature
3. Pain receptors (Nociceptors): Two types

Aδ fiber nociceptors C-fiber nociceptors
1. Myelinated with high conduction velocity. 1. Non-myelinated with low conduction velocity.
2. Subserve fast pain → bright, sharp and localized 2. Subserve slow pain → dull, intense and diffuse
pain. pain.
3. Less in number. 3. Relatively more in number.
4. Stimulus: Only noxious. 4. Noxious, mechanical and thermal.
5. Synaptic transmitter: Glutamic acid. 5. Substance P.
6. Mechanosensitive i.e. conduction in these fibers 6. Chemical sensitive; conduction get blocked by
blocked by pressure. local anaesthetics, kinins, histamine etc.
Electrical and Ionic Events in Receptors (Fig. 10.17)

1. Receptor (or generator) potential
(i) Definition: Local potential change produced by natural excitation of a receptor
(ii) Source: Originates from the unmyelinated nerve ending and not from the capsule or from 1st
node of Ranvier.
2. How action potential is produced in the sensory nerve?
Generator potential → depolarizes the sensory nerve at the 1st node of Ranvier → convert generator
pot. into action potential.
10
Myelinated axon
Trigger zone
Transduction site Axon
terminal
Stimulus
Amplitude
Membrane potential
n
20
i
– 20
(mV)
– 40
Threshold
Duration
a
– 60
(A) Moderate – 80
stimulus 0 5 10 0 5 10 0 5 10
Time (sec)
J
Membrane potential
.
20
0
(mV)
– 20
– 40
K
– 60
.
– 80
(B) L
onger and 0 5 10 0 5 10 0 5 10
stronger stimulus
A
1 2 3 4
Recepor potential Recepor Frequency of action potentials Neurotransmitter
strength and potential is is proportional to stimulus release varies with
duration vary with integrated at intensity. Duration of a series of the pattern of action
the stimulus. the trigger zone. action potentials is proportional potentials arriving at
to stimulus duration. the axon terminal.
Fig. 10.17 Relation amongst intensity of stimulus, size of generator potential and frequency of action potential
3. Weber Fechner Law

(i) Magnitude of the generator potential α intensity of stimulus;
(ii) Frequency of action potential in a sensory nerve α magnitude of the generator potential.
Finally the magnitude of the sensation felt is proportional to the log of the intensity of the stimulus.
4. Ionic basis of generator potential
Stretching of the membrane of unmyelinated nerve → ↑ Na+ influx.
Properties of Receptors
1. Law of adequate stimulus
2. Adaptation Varies with the type of receptors (tonic and phasic). (Fig. 10.18)
Tonic receptors Phasic receptors

1. Poor, slow and incompletely adapting 1. Rapidly adapting.
2. Can continue to transmit informations for many 2. Transmit signals only when the stimulus
hours even at a constant intensity of stimulus strength is changed.
or over many days.
3. Generator potential prolonged and decays slowly. 3. Short and decays rapidly.
4. Important to sustain life 4. Important to transmit informations
5. Examples: Muscle spindles, baroreceptors, pain 5. Touch, olfactory and pressure receptors
receptors and chemoreceptors.
(A) S
lowly adapting (B) R
apidly adapting
tonic receptor phasic receptor
Stimulus
Stimulus
Receptor Generator
potential
Prolonged; Short; decays
decays slowly rapidly
Axon of Action
sensory potentials
n
neuron in sensory
neuron
i
Time
a
Fig. 10.18 Generator potential in (A) Tonic and (B) Phasic receptors; and
action potential activity in the corresponding sensory nerve
J
3. Muller’s doctrine of specific nerve energies
.
4. Law of projection: Phantom limb
5. Law of intensity discrimination
K
Reflexes
.
Definition
The Reflex Arc (Fig. 10.19)
A
1. Functional unit of the nervous system.
2. Components: receptor, an afferent and efferent neurons, and an effector organ.
Stretching of
muscle stimulates Activation of
muscle spindles sensory neuron
Central synapse
(neurotransmitter
Opposes
Muscle glutamic acid)
Information
Contraction processing at
of muscle Activation of motor neuron
being motor neuron
stretched
Fig. 10.19 Pathway for stretch reflex
Classification of Reflexes: Mono and polysynaptic reflexes

Monosynaptic reflexes Polysynaptic reflexes
1. Only one synapse is present between the 1. Two or more interneurons are present between
afferent and efferent neurons. the afferent and efferent neurons.
2. Examples: Deep/Tendon reflexes; all stretch 2. Withdrawal reflexes, superficial reflexes
reflexes
12
Monosynaptic Reflexes: Stretch Reflexes

1. Definition
2. Components
(i) Stimulus: stretch to the muscle
(ii) Receptor: muscle spindle
(iii) Response: Contraction of the muscle being stretched
(iv) Neurotransmitter: Glutamic acid
3. Example: Deep (or tendon) reflexes
4. Reaction time: 19–24 msec.
5. Central delay: 0·6–0·9 msec.
n
6. Significance
(i) Fundamental reflex in control of body posture.
i
(ii) Highly developed in antigravity muscles which oppose force of gravity.
a
The Muscle Spindle
Structure
J
1. Macroscopic structure, its number varies with type of muscle e.g.
(i) Small distal muscles for delicate movements: 150/g.
.
(ii) Large muscles contain: 5/g.
2. Each muscle spindle contain 8–12 intrafusal fibers, 2 types: nuclear bag (dynamic and static) and
nuclear chain fibers.
K
Innervation (Fig. 10.20)
.
1. Sensory supply
(i) Primary (or annulospiral) endings: (a) dynamic nuclear bag fibers gets stimulated when the
muscle is being stretched (b) static nuclear bag fibers and nuclear chain fibers get stimulated
A
by sustained stretch of the muscle.
(ii) Secondary (or flower spray) endings: respond mainly to sustained stretch.
Primary Afferent
(Group Ia) afferent (sensory)
nerve
Efferent fiber
γ1 Efferent Secondary
(dynamic) γ2 Efferent (Group II)
fiber (static) fiber afferent
I
Static n
nuclear- t
bag fibers r
a
f
u
Dynamic s
a
nuclear- l
bag fibers
f
Nuclear- i
chain b
e
fibers r
Primary ending Secondary ending
s
(annulospiral ending)
Fig. 10.20 Muscle spindle and its neural connections
Note: Fibers from both primary and secondary endings terminate directly on α-motor neurons supplying the
extrafusal fibers of the same muscle → direct contraction of the muscle.
2. Motor supply
(i) γ1-fibers supply ends of dynamic nuclear bag fibers.
(ii) γ2-fibers supply ends of static nuclear bag fibers and nuclear chain fibers.
The spindle sensitivity varies with the rate of γ-efferent discharge.
(i) Stimulation of γ1-efferent → ↑ spindle sensitivity to rate of change of stretch.
(ii) Stimulation of γ2-efferents → ↑ sensitivity to steady, maintained stretch.
Functions
1. Length-servo mechanism: (a) The motor control system in the brain controls muscle movements via
α‑γ coactivation (b) muscle spindle and its reflex connections via α-γ linkage constitutes a negative
feedback device which operate to maintain muscle length during body movements. (Fig. 10.21)
n
2. Follow up servo mechanism: Muscle spindles maintain body posture by sustained contraction of the
i
muscle.
Normal Muscle Length
(Extrafusal muscle fibers)
a
Muscle length decreases If Length
(due to muscle contraction) increases
. J
Stimulates α-motor neurtons Muscle Spindle Stretches
in the spinal cord and its discharge increases
K
Stimulates sensory nerve
(Group Ia fibers)
.
Fig. 10.21 Operation of length servo mechanism
(system of negative feedback device)
A
Higher Control of Stretch Reflex
The brain areas act by ↑ or ↓ muscle spindle sensitivity by way of altering the γ-MN discharge. (Fig. 10.22)
Facilitatory areas Inhibitory areas
1. Facilitatory reticular formation → spontaneous 1. Inhibitory reticular formation (do not discharge
discharge of γ-MN. spontaneously).
2. Vestibular nucleus → stimulate α-MN. 2. Cerebral cortex
3. Cerebellum → stimulate inhibitory
reticular formation
4. Basal ganglia
14
Motor cortex Basal ganglia
(–)
(–)
(–)
Cerebellum
(–)
(–) (–)
(+) (+) (+)
Vestibular
nucleus
(–)
(+) α−MN
(+) γ−MN
n
(–) γ−MN
Facilitatory reticular Inhibitory reticular
i
formation (it is a large area formation (it is a smaller
which discharge spontaneously area which does not
in response to afferent input) discharge spontaneously)
a
Fig. 10.22 Brain areas that facilitate and inhibit stretch reflexes
(+) and (–) facilitatory and inhibitory areas respectively. (MN:
Motor Neuron)
. J
Note: Normally stretch reflex remain inhibited.
Other factors which increase the γ-efferent discharge

1. Anxiety → hyperactive tendon reflexes
K
2. Unexpected movement
.
3. Noxious stimuli to skin
4. Jendrassik’s manoeuvre
A
Muscle Tone
1. Definition
2. Cause/basis: Due to low frequency and asynchronous discharge of γ-MNs.
Hypotonia Hypertonia
(i) ↓ in resting muscle tone. (i) ↑ resting muscle tone.

(ii) Causes: (ii) (a) any factor which ↑ γ-MN discharge (see to
(a) destruction of reflex arc. above).
(b) stimulation of inhibitory areas in higher (b) destruction of inhibitory areas in the brain.
centre. (c) stimulation of facilitatory areas in the
(c) inhibition of facilitatory areas in the brain. brain.
(d) during sleep.
(e) sedative
Note: If hypertonia is confined to only one groups of muscle, it is called spasticity; if it involves both the
extensors as well as flexors, it is referred as rigidity
Inhibition of Stretch Reflexes

Two mechanisms: reciprocal innervation (Fig. 10.23) and inverse stretch reflex (Fig. 10.8).
Clinical Significance
1. Lengthening reaction or Clasp Knife effect
2. Clonus (Fig. 10.24)
Protagonist
muscle (Flexor)
Motor Inhibitory
neuron of interneuron
protagonist (NT: Glycine)
muscle
Motor neuron of
antagonist muscle
Protagonist
muscle
(Flexor)
i n
Antagonist muscle (Extensor)–
Reciprocal inhibition
a
Fig. 10.23 Pathway for reciprocal innervation
J
Series of rhythmic plantar Sudden, maintained dorsi
flexion at the ankle flexion of foot
K .
A .
Polysynaptic Reflexes–The Withdrawal Reflex
Fig. 10.24 Ankle clonus
1. Definition
2. Response (Fig. 10.25)
(i) Flexor reflex.
(ii) With a stronger stimulus, in addition called crossed extensor reflex.
16
Ascending
pathways to brain
Spinal cord
Sensory
neuron Spinal cord
Inhibitory
Inhibitory interneuron
interneuron
α-motor α-motor neurons
neurons
n
Nociceptor
i
Painful stimulus
a
(–)
Extensor inhibited
(+) (–)
Flexors contract
J
(+) Flexors inhibited
(moving foot
away from painful
.
stimulus) Extensors contract
(to support the body
weight)
K
Flexor reflex Extensor reflex
.
Ipsilateral limb Contralateral limb
(A) (B)
Fig. 10.25 Pathway for withdrawal reflex: flexor reflex (A) and crossed extensor reflex (B) {(+): Excitation; (–): Inhibition}
A
3. Mechanism: (Fig. 10.26)
(i) Irradiation of the stimulus (impulse)
(ii) Recruitment of motor units
Reverberating
circuits
Afferent (sensory)
neuron
Interneurons
Efferent (motor) neuron
Fig. 10.26 Polysynaptic reflex pathway showing connections

between afferent and efferent neurons in the spinal cord
4. Significance: protective reflex

5. Characteristic features
(i) Prepotent (more stronger than other)
(ii) A strong stimulus → recruitment and after discharge
(iii) Local sign
(iv) Summation, occlusion and subliminal fringe of reflex activity
General Properties of Reflexes

1. Adequate stimulus
2. Final common pathway: α-MN. (Fig. 10.27)
i n
Ipsilateral inputs Contralateral inputs
1. Stretch reflex, tone and posture

(muscle spindle)
Spinal
a
2. Flexion reflex, noxious stimuli (skin) α-motor neuron
(+)
(–) Secondary endings
J
(+) (flower spray-muscle spindle)
(–)
3. Relax antagonists (reciprocal
innervation; muscle spindle) (–) (+)
.
(–)
(–) Crossed extensor reflex
4. Secondary endings
(flower spray-muscle spindle) (–)
. K
5. Tendon reflex (Golgi tendon organ) Tendon reflex
6. Recurrent inhibition through (golgi tendon organ)
Renshaw cell
A
Final common pathway
Fig. 10.27 Summary of the major inputs to the cell body of a single spinal α-motor neuron (the final common pathway)
(Note: Only lower motor neurons, provide output from the CNS to skeletal muscle fibers)
3. Central excitatory and inhibitory states

Example: Mass reflex
4. Habituation and Sensitization of reflex response
Reflex responses can be modified by experience
18
The Sensory System

Components
1. Sensory receptors: Sensory Unit (Fig. 10.28)
2. Neural pathways
Central terminals
Afferent nerve fiber

Central process
Neuron cell body
Peripheral process
i n
Peripheral terminals
with receptors
a
Receptive field
Fig. 10.28 Sensory unit and receptive field
J
3. Somatosensory cortex (Fig. 10.29)
.
Somatosensory cortex
(postcentral gyrus)
Frontal lobe
. K
Parietal
lobe
A
Temporal
lobe
Occipital lobe
Fig. 10.29 Location of somatosensory cortex
Note: In most sensory systems, the control is organized by lateral inhibition → accurate localization. (Fig. 10.30)
Action
potentials at
the end of
pathway
i n
Action
potentials at
the beginning Excitatory synapses
a
of pathway Inhibitory synapses
Fig. 10.30 Afferent pathways showing lateral inhibition.

Note: The central fiber (firing at highest frequency) inhibiting the
J
lateral neurons more strongly via inhibitory interneurons.
.
Ascending (Sensory) tracts (location and sensations conveyed) (Fig. 10.31)
A. Tracts in dorsal (posterior) white column
K
1. Fasciculus gracilis
.
2. Fasciculus cuneatus
(i) Fine touch (touch with low threshold- well localized).
(ii) Tactile localization and discrimination.
A
(iii) Proprioceptive and kinesthetic sensation
(iv) Vibration sense
(v) Sense of deep pressure.
Convey fine touch;
Fasciculus gracillis Dorsal tactile localization
(posterior) and discrimination,
Fasciculus cuneatus columns pressure, vibration
and proprioception
L S S L
T T
C C
Dorsal (posterior) spinocerebellar

tract (carry unconscious
kinesthetic impulses)
S L
Ventral (anterior) spinocerebellar L S
tract {carry unconscious T
T
C
C
kinesthetic impulses}
Lateral spinothalamic tract Ventral (anterior)

(convey pain and temperature) spinothalamic tract
{convey gross/crude touch}
Fig. 10.31 A cross-section of the spinal cord showing location of major ascending tracts and sensations they convey.
20
B. Tracts in Lateral White Column

1. Lateral spinothalamic tract (LSTT): Pain and temperature (both hot and cold)
2. Dorsal (posterior) and ventral (anterior) spinocerebellar tract: Unconscious kinesthetic
sensations.
C. Tracts in Ventral (anterior) white column

Ventral (anterior) spinothalamic tract (ASTT): Gross/Crude touch.
Important points: Synthetic sensation

1. Vibration sense
2. Two-point discrimination
n
3. Stereognosis
i
Pathways
a
Dorsal (posterior) Lateral spinothalamic Ventral (anterior)
column pathway pathway spinothalamic pathway
(Fig. 10.32) (Fig. 10.33) (Fig. 10.34)
J
Sensations Sensations Sensations
[2: (i) to (vi)] (Pain, Temp.) (Crude touch)
.
1st order neuron
F. gracilis and cuneatus 1st order
End around cell in End around cells in dorsal horn
(medial to lateral: S-L-T-C) neuron dorsal horn (medial to (Ist Relay)
(ascend in dorsal lateral: C-T-L-S) (Ist Relay)
K
column) (cross and
(cross and ascend ascend in
.
Nu. gracilis and cuneatus 2nd order neuron
in LSTT) ASTT)
in medulla (Ist Relay) 2nd order
(cross) neuron
A
Ventroposterior nucleus of thalamus (2nd Relay)
(via internal capsule) 3rd order neuron
Somatosensory Cortex (post-central gyrus) area 3, 1, 2
Ventroposterior nucleus Internal capsule

of thalamus
Somatosensory cortex
(postcentral gyrus)
Cerebrum
Third-order
neuron
n
Second-order
i
Nucleus gracilis
neuron
Nucleus cuneatus
a
medulla
J
First-order
neuron Fasciculus cuneatus
.
Fasciculus gracilis
Posterior white column
Spinal
cord
. K
Discriminative touch, proprioceptive,
A
pressure or vibration receptors
Fig. 10.32 Sensory pathway for fine touch, tactile localization and
discrimination, pressure, proprioception and vibration – the
dorsal (posterior) column pathway
22
Internal capsule Internal capsule

Ventroposterior Somatosensory cortex Ventroposterior Somatosensory cortex
nucleus of (postcentral gyrus) nucleus of (postcentral gyrus)
thalamus thalamus
Third-order Third-order
neuron neuron
Cerebrum
i n
Second-order Second-order
neuron neuron
a
medulla
. J
Posterior Posterior
grey horn grey horn
Lateral white
K
First-order column First-order Anterior white
neuron Spinal neuron column
.
Lateral cord
Spinothalamic
tract
Anterior
Spinothalamic
A
Warmth, cold and Gross tract
pain receptors touch receptor
Fig. 10.33 Sensory pathway for pain and temperature - the lateral Fig. 10.34 Sensory pathway for gross (crude) touch - the ventral
spinothalamic pathway (anterior) spinothalamic pathway
Termination of afferent neurons in dorsal horn (Lamina of Rexed’d) (Fig. 10.35)

Aα : Proprioceptors
Aβ : Touch, pressure Mechanoceptors

Aδ : Touch
Aδ : Nociceptors (pain)
Thermoreceptors (temperature)
nociceptors (pain)
I C
Substantia thermoreceptors; some
II of mechanoreceptors
gelatinosa
of Rolando III
IV
V
VI
VII
Fig. 10.35 Termination of primary afferent neurons in the various layers of the dorsal
horn of the spinal cord (Numeral indicate Rexed’s laminae) (Rexed, B. 1952)
Note: Lamina VII receive input from both sides of the body, whereas other
laminas receive only unilateral input.
Somatosensory Cortex (Fig. 10.36)

Primary sensory area: S-I Secondary sensory area: S-II
1. Location: Postcentral gyrus 1. Superior wall of lateral cerebral sulcus.
2. Supplied by afferent from the opposite side of 2. Supplied by afferents from both sides of the
the body but from both sides of the face. body.
3. Shows detailed point-to-point localization of 3. Like S-I, but there is more overlap.
fibers of the body parts.
4. Inverted representation of body parts. 4. Antero-posterior representation of body parts;
5. Extent of representation: body parts that are 5. No such feature.
most densely innervated (Fig. 10.37)
6. Its removal → fine touch and proprioception most 6. Removal → deficits in discrimination power.
n
affected
i
Central
Postcentral
sulcus
a
gyrus
6 1
7
4
J
Anterior
.
2 Posterior
3 5
Central sulcus
S.I
K
3 1
2
Le un
.
g k
Tr ead
7
H m
Ar and
H ce
Fa eth ue
Te ng
To
40
A
Leg
S.II
Face Arm
Lateral sulcus
(sylvian sulcus)
Fig. 10.36 Brain areas concerned with somatic sensation

[Inset: Sagittal section (i.e. in anteroposterior direction) of
fronto-occipital region]
Note: Areas SI and II exhibits cortical plasticity.

24
i n
J a
.
Fig. 10.37 Location of pathway termination of different parts of the
K
body in the somatosensory cortex
.
Individual Somatic Sensations
A
A. Touch-Pressure
B. Proprioception and Kinesthesia
C. Temperature
D. Pain
1. Definition
2. Associated with emotions (fear; anxiety); withdrawal reflex; autonomic changes.
3. Types
Superficial (cutaneous) pain Deep pain
(i) Involves the skin and s/c tissue. (i) Involves muscles and hollow viscera.
(ii) Sharp, well-localized; conducted via Aδ fibers (ii) Dull, poorly-localized; conducted via ‘C’ fibers
(iii) Associated with reflex withdrawal, ↑ HR, (iii) Produces faintness, nausea, vomiting,
↑ BP and ↑ respiration. sweating, ↓ BP, ↓ HR and ↓ respiration.
(iv) Usually does not radiate. (iv) It is both local and radiates to the distant site.
4.Pain receptors
5.Neural pathways
6.Neurotransmitter: Glutamic acid and Substance P
7.Fast and Slow Pain: → Double pain sensation
(i) Fast component due to activation of Aδ fibers → bright, sharp and localized pain.
(ii) Slow component due to activation of ‘C’ fibers → dull, intense, diffuse and unpleasant feeling of
pain.
The two components are separated by 1–1·5 sec.
8. Ischaemic muscular pain

(i) Muscular activity → accumulation of Lewis P-Factor.
(ii) Examples
(a) Intermittent claudication
(b) Pain of angina pectoris
9. Referred and Radiating pain (Fig. 10.38)
(i) Definition
Heart
Liver and
n
Lung and
Liver and diaphragm gallbladder
i
gallbladder
Heart Stomach
Pancreas
Gallbladder
a
Stomach Liver and
Small intestine
Ovary gallbladder
Kidney Urinary Kidney
J
bladder
Ureter
.
(A) Anterior view (B) Posterior view
K
Fig. 10.38 Referred pain
.
(ii) Examples
(a) Phantom limb pain, (b) Stone in gall bladder, (c) Stone in ureter., (d) Angina pectoris
(iii) Mechanism: Dermatomal rule
A
(iv) Theories (Fig. 10.39)
(a) Convergence theory
(b) Facilitation theory
(A) Convergence theory (B) Facilitation theory
Spinothalamic tract
(to brain)
Somatic structure–
skin (usual stimulus)
Spinothalamic neurons
Painful stimulus to
a visceral structure
(uncommon stimulus)
Fig. 10.39 The two theories of referred pain: convergence (A) and
facilitation theory (B)
26
10. Inhibition of Pain: Analgesia - two mechanisms.

(i) Stimulation produced analgesia:
Types
(a) Segmental inhibition: Gate control theory of pain (Fig. 10.40)
Clinical applications
• Stress analgesia
• Acupuncture
• Counter irritants
• Transcutaneous electrical nerve stimulation (TENS) therapy.
Central control
n
Gate Control System
i
(L)
Pain perception
(+) (–) (+)
Action
a
SG T-Cell (+)
system (LSTT)
Input
(–) (–) (+) Responsible for
J
(S) perception of pain and
its motor responses
.
Dorsal horn
L : Large peripheral fibers such as touch fibers in dorsal column

S : Small peripheral fibers such as Aδ and 'C' group of fibers
K
Fig. 10.40 Gate control theory of pain: Factors involved in the transmission of impulses from peripheral nerve
to control transmission cells (T-cells) in the dorsal column.
.
SG: substantia gelatinosa cells. LSTT: Lateral spinothalamic tracts
(b) Supraspinal inhibition: (Fig. 10.41)
A
Substantia nigra Periaqueductal
(Dopaminergic grey matter
pathway) (Serotonin-5 HT
containing pathway)
Raphe
nucleus

Spinal cord
Rexed laminae I, IV and V
Fig. 10.41 The proposed relationship of three brain sites at which

electrical stimulation or morphine administration produces
analgesia
(ii) By release of endogenous opioid peptides: Enkephalins and Endorphins (Fig. 10.42)
Noxious stimulation of
Aδ or 'C' group of fiber
Enkephalin
secreting neuron
Opiate receptors Substance P secreting

primary afferent neuron
Spinothalamic neuron
in dorsal horn
Fig. 10.42 Location of opiate receptors and their relationship
i n
a
with Enkephalin secreting neuron (mechanism of presynaptic
inhibition)
J
11. Hyperalgesia
(i) Definition
.
(ii) Cause: Tissue damage; and nerve lesion.
(iii) Types: Primary and secondary
K
Motor Areas and Descending Tracts
.
Motor Areas: Areas 4, 6 and 8 (Fig. 10.43)
Area 4: Motor cortex
A
1. Location
(i) Whole of precentral gyrus, and
(ii) Medial surface above cingulate sulcus (Supplementary motor area).
2. Histologically divided into
(i) Area 4α
(ii) Area 4γ -
(iii) Area 4s: Suppressor area
Motor cortex
4s 4α 4γ
Central sulcus
Frontal eye field
Fig. 10.43 Localization of major motor areas of cerebral cortex

28
3. Give rise to origin of pyramidal tracts

4. Body representation (Fig. 10.44)
(i) Inverted, from the opposite side of the body.
(ii) Size of representation: proportional to the skill with which part is used in fine voluntary
movements.
(iii) Face, pharynx, vocal cords and muscles of jaws - bilaterally represented.
Supplementary motor cortex Primary motor cortex
Shoulder
Hand
Elbow
Trunk
Wrist
Arm
Hip
Central sulcus
n
Leg
Cerebral hemisphere
i
Pre-central sulcus
(medical surface)
Thumb
Neck Premotor
Toes Eye cortex
a
Face
Lips
J
Tongue
Jaw
.
Somatosensory Corpus callosum
cortex
Pharynx
K
(A) Right cerebral hemisphere (B)
.
Fig. 10.44 (A) Representation of the body in the primary motor cortex and (B) Primary and supplementary motor area.
(Note: The large area represented to the thumb and fingers and to the face.)
A
5. Functions
(i) Carry out postural adjustments and gross movements
(ii) Sensory motor coordination
(iii) Carry out skilled work
6. Supplementary motor area → involved in voluntary movements which are complex and involve
planning.
7. Shows motor cortical plasticity.
Area 6: Premotor Cortex
1. Location: Anterior to area 4.
2. Contributes to: PT & EPT
3. Receive inputs from SI and SII.
4. Shows point-to-point representation of body parts.
5. Functions: Involved in complicated motor functions e.g.
Area 8: Frontal Eye Field
Lies in middle frontal gyrus anterior to area 6, maintain binocular vision.
Descending Tracts or Motor Pathways: Pyramidal and Extrapyramidal tracts

A. Pyramidal tracts (PT) (Fig. 10.45)
Corticospinal and cortibulbar tracts
1. Origin
(i) 30% from area 4.
(ii) 30% from area 6.
(iii) 40% from areas S-I and S-II.
Motor cortex
Cerebrum
Internal
capsule
i n
Mid brain
Cerebral peduncle Upper motor
a
neurons
Pons
J
Decussation in medulla
Medulla
.
(80–85% cross to the
opposite side)
Lateral white
Anterior grey horn
Spinal column
Anterior white column
K
cord
Lateral Anterior
.
corticospinal tract corticospinal tract
Lower motor
neurons
A
To skeletal muscles To skeletal
muscles
Fig. 10.45 Corticospinal tract: Pyramidal pathways
2. Course:
(i) internal capsule: point to point representation of body parts. (Fig. 10.46)
(ii) the mid brain: middle 3/5th of crus
(iii) the pons: tract is broken up. (Fig. 10.47)
30
Anterior
Caudate nucleus
Frontopontine
Anterior limb of tract
Internal capsule Anterior thalamic
radiation
Corticospinal tract
Lenticular nucleus
Corticobulbar tract
Putamen
Anterior 2/3rd of e
posterior limb of Fac
Arm k Globus
internal capsule Tru
n
n
pallidus
Leg
Thalamus
i
Auditory
radiation
a
Medial geniculate body
Lateral geniculate body
J
Midline
.
Optic
radiation
Posterior
Fig. 10.46 Arrangement of pyramidal tract fibers in the internal capsule
K
Superior cerebellar
.
peduncle
Inferior colliculus Rubrospinal tract
Aqueduct of sylvius IV ventricle
Medial lemniscus
A
Nuclei of III and IV nerve
Medial longitudinal
Medial longitudinal bundle bundle
Temporo Superior cerebellar peduncle Medial lemniscus
pontine tract
Substantia nigra
Pyramidal
tract
Frontopontine fibers Fibre of
Vth nerve Middle cerebellar
Nuclei pontis Trapezoid body peduncle
(A) (B)
Fig. 10.47 Arrangement of pyramidal tract fibers in the mid brain (A) and pons (B)
(iv) In the medulla

(a) reunite → Pyramid (bulge)
(b) 80–85% fibers cross to opposite side (lateral corticospinal tract or crossed / indirect PT).
(c) 15–20%, do not cross (anterior corticospinal tract or uncrossed / direct PT).
3. Functions of PT
(i) Lateral corticospinal tracts: Control voluntary movements of distal limb muscles to carry out
skilled work.
(ii) Anterior corticospinal tracts: Control of muscles of the trunk and proximal portions of the
limbs to carry out postural adjustments and gross movements.
(iii) Form a part of the pathways for superficial reflexes.
(iv) Sensory-motor coordination. .
(ii) Corticobulbar (corticonuclear) tracts
(a) Responsible for voluntary control of muscles of larynx, pharynx, palate, upper and lower
face, jaw, eye etc.
(b) Bilateral lesion of these tracts → paralysis above-mentioned muscles (called pseudobulbar
palsy).
4. Characteristic features of PT
(i) Phylogenetically, the anterior pathways are old; lateral pathway are new.
(ii) 55% end in the cervical, 20% in the thoracic and 25% in the lumbosacral region.
(iii) Longest tract, descends down without any relay → advantage of speed and specificity.
(iv) 85–90% (≤ 1 µm diameter) and 50% are unmyelinated.
(v) PT & EPT that influence activity of LMNs constitute the UMNs. (Fig. 10.48)
Motor cortex Upper motor

neuron
Lower motor
neuron
n
Brain stem (cranial nerve)
i
Muscle
Corticospinal tract
J a
Spinal cord
.
Lower motor
neuron
(spinal nerve)
K
Muscle
.
Fig. 10.48 Lower and upper motor neuron
A
(vi) Most common site of lesion: internal capsule.
(vii) Apoplexy or Stroke means a sudden attack of paralysis: (Fig. 10.49)
(a) damage to area 4 → monoplegia
(b) injury at the internal capsule level → hemiplegia
(c) injury at the brain stem level → either paraplegia or quadriplegia.
B. Extrapyramidal tracts (EPT)

1. Definition
2. Have many synapses in their descending path
32
i n
Hemiplegia Paraplegia Quadriplegia
Paralysis of one side Paralysis of both Paralysis of all
of the body. The the lower limbs four limbs
a
arm is usually more
involved than the leg
. J
. K
A
3. Major EPT (Fig. 10.50)
Tracts
(i) Rubrospinal
Monoplegia
Paralysis of one limb
only usually an arm.
Triplegia
Paralysis three limbs usually
both arms and a leg.
Fig. 10.49 Types of Apoplexy (or stroke)
Origin
Red nucleus in mid brain
Function
Facilitatory influence over flexor muscle tone and
(crossed) inhibit extensor MNs.
(ii) Tectospinal and Superior colliculus (optic Mediate reflex postural movements in response to
tectobulbar center in mid brain) visual and auditory stimuli.
(crossed)
(iii) Reticulospinal Reticular formation in ↑ or ↓ γ-MNs → alteration in voluntary muscle tone;
brain stein (crossed mainly) blood pressure and respiration.
(iv) Vestibulospinal Lateral vestibular nucleus Facilitatory influence over antigravity muscles
in medulla (uncrossed) (mainly control muscle tone in extensor group).
(v) Medial Medial vestibular nucleus Integration of eye and neck movements; coordination
longitudinal superior colliculus and of reflex ocular movements.
bundle reticular formation
Pyramidal cell
(of Betz)
Cerebrum
Red nucleus
Midbrain Superior
colliculus
n
Cerebellum
i
Vestibular nucleus
a
Medulla
Pyramidal crossing
J
Tectospinal tract
.
Vestibulospinal tract
Pyramidal tract
(indirect, crossed)
Rubrospinal tract
K
Pyramidal tract
(direct, uncrossed)
.
Fig. 10.50 The major descending (motor) tracts and their origin within the brain
4. Functions
A
(i) Control the movement of the eye balls.
(ii) Control muscle tone, posture and equilibrium.
(a) Rubrospinal (tone and posture)
(b) Tectospinal (visuospinal reflexes)
(c) Vestibulospinal (equilibrium and balance)
(iii) Control complex co-ordinated movements of arms and legs during walking,
(iv) Exert tonic inhibitory control over the lower centres. (Therefore, EPT damage → rigidity due to
release phenomenon)
5. Functional differences between PT and EPT
Differences between lower and upper motor neuron lesions

LMNL UMNL
1. Cause: Lesion of LMNs 1. Lesion of UMNs

2. Features 2.
(i) Usually single muscle is affected. (i) Involves a group of muscles.
(ii) Produces flaccid paralysis (ii) Spastic paralysis due to release phenomenon
(iii) Disuse atrophy of the muscle → fibrous and denervation hypersensitivity.
muscle. (iii) Muscle atrophy is mild
(iv) All reflexes (superficial or deep): absent. (iv) (a) deep reflexes: ↑↑ (due to ↑ γ-MN
discharge → hyperactive stretch reflex.
(b) superficial reflexes: lost.
(v) Babinski sign: not elicited (v) Babinski sign Elicited (abnormal) (Fig. 10.51)
34
Up
Toes down
(flexion) Fanning
of toes
(A) (B)
Fig. 10.51 Testing plantar response (A) Normal plantar response;
(B) Extensor plantar response (Babinski sign abnormal)
n
Important Note:
i
1. The normal plantar response appears with the development of PTs; if once it becomes abnormal, it will
remain abnormal for the rest of the life thereafter (Disdvantage: Person neither can run fast nor can travel
long distances).
a
2. Causes of abnormal Babinski Sign: (i) Infants (< 1 year of age) due to incomplete myelination of PT;
(ii) During deep sleep; (iii) Inhibition of PTs; (iv) Cheyne-stokes respiration.
. J
Autonomic Nervous System (ANS)
1. Definition
2. Main aim: To maintain the optimal internal environment of the body.
K
3. Also called vegetative or efferent or involuntary nervous system (vegetative because concerned with
.
growth i.e. vegetative aspect of day-to-day living).
Note: Form basis of polygraph (lie detector) test.
A
Organization of ANS (Sympathetic and Parasympathetic)
Main differences between two divisions of the ANS (Fig. 10.52)
Sympathetic component Parasympathetic component

1. Thoracolumbar outflow (T1 to L2 or 3) (80% of its 1. Craniosacral outflow: III, VII, IX and X cranial
fibers are in skeletal muscle). nerves and S2,3,4 spinal nerves (75% of its fibers
are in vagus nerve).
2. Preganglionic fibers: short, myelinated. 2. Long, myelinated.
3. Postganglionic fibers: long; unmyelinated: 3. Short and unmyelinated.
4. Sympathetic activity is spread over many 4. Its effect is localized.
segments.
5. 5.
(i) It prepares the individual to cope with the (i) It is concerned with vegetative aspect of
emergency: flight or fight reactions. day‑to‑day living.
(ii) Principally involved with expenditure of (ii) Conservation of body energy.
body energy. (iii) Therefore, this division is referred as
(iii) Catabolic nervous system. anabolic nervous system.
6. The major transmitter released between pre 6. The major neurotransmitter released at pre and
and postganglionic fibers is A-ch whereas at postganglionic nerve endings is A-ch.
postganglionic endings it is usually NE.
Note: Two divisions of ANS act in opposite manner

Sphenopalatine
ganglion
Sub maxillary and
sublingual ganglion
Lacrimal gland Parasympathetic preganglionic fibres
Eye Parasympathetic postganglionic fibres
Ciliary Sympathetic preganglionic fibres
ganglion
Olfactory glands Sympathetic postganglionic fibres
Eye
Parotid gland III Midbrain
Otic ganglion Pons
Brain VII
stem IX Medulla
Submandibular Olfactory glands
n
X
and
sublingual
i
Vagus nerve Parotid gland
salivary glands
Submandibular and
Cervical
Superior sublingual salivary glands
a
cervical ganglion
Middle cervical ganglion
Inferior cervical ganglion
J
Heart
T1
.
2
Sympathetic Lungs
3 trunk
4
Stomach
K
5 Heart
Lungs
Thoracic
6 Coeliac ganglion
.
Spinal cord 7
8
Stomach Spleen
9
A
10 Adrenal gland
Small 11 Superior
intestine Kidney
12 mesenteric
ganglion
L1 Small intestine
Colon
Lumbar
L2
L3
L4
L5 Inferior mesenteric
S1 ganglion Colon
2
3 Sacral
Urinary 4
bladder 5
Parasympathetic sympathetic
(Craniosacral division) (Thoracolumbar division)
[III, VII, IX, X CNs and S2,3,4] [T1 to L2 or 3]
Fig. 10.52 Distribution of the parasympathetic (left) and sympathetic (right) divisions of the autonomic nervous system.
36
On the basis of neurotransmitters, ANS neurons are either cholinergic or adrenergic. (Fig. 10.53)
Cholinergic neurons Adrenergic neurons
1. Secrete Ach at endings. 1. Secrete Ep. or NE

2. Examples 2. Examples
(i) All preganglionic ANS fibers ending. (i) Post ganglionic synpathetic adrenergic
(ii) Post ganglionic parasymphathetic endings. endings.
(iii) Post ganglionic symphathetic cholinergic endings (ii) Cerebral cortex, cerebellum.
(sweat glands, skeletal muscle blood vessels). (iii) Hypothalamus
(iv) NMJ (neuromuscular junction). (iv) Brain stem
n
(v) Cerebral cortex; thalamus; PGO spike (v) Spinal cord.
(vi) Amacrine cells-retina. (vi) Adrenal medulla.
i
CNS Effector
a
Somatic nervous system Skeletal muscle
organ
Efferent (motor) nerve A-ch
J
CNS Effector Smooth muscle,
ANS parasympathetic division
.
organ heart, glands
Preganglionic fiber Ganglion

Postganglionic fiber
K
CNS Effector Smooth muscle,
ANS sympathetic (adrenergic) organ heart, glands
.
A-ch NE (mainly)
A-ch
Ganglion
CNS
Sympathetic (to adrenal medulla) 80% Ep and 20% NE secreted
A
directly into the blood.
Adrenal medulla
(act as a ganglion)
Sympathetic (cholinergic) CNS Effector Sweat gland, blood vessels
Preganglionic fiber organ in skeletal muscle and skin
A-ch
Ganglion A-ch Postganglionic fiber
Fig. 10.53 Transmitter used in various components of the peripheral nervous system (Ep: Epinephrine, NE: Nor-epinephrine)
Drugs which excite or inhibit ANS acts via adrenergic and cholinergic receptors.
Adrenergic and Cholinergic receptors in the ANS
Receptor Location Response
Adrenergic Receptors
α1 Widespread, found in most tissues; not in Excitation, stimulation of metabolism.
the heart.
α2 Sympathetic and parasympathetic Inhibition of neurotransmitter release.
neuroeffector junction
β1 Heart, kidneys, liver, adipose tissues. Stimulation, increased energy consumption.
β2 Smooth muscles in vessels of heart and Inhibition, relaxation.
skeletal muscle, intestinal muscles, walls of
lungs and bronchi.
β3 Brown adipose tissue Excitation, lipolysis → release of FFA
(thermogenesis)
Receptor Location Response

Cholinergic Receptors
Nicotinic • All autonomic (sympathetic and Stimulation/excitation → impulse in post
parasympathetic) synapses between pre synaptic membrane.
and postganglionic neurons;
• Neuromuscular junctions.
• Adrenal medulla. Excitation → muscle contraction.
Ep and NE secretion
Muscarinic • All parasympathetic neuroeffector Variable (stimulation or inhibition).
junctions,
n
↑ sweating and ↑ blood flow in skeletal
i
• Cholinergic sympathetic neuroeffector muscle.
junctions.
a
Important Note: Activation of α1 and β1 receptors generally produce excitation and that of α2 and β2 causes
inhibition.
. J
Spinal Cord Lesions
Transection 3 types: complete, incomplete and hemisection.
K
A. Complete Transection of Spinal Cord
.
Immediate effects
Stage of spinal shock (or stage of flaccidity):
A
Features
1. Portion above the cut-unaffected; below the section: deprived of all activities. (diaschisis).
2. Duration of shock: 3 weeks
3. Cause: Stoppage of tonic bombardment of spinal motor neurons by excitatory impulses in the
descending pathway.
4. Flaccid paralysis
5. ↓ VR → cold blue extremities; dry, scaly skin and bed sores.
6. Subnormal body temperature.
7. Muscle tone: completely lost.
8. All reflexes (superficial and deep): +++ ↓ or lost.
9. All sensations below transection: lost.
10. Urinary bladder and rectum: paralysed.
11. Penis: flaccid, erection impossible.
12. BP ↓s (fall is less marked as the section shifts more distally towards L2)
Later effects (after 1 wk)

Stage of reflex activity
1. Autonomic reflexes recover within days or weeks
(i) retention of urine (sphincter vesical recover very soon than detrusor muscle)
(ii) paralysed blood vessel tone returns
2. Muscle tone returns slowly, reflex in character →
(i) paraplegia in flexion (limbs adopt a position of flexion) (Fig. 10.54)
(ii) spinal man cannot stand unsupported.
(iii) No muscle wasting.
38
(A) (B)
i n
J a
Fig. 10.54 Paraplegia in flexion (A) and extension (B)
3. Reflex movements: return in approx. 2 weeks. Cause
.
(i) denervation hypersensitivity to the mediators; (ii) growing of collateral
Features
(i) Abnormal Babinski response
K
(ii) Mass reflex - advantage
.
(iii) Deep (or tendon) reflexes: sluggish
(iv) After 6 months, marked activity ↑ extensor reflexes.
(v) Coitus (sexual) reflex: absent.
A
Note: Malnutrition or infection → failure of reflex functions.
B. I ncomplete or Irregular Transection of the Spinal Cord

Stage of spinal shock: As above
Stage of reflex activity: → paraplegia in extension. (Fig. 10.54)
Features
1. All features of UMNL
2. Involuntary movement: infrequent.
3. Reflex movements
(i) extensor thrust reflex: positive; (ii) Crossed extensor reflex: positive.
C. H
emisection of the spinal cord: Brown Sequard Syndrome (Fig. 10.55 and 10.56)
(ANS functions remain normal)
On the same side On the opposite side
1. Below the level of hemisection 1. Below the level of hemisection
(i) Extensive motor loss of UMNL type (i) Either no paralysis or paralysis of few muscles of
(ii) Little sensory loss UMNL type.
(ii) Extensive sensory loss
2. At the level of hemisection 2. At the level of hemisection
(i) Sensory changes (i) Sensory changes: Some loss of pain
LMNL type
(ii) Motor changes (ii) Motor changes: Nil
3. Above the level of hemisection 3. Above the level of hemisection
A band of hyperaesthesia Hyperaesthesia may be referred.
Thalamus Midline
Site of lesion Nucleus gracilis

and cuneatus
Crossed pyramidal
tract
Direct pyramidal
Ventral and lateral
n
tract
spinothalamic tract
i
Fasciculus gracilis
and cuneatus
J a
Fig. 10.55 Hemisection of the spinal cord
.
Area of cord
damage
. K
A Loss of pain, temperature and
light touch on opposite side
Loss of motor function and vibration,

position and deep touch sensation on
same side as the cord damage
Fig. 10.56 Brown sequard syndrome i.e. motor & sensory changes below the level of hemisection
Sensory Disturbances
A. Syringomyelia (Syrinx = cavity; myelia = S. cord) (Fig. 10.57)
1. Cause: Extensive growth of neuroglial tissue round the central canal of the spinal cord with
cavity formation.
2. Common site: Cervical region
40
Loss of pain and

temperature sensation
Fig. 10.57 Syringomyelia involving the cervico-thoracic portion of
i n
a
the spinal cord
3. Features:
J
(i) Loss of pain and
temperature.
.
dissociated
(ii) Touch is retained (as it anaesthesia
has double pathway)
(iii) At the level of lesion: (a) initially flaccid paralysis of the muscle (usually of the hands),
K
(b) later involvement of PT → spastic paralysis of the legs.
.
B. Tabes dorsalis (Fig. 10.58)
1. Cause: Usually syphilis → degeneration of dorsal nerve roots.
A
Pale dorsal
(A) columns
(B)
Charcot joints Perforating ulcer Gangrene of

at pressure point peripheral parts
Fig. 10.58 Tabes dorsalis (A) Pale dorsal columns;

(B) Characteristic features of tabes dorsalis
2. Features
(i) Lightning pain
(ii) (a) perforating ulcers at pressure points.
(b) anaesthesia round the anus, over legs, upper chest and hands.
(c) Charcot joint.
(iii) Loss of position sense and vibration sense.
(iv) Deep (or tendon) reflexes: lost.

(v) Marked disturbance of voluntary movements.
C. Disseminated (multiple) sclerosis (Fig. 10.59)

1. Cause: Patchy widespread destruction of myelin in the CNS.
2. Sign and symptoms manifest according to the ascending and descending pathways involved.
(It is a crippling disease).
Axon of a
Myelin sheath normal neuron
intact
i n
a
Demyelination
in progress
J
Fig. 10.59 Disseminated (multiple) sclerosis
.
The Vestibular Apparatus (Labyrinth)
K
Components (Fig. 10.60)
.
1. Three semicircular canals containing a projection ridge, the crista.
2. Otolith organ (saccule and utricle), contain a projecting ridge, the macula.
A
Ductus
endolymphaticus
Semicircular canals
Superior
(anterior)
Inferior
(posterior)
Horizontal
(lateral)
Cochlea
Saccule
Utricle
Ampulla
Cochlear duct
indicates the position of receptors (hair cells)
Fig. 10.60 The vestibular apparatus: the semicircular canals, saccule

and utricle
Structure of the receptor: crista and macula (Fig. 10.61)

1. (a) Tall columnar epithelium
(b) stiff hair cells containing stereocilia
(c) cupula terminalis.
42
Otolith
membrane
Perilymph Cupula
Cupula Hair cell
terminalis
Nerve fibers
Endolymph (B)
Hair
(long and stiff) Projecting ridge Kinocilium
Stereocilia
Ampulla wall Hair cells

Supporting cell
n
Hair cell
i
Nucleus
Vestibular
a
Nerve fibers (vestibular
nerve fiber
division of VIII nerve)
(A) (C)
J
Fig. 10.61 Structure of (A) crista (of semicircular canals) and macula (of saccule and utricle); (B) the otolith membrane and (C) the hair cell
.
2. Kinocilium
3. Cupula contains the Otoliths (or otoconia)
4. When the head is in the normal erect position, macula of each utricle is in the horizontal plane with
K
cupula rising vetically and macula in each saccule lies in the vertical plane with cupula projecting
.
horizontally.
Oculomotor (III) To cerebral
nerve nucleus cortex
A
Trochlear (IV)
nerve nucleus
Thalamus
Abducens (VI)
nerve nucleus
To Medial longitudinal
Superior
cerebellum bundle
Vestibular nuclei
Lateral Reticular
formation
Medial Inferior
cerebellar
Inferior peduncle
Vestibular
ganglion
Anterior
vestibulospinal
tract
From utricle,
semicircular
canals
Lateral
vestibulospinal tract Midline
Fig. 10.62 The neural pathways from the vestibular apparatus

5. Nerve endings in the crista and macula continue as vestibular division of VIII cranial nerve. Fibers
from here pass: (Fig. 10.62)
(i) to the cerebellum (flocculonodular lobe) of both sides; and
(ii) to cranial nerve nuclei (III, IV and VI) of both sides
(iii) down the vestibulospinal tracts to end directly round ventral horn cells of both sides in the
spinal cord.
(iv) to opposite thalamus and temporal lobe.
Functioning of the Vestibular Apparatus

A. Mode of action of Otolith organ: saccule and utricle (Fig. 10.63)
n
1. Provide information about (static equilibrium) during linear acceleration. The saccule responds
to vertical acceleration (lateral tilt of the head) and the utricle to horizontal acceleration (nodding of
i
head up and down as in signifying ‘yes’).
Macula of
a
saccule and Gravity Gravity
utricle
Otolith organ
Otolith organ
J
Hair cell
.
Vestibular
nerve fiber
K
(A) Head in neutral (upright) position (B) Head tilted posteriorly (backwards)
.
Fig. 10.63 Mode of action of otolith organ (saccule and utricle) (A) Resting state; (B) Linear acceleration
2. The maculae are stretch receptors, the effective stimulus being the pull of the gravity on the
cupula → hair cells deformation → (+) nerve fibers (Fig. 10.64)
A
Action
potential in
vestibular
nerve
Resting state Stimulation Inhibition

(Head in upright (depolarization) (hyperpolarization)
position)
(During tilting of the head)
Fig. 10.64 Mode of action of otolith organ (saccule and utricle)

(RMP of the hair cells is –60 mV)
3.
The saccules are affected by a lateral tilt of the head, (to rest on the shoulder)
4.
The utricular maculae are affected by nodding the head up and down as in signifying ‘yes’:
5.
A tilt of as little as 2.5° stimulates the maculae.
6.
The maculae also discharge tonically in the absence of head movement, because of the pull of
gravity on the otoliths.
Thus the receptors show little adaptation.
B. Mode of action of the Semicircular Canals

1. Provide information about dynamic equilibrium i.e. detect angular (rotational) acceleration
during sudden rotation of the head along three perpendicular axes.
44
2. The effective stimulus to each ampulla is rotation of the head in the plane of its canal.
(B) Direction of movement of the
head towards left
(A)
Semicircular Ampulla
Left Right
canal Cupula
Utricle Utricle
Axis of Axis
hair cells of hair
cells
Crista
Direction of movement
Nerve fibers (vestibular of endolymph
Ampulla division of VIII nerve)
i n
Horizontal semicircular canals
Vestibular divison
a
of VIII nerve
Membrane
Membrane
J
potential
potential
Note
(mV)
(mV)
.
The left ampulla is stimulated (+) whereas the right ampulla
Time Time
is inhibited (–).
Increase in frequency Decrease in frequency
of action potential of action potential
K
Fig. 10.65 (A) Mode of stimulation of semicircular canals; (B) mode of action of horizontal (lateral) semicircular canal when the head is
.
moved towards the left
3. Example, in case of rotation of the head towards left side in the horizontal plane the initial
endolymph movement is thus towards the left ampulla and away from the right ampulla; both
A
cupulae swing to the right. Vestibular action potentials show that the frequency of the impulses
from the left ampulla is increased while that from the right ampulla is decreased. (Fig. 10.65)
4. The stimulus to the cristae is due to the swinging (from side to side) of the cupula set up by
the endolymph.
5. The frequency of action potential in the afferent nerve fibers is related to the rate of acceleration
of rotational movement.
6. With the head erect at rest; there is a steady spontaneous discharge of impulses from all the six
ampullae.
Important Note: The semicircular canals give information about movements, and the otolith organ about the
position of the head.
C. Role of vestibular apparatus in regulation of posture

Afferents: from vestibular apparatus receptors, eyes, joints and skin receptors.
1. Sense organ of balance (equilibrium) and orientation of head in space.
Mechanism: Maintains tone in antigravity muscle; and
2. Helps in conscious awareness of the position and acceleration of the body.
3. Controls eye movements, vestibulo-ocular reflex.
Note: Reading newspaper or magazine in a moving bus puts maximum strain to the vestibulo-visual fixation
mechanism. That is why, reading prints in a moving bus is so difficult.
4. Initiate otolith reflexes that prevents leg injuries when a person walks down stairs.
Vestibular Dysfunction: Motion Sickness

1. Cause: All forms of travel where there is irregular motion
2. Features: Tendency to yawning, ↑ salivation, GIT discomfort, nausea, retching, vomiting, pallor,
headache, vertigo and mental depression.
Control of Body Movement and Posture

Levels of Motor Control System
Its motor neurons are organized at three levels: Highest, middle and lowest. (Fig. 10.66)
Middle level
n
Highest level Lowest level
(subcortical centre)
i
1. Parts involved: cerebral and 1. Sensory and motor cortex, 1. Brain stem and spinal cord.
limbic cortex; motor cortex cerebellum, basal ganglia
a
and association cortex. and brain stem nuclei.
2. Function: form complex plans 2. Receive afferents from 2. (i) Brain stem: Major relay station
J
and is responsible for: sensory system and converts for all motor commands
(i) generating idea for complex plans to a smaller and also responsible for
.
voluntary movements; motor plans so that tasks are maintaining normal body
(ii) issuing motor properly carried out. posture during movements.
commands via (i) Basal ganglia: plan (ii) Spinal cord: Final common
descending pathways to movements pathway through which a
K
middle and lower levels (ii) Subcortical and brain stem proper movement is carried
.
for their execution. nuclei: adjust posture out.
(iii) Cerebellum: Coordinates
movements.
A
Association Cortex
A. Highest level
other brain regions (cerebral cortex)
Generate commands for voluntary movements
Sensory motor
cortex
B. Middle level
Basal 1. Subcortical Nuclei Cerebellum (Subcortical centres)
ganglia 2. Brainstem nuclei
Plan movements Adjust posture Coordinates movements
via descending
pathways Spinal Cord
Execute movements C. Lowest level

(Brain stem and
Motor neurons
spinal cord)
Muscle Receptors in
fibers muscles, tendons,
joints, skin
Adjusts and smoothens movements
Fig. 10.66 The levels of organization of the neural system controlling body movement
46
Important Notes:
1. The motor programme is continuously adjusted by a control feedback from receptors in the periphery.
2. The motor systems “learns by doing” ; this involves “synaptic plasticity”
Control of Body Posture

1. Definition of normal posture: (Fig. 10.67)
i n
J a
.
Fig. 10.67 Normal body posture
K
2. Basic mechanism: Localized stretch reflexes → contraction of antigravity muscles and reciprocal
.
inhibition of the antagonistic muscles.
3. Postural reflexes
(i) Components of reflex arc: (Fig. 10.68)
A
(a) Afferent pathways: from eyes, vestibular apparatus and the proprioceptors.
(b) Efferent pathways: α-MNs to the skeletal muscle.
(c) Integrating centres: brain and the spinal cord.
Cerebrum
Pyramidal tract
Eye
Thalamus
Red nucleus and nuclei

of reticular formation of
brain stem
Lateral vestibular
(Deiter's) nucleus
Vestibular
Cerebellum apparatus
Neck muscle
Proprioceptors
Trunk muscle
Ventral horn cell

(α-motor neuron) Limb muscle
Fig. 10.68 Major components of ‘postural reflexes’ which

maintain body posture and balance
(ii) Functions: Maintain the

(a) body in an upright balanced position, and
(b) provide the constant adjustments necessary to maintain a stable background for voluntary
activity.
(iii) Mechanism: Caused by variation in the threshold of the spinal stretch reflex.
(iv) Main levels of motor integration
Level of integration Principal function/principal postural reflexes
(i) Spinal cord Control of spinal reflexes (stretch reflex-positive and negative
supporting reactions)
(ii) Medulla Regulation of heart, respiration and antigravity reflexes.
n
(iii) Midbrain Regulation of righting reflexes.
i
(iv) Midbrain, thalamus Regulation of locomotor reflexes.
(v) Hypothalamus, limbic system Emotional functions.
(vi) Cerebral cortex Initiation of voluntary movements, emotions and memory;
a
involved in conditioned reflexes.
J
Note: Role of postural reflexes are studied in animal after removal of a portion of neural axis.
.
Posture in spinal preparation
1. During stage of spinal shock: Spinal man cannot stand unsupported (without support).
2. During stage of reflex activity: Stretch reflexes become hyperactive so the resulting posture is
K
modified by:
.
(i) local static postural reactions e.g. positive supporting reaction (magnetic reaction) and negative
supporting reaction.
(ii) Segmental static postural reflexes e.g. crossed extensor response.
A
Posture in Decerebrate Preparation (Sherrington/classical decerebation) (Fig. 10.69)
(A)
Opisthotonos
(B)
Fig. 10.69 (A) Decerebrate cat with intact labyrinths, suspended

to show extensor rigidity. (B) Decerebrate cat following
labyrinthectomy, the head drops forward which causes flexion of
the forelimbs with associated extension of the hind limbs.
48
1. Hypertonia in extensor group of muscles, called decerebrate rigidity (limbs hyperextended, head
extended and back is concave)
2. It has no righting reflexes
3. Mechanism: ↑ γ-MNs discharge → ↑ muscle spindle sensitivity.
Cause:
(i) release of spinal γ-MNs from an inhibitory extra pyramidal tract discharge;
(ii) ↑ discharge from facilitatory reticular formation → ↑ γ-MNs discharge.
Important Note: ↑ γ-MNs discharge → ↑ muscle spindle sensitivity to stretch → rigidity, popularly called as
γ-Rigidity.
n
4. Significance of decerebrate rigidity → contraction of antigravity muscles → helps supporting the body
i
against gravity.
5. Postural reflexes: Tonic labyrinthine and tonic neck reflexes are more than found in spinal preparation
and help adjustment of posture of the trunk and limbs. Thus keep the head in upright position;
a
(i) Tonic labyrinthine reflexes; and
(ii) Tonic neck reflexes. (Fig. 10.70)
J
(i) and (ii) → more contraction of limb extensor muscles.
Decorticate posture
.
True decerebrate posture (Damage to upper border
(Damage to upper border of the pons) of the midbrain)
K
Neck and head:
.
Extended Head is flexed
Upper extremities:
A
extended with fingers Upper extremities:
flexed and forearms flexed
pronated.
Lower extremities: Lower extremities:

extended with toes extended with toes
pointed inward pointed slightly inwards
Person is lying supine The head is turned to the right and

left causing alterations in the position
of the hands and arms through
activation of tonic neck reflexes
Fig. 10.70 Decerebrate and decorticate rigidity in human
Posture in Mid Brain Preparation → Extensor rigidity. (as seen in decerebrate preparation) with intact
righting reflex.
Features
1. Individual can rise to the standing position, walk and right themselves.
2. By means of righting reflexes, individual can bring his head right way up and get the body into
erect position under all circumstances.
3. Examples of righting reflex
(i) Labyrinthine righting reflex
(ii) Body righting reflex

(iii) Neck righting reflex
(iv) Limb righting reflex
(v) Optical righting reflex.
4. Other mid brain reflexes
(i) Pupillary light reflex
(ii) Nystagmus
(iii) Vestibular placing reaction.
Posture in Decorticate Preparation → Decorticate rigidity
Cause: Due to loss of cortical area that inhibit spinal γ-MNs discharge via reticular formation
n
Features
i
Postural reflexes:
(i) Neck reflexes and righting reflexes present.
(ii) Hopping and placing reaction-lost
a
Note: Decorticate animals are easier to maintain.
. J
The Reticular Formation
Definition
1. Characterised by interlacing network of fibers in the brain stem with more than 50 reticular
K
nuclei.
2. Absolutely essential for life:
.
3. Components:
(i) Ascending reticular system: Reticular Activating System (RAS) (Fig. 10.71)
(a) Polysynaptic cholinergic pathway.
A
(b) Receive afferents from:
(Note: No inputs from sense of smell).
Specific sensory area
(somatosensory cortex)
Cerebral cortex
Thalamus
Subthalamus and
Midbrain Bulb of
hypothalamus
Pons medulla
Ascending reticular Brain stem

activating system in Afferent and collaterals
brain stem from ascending
specific sensory system
(cutaneous, eye and ear)
Fig. 10.71 Distribution of afferent collaterals to ascending reticular
activating system in brain stem
50
(c) Widely distributed to all parts of the cerebral cortex.

(d) Functions
• Produces the conscious state
• Responsible for EEG.
(ii) Descending reticular system: Reticulospinal tract (Fig. 10.72)
Components:
(a) The descending inhibitory reticular projection: Causes the reduction of movements either
reflexly by pyramidal stimulation or by stimulation of the inhibitory areas of motor cortex
and cerebellum.
n
Motor cortex
i
(–)
Caudate nucleus Cerebellum

(basal ganglia) (–)
a
Important Note 2
Fastigial
(–) nucleus
The anaesthetics (like ether) and 3
J
(+) + Vestibular
sedatives in high dose (such as (+) nucleus
barbiturate) produce unconsciousness
.
by depressing conduction in the 1 (–)
RAS. This is achieved by decreasing 6
Pons 5
building up of EPSPs to the firing 4
level of the postsynaptic neurons in Facilitatory reticular Medullary inhibitory
K
formation Medulla bulb
multisynaptic paths of RAS. reticular formation
.
Fig. 10.72 Inhibitory (1 to 4) and facilitatory (5, 6) systems concerned in spasticity
(b) The descending facilitatory reticular projection
A
• Causes facilitation of cortically induced movements by the reticulospinal pathways.
• The vestibular nuclei also produce facilitatory influence of the spinal motor neurons
via vestibulospinal tract which influences the tone of extensor (antigravity) group of
muscles.
The Cerebellum
Functional classification: (Fig. 10.73)
1. Vestibulocerebellum
2. Spinocerebellum
3. Neocerebellum (greatest developed in human)
Spinocerebellum
To medial descending system,
i.e. Vestibulospinal and Control axial
reticulospinal tracts (i.e. trunk) and
limb muscles and
To lateral descending system, postural reflexes
i.e. corticospinal tracts
Neocerebellum Control skilled
voluntary movements
To motor cortex, area 4 and 6
To vestibular nuclei
Control body posture,
Vestibulocerebellum equilibrium and eye
movements
Fig. 10.73 Functional divisions of the cerebellum

Cerebellar Cortex (Fig. 10.74)

Outer GM; inner WM with deep cerebellar nuclei.
Purkinje cells Stellate cell
n
Basket cell
i
Parallel fibres
a
Golgi cell
Granule cell
. J
Climbing fibres
Mossy fibres
K
Cortex White Inner Outer
matter granule molecular
.
cell layer layer
Middle Purkinje
cell layer
Fig. 10.74 Histology of cerebellar cortex (cross section of cerebellar folium)
A
1. Structure: 3 layers
(i) Outer molecular layer contains
(a) Nerve fibers: Dendrites of Purkinje cells and axons of granule cells and the climbing fibers.
(b) Nerve cells: Stellate and Basket cells.
(ii) Middle Purkinje cell layer contain Purkinje cell (the biggest neuron in the body). Its axons form
the only output to the deep cerebellar nuclei.
(iii) Inner granule cell layer contain granule cells (its axons bifurcate to form parallel fibers) and golgi
cells.
2. Inputs: Afferent fibers
(i) Climbing fibers carrying proprioceptive inputs.
(ii) Mossy fibers: Their output is excitatory.
[Important, the sequence, mossy fibers – stimulate dendrites of granule cell – parallel fiber axons –
stimulate dendrites of Purkinje basket and stellate cells provides excitation of the Purkinje cell.]
3. Neural Circuits (Fig. 10.75)
(i) The output of granule cell (via parallel fibers) is always excitatory.
(ii) The output of Purkinje cells, golgi cells, basket cells and stallet cells is always inhibitory (NT:
GABA).
52
Parallel fibre (PF)

Summary
GoC (+)
Stellate cell (SC)
PF
Basket cell (BC)
(–) Gr.C
Outer Molecular layer (A) N
egative
feedback loop
BC (–) PC
(+) (+)
Middle Purkinje cell layer
n
Purkinje
cell (PC) GrC
i
(B) F
eed forward
inhibition
Inner Granule cell layer
a
Golgi cell (GoC)
J
Granule cell (GrC)
.
lutamatergic
G
(Excitatory ending : GrC)
aba-ergic cells
G
(Inhibitory endings : SC, Deep
Mossy fibres
PC, GoC, BC) cerebellar
K
(Axons of spino, vestibulo and
nuclei
Interneurons corticoponto-cerebellar tracts)
Input
.
Axons Climbing fibre
Output (Afferents from inferior
olivary nucleus)
Fig. 10.75 Neural connections within the cerebellar cortex. (Inset: Summary)
A
(iii) The granule cell output is rapidly stopped by a negative feedback loop i.e. granule cell → (+) golgi
cells → (–) granule cell.
(iv) Basket cell → (–) Purkinje cells (NT: GABA). However, the basket cells and the Purkinje cells are
excited by the same excitatory input (parallel fibers). This arrangement is called feed-forward
inhibition and helps to limit the duration of the excitation produced by any given afferent
impulse.
(v) Purkinje fibers → (–) deep cerebellar nuclei (NT: GABA). These nuclei also receive excitatory
inputs in collateral from the mossy and climbing fibers. However, the ultimate impulse coming
out of the deep cerebellar nuclei is excitatory (NT: GA)
(vi) Functions
(a) Controlling or timing the excitatory output of the deep cerebellar nuclei to the brain stem and
thalamus. This helps the cerebellum in coordinating the muscle movements.
(b) The inhibitory transmitter: is GABA, whereas the excitatory transmitter is glutamic acid
(GA).
Connections of Cerebellum
1. Afferent Connections (via Mossy and climbing fibers) (Fig. 10.76)
(i) Dorsal and ventral spinocerebellar tract.
(ii) Olivocerebellar tract.
(iii) Vestibulocerebellar tract.
(iv) Cuneocerebellar tract.
(v) Tectocerebellar tract.
(vi) Cortico-ponto-cerebellar tract.
(vii) Rubrocerebellar tract arises.
(viii) Reticulocerebellar tract.
Cerebral cortex
Midline
Area 4
Motor
Thalamus (ventrolateral nucleus) cortex
Area 6
Red nucleus
Tectum (superior and

inferior colliculi)
7 Corticopontine fibres
n
8 Rubro cerebellar tract
i
Superior cerebellar peduncle
6 Tectocerebellar tract
a
Dentate nucleus
Cerebellar cortex
J
Middle cerebellar peduncle
Ponto cerebeller fibers
.
3 Olivo Cerebellar tract
Pontine nuclei
5 Cuneocerebellar tract
. K
Medulla
Inferior cerebellar peduncle
Inferior
olive Important Note
4 Vestibulocerebellar tract
A
9 Reticulocerebellar tract The olivocerebellar pathway
projects to the cerebellar cortex
Nucleus gracilis and cuneatus via climbing fibers, the rest paths
2 V
entral
Reticular formation
spinocerebellar project via mossy fibers.
tract
1 Dorsal spinocerebellar tract
Fig. 10.76 Principal afferent cerebellar connections
Note: There is point-to-point representation of motor areas in the cerebellum.
2. Efferent Connection (Fig. 10.77)

(i) Purkinje cell axons pass to the deep cerebellar nuclei (Dentate, Emboliform, Fastigial and Globose).
Their influence on these nuclei is purely inhibitory via release of GABA.
54
Midline
Cerebral cortex
Thalamus (ventro- Area 4

lateral nucleus) Motor
cortex
Area 6
Red
nucleus
Vestibular nucleus
Superior
cerebellar
penduncle Cerebellar
n
cortex
i
Nucleus interpositus
(Emboliform &
a
globose)
Inferior
J
cerebellar
penduncle
Dentate nucleus
.
Flocculonodular
lobe
Fastigial
K
nucleus
.
Fig. 10.77 Principal efferent cerebellar connections
(ii) CF of deep cerebellar nuclei:

(a) Provide excitatory output for the spinocerebellum and neocerebellum.
A
(b) Project
• to the vestibular and reticular nuclei:
• to the nuclei of III, IV and VI cranial nerves (controlling the extrinsic eye muscles); and:
• to the red nucleus.
(c) Dentate nucleus influences corticospinal tract;
(d) Fastigial nucleus influences vestibulospinal and reticulospinal tracts;
(e) Emboliform and globose nuclei influences the rubrospinal tracts.
Functions of the Cerebellum

1. Control of body posture and equilibrium by the vestibulo-cerebellar connections.
2. Inhibit muscle tone and stretch reflexes
However, cerebellar lesion also → hypotonia. Mechanism: Anterior lobe → (–) γ-MNs discharge to
muscle spindle → ↓ excitability of the stretch reflex.
3. Coordination of movements: result of appropriate regulation of time, rate, range (extent), force and direction
of muscular activity.
(i) Control of involuntary movements
(ii) Control of voluntary movements: The 3 lobes of vestibulo, spino and neocerebellum acts as a
comparator of a servo-mechanism. How? (Fig. 10.78)
Pathway
(a) Afferents:
• Sensory information from all parts of the body via climbing fibers, and
• Pyramidal and Extrapyramidal impulses which are transmitted to the muscles via cortico-
ponto-cerebellar pathways.
Motor cortex
Mid line
Pyramidal Thalamus
tract (cortico (Ventrolateral nucleus)
spinal tract)
Cerebellum
Pontine Dentate nucleus

nucleus
Reticular nucleus
n
Reticulospinal
Rubrospinal tract
tract
i
Spinocerebellar
tract Proprioceptors
Ventral horn cell of the muscles
of the body
a
Skeletal muscle
Fig. 10.78 Pathway – “Comparator of a servo-mechanism” function
J
of the cerebellum (Note: Cortico-ponto-dentato-thalamo-
cortical circuit: red arrows)
.
(b) Efferents: via deep cerebellar nuclei back to above areas in the brain.
Thus corrects the error in the movements by adjusting the activity in the descending
pathways.
K
Important Notes:
.
1. The cerebellum’s role in control of movements is comparing informations what the muscles should be doing
with information about what they are actually doing (learning of motor skills).
2. Each cerebellar hemisphere influences the opposite cerebral cortex (via dentato-thalamo-cortical path i.e. cortico-
A
ponto-dentato-thalamo-cortical circuit);
3. Motor cortex via the corticospinal tracts, controls the movements of the opposite side of the body. Because
of the double decussation, each cerebellar hemisphere controls voluntary movements on its own side of the
body.
Cerebellar Dysfunctions
(Neocerebellum damage→most of the dysfunctions)
Characteristic Features (Fig. 10.79)
1. Disturbance of Posture
(i) Atonia or hypotonia on the affected side.
(A) (B) (E)
(C) (D)
Fig. 10.79 Characteristic features and tests in cerebellar dysfunction. (A) Intentional tremors;
(B) Finger nose test; (C) Adiadokokinesia; (D) Heel-knee test; (E) Drunken gait
56
(ii) Attitude: The trunk is bent with the concavity towards the affected side.
(iii) Nystagmus.
(iv) Deep (or tendon reflexes): weak and pendular
2. Disturbances of Voluntary Movement
(i) Asthenia
(ii) Ataxia →
(a) Decomposition of the movement:
(b) Asynergia:
(c) Dysmetria: → movements overshoot their intended mark, i.e. past pointing (or hypermetria) or
fall short of it.
(iii) Intention tremor: Coarse (frequency of 4-6/sec.)
n
(iv) Gait: Drunken gait.
i
(v) Speech: Slow and lalling
Note: Clinically these disturbances can be demonstrated by finger-nose test; rebound phenomenon; adidokokinesia and
a
heel-knee test.
J
The Thalamus
.
Anatomical Classification of Thalamic Nuclei (Fig. 10.80)
Three groups:
1. Lateral nucleus
K
(i) Ventral: anterior, lateral, posterior, medial and lateral geniculate bodies.
(ii) Dorsal: anterior, posterior, pulvinar.
.
Internal medullary lamina Massa intermedia
Nuclei of midline
A
Anterior group Right Left
of nuclei Dorsomedial thalamus thalamus
nuclei
Hypothalamus
Ventral anterior Pulvinar

nucleus
Location of thalamus
Lateral dorsal nucleus
Medial geniculate
Lateral ventral nucleus Lateral bodies
Lateral posterior nucleus

Posterior ventral nuclei
(3 divisions)
Dorsal group
Lateral group of nuclei
Ventral group
Fig. 10.80 Thalamus and its principal nuclei
2. Anterior nucleus
3. Medial nucleus: (a) dorsomedial; (b) midline
Functional Connections of Thalamic Nuclei (Fig. 10.81)
1. Non-specific projection nuclei: midline and intralaminar nuclei receive impulses from RAS and project
diffusely to the whole of the neocortex → alerting effect of RAS.
2. Specific projection nuclei: divided into 3 groups:
(i) Specific sensory relay nuclei e.g.
(a) Medial and lateral geniculate bodies - relay auditory and visual informations respectively.
(b) Posteroventral groups of nuclei - receive somesthetic sensory information and relay to the
postcentral sensory cortex areas S I and S II.
Prefrontal cortex
Cingulate gyrus (area 24) (areas 8, 9, 10, 11)
Other
thalamic
nuclei Hypothalamus
Superior parietal lobule

Mammillary body
of hypothalamus
Cortex (area 18, 19)
n
Inferior parietal lobule
i
Substantia nigra;
globus pallidus
J a
Cochlear nuclei inferior colliculus
Dentate nucleus of
.
Spinothalamic Auditory cortex (area 41, 42)
cerebellum; globus pallidus
tract; medial
lemniscus Optic tract
Calcarine cortex (area 17)
K
Motor cortex (area 4 and 6)
Trigeminal lemniscus
.
Sensory cortex (area 3, 1, 2)
Fig. 10.81 Major thalamic projections to the cerebral cortex (also see Fig. 90.1)
(Note: The majority of cortical areas reciprocally project fibers back to the thalamic nuclei)
A
(ii) Nuclei concerned with motor control
(a) Ventrolateral group: receive inputs from basal ganglia and cerebellum and project to the
motor cortex (area 4, 6).
(b) Anterior group: receive inputs from mammillary bodies and project to the limbic cortex;
concerned with recent memory and emotion.
(iii) Dorsolateral nuclei receive inputs from hypothalamus and thalamus and are projected to prefrontal
cortex. These are concerned with integrative functions such as language (speech).
Functions of The Thalamus

1. A great sensory relay station (except the sense of smell).
2. Responsible for maintaining conscious and alerting responses of RAS.
3. Responsible for subcortical perception of pain.
4. Controls muscular movements.
5. An integrating centre for sleep.
6. Concerned with recent memory, emotion and with language (speech) via papez circuit.
7. Role in genesis of sinchronized activity of EEG.
Thalamic Syndrome
Cause:
Damage to posterior ventral and lat. nu. of thalamus → signs and symptoms on opposite side of body
with emotional disturbances →
1. overreaction to painful stimuli
2. loss of tactile localization and discrimination, kinesthetic sensation, therefore, difficulty to locate
body part with eyes closed (called Thalamic phantom limb).
58
3. Thalamic hand: wrist flexed with fingers hyperextended.

4. Marked muscular weakness, ataxia, intentional tremors.
The Electroencephalogram (EEG)
Definition
Normal EEG rhythm: Main features
EEG Rhythm Frequency (Hz) Amplitude (µV) Associated features

1. Alpha (α) 8–12 50–100 Present in all normal individuals in awake state;
n
maximally in the occipital and parieto-occipital areas
when the eyes are closed.
i
2. Beta (β) 14–30 5–10 Generally seen in frontal region (normal awake
pattern); commonly seen in infants.
a
3. Theta (θ) 4–7 10 Often found over the parietal and temporal areas
(normal in children and in early sleep).
J
4. Delta (δ) 1–4 20–200 Usually appear during sleep; can be produced by
overbreathing; or evidence of organic brain diseases
.
when seen in awake state.
Important Note: In general, lower EEG frequencies indicate less responsive behaviour, such as sleep, whereas higher
frequencies indicate arousal.
K
α-Rhythm: Characteristic features (Fig. 10.82)
.
1. Present at rest when the eyes are closed; associated with decreased level of attention; subject feels
relaxed and happy.
2. Its frequency:
A
(i) ↓ed by hypoglycemia; ↓ body temperature; ↑ pCO2; sleep and ↓ GCs.
(ii) ↑ed by hyperglycemia; ↑ body temperature; ↓ pCO2; alerting states and ↑GCs.
100 µV
(A) α-rhythm: Related with eyes closed
100 µV
Eyes open Eyes closed

(B) α-block : Alert/arousal phenomenon
Time 1 sec
Fig. 10.82 Normal electroencephalogram (EEG)
3. The replacement of regular α-rhythm with fast, high frequency, irregular low amplitude (voltage)
activity is called alpha-block, or desynchronization of EEG. It is produced by any sensory stimulation
and is correlated with the aroused, alert state, (arousal or alerting response).
Physiological basis of EEG (Fig. 10.83)

Summated graded post synaptic potentials of rhythmically discharging cell bodies (neurons) in the most
superficial layers of the cerebral cortex.
Presynaptic
terminations on
the dendrites
100
µV
Wave Activity
(sum of graded
potentials)
Dendrites
Flow of
current
200 µV
i n
Axon
a
All or none
action potential
J
Fig. 10.83 The electrical activity as recorded from the
dendrites compared to that recorded from an axon
.
Uses of EEG
1. Localization of pathological conditions eg:
K
(i) Subdural haematoma or fluid collection → ↓ EEG activity over this area.
.
(ii) Lesion in the cortex → local irregular or slow waves in the EEG.
2. Diagnosis of epilepsy → localized high voltage waves in the EEG.
A
Sleep
Definition
Factors affecting
Types of Sleep
1. Non-rapid eye movement (NREM) sleep or slow wave sleep; and
2. Rapid eye movement (REM) sleep or paradoxical sleep.
Behavioural and EEG changes during sleep

Stage Behavioural Observation EEG Changes
1. Relaxed awake Relaxed with eyes closed Mainly α-rhythm.
2. Relaxed Sleepy but not asleep, eye lids narrows, Amplitude and frequency of α-wave ↓s.
drowsiness head starts to droop.
3. NREM sleep
(i) Stage 1 Light sleep: easily aroused by stimuli; Further ↓ in amplitude and frequency of
awareness further ↓s. α-wave.
(ii) Stage 2 True sleep: Further lack of sensitivity to
Apperance of sleep spindles 14–15 Hz,
arousal 50 µV due to reverberating activity b/w
thalamus and cerebral cortex.
(iii) Stage 3 Sleep deepens Occasional sleep spindles with δ-waves
(iv) Stage 4 Deep sleep: High threshold of awakening; Slow high voltage δ-waves.
not associated with dreaming.
4. REM Sleep Deepest sleep: greatest relaxation; Desynchronized (like of alert awake
difficulty of arousal by sensory stimuli; state), therefore, also called Paradoxical
generalised hypotonia (except in eyes → sleep.
REM); associated with dreaming.
60
Awake: Relaxed with

eyes closed (α-rhythm)
Stage 1
Sleep spindles
Stage 2
(true sleep) NREM
sleep
Stage 3
n
Stage 4
(deep sleep)
i
REM sleep: resembles
that of alert awake state
a
(deepest sleep)
1 sec 50 µV
Fig. 10.84 Pattern of EEG record during various stages of sleep
J
Characteristic features (NREM and REM sleep compared)
.
NREM Sleep REM Sleep
1. EEG: ↓ frequency and ↑ in voltage with each 1. EEG: desynchronized pattern (paradoxical effect).
succesive stage.
K
2. Muscle tone progressively ↓s. 2. +++ ↓ in generalized muscle tone, (snoring).
.
3. Eyes begin slow, rolling movements until they 3. Small jerky eyes movements that rapidly bring
finally stop in stage 4 (deep sleep). the eyes from one fixation point to another
(watching visual images of dreams).
A
4. Not associated with dreaming. 4. Closely associated with dreaming, teeth
grinding (Bruxism) in children; engorgement
of sexual erectile tissues; facial or limb muscles
twitches.
5. Significance: Associated with pulsalite release of 5. (i) Necessary for mental well-being and
GH and gonadotrophins, ↓ HR, ↓ BP, maturation of brain.
↓ respiration, therefore, (period of body’s rest (ii) Make learning and memory possible.
and metabolic restoration). (iii) Plays important role in homeostatic
mechanism. (Its complete loss → weight loss
and death)
6. Genesis: 6. (i) Discharge of NE from neurons in pontine
(i) (–) of RAS inputs → synchronized activity reticular formation and in locus ceruleus
in EEG. (in 4th ventricle of brain).
(ii) Rhythmic discharge from thalamus → (ii) Discharge of cholinergic neurons → PGO
(a) synchronized mechanism (due to (ponto geniculo occciptal) spikes → shift
stoppage of discharge of 5HT NREM to REM sleep.
(b) release of prostaglandin D2.
(Note: Sedatives or tranquillizer → ↓ REM sleep → psychological disturbances).
Sleep Cycle (Fig. 10.85)

1. 8 hours sleep and 16 hours awake.
2. NREM followed by REM sleep.
3. Average total sleep period comprises 4 or 5 such cycles, each cycle lasting 90 to 100 minutes (80
min NREM and 20 min REM).
4. NREM sleep constitutes about 80% of the total sleeping time and REM sleep about 20%.
5. REM sleep ↑s towards the morning.
24 hour-sleep/dream cycle
Midnight
3 a.m.
6 a.m.
n
9 a.m.
i
12 Noon REM Dreaming Sleep
NREM Deep Sleep
a
Awake
Fig. 10.85 Sleep-waking cycle: Circadian rhythm (Based on normal
J
8 hour night of sleep and a 90 minute sleep cycle rhythm)
.
Control of Sleep-Waking Cycle
A. Neural Mechanism
1. Controlled by biological clock in the hypothalamic suprachiasmatic nucleus which receive input
K
from eye via retina hypothalamic fibers. → circadian rhythm of 8 hours sleep and 16 hours awake
.
cycle.
Note: Light dark cycle; temperature and meal timing provide hint for occurrence of its setting.
A
2. Involves interaction between arousal and sleep-promoting systems in the brainstem. (Fig. 10.86)
(i) arousal system activated by: stimulation of sensory receptors, reticular formation and raphe
nuclei of pons and medulla.
(ii) sleep-producing system activated by: ↓ activity of RAS and stimulation of anterior and dorsal
hypothalamus.
Cerebral cortex
Arousal
REM: paradoxical sleep
NREM: slow wave sleep
Fig. 10.86 Brainstem structures involved in arousal, NREM and

REM sleep
B. Humoral or Chemical mechanism

Sleep inducing chemical substances include: NE; 5HT antagonists; A-ch, adenosine, hypotoxin; delta-
sleep producing peptide (DSIP) and sleep promoting factors (Factor S).
62
Summary: Sleep Waking Cycle

NREM NE & Ach REM
Never
possible
RAS 5 HT
inhibition and
RAS RAS
WAKING
n
Note: Caffeine, an adenosine antagonist → alerting effects.
i
Sleep Disorders
a
1. Insomnia: Unable to initiate and/or maintain sleep.
2. Fatal familial insomnia: persistent insomnia, dementia, impaired autonomic and motor functions.
3. Somnambulism or sleep-walking. Common in children, wake with eyes open; avoid obstacles; when
J
awakened can’t recell episode. Usually occur during NREM sleep.
.
4. Nocturnal enuresis i.e. involuntary voiding of urine during sleep at night.
5. Narcolepsy: Starts with sudden onset of REM sleep due to brain diseases → Uncontrollable urge to
sleep during day time activities with loss of muscle tone (cataplexy).
K
6. Sleep apnoea
7. REM behaviour disorder: REM sleep not associated with hypotonia.
.
The Basal Ganglia
A
It is the primary motor area in lower animals and called the head ganglia of neural control.
Parts (Fig. 10.87)
1. Caudate nucleus (CN),
Corpus striatum or neostriatum
2. Putamen
3. Globus pallidus or paleostriatum,
4. Subthalamic nucleus, and
5. Substantia nigra.
Caudate head
Corona radiata
(corticospinal fibres) Thalamus
Putamen
Globus pallidus
Caudate tail
Internal
capsule
Caudate
head Thalamus
Putamen and
globus pallidus
Cerebral Caudate tail
peduncle
Amygdaloid
nucleus
Fig. 10.87 Relationship between basal ganglia, thalamus and cerebral cortex
in sagittal section and coronal section (inset)
Connections
A. Afferents
1. Whole of cerebral cortex Excitatory Neostriatum
2. Thalamus Cholinergic (A-ch) neurons (CN + putamen)
(Ventrolat. and med. nu.)
B. Internuclear
Inhibitory Dopaminergic
1. Substantia nigra Neostriatum
(nigrostriatal tract)
Inhibitory GABA-ergic
n
2. Neostriatum Susbstantia nigra
i
3. Neostriatum Globus pallidus
a
4. Globus pallidus Subthalamic nucleus
. J
Excitatory
5. Subthalamic nucleus Globus pallidus and
glutaminergic
substantia nigra
. K
Summary: C
onnections of the basal ganglia
(ES, IS: External and internal segment;
PC, PR: Pars compacta and reticulata)
A
Cerebral Cortex
Neostriatum
Thalamus
Globus ES IS
pallidus
Subthalamic Nucleus PC PR
Superior
Substantia colliculus
Nigra
Excitatory neurons: A-ch ; glutamic acid ;

Inhibitory neurons: GABA (– – –); dopamine (– – –)
C. Efferents
Globus pallidus and Substantia nigra Thalamus
64
D. Feedback circuit
Cerebral Cortex
(Excitatory
(Excitatory cholinergic)
cholinergic) Neostriatum
Inhibitory
GABA-ergic
Thalamus
i n
Globus pallidus and
Inhibitory
substantia nigra
GABA-ergic
a
Important Note: This feedback circuit is integrated in the ventrolateral nucleus of the thalamus with another
circuit i.e. cortico-ponto-dentato-thalamo-cortical circuit and inhibits excessive activity of the motor cortex, areas 4
J
and 6.
.
Functions of Basal Ganglia
Neurons in the basal ganglia discharge before movements begin.
K
1. Subthalamic Nucleus and Globus Pallidus
.
Involved in the planning and programming of movements by preventing oscillation (unwanted
movements) and after discharge in the motor system.
A
Important Note: The neurons in the basal ganglia are stimulated mainly by A-ch and are inhibited by the
dopamine and GABA.
2. Caudate Nucleus
Inhibits the stretch reflex (muscle tone) throughout the body by stimulation of the inhibitory RF →↓
γ Mn discharge.
This is why damage to the basal ganglia produces rigidity.
3. Neostriatum
Regulates the subconscious gross movements such as performing a skilled task without fully recognising
what you are doing.
4. Globus Pallidus
Provides appropriate muscle tone for performance of skilled movements.
5. Substantia Nigra
Centre for coordination of those impulses which are essential for skilled movements.
6. Responsible for control of normal automatic and associated movements such as swinging of arms
during walking. These movements are initiated in motor cortex, area 6.
7. With limbic system regulate emotional behaviour.
Diseases of the Basal Ganglia

A. Parkinson’s Disease (Paralysis Agitans): Shaking palsy
Stooped posture Masked facial

expression
Rigidity
Forward tilt of trunk
Flexed
elbows Reduced arm swinging
and writs
– Persistent tremors
– Repetitive pill rolling
movement
i n
Slightly flexed
hips and knees
Trembling of
a
extremities
Shuffling, short-stepped
gait
J
Fig. 10.88 Characteristic features of Parkinson’s disease
.
Characteristic features (Fig. 10.88)
K
Cause
1. Occurs in late middle age common in males
.
2. Degeneration of dopaminergic nigrostriatal tract → ↓ concentration of dopamine (and balance shifts
to excitatory transmitter i.e. A-ch)
A
A-ch → (+) NEOSTRIATUM (–) ← Dopamine
Normally balanced
3. Dopaminergic neurons and dopamine receptors are steadily lost with aging in basal ganglia.
Symptoms appears when > 60% of these neurons are lost.
4. Hyperkinetic features
(i) Rigidity (extrapyramidal type)
(a) Affects large proximal group of muscles of the limbs, involving both protagonists (flexors)
and antagonists (extensors).
(b) Flexion attitude; in advanced cases → Statue.
Causes of rigidity: ↑ discharge of γ-efferents supplying the muscle spindle.
(ii) Tremor (present in > 85% of patients)
(a) Regular, rhythmic, alternate contraction of antagonist and agonist muscles @ 6‑8 times/sec.;
(seen as pill-rolling movements).
(b) Common sites: fingers, hands, lips or tongue.
(c) Resting (static) tremor. Mechanism: voluntary movements from motor cortex → (+) α and
γ MNs → (+) stretch reflex →↓ involuntary movements called as damping effect.
(d) Increases in emotional states, excitement or anxiety due to secretion of Ep. from the adrenal
medulla → (+) RAS
(e) Tremor disappears during sleep due to decreased activity of the RAS).
5. Akinesia or hypokinesia or bradykinesia
Cause: Due to dopamine deficiency (mainly); in addition predisposed by presence of rigidity.
(i) Difficulty in initiating fine voluntary movement.
(ii) Slow and monotonous speech.
66
(iii) The face becomes mask-like.

(iv) Loss of subconscious associated movements.
(v) Gait: festinant type shuffling gait.
(vi) Tendon jerks: More difficult to elicit.
Differences between spasticity and rigidity

Spasticity Rigidity
Cause: 1. Lesion of the basal ganglia, (sp. caudate nu)

1. Seen following the lesion of PT (commonest site (called the extrapyramidal rigidity).
internal capsule).
i n
2. Involves only one group of the muscle either 2. Involves both the agonist as well as antagonist
agonist or antagonist. Usually antigravity muscles → generalized attitude of flexion.
muscles.
a
3. Stretch sensitive. (↑ tone developed 3. No such phenomenon is seen here.
proportional to speed of applied stretch)
J
4. Hypertonia: Clasp-knife type. 4. Two types: Lead-pipe and cog-wheel rigidity
.
B. Chorea and Athetosis
1. CF: spontaneous involuntary movements due to interruption of inhibitory pathway from area 4s via
caudate nucleus to the thalamus.
K
2. Chorea: due to involvement of caudate nucleus → rapid irregular involuntary movements of short
.
duration; ↓ muscular tone and weakness.
3. Athetosis: due to lesion of lenticular nucleus → continuous slow twisting movements.
C. Wilson’s Disease (or progressive hepatolenticular degeneration)
A
1. Cause: ↓ ceruloplasmin → ↑ copper content of substantia nigra → +++ degeneration of lenticular
nucleus with cirrhosis of liver.
2. Features: Muscular weakness, rigidity, tremors, cirrhosis of liver → jaundice and emotional
disturbances.
D. Kernicterus
Rh-incompatibility in a newborn → hemolytic disease → ↑ indirect bilirubin → cross BBB →
damages globus pallidus → fatal condition; if child survives → rigidity, chorea, athetosis and mental
deficiency.
The Hypothalamus
Hypothalamic areas and nuclei (Fig. 10.89)
1. Pre optic area: Pre optic nucleus
2. Anterior area: Supra optic nu.; suprachiasmatic nu., paraventricular nu., anterior nu.
3. Middle area: Ventromedial nu., dorsomedial nu., arcuate nu.
4. Posterior area: Mamillary bodies; posterior nu.
5. Lateral area: Lateral nu.
Transverse section
Massa
Paraventricular intermedia
Nucleus of thalamus
Anterior Nucleus
Preoptic Nucleus Posterior
Suprachiasmatic nucleus
nucleus
Mammillary
Supraoptic nucleus body
Optic chiasma
Infundibulum
Dorsomedial
n
nucleus
i
Pituitary gland
Ventromedial
nucleus
a
Arcuate nucleus
Preoptic area
J
Anterior (supraoptic) area
Middle (tuberal) area
.
Posterior (mammillary) area
(Lateral area – not shown)
Fig. 10.89 Relationship among the hypothalamic nuclei
. K
Connections
1. Main afferent: With the limbic system (amygdala and hippocampus); thalamus, basal ganglia, retina,
midbrain and medulla (Ep. NE and 5 HT fibers)
A
2. Main efferents projected to the limbic system, midbrain, thalamus, posterior pituitary, RF in brain
stem and the spinal cord.
Functions of the Hypothalamus

1. Regulation of body temperature
2. Regulation of the anterior pituitary gland activity through the release of releasing factors and release-
inhibiting factors
3. Regulation of the posterior pituitary hormone secretion
4. Control of circadian rhythm (or diurnal variation) Examples: secretion of ACTH, GH, sleep waking
cycle, body temperature rhythm and gonadotrophin secretion. The menstrual cycle (about 28 days).
Neural basis:
Suprachiasmatic nuclei receive important inputs from:
(i) the eyes; and
(ii) the lateral geniculate nuclei.
Function is to synchronize the various body rhythms to the 24 hour light-dark cycle; and initiate
neural and hormonal signals that form circadian rhythm.
5. Control of sleep-waking cycle: By the biological clock function of the hypothalamic suprachiasmatic
nucleus.
6. Control of the ANS:
(i) Anterior hypothalamus → parasympathetic response.
(ii) Lateral hypothalamus → sympathetic responses.
7. Control of hunger and feeding: Theories
(i) Glucostatic Theory (Fig. 10.90)
(a) Ventromedial nucleus (satiety center). It functions by inhibiting the feeding centre.
68
(b) The feeding centre (in lateral hypothalamus) chronically active; its activity is inhibited by the
activity in the satiety centre.
(c) The activity of the satiety centre is governed by the level of glucose utilization across the
glucoreceptors (or glucostats) in the centre. Therefore, if the glucoreceptors are supplied with
sufficient glucose, their activity is increased → inhibits the feeding centre and the individual
feels satisfied.
Higher CNS Centres
(cognition and emotional factors)
n
Hypothalamus
i
Leptin Hypothalamus
(+)
ents
a
Reduced Affer Feeding (+)
gastric centre
activity (+) (+) (–)
J
Satiety
centre Cold Leptin
(CCK, secretin, GIP) Heat Lateral hypothalamic
.
Blood- area: Hunger centres
HCI Enterogastrones Glucose Blood
leptin
• Glucose Incretin Insulin Energy
• Gut stores Leptin
K
glucacon release Ventromedial nuclei:
• GIP Fat tissue Satiety centres
.
Fig. 10.90 Control of hunger and feeding (Negative feedback and feedforward factors) (Note: Incretin is a hormone that
stimulates insulin secretion in response to meals e.g. Glucagon Like Peptide-1 (GLP-1) and GIP
A
Note: In DM due to insulin deficiency → ↓ glucose utilization of glucoreceptors → unchecked activity of feeding
centre → polyphagia.
(ii) Lipostatic Theory: (Fig. 10.91)
FAT DEPOTS
(Increased fat Increased leptin Increased plasma
deposition) synthesis leptin concentration
Important Note
(stimulate) Decrease in plasma leptin produced by
fasting is associated with inhibition of
Hypothalamus the onset of puberty, decreased thyroid
(increased activation function, and increased glucocorticoid
of leptin receptors) secretion. These are adaptive responses
Increased food intake inhibit to the shortage of calories signaled by the
and decreased energy decrease in leptin.
expenditure
Fig. 10.91 Feed-back loop i.e. control of fat depots by leptin
Note: Any defect in the leptin receptor genes → obesity.
(iii) Gut peptide theory: Food in the GIT → release of CCK, glucagon, gastrin releasing peptide (GRP);
YY neuropeptide and somatostatin → via hypothalamus → ↓ food intake.
(iv) Thermostatic theory: ↓ core temperature stimulates the food intake whereas a rise inhibits it.
8. Control of water intake i.e. Thirst and water loss.

Pathways controlling thirst
(i) True thirst assoc. with ↓ ECFV or ↑ plasma osmolality. (Fig. 10.92)
Mechanism: Decrease in ECFV via the renin-angiotensin system → angiotensin II → (+) OVLT
area of the circumventricular organs in the brain → ↑ thirst.
(ii) Other pathway: Dryness of mouth and throat → ↑ thirst.
Neurotransmitters and thirst

(i) A system of cholinergic neurons subserve drinking which converge on the lateral preoptic area
of hypothalamus.
(ii) The renin-angiotensin system is concerned with drinking caused by β-adrenergic stimulation.
n
9. Control of emotional behaviour: The hypothalamus integrates the endocrine, autonomic and some
i
of the motor activities that form appropriate emotional behaviour.
10. Integrated control of the CVS by corticohypothalamic descending pathways which discharge by emotions
→ emotional effects on the CVS.
a
Haemorrhage
J
Vomiting Plasma ECFV Speaking
Diarrhoea osmolality Smoking
.
Angiotensin II Breathing through mouth
ECFV Osmoreceptors Eating dry food

(located in the Via OVLT
K
Blood volume anterior hypo- Dry mouth and throat
.
thalamus
Baroreceptors
(venous and
A
arterial)

(+) (+) (+) (+)
Hypokalemia T H I R S T Metering of water

(+) (–)
Hypercalcaemia intake by GIT
Fig. 10.92 Inputs reflexly controlling thirst {(+): Stimulation; (–): Inhibition}
The Cerebral Hemisphere (Cerebrum)

1. Cerebral Cortex: 2–4 mm thick with total surface area 2200 cm2.
Frontal lobe
Central sulcus
Frontal pole
(sulcus of Rolandic)
Parietal lobe
Parietal-occipital sulcus
Occipital lobe
Occipital pole
Lateral sulcus
(sylvian sulcus)
Temporal lobe
Temporal pole
Fig. 10.93 Principal lobes of cerebral hemisphere

70
2. 4 major lobes: frontal, parietal, occipital and temporal; consisting of 47 functional Brodmann areas. (Fig. 10.93)
3. Histology: Typical cortex contains 6 layers. The areas of the cortex where number of layers are
less than six are called Allocortex and where number of layers are six are called Neocortex; with
evolution actual extent of allocortex has changed little. (Fig. 10.94)
Note: Human brain: Immense growth of the 4 major neocortical lobes (specially parietal and temporal lobes)
Rat Cat Monkey
n
Human
i
Cingular gyrus
a
Entorhinal
gyrus
J
Piriform Hippocampal
cortex gyrus
.
Uncus (Anterior end of
hippocampal gyrus)
Neocortex (neopallium) Allocortex (archipallium) and
K
Juxtallocortex (mesopallium)
Fig. 10.94 Relative extent of the allocortex and neocortex in
.
different mammals compared
A
Parietal Lobe (Fig. 10.95)
1. Location:
2. Major areas: SI, SII, areas 5, 7 and 40.
Supplementary motor area
Sulcus cinguli
4
5
Medial edge
SI of hemisphere
2 7
Precentral 3
sulcus 1
S.II
Fig. 10.95 Connections of the parietal lobe areas involved in

somatic sensation
3. Connections
(i) Association fibers joins different areas of cerebral cortex.
(ii) Commissural fibers connect the corresponding SI & II.
(iii) SI and II sends fibers to the caudate nucleus, putamen and motor areas 4 and 6.
(iv) ‘SI’ sends fibers to the thalamus, midbrain, pons, cerebellum, brainstem and dorsal horn in the
spinal cord.
4. Functions
(i) Post Central Gyrus (Areas 3, 1 and 2): Appreciation of the elementary sensations.
(ii) Areas 5 and 7: Discrimination between intensity of different stimuli.
(iii) Area 40: Stereognosis area.
(iv) Angular gyrus. recognition of spatial relationship, i.e.
(a) Tactile localization;
(b) Tactile (two point) discrimination; and
(c) The extent and direction of small joint displacements.
(a), (b) and (c) help the relations of a stimulus in one, two or three-dimensional space to be
clearly defined.
5. Applied Aspect
n
(i) Unilateral removal of parietal lobe on one side →
i
(a) loss of sensation on opposite side
(b) ataxia; and
(c) loss of body images (Fig. 10.96)
a
(A) (B)
. J
. K

(ii) A Fig. 10.96 Body images [Model (A) and patient copy (B)]
Bilateral removal of areas 3, 1, 2.

(a) visual placing retained but tactile placing is completely lost.
(b) withdrawal reflexes: exaggerated and explosive → violent withdrawal reflex.
(iii)
Removal of areas 7.
(a) Unilateral: opposite receptive field (both visual and somatic) lost → failure to care for half
of body inspite of normal vision and somatic sense.
(b) Bilateral: No visual placing but (normal tactile placing → constructional apraxia and spatial
disorientation.
Prefrontal Lobe (or Orbito-frontal region)

1. Location: Anterior to motor areas 4, 6 and 8.
2. Major areas: 9 to 13, 24, 32, 44 and 47.
3. Connections
(i) Afferents: Mainly from the thalamus (anterior and dorsomedial nucleus) (Fig. 10.97)
72
Anterior Nucleus cingulate gyrus (area 24)

of thalamus (in the prefrontal lobe)
via mammillothalamic
tract
Mammillary bodies of Hippocampus

the hypothalamus via fornix
Papez Circuit (i.e. prefrontal lobe-area 24 forms a close circuit connections with thalamus)
n
Sulcus cinguli
Cingulate gyrus
i
Callosal sulcus
Anterior
a
Nucleus of thalamus
Dorso medial
Fibers from hypothalamus to
J
Mammillary body dorsomedial nucleus of thalamus
.
Mammillothalamic tract Cerebral peduncle
Optic chiasma Hypothalamus
Pituitary complex
K
Anterior Commissure
.
(A) Afferent connections (medial aspect of right cerebral hemisphere)
Fronto-occipital
projections
A
Caudate nucleus
Dorsomedial nucleus
of thalamus
Tegmentum
Mammillary body
Tract from
hypothalamus to Temporal
posterior pituitary lobe
(B) Efferent connections (C) Intercortical connections: Association tracts
(medial aspect of right cerebral hemisphere) (lateral aspect of left cerebral hemisphere)
Fig. 10.97 Major connections of the prefrontal lobe
(ii) Efferents: Mainly to the caudate nucleus, pons, cerebellum, mid-brain, thalamus, RF and the
hypothalamus. (mammillary bodies)
(iii) Intercortical:
(a) Area 8 to area 18 (fronto occipital projection). Its damage → visual agnosia (can’t recognise
objects even with normal vision).
(b) Area 44, 47 and 18 → temporal lobe.
4. Functions
(i) Control of the ANS via the hypothalamus and the brain stem;
(ii) Control of the higher intellectual activities; (such as speech, learning and memory). (Removal
→ apathy initially then hyperactive states and memory loss)
(iii) Control of personality;
(iv) Control of emotional affects; (removal → loss of discrimination power)
(v) Control of behaviour and social consciousness; and loss of moral sense of right or wrong.
(vi) Responsible for the resting EEG.
5. Applied Aspect
(i) Prefrontal Lobectomy in Man
(a) Unilateral removal → no impairment of movements; little change in the personality.
(b) Bilateral removal → +++ ↓ in social behaviour.
(ii) Prefrontal leucotomy in man: → Frontal Lobe Syndrome, which is characterized by:
(a) Flight of ideas.
(b) Euphoria Failure to realise others emotions.
(c) Recent memory impaired with loss of moral and social sense.
(d) Attention and power of concentration lost and restlessness develops.
n
(e) Lack of initiative →↓ mental drive.
i
(f) Emotional instability.
6. Clinical Significance
a
Temporal Lobe
Functions
J
1. Concerned with hearing.
.
2. Provide sense of equilibrium.
3. Concerned with speech (language) and memory.
K
Applied Aspect
1. Unilateral removal → no deafness but results in tinitus and auditory hallucinations.
.
2. Bilateral removal (in monkeys) → Kluver-Bucy syndrome.
Features: (mainly due to destruction of limbic system specially amygdala nucleus).
(i) Animals are obedient, hyperphagic and males are hypersexual.
A
(ii) Ominophagic with loss of pre-operative fear from snakes.
(iii) Visual agnosia.
(iv) +++ ↑ in oral activity due to:
(v) Hypermetamorphosis
The Limbic System

1. Definition
2. Components (Fig. 10.98)
(i) Limbic Lobe i.e. cingulate gyrus, isthmus, hippocampal gyrus and uncus (anterior end of
hippocampal gyrus in the temporal lobe).
(ii) Subcortical nuclei include:
(a) Amygdala (group of nuclei on the tip of temporal lobe)
(b) Septal nuclei (group of nuclei on the tip of cingulate gyrus)
(c) Hypothalamus; and
(d) Anterior thalamic nuclei.
74
Cingular gyrus
Frontal lobe
Retrosplenic cortex
Subcallosal gyrus
Piriform cortex Entorhinal cortex
Parahippocampal gyrus
Uncus (anterior end of
n
hippocampal gyrus) Temporal lobe
i
Neocortex (neopallium)
a
Allocortex (archipallium) and juxtallocortex (mesopallium)
Fig. 10.98 The medial surface of right cerebral hemisphere showing: The limbic lobe
. J
Note: The limbic cortex is made up allocortex.
3. Connections
K
(i) Fornix,
(ii) Papez circuit,
.
4. Functions
(i) Controls autonomic function.
(ii) Role in the emotions of rage (violent anger) and fear; and the motivation.
A
(iii) Concerned with behavioural aspect of hunger and sex.
(iv) Concerned with olfaction and memory.
5. Unique features
(i) Emotions cannot be turned on and off at will.
(ii) Shows prolonged after discharge following stimulation.
A. Emotion
Definition
Two major components: mental and physical.
Mental component: It consists of cognitive, affective and conative changes.
For example: I hear a noise, which I recognize as that of an exploding bomb (cognition); I feel frightened
(affect), and I want to take shelter (conation).
The physical change: generalised and involve the autonomic and somatic nervous systems. For
example:
Fear and Rage: Related natural protective responses to threat in the environment.
1. Fear reaction
2. Rage reaction
Genesis and Expression of Emotion: by Papez circuit.
The normal emotional state is determined by afferent impulses that adjust the balance between the
hypothalamus and limbic system, one promoting placidity (tameness) and the other rage (violent
anger).
1. Role of Limbic System: Emotional informations including information gathered from memory and
understanding, is passed to the hypothalamus.
2. Role of Hyptothalamus: Integrates the endocrine, autonomic and motor activities that form appropriate
emotional behaviour.
3. Role of Cerebral Cortex:
(i) processing the conscious experience of emotional feeling;
(ii) provides neural mechs. that direct the motor responses;
(iii) modulation, direction, understanding, and inhibition of emotional behaviour.
Thus the limbic system participates in:
The elaboration and integration of the activity whereby emotion is expressed; and
B. Motivation
1. “that which moves the will” and is responsible for goal directed quality of behaviour.
n
2. Concept of reward (approach system) and punishment (avoidance system)
i
(i) Rewards. They make the behaviour that leads to them occur more often.
(ii) Punishments leads to behaviours in which an individual tries to escape from a painful or life-
threatening situation.
a
3. Mechanism
(i) Reward system areas in the brain are located in the:
J
(a) medial forebrain bundle (mainly) in lat. hypothalamus
(b) midbrain
.
(c) prefrontal cortex
(d) nucleus accumbens at base of neo-striaturm. (Fig. 10.99)
(e) brain stem
(Stimulation of these areas → pleasurable sensations)
. K
Medial
prefrontal cortex
A
Nucleus Ventral
accumbens Tegmental
area
Amygdala
Hippocampus
dopaminergic projection
glutaminergic projection
Fig. 10.99 Major excitatory projections to nucleus accumbens
which is the key brain area involved in addiction.
(ii) Brain areas:

(a) posterior hypothalamus
(b) dorsal midbrain
(c) entorhinal cortex in hippocampus (Stimulation of these sites → sensation of fear to terror)
Important Notes:
1. Reward system a. NT involved-dopamine (mainly and NE).
2. Habit-forming substances act by increasing dopaminergic activity via D3-receptors in the reward system of
the brain. Antipsychotic agents ↓ the activity of dopamine by blocking D3–dopaminergic receptors.
Higher Functions of the Nervous System

(Language/Speech; Learning; Memory and Judgement)
Include the major functions of its four lobes
1. Control of higher intellectual activities.
2. Control of sensory (general and special) motor and autonomic functions.
3. Control of language (speech), learning and memory.
76
Language (Speech)
Defintion: To understand the spoken and printed words and express ideas in speech and writing.
Categorical versus representational hemisphere
Categorical Hemisphere Representational Hemisphere

1. Specialized for higher functions of the 1. Specialized in the area of spatio-temporal relations
nervous system. such as with the recognition of faces, identification
of objects by their form.
2. Its disorder produces: 2. Its disorder or lesion produces:
(i) Language disorders. (i) Astereognosis.
(ii) Patients are disturbed about their (ii) Patients are unconcerned of their disability,
n
disability and often depressed. cheerful and have trouble recognizing emotions
i
of other individuals.
(iii) Agnosia.
Note: Hemispheric specialization is related to handedness, (genetically determined). In right handed individuals,
a
90% of population, the left hemisphere is the dominant or categorical hemisphere). In 30% left handed individuals,
it is right cerebral hemisphere dominant.
. J
Types of Speech: Spoken and Written
1. Spoken speech: understanding the spoken words and expressing ideas in speech.
Motor area
K
Central sulcus
Motor speech centres
Supra-marginal
.
Exner's area
gyrus
Sensory speech
(motor writing Dejerine’s area
centre)
centres
(area 39)
Broca's area
Wernicke's area
A
(area 44)
(area 22)
Arcuate fasciculus
Fig. 10.100 Sensory and motor speech centers
Mechanism (Fig. 10.100)

(i) To hear sounds. An intact auditory pathway.
(ii) To understand spoken words: auditory-psychic areas (area 20, 21).
(iii) To express the ideas in speech: auditory speech center, (Wernicke’s area, area 22).
Wernicke’s area lies in the superior temporal gyrus in the dominant hemisphere; interpretation and
understanding of auditory and visual informations.
2. Written speech: means understanding written words and expressing the ideas in writing.
Mechanism
(i) To see the words: An intact visual pathway from the eyes to the primary visual cortex, area 17.
(ii) To correctly interpret written words: visuo-psychic areas (area 18, 19).
(iii) To express the ideas in writing: visual speech center, (Dejerine Area, area 39).
Dejerine area lies behind the Wernicke’s area. Printed words converted into the auditory forms of
the words in the Wernicke’s area (internal speech).
Note: Wernicke’s and Dejerine areas are together called the sensory speech centers.
Mechanism of Expression of Speech (Fig. 10.101)

Speech Pathways: Requires motor speech centers for both spoken and written speech: Broca’s and Exner’s
areas.
1. Broca’s Area (Area 44): Lies in the inferior frontal gyrus, in the dominant hemisphere; processes
the information received from Wernicke’s area into a detailed and coordinated pattern for
vocalization.
2. Exner’s Area: Motor Writing Center: Located in the middle frontal gyrus in the dominant hemisphere.
It processes the informations from Broca’s area into detailed and coordinated pattern, to produce
written speech.
(i) Pathways for Expression of Spoken Speech: Spoken Speech → Primary auditory area (area 41) →
Wernicke’s area (area 22) → Broca’s area (area 44) → Motor cortex → Appropriate movements
n
of lips, tongue and larynx to produce speech.
i
(ii) Pathways for expression of both spoken and written speech: Printed words → Primary visual
area (area 17) → Visual association area (area 18) → Dejerine area (area 39) → Wernicke’s area
(area 22) → Broca’s area (area 44) → Exner’s area → Motor cortex → Appropriate movements
a
of muscles for vocalization and writing.
(4) Motor cortex (6) Exner's area (7) Motor cortex
J
Exner's area Central sulcus Central sulcus
.
Dejerine’s area (3) Dejerine's area
(area 39) (area 39)
(3) B
roca's area (5) Broca's
K
(area 44) area (2) Visual association
(area 44) area (area 18)
.
(1) Primary visual
area (area 17)
(1) P
rimary auditory
area (area 41) (2) Wernicke's area (4) Wernicke’s area
(area 22)
A
(A) (B)
Fig. 10.101 Pathways involved in expression of spoken speech (1 to 4) (A); and written speech (1 to 7) (B)
Speech Disorders
1. Aphasias:
2. Dysarthria
Types:
A. Sensory (or fluent) aphasia
esion in Wernicke’s area → talk excessively
Cause: L
Types:
(i) Pure word blindness: heroglyphics
(ii) conductive aphasia–person cannot speak.
B. Motor (or non-fluent) aphasia
Cause: Lesion of Broca’s area → uses automatic 2 or 3 words.
Features: inability to write (agraphia); patient is dumb.
C. Global aphasia: Sensory plus motor aphasia due to lesion in both Wernicke’s and Broca’s area. →
Loss of all the functions of speech.
Learning: Conditioned Reflexes

Definition
The ability to alter (change) behaviour on the basis of experience is called learning.
Conditioned reflexes. Two classes: inborn and acquired.
78
A. T
he inborn or unconditioned reflex: Superficial, deep (or tendon) and organic reflex (e.g. deglutition,
defecation, sucking, grasping and micturition reflex).
B. The Acquired or conditioned Reflex
Features
1. A reflex response to a stimulus that can be developed (acquired).
2. Peculiar to the individual.
3. Depends for its appearance on the formation of new functional connections in the CNS.
4. Example: Pavlov’s classical dog experiment. (Fig. 10.102)
Before conditioning
i n
Response
a
Unconditioned Salivation
stimulus Unconditioned
(inborn)
J
response
Before conditioning
.
Response
K
Neutral No salivation
.
stimulus No conditioned
response
A
Before conditioning
Response
Salivation
Unconditioned
response
After conditioning
Response
Conditioned Salivation
stimulus Conditioned
response
Fig. 10.102 Pavlov’s classical dog experiment
5. Mech. of development: on inborn reflexes by means of synaptic plasticity.

6. Factors which influence conditioned reflex to develop are:
(i) alertness and good health.
(ii) CS must begin to operate before the US is applied and must be allowed to overlap it.
(iii) interval between the CS and US should not > 90 sec; if more, the response is called delayed
conditioned reflex.
(iv) Necessity for reinforcement

(a) Extinction (disappearance) or internal inhibition.
(b) External inhibition.
Notes:
1. Pleasant or positive reinforcement
2. Unpleasant or negative reinforcement.
(v) Operant (environment) conditioning. conditioned avoidance reflex. This is based on phenomenon
of sensitization and habituation.
(vi) Discriminate conditioning.
7. Biochemical basis of conditioned reflex: Involve synaptic plasticity.
n
8. Physiological Basis of Conditioned Relflexes:
i
(i) Formation of a new functional connection in the nervous system Eg., in Pavlov’s classical
experiments.
(ii) Site of formation of functional connections:
a
(a) intracortical level (mainly).
(b) Subcortical level.
J
9. Clinical Significance
(i) Detecting crimes.
.
(ii) Somatic, visceral and other neural changes can be made to occur as conditioned reflex
responses.
(iii) Cortical plasticity
(iv) Split brain animals:
. K
Memory
1. Definition
2. Types:
A
(i) Declarative or Explicit memory
(ii) Non-declarative or Implicit or reflexive (or unconscious) memory:
3. Types of Declarative memory
(i) Recent or short-term memory
(ii) Remote or long-term memory
Note: Retrograde amnesia, which persists from few hours to even years, but remote memory is not affected.
4. Physiology of memory
(i) Encoding or consolidation of memory
(ii) Encoding process involves the hippocampus and entorhinal, perirhinal and parahippocampal
areas. These connections contain cell bodies and fibers of the cholinergic system.
(iii) Memory stored as a biochemical change in the neurons of the temporal lobe. Mechanism:
5. Drugs that facilitate memory
(i) Caffeine.
(ii) Physostigmine.
(iii) Amphetamine.
(iv) Nicotine.
Alzheimer’s Disease
It is characterised by progressive loss of memory and cognitive function in middle-aged individuals.
Initial Changes
1. Memory failure for recent events.
2. Lack of spontaneous activity and initiative with loss of intellecual functions.
80
3. Extrapyramidal and akinetic hypertonic symptoms.

4. Loss of spatial orientation.
Later Changes (after 2 or 3 years)

1. Dementia (memory loss)
2. Aphasia.
3. Apraxia
4. Agnosia
Note: Similar feature in the old age (> 65 years) are called senile dementia.
n
Cause: Degeneration of cholinergic nerve terminals in the cerebral cortex and hippocampus specially in
i
the nuclei of septal region of the forebrain that forms a major source of cholinergic innervation of the
cerebral cortex. (Fig. 10.103)
a
The sequence of events in the affected neurons
Mutation of amyloid precursor protein gene
J
↓
Parietal cortex
Aggregation of β-amyloid peptides
.
Frontal cortex ↓
Formation of extracellular plaques
(Senile plaques: toxic polypeptide)
↓
Inflammatory reaction with oxidative damage
K
↓
Altered nerve fibers and reactive
.
Hippocampus glial cells (Gliosis)
Septal nuclei ↓
Formation of intracellular neurofibrillary tangles
↓
Degeneration of cholinergic neurons in the cerebral
A
cortex and hippocampus
↓
Alzheimer’s disease
(A)
(B)
Fig. 10.103 The major cholinergic pathways involved (A) and pathogenesis (B) in Alzheimer’s disease

Unit 10 The Nervous System

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Unit 10 The Nervous System

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Unit

The Nervous System

Pons Medulla Cerebellum

Olfactory bulb Septum

Thalamus Globus pallidus

Ventral Spinal cord Dorsal

Fig. 10.1 Organization of the nervous system

Types (Fig. 10.2)

Structure (Fig. 10.3)

Fig. 10.3 Structure of a synapse

Functional classification of synapses

4. Synaptic delay: 0.5 msec. 4. absent

Electrical events at synapses

Fig. 10.4 Ionic basis of EPSPs (Excitatory transmitter (E) increases

Fig. 10.5 Ionic basis of IPSPs ((Inhibitory transmitter (I) increases

Genesis (how action potential is produced in postsynaptic neuron?)

Inhibition at Synapses: Presynaptic and Postsynaptic inhibition

(c) Examples: Inhibition of stretch reflexes

Fig. 10.8 Pathway responsible for the stretch reflex ( ) and

(ii) Indirect inhibition

Renshaw cell A-ch Ventral horn

Fig. 10.9 Renshaw cell inhibition or negative feedback inhibition

Fig. 10.10 ‘Convergence’ of neural input from many neurons onto

EPSPs spread from several

Postsynaptic neuron fires 15 EPSP EPSP

Fig. 10.12 Temporal summation

Axo-axonal ending mediating

(i) Post-tetanic potentiation Postsynaptic

Fig. 10.14 Synaptic plasticity: Presynaptic and postsynaptic sites

Fig. 10.15 Cutaneous receptors: sensory receptors in the skin

2. Thermoreceptors or temperature receptors: (cold and warm). (Fig. 10.16)

3. Pain receptors (Nociceptors): Two types

Electrical and Ionic Events in Receptors (Fig. 10.17)

3. Weber Fechner Law

Tonic receptors Phasic receptors

The Reflex Arc (Fig. 10.19)

Muscle glutamic acid)

Fig. 10.19 Pathway for stretch reflex

Classification of Reflexes: Mono and polysynaptic reflexes

Monosynaptic Reflexes: Stretch Reflexes

Fig. 10.20 Muscle spindle and its neural connections

Facilitatory areas Inhibitory areas

Motor cortex Basal ganglia

Other factors which increase the γ-efferent discharge

(i) ↓ in resting muscle tone. (i) ↑ resting muscle tone.

Inhibition of Stretch Reflexes

Efferent (motor) neuron

Fig. 10.26 Polysynaptic reflex pathway showing connections

4. Significance: protective reflex

General Properties of Reflexes

1. Stretch reflex, tone and posture

3. Central excitatory and inhibitory states

The Sensory System

Afferent nerve fiber

Fig. 10.28 Sensory unit and receptive field

Fig. 10.29 Location of somatosensory cortex

Fig. 10.30 Afferent pathways showing lateral inhibition.

Dorsal (posterior) spinocerebellar

Lateral spinothalamic tract Ventral (anterior)

B. Tracts in Lateral White Column

C. Tracts in Ventral (anterior) white column

Important points: Synthetic sensation

Ventroposterior nucleus Internal capsule

Internal capsule Internal capsule

(c) Examples: Inhibition of stretch reflexes

1. Stretch reflex, tone and posture

C. Tracts in Ventral (anterior) white column

(b) Supraspinal inhibition: (Fig. 10.41)

B. I ncomplete or Irregular Transection of the Spinal Cord

B. Mode of action of the Semicircular Canals

C. Role of vestibular apparatus in regulation of posture

Execute movements C. Lowest level