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CNS Lecture Note

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2 views359 pages

CNS Lecture Note

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joyceonore620
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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CNS PHYSIOLOGY

INTRODUCTION: BASIC CONCEPTS


 Body’s NS is organised into CNS & PNS
 Sensory elements of the PNS detect changes in the
Internal & external environ.
 They then Send info to the CNS
 The CNS receives, process & respond to the info
 May generate an output that is sent to effectors
through motor elements of the PNS
 Neurons and neuroglia are the principal types of
cells found in the nervous sys.

 Neurons are commonly called nerve cells

 Neuroglia provide structural and metabolic


support for the neurons
 Nerve
impulse is a wave of depolarisation
immediately followed by repolarisation.

 This is collectively called an ACTION POTENTIAL.

 Changesin ion conductance across the nerve


membranes are responsible for the initiation and
propagation of Action Potential.
 Functionalconnection btw a neuron and its
effector cell is called synapse.

 Neurons communicate with each other via


synaptic transmission.

 Neurotransmitters can be grouped according


to their molecular weight
INTRODUCTION: FUNCTIONS OF THE
NERVOUS SYSTEM
 The primary fxn of the NS is to maintain
homeostasis through the control of the other body
system
 E.g. during exercise, the NS coordinate the
activities of
Muscular system
Heart
Respiratory system
ORGANISATION OF THE NERVOUS
SYSTEM
Functional composition of the PNS.
Comparison of Somatic &
Autonomic Nervous System
 The nervous system dev from ectoderm, an
embryonic tissue that forms a neural plate
 The neural plate differentiates into a neural
crest and a neural tube
 The neural tube differentiates into CNS, i.e.
the brain and spinal cord
 The neural crest gives rise to most of the
PNS with 12 pairs of cranial nerves & 31
pairs of spinal nerves
THE CENTRAL NERVOUS SYSTEM
 Thebrain dev at the cranial end of
the embryonic neural tube

 Bythe end of the first month, three


primary vesicles are formed:
Forebrain – prosencephalon
Midbrain – mesencephalon
Hindbrain - rhombencephalon
Five secondary vesicles are formed:
 Forebrain gives raise to
1.Telencephalon (Cerebral hemisphere)
2.Diencephalon (Thalamus & hypothalamus)
 Midbrain remains
3.Mesencephalon (Midbrain)
 Hindbrain
4.Metencephalon (Pons & cerebellum)
5.Myelencephalon (Medulla oblongata)
Cerebral cortex (Neocortex)

 This is the grey matter that forms the


outermost layer of the cerebral hemisphere
 It is functionally divided into:
Primary somatic motor cortex
Premotor cortex
Somatosensory cortex
Visual cortex
Auditory cortex
Other areas of neocortex

 Wernicke’s area and Broca’s area


 Frontal cortex
 Limbic cortex
REFLEX ARC

 Reflex activity is the response to a peripheral


nervous stimulation that occurs without our
consciousness.
 It is a type of protective mechanism
 Reflex arc is the anatomical nervous pathway
for a reflex action
A simple reflex arc includes five
components
Bell–Magendie law

• The spinal nerves’ anterior


roots consist of motor
fibres while the posterior
roots contain sensory
fibres.

• The movt. of the impulses


is only in one direction
CLASSIFICATION OF REFLEXES

 1. Depending upon whether inborn or acquired


 2. Depending upon situation – anatomical classification
 3. Depending upon purpose – physiological
 classification
 4. Depending upon number of synapse
 5. Depending upon whether visceral or somatic
 6. Depending upon clinical basis
1. Depending upon whether inborn or acquired
i. Inborn Reflexes or Unconditioned Reflexes
ii. Acquired Reflexes or Conditioned Reflexes
2. Depending upon situation – anatomical
classification
i. Cerebellar Reflexes
ii. Cortical Reflexes
iii. Midbrain Reflexes
iv. Bulbar or Medullary Reflexes
v. Spinal Reflexes
3. Depending upon purpose – physiological
classification
i. Protective Reflexes or Flexor Reflexes
ii. Antigravity Reflexes or Extensor Reflexes
4. Depending upon number of synapse
i. Monosynaptic Reflexes e.g. stretch reflex
ii. Polysynaptic Reflexes e.g. flexor reflex
5. Depending upon whether visceral or somatic
i. Somatic Reflexes
ii. Visceral or Autonomic Reflexes
6. Depending upon clinical basis
i. Superficial reflexes
ii. Deep reflexes
iii. Visceral reflexes
iv. Pathological reflexes eg
1. Babinski sign
2. Clonus
3. Pendular movements
(Neuregulin)
NEUROGLIA

 Thisis the supporting cell of the nervous system.


 Neuroglial cells are non-excitable and do not
transmit nerve impulse
 They are called non-neural cells or glial cells
 They are 10 to 15 times more than neural cells
 They constitute the site for most tumours of nervous
system
CLASSIFICATION OF NEUROGLIAL CELLS
 They are classified into:
A. Central neuroglial cells
1. Astrocytes
2. Microglia
3. Oligodendrocytes
B. Peripheral neuroglial cells
1. Schwann cells
2. Satellite cells
A1: Astrocytes

Astrocytes are star-shaped neuroglial


cells present in all the parts of the
brain
There are two types of astrocytes:
 i. Fibrous astrocytes
 ii. Protoplasmic astrocytes.
Functions of Astrocytes
i. Forms the supporting network in brain and spinal
cord
ii. Form the blood-brain barrier
iii. Maintain the chemical environment of ECF
around CNS neurons
iv. Regulate recycling of neurotransmitter during
synaptic transmission
A2: Microglia

 These are phagocytic cells that migrate to the site


of infection or injury and are often called the
macrophages of CNS.
 Functions of Microglia
Engulf and destroy the microorganisms and cellular
debris by means of phagocytosis
Migrate to the injured or infected area of CNS and act
as miniature macrophages.
A3: Oligodendrocytes

 Theyare the cells that produce myelin


sheath around the nerve fibers in CNS

 Functions of Oligodendrocytes
Provide myelination around the nerve fibers
in CNS where Schwann cells are absent
Provide support to the CNS neurons
B1: Schwann Cells

 They are the major glial cells in PNS


 Functions of Schwann Cells
Provide myelination around the nerve fibers in PNS
Play important role in nerve regeneration
Remove cellular debris during regeneration by
phagocytosis.
B2: Satellite Cells

 They are the glial cells present on the exterior


surface of PNS neurons.
 Functions of Satellite Cells
Provide physical support to the PNS neurons
Helpin regulation of chemical environment of ECF
around the PNS neurons.
MENINGES
 The brain and spinal cord are covered by sheaths
called meninges, which are membranous in
nature.
 Meninges are made up of:
Dura mater
Arachnoid mater
Pia mater
 Meningesare responsible for protection and
nourishment of the nervous tissues.
CEREBROSPINAL FLUID
 Cerebrospinal fluid (CSF) is the clear, colorless fluid
that circulates through ventricles of brain,
subarachnoid space and central canal of spinal
cord.
 It is a part of extracellular fluid (ECF)
 Volume is about 150mL, specific gravity is 1.005,
alkaline in nature.
 Site of Formation: choroid plexuses, situated within
the ventricles.
 Injection of isotonic or hypotonic saline leads to
increase secretion.
 Injection of hypertonic saline leads to decrease
secretion.
 Functions Of Cerebrospinal Fluid:
1. Protective Function
2. Regulation of Cranial Content Volume
3. Medium of Exchange
Absorption Of Cerebrospinal Fluid

 Itis mostly absorbed by the arachnoid villi into


dural sinuses and spinal veins.
 Small amount is absorbed along the perineural
spaces into cervical lymphatics and into the
perivascular spaces.
 The mechanism of absorption is by filtration
BLOOD-BRAIN BARRIER
 This is a neuroprotective structure that prevents the
entry of many substances and pathogens into the
brain tissues from blood.
 It exists in the capillary membrane of all parts of the
brain, except in some areas of hypothalamus.
 There is absence of fenestra in the capillary beds
 Astocytes form foot processes enveloping the
vasculature almost completely.
Functions Of Blood-brain Barrier

 BBB acts as both a mechanical barrier and


transport mechanisms
 Substances which can Pass through Blood-Brain
Barrier include:
 1. Oxygen 2. Carbon dioxide 3. Water 4. Glucose
5. Amino acids 6. Electrolytes 7. Some drugs 8. Lipid-
soluble anesthetic gases 9. Other lipid-soluble
subs.
Substances which cannot Pass
through Blood-Brain Barrier

 1. Injurious chemical agents


 2. Pathogens such as bacteria
 3. Drugs such as Penicillin, the catecholamines
and dopamine also cannot pass through BBB.
 4. Bile pigments
NEUROTRANSMITTERS

 Itis a chemical substance that acts


as a mediator for the of nerve impulse
from one neuron to another neuron
through a synapse

 Discoveredby an Austrian scientist


named Otto Loewi in 1921
Criteria For Neurotransmitter

1. It must be found in a neuron


2. It must be produced by a neuron
3. It must be released by a neuron
4. After release, it must act on a target area and
produce some biological effect
5. After the action, it must be inactivated
Classification Of Neurotransmitters

 Based on Chemical Nature


1. AminoAcids e.g. GABA, glycerine, glutamate,
aspartate
2. Aminese.g. Noradrenaline, adrenaline, dopamine,
serotonin, histamine
3. Others:They don’t fit into the above e.g. acetylcholine,
nitric oxide
 Based on Function
1. Excitatory neurotransmitters e.g. acetylecholine and
noradrenaline. Causes Na ion influx excitatory
postsynaptic potential (EPSP)
2. Inhibitory neurotransmitters e.g gammaaminobutyric
acid (GABA) and dopamine. Causes efflux of K ion
inhibitory postsynaptic potential (IPSP).
Inactivation Of Neurotransmitter
1. It can move out of synaptic cleft to the
area where it has no action
2. It is destroyed or disintegrated by
specific enzymes
3. It is engulfed and removed by astrocytes
(macrophages)
4. It is removed by means of reuptake into
the axon terminal.
NEUROMODULATORS

 Theseare chemical messenger, which modifies


and regulates activities that take place during the
synaptic transmission. E.g.
 Enkephalins
 Dynorphins
 Endorphins
NERVE REGENERATION AND
DEGENERATION

 Degenerative changes are what occurs when a


nerve fiber is injured.
 Causes for Injury include:
1. Obstruction of blood flow
2. Local injection of toxic substances
3. Crushing of nerve fiber
4. Transection of nerve fiber.
 Degenerative changes are classified into
three types:

1. Wallerian degeneration
2. Retrograde degeneration
3. Transneuronal degeneration
1. Wallerian Degeneration Or
Orthograde Degeneration

 Thepathological change that occurs in the


distal cut end of nerve fiber.

 Starts within 24 hours of injury.

 Change occurs throughout the length of distal


part of nerve fiber simultaneously.
i. Axis cylinder swells and breaks up into
pieces.
ii. Myelin sheath disintegrated into fat
droplets. This occur from 8th to 35th day
iii. Neurilemmal sheath is unaffected, but
the Schwann cells multiply rapidly
iv. Macrophages comes and remove the
debris of axis cylinder and fat droplets of
disintegrated myelin sheath
2. Retrograde Degeneration
 Itis the pathological changes, which occur in the
nerve cell body and axon proximal to the cut end.
 In the cell body:
Nissl granules disintegrates
Cell body swells
Neurofibrils disappear as the nucleus is displaced to
the periphery
Nucleus may be extruded out of the cell
 In the axon: Similar to distal changes
3. Transneuronal Degeneration

 Cutting an afferent nerve fiber leads to


degenerative changes in the neuron with which
the afferent nerve fiber synapses.
 Examples:
i.
Chromatolysis in the cells of lateral geniculate
body occurs due to sectioning of optic nerve
REGENERATION OF NERVE FIBER

 This refers to regrowth of lost or destroyed part of a


tissue.
 The injured and degenerated nerve fiber can
regenerate.
 It starts as early as 4th day after injury, but
becomes more effective only after 30 days
 It is completed in about 80 days.
Criteria For Regeneration

1. Gap between the cut ends of the nerve should not


exceed 3 mm
2. Neurilemma should be present; as neurilemma is
absent in CNS, the regeneration of nerve does not
occur in CNS
3. Nucleus must be intact
4. Two cut ends should remain in the same line.
Stages Of Regeneration
1. Regenerative sprouts fibrils grow from the
proximal cut end of the nerve.
2. Fibrils move towards the distal cut end of the
nerve fiber
3. Some of the fibrils enter the neurilemmal tube of
distal end and form axis cylinder
4. Schwann cells line up in the neurilemmal tube to
guide the fibrils into the tube.
5. Schwann cells also synthesize nerve
growth factors, which attract the fibrils form
proximal segment.
6. Myelin sheath is formed by Schwann cells
slowly. Myelination is completed in 1 year.
7. In the cell body, first the Nissl granules
appear followed by Golgi apparatus
8. Cell looses the excess fluid; nucleus
occupies the central portion
9. Functional recovery occurs after a long
period.
SENSORY SYSTEM RECEPTORS
 Sensory info from the body reaches the NS
through a series of sensory pathways associated
with specific sensory modalities.
 These pathways consist of sensory receptors and
their projections to designated receiving areas in
the cortex.
 A unified perception of our physical world
emerges from the coordinated response of these
10 receiving areas and 20 association areas
Types of Receptors

 The five types of receptors are


1. Mechanoreceptors
2. photoreceptors,
3. chemoreceptors,
4. thermoreceptors, and
5. nociceptors.
PROPERTIES OF SENSORY RECEPTORS
 There are separate pathways for the special
senses of vision, hearing, taste, and olfaction
and for the vestibular sense of equilibrium

 The other senses comprise the somatosensory


system, whose receptors are found throughout
the body and provide four general sensations:
Types Of Somatic Sensations

 1. Epicritic sensations

 2. Protopathic sensations

 3. Deep sensations

 4. Synthetic Sensations
1. Epicritic Sensations

i. Fine touch or tactile sensation


ii. Tactile localization
iii. Tactile discrimination
iv. Temperature sensation with finer
range between 25°C and 40°C.
2. Protopathic sensations

i. Pressure sensation
ii. Pain sensation
iii. Temperature sensation with a wider
range, i.e. above 40°C and below
25°C.
3. Deep Sensations
i. Sensation of vibration or pallesthesia, which is the
combination of touch and pressure sensation
ii. Kinesthetic sensation or kinesthesia: Sensation of
position movement of the body
iii. Visceral sensations arising from viscera
4. Synthetic Senses

 Two or more basic sensations are


integrated at the cortical level
 Examples:
Vibration sense
Stereognosis
Two-point discrimination
THERMORECEPTORS
 Changes in ambient temperature are monitored
by separate cold and warm thermoreceptors in
the skin.
 Each receptor has a receptive field size of
approximately 1 mm in diameter with little
overlap between adjacent receptive fields
 They are both sensitive to abrupt change in
temp
 They are limited in their response range
 Heat receptors are active at temperatures of
25 to 45C
 Cold receptors respond preferentially to
temperatures of 18 to 25C and cease firing
entirely below 10C
 Other thermoreceptors are found in the
hypothalamus and spinal cord to monitor
internal temperatures.
 A stable core temperature close to 37C is
particularly important for maintaining normal
brain function.
 Temperatures above 40.5C cause serious
dysfunction
 Brain temperatures below 30C depress all
neuronal activity, including that necessary for
maintaining minimal respiratory rate
PHYSIOLOGY OF PAIN

 Pain is defined as an unpleasant and emotional


experience associated with or without actual
tissue damage.
 Pain sensation is described in many ways like
sharp, pricking, electrical, dull ache, shooting,
cutting, stabbing, etc.
 Often it induces crying and fainting.
Pain may be acute or chronic.
Acute pain is a sharp pain of short duration
with easily identified cause
Chronic pain is the intermittent or
constant pain with different intensities.
It lasts for longer periods.
It is difficult to treat and it needs professional
expert care.
BENEFITS OF PAIN SENSATION

1. Pain gives warning signal about a problem or


threat.
2. Pain prevents further damage by causing reflex
withdrawal from the source of injury.
3. Pain forces the person to minimize activities thus
enabling rapid healing of injured part.
4. Pain makes one take required treatment to
prevent major damage.
TYPES OF PAIN

Painhas been classified into two


major types:
fastpain and
slow pain.
Fast Pain
 Fast pain is felt within about 0.1 second after a
pain stimulus is applied
 It is also described as sharp pain, pricking pain,
acute pain, and electric pain.
 This type of pain is felt when a needle is stuck into
the skin, when the skin is cut with a knife, or when
the skin is acutely burned.
 Fast-sharp pain is not felt in most deeper tissues of
the body.
Slow Pain
 Slow pain begins only after 1 second or more and
then increases slowly over many seconds and or
even minutes.
 Also referred to as slow burning pain, aching pain,
throbbing pain, nauseous pain, and chronic pain.
 This type of pain is usually associated with tissue
destruction.
 It can occur both in the skin and in almost any
deep tissue or organ.
Pain Receptors
The pain receptors in the skin and other
tissues are all free nerve endings.
They are widespread in the superficial layers
of the skin as well as in certain internal
tissues, such as the periosteum, the arterial
walls, the joint surfaces, and the falx and
tentorium in the cranial vault
Pain Stimulation
Pain can be elicited by multiple types of
stimuli
Mechanical
Thermal, and
Chemical stimuli
Ingeneral, fast pain is elicited by mechanical
and thermal types of stimuli, whereas slow
pain can be elicited by all three types
Pain Substances
 Chemicals that excite the chemical type of pain are:
 Bradykinin
 Serotonin
 Histamine
 Potassium ions
 Acids
 Acetylcholine
 Proteolytic enzymes
 In
addition, prostaglandins & substance P enhance the
sensitivity of pain endings but don’t directly excite them.
PATHWAYS OF PAIN SENSATION

1. Pathway from skin and deeper


structures
2. Pathway from face
3. Pathway from viscera
4. Pathway from pelvic region.
1. FROM SKIN AND DEEPER STRUCTURES
 Receptors:
Receptors of pain sensation are the free nerve endings.
 First Order Neurons:
Cells in posterior nerve root ganglia
Fast pain is carried by Aδ type afferent fibers which
synapse with neurons of marginal nucleus in the
posterior gray horn
Slow pain is carried by C type afferents, which synapse
with neurons of substantia gelatinosa of Rolando in the
posterior gray horn
Second Order Neurons
Neurons of marginal nucleus and substantia
gelatinosa of Rolando.
Fibers from these neurons ascend in the form of
the lateral spinothalamic tract.
Fibers of fast pain arise from neurons of
marginal nucleus crossing the midline via the
anterior grey commissure to the lateral white
column of the opposite side and ascends.
Fibers of slow pain, cross the midline and run
along the fibers of fast pain as
paleospinothalamic fibers.
One fifth of these fibers terminate in ventral
posterolateral nucleus of thalamus.
Remaining fibers terminate in any of the
following areas:
i. Nuclei of reticular formation in brainstem
ii. Tectum of midbrain
iii. Gray matter surrounding aqueduct of Sylvius
Third Order Neurons
these are the neurons in:
i. Thalamic nucleus
ii. Reticular formation
iii. Tectum
iv. Gray matter around aqueduct of Sylvius.
Axons from these neurons reach the sensory
area of cerebral cortex. Some fibers from
reticular formation reach hypothalamus.
VISCERAL PAIN

 Painfrom viscera is unpleasant. It is poorly


localized

 Causes of include:
Ischemia
Chemical Stimuli
Spasm and Overdistention of hollow organs
REFERRED PAIN

Referred pain is the pain that is perceived at a


site adjacent to or away from the site of
origin.
Deep pain and some visceral pain are
referred to other areas.
But, superficial pain is not referred.
EXAMPLES OF REFERRED PAIN
1. Cardiac pain is felt at inner part of left arm and
left shoulder
2. Pain in ovary is referred to umbilicus
3. Pain from testis is felt in abdomen
4. Pain in diaphragm is referred to shoulder
5. Pain in gallbladder is referred to epigastric
region
6. Renal pain is referred to loin.
MOTOR UNIT
 Single motor neuron, its axon terminals and the
muscle fibers innervated by it are together
called motor unit.
 Each motor neuron activates a group of muscle
fibers through the axon terminals.
 Stimulation of a motor neuron causes
contraction of all the muscle fibers innervated
by that neuron.
Examples
 Laryngeal muscles: 2 to 3 muscle fibers per
motor unit
 Pharyngeal muscles: 2 to 6 muscle fibers per
motor unit
 Ocular muscles: 3 to 6 muscle fibers per motor
unit
 Back muscle: 120 to 165 muscle fibers per motor
unit
PROPRIOCEPTORS
These are receptors, which detect and
give response to movement and change
in position of different parts of the body.

These receptors are also called


kinesthetic receptors or joint position
sense
Different Proprioceptors

 1. Muscle spindle
 2. Golgi tendon organ
 3. Pacinian corpuscle
 4. Free nerve ending
 5. Proprioceptors in labyrinth.
MUSCLE SPINDLE
 Muscle spindle is a spindle-shaped
proprioceptor situated in the skeletal muscle.
 It is formed by modified skeletal muscle fibers
called intrafusal muscle fibers.
 Each muscle spindle is formed by 5 to 12
intrafusal muscle fibers
 The enclosing capsule is attached to either
side of extrafusal fibers or the tendon of the
muscle
NERVE SUPPLY TO MUSCLE SPINDLE

It is the only receptor


in the body, which has
both sensory and
motor nerve supply.
FUNCTIONS OF MUSCLE SPINDLE
Muscle spindle gives response to change in the length
of the muscle
 1. It forms the receptor organ for stretch reflex
 2.It plays an important role in maintaining muscle
tone.
GOLGI TENDON ORGAN
 Golgi tendon organ is situated in the tendon of
skeletal muscle near the attachment of
extrafusal
 It is placed in series between the muscle fibers
and the tendon.
 Golgi tendon organ is formed by a group of
nerve endings
MUSCLE TONE
 Muscle tone is defined as the state of continuous
and passive partial contraction of muscle with
certain vigor and tension.
 It
plays an important role in maintenance of
posture.

 Development of Muscle Tone


Regulation of Muscle Tone
Itis by some supraspinal centers in
different parts of brain.
Some of these centers increase the
muscle tone (facilitatory)
While other centers decrease the
muscle tone (inhibitory)
Supraspinal facilitatory centers
1. Motor area 4 in cerebral cortex
2. Cerebellum
3. Descending facilitatory reticular system
4. Red nucleus
5. Vestibular nucleus
Supraspinal inhibitory centers

1. Suppressor areas of cerebral cortex


2. Basal ganglia
3. Descending inhibitory reticular
system.
 Facilitatory Tracts
Vestibulospinal tract/VST
Medial reticulospinal tract/medial RST

 Inhibitory Tracts
Corticospinal tract/CST
Corticoreticular and dorsal reticulospinal tract
STRETCH REFLEX
 It
is the basic reflex involved in maintenance of
posture
 Serves to maintain the body in an upright position.
 They therefore more pronounced in extensor muscles
POSTURAL REFLEXES
 Postural reflexes are generally classified into two
groups:
A. Static reflexes
 I. General static reflexes or righting reflexes
 II. Local static reflexes or supporting reflexes
 III. Segmental static reflexes
 IV. Statotonic or attitudinal reflexes.
B. Statokinetic reflexes
I.General Static Reflexes or Righting Reflexes
 General static reflexes are otherwise called righting
reflexes because these reflexes help to maintain an
upright position of the body.
Righting reflexes are divided into five types:
1. Labyrinthine righting reflexes acting on the neck
muscles
2. Neck righting reflexes acting on the body
3. Body righting reflexes acting on the head
4. Body righting reflexes acting on the body
5. Optical righting reflexes.
II. Local Static Reflexes or Supporting
Reflexes
 Local
static reflexes or supporting reactions support the
body in different positions
They are classified into two types:
1. Positive supporting reflexes
2. Negative supporting reflexes.
III. Segmental Static Reflexes
Segmental static reflexes are very essential for walking.
➢ During walking, in one leg, the flexors are active and
the extensors are inhibited.
 It is known as crossed extensor reflex.
 Segmental static reflexes are demonstrated in spinal
animal. And, the centers for these reflexes are situated
in the spinal cord.
IV. Statotonic or Attitudinal Reflexes
 Statotonic
or attitudinal reflexes are developed
according to the attitude of the body and are of two
types:
1. Tonic labyrinthine and neck reflexes acting on the
limbs
2. Labyrinthine and neck reflexes acting on the eyes.
STATOKINETIC REFLEXES

 Statokinetic
reflexes are the postural reflexes that
maintain posture during movement.
 These reflexes are concerned with both angular
(rotatory) and linear (progressive) movements.
 The vestibular apparatus is responsible for these
reflexes.
Basal Ganglia
 Basalganglia are
the scattered
masses of gray
matter submerged in
subcortical
substance of
cerebral hemisphere
 Its a group of nuclei, act as a unified functional
unit.
 Its a subcortical nuclei of grey matter located
in the interior part of cerebrum / base of the
forebrain
 Connected with cerebral cortex, thalamus, and
other brain areas.
 Play a role in action selection, decision of
possible behaviors to execute at a given time
Basal ganglia include three primary
components:
 1. Corpus striatum
 2. Substantia nigra
 3. Subthalamic nucleus of Luys.
1. Corpus striatum

 Corpus striatum is incompletely divided


into two parts by internal capsule:
 i. Caudate nucleus
 ii. Lenticular nucleus.
Caudate Nucleus
 Caudate nucleus is an
elongated arched gray
mass, lying medial to
internal capsule
 It
is related to lateral
ventricle
 Thetail is long, arched &
ends in amygdaloid
nucleus
Lenticular Nucleus

 It is a wedgeshaped gray mass,


situated lateral to internal capsule.
 It is divided into 2:
a. Outer putamen
b. Inner globus pallidus.
2. SUBSTANTIA NIGRA

 It is situated below red nucleus.


 It is made up of large iron-containing pigmented
cells.

3. SUBTHALAMIC NUCLEUS OF LUYS

 Subthalamic nucleus is situated lateral to red


nucleus and dorsal to substantia nigra.
Basal ganglia Input

1. Parietal cortex (primary and secondary somatosensory


information, secondary visual information),
2. Temporal cortex (secondary visual and auditory
information),
3. Cingulate cortex (limbic and emotional status
information),
4. Frontal cortex (primary and secondary motor
information),
5. Prefrontal cortex.
FUNCTIONS OF BASAL GANGLIA
1. CONTROL OF MUSCLE TONE
 It decrease the muscle tone by inhibiting gamma motor
neurons through descending inhibitory reticular system in
brainstem
 Thus, lesion leads to increase muscle tone, leading to rigidity
2. CONTROL OF MOTOR ACTIVITY
i. Regulation of Voluntary Movements: These are initiated by
cerebral cortex but controlled by basal ganglia
ii. Regulation of Conscious Movements: I.e. Cognitive control.
Fibers in connection with cerebral cortex are concerned with
regulation of conscious movements
iii. Regulation of Subconscious Movements
3. CONTROL OF REFLEX MUSCULAR ACTIVITY
 Basalganglia are responsible for the coordination and
integration of impulses for particularly visual and
labyrinthine reflexes
4. CONTROL OF AUTOMATIC ASSOCIATED MOVEMENTS
 Egthe swing of the arms while walking, appropriate
facial expressions while talking or doing any work.
5. ROLE IN AROUSAL MECHANISM
 Globus pallidus and red nucleus are involved in arousal
mechanism because of their connections with reticular
formation.
6. ROLE OF NEUROTRANSMITTERS IN THE FUNCTIONS OF
BASAL GANGLIA
1. Dopamine - substantia nigra to corpus striatum
2. Gammaaminobutyric acid (GABA) - corpus striatum &
substantia nigra
3. Acetylcholine - cerebral cortex to caudate nucleus &
putamen
4. Substance P - globus pallidus reaching substantia nigra
5. Enkephalins - globus pallidus reaching substantia nigra
6. Noradrenaline - basal ganglia and reticular formation
7. Glutamic - subthalamic nucleus to globus pallidus &
substantia nigra.
Dopamine: Neuromodulatory neurotransmitter, excites areas of
the caudate/putamen with D1 receptors to promote the
direct pathway, inhibits areas of the caudate/putamen with
D2 receptors to inhibit the indirect pathway
Glutamate: Excitatory neurotransmitter
Subthalamic nucleus projects glutamate to stimulate the
ventrolateral thalamus. Ventrolateral thalamus projects
glutamate to stimulate the primary localized motor cortex
GABA: Inhibitory neurotransmitter:
Caudate/Striatum (direct) projects GABA to inhibit the Gpi GPi
projects GABA to inhibit the ventrolateral nucleus
Caudate/Striatum (indirect) projects GABA to inhibit the GPe
GPe projects GABA to inhibit the subthalamic nucleus
156

RED: Excitatory glutamatergic pathways,


BLUE: Inhibitory GABAergic pathways,
Magenta: Modulatory dopaminergic pathways
GPe: globus pallidus external; GPi: globus pallidus internal; STN: subthalamic nucleus; SNc: substantia
nigra compacta; SNr: substantia nigra reticulata
Disorders of movement in Basal 157

ganglia disease

1. Hyperkinetic: Excessive abnormal


movement i.e. chorea, athetosis, ballism

2. Hypokinetic: Slow movements i.e. akinesia,


bradykinesia .
HYPERKINESIA 158

Chorea: Rapid involuntary “ dancing” movements


Athetosis: Continuous , slow writhing movements .
Ballism (Hemiballismus): Involuntary flailing , intense and
violent movements
HYPOKINESIA 159

Akinesia: Difficulty in initiating movement


Braykinesia :Slowness of movement.
DISORDERS OF BASAL GANGLIA
1. PARKINSON DISEASE:
 It is a slowly progressive degenerative disease of
N S associated with destruction of brain cells,
which produce dopamine.
 Great boxer Mohammed Ali was affected by
parkinsonism because of repeated blows he
might have received on head
Causes
 Lackof dopamine caused by damage of basal ganglia
(especially substantia nigra has dopaminergic fibers).
 Damage of basal ganglia is usually due to the following
causes:
 i. Viral infection of brain like encephalitis
 ii. Cerebral arteriosclerosis
 iii. Injury to basal ganglia
 iv. Destruction of dopamine in basal ganglia. May occur due
to long-term treatment with antihypertensive drugs like
reserpine (drug-induced parkinsonism)
 v. Unknown causes (idiopathic parkinsonism).
Signs and Symptoms
i. Tremor
ii. Slowness of movements
iii. Poverty of movements
iv. Rigidity
v. Gait (Festinant Gait)
vi. Speech problems
vii. vii. Emotional changes
viii.viii. Dementia
 Chorea movement https://youtu.be/_WVYsSBadGY
 Athetosis https://youtu.be/J_wIDm1_ax4
 Ballism (Hemiballismus) https://youtu.be/V6cxZa6gy6g
Treatment
 It is treated by dopamine injection.
 Dopamine does not cross the blood-brain
barrier, so levodopa (L-dopa), which crosses the
blood-brain barrier is injected
 L-dopa is converted to dopamine in the brain &
liver
 Carbidopa is also given to prevent the
conversion of L-dopa to dopamine
 But carbidopa cannot the blood-brain barrier.
2. WILSON DISEASE: Due to damage of the lenticular nucleus
particularly, putamen
3. CHOREA: Due to the lesion in caudate nucleus and putamen.
4. ATHETOSIS: Due to lesion in caudate nucleus and putamen
5. CHOREOATHETOSIS: Due to combined effects of chorea and
athetosis.
6. HUNTINGTON CHOREA: Due to lesion in corpus striatum and
substantia nigra
7. HEMIBALLISMUS: Due to degeneration of subthalamic nucleus of
Luys.
8. KERNICTERUS: Due to severe jaundice & staining of the basal
ganglia.
CEREBELLUM
 The cerebellum sits astride the main sensory and
motor systems in the brainstem
 It is connected to the brainstem on each side by:
superior peduncle
middle peduncle, and
inferior peduncle.
 The cerebellum weighs only 10% as much as the
cerebral cortex, but its surface area is about 75%
of that of the cerebral cortex.
Divisions of the cerebellum

 The
vestibulocerebellum is dominated by vestibular input
and controls balance and eye movements.
 The
spinocerebellum is dominated by spinal cord input
and controls synergy of movement.
 The
pontocerebellum is dominated by cerebral input, via
pontine nuclei, and controls the planning and initiation of
movements
Thecerebellar cortex contains five types of
neurons:
Purkinje, granule, basket, stellate, and Golgi
cells
It has three layers:
an external molecular layer,
a Purkinje cell layer that is only one cell thick,
and an internal granular layer.
Purkinje cells

They are among the biggest neurons in the


body.
They have very extensive dendritic arbors
that extend throughout the molecular layer.
Their axons, which are the only output from
the cerebellar cortex, generally pass to the
deep nuclei
Granule cells

 They receive input from the mossy fibers and


innervate the Purkinje cells.
 They have their cell bodies in the granular layer.
 Each sends an axon to the molecular layer,
where the axon bifurcates to form a T.
 The branches of the T are straight and run long
distances. Thus they are called parallel fibers.
Basket cells

 They are located in the molecular layer


 They receive input from the parallel fibers,
and projects to many Purkinje cells.
 Their axons form a basket around the cell
body and axon hillock of each Purkinje
cell they innervate
Stellate cells

They are similar to the basket cells


but more superficial in location
Golgi cells
 They are located in the granular layer.
 Their dendrites, which project into the molecular
layer, receive input from the parallel fibers.
 Their cell bodies receive input via collaterals from
the incoming mossy fibers and the Purkinje cells.
 Their axons project to the dendrites of the granule
cells.
The first two cells are excitatory while the last
three are inhibitory
 Thetwo main inputs to the cerebellar cortex are
climbing fibers and mossy fibers.
 Both are excitatory
 The climbing fibers come from a single source, the
inferior olivary nuclei.
 Proprioceptive input to the inferior olivary nuclei comes
from all over the body.
 Mossy fibers provide direct proprioceptive input from all
parts of the body
 They
end on the dendrites of granule cells in complex
synaptic groupings called glomeruli.
The transmitter secreted by the stellate,
basket, Golgi, and Purkinje cells appears to
be GABA
Whereas the granule cells probably secrete
glutamate.
Functional divisions of cerebellum
 Vestibulocerebellum - Afferent fibres are:
 Vestibulocerebellar tract
 Spinocerebellum - Afferent fibres are:
1. Dorsal spinocerebellar tract 2. Ventral spinocerebellar tract
3. Cuneocerebellar tract 4. Olivocerebellar tract
5. Pontocerebellar tract 6. Tectocerebellar tract
7. Trigeminocerebellar tract
 Corticocerebellum - Afferent fibres are:
1. Pontocerebellar tract
2. Olivocerebellar tract
Function of Principal Afferent Systems
to the Cerebellum
 Vestibulocerebellar
Vestibular impulses from labyrinths, direct and via
vestibular nuclei
 Dorsal spinocerebellar
Proprioceptive and exteroceptive impulses from body
 Ventral spinocerebellar
Proprioceptive and exteroceptive impulses from body
 Cuneocerebellar
Proprioceptive impulses, especially from head
and neck
 Tectocerebellar
Auditory and visual impulses via inferior and superior
colliculi
 Pontocerebellar
Impulses from motor and other parts of cerebral
cortex via pontine nuclei
 Olivocerebellar
Proprioceptive input from whole body via relay in
inferior olive
Functions of Major Parts of the
Cerebellum
 Vestibulocerebellum
Regulates tone, posture and equilibrium by receiving
impulses from vestibular apparatus.
Information regarding gravity, linear movement and
angular acceleration to vestibulocerebellum comes
through vestibulocerebellar tract.
Vestibulocerebellum, in turn, sends signals to spinal
cord via vestibulospinal and reticulospinal tracts.
Spinocerebellum
 Regulates tone, posture and equilibrium by receiving sensory
impulses form tactile receptors, proprioceptors, visual receptors
and auditory receptors.
 Tactile and proprioceptive impulses are localized in the
spinocerebellum
 In cerebral cortex, different parts of the body are represented in
an inverted manner.
 But in cerebellum, different parts are represented in upright
manner.
Corticocerebellum
 It is concerned with the integration and regulation of well-
coordinated muscular activities.
These include:
i. Damping action
ii. Control of ballistic movements
iii. Timing and programming the movements
iv. Servomechanism
v. Comparator function
Cerebellar Lesions
 Cerebellar lesions may be due to tumor, abscess or an
injury.
 Excess alcohol ingestion also leads to cerebellar lesions.

DISTURBANCES IN TONE AND POSTURE


1. Atonia or Hypotonia
2. Attitude
3. Deviation Movement
4. Effect on Deep Reflexes
DISTURBANCES IN EQUILIBRIUM
 While Standing:
 The legs are spread to provide a broad base and the body sways
side-to-side with oscillations of the head.
 While Moving – Gait:
A
staggering, reeling and drunken-like gait is observed.
DISTURBANCES IN MOVEMENTS
1. Ataxia
2. Asynergia
3. Asthenia
4. Dysmetria
5. Intention tremor
6. Astasia
7. Nystagmus
8. Rebound phenomenon
9. Dysarthria
10. Adiadochokinesis
CEREBRAL CORTEX

 Itis also called pallidum and it consists of two


hemispheres.
 Surface area in human beings is 2.2 sq m.
 Cerebral hemispheres are separated by a deep
vertical fissure.
 The separation is complete anteriorly and
posteriorly.
 But in middle portion, the fissure extends only up to
corpus callosum.
 Cerebral cortex consists of outer gray matter
and inner white matter.
 Histologically it is divided in 6 layers from
outside to inside:
1. Molecular or Plexiform Layer
2. External Granular Layer
3. Outer Pyramidal Layer
4. Internal Granular Layer
5. Ganglionic Layer or Internal Pyramidal Layer
6. Fusiform Cell Layer
Cerebral Dominance And Handedness

 Cerebral dominance is related to handedness


 More than 90% of people are right handed
 In these individuals, the left hemisphere is
dominant and it controls the analytical process,
speech, reading and writing.
 Hence, left hemisphere of these persons is called
dominant hemisphere.
 Right hemisphere is called representational
hemisphere
Brodmann Areas

 Brodmann area is a region of cerebral cortex
defined on the basis of its cytoarchitecture.

 Brodmannareas were originally defined and


numbered in 1909 by Korbinian Brodmann
depending upon the laminar organization of
neurons
Frontal Lobe Of Cerebral Cortex

 Frontallobe is divided into two parts:


A. Precentral cortex
B. Prefrontal cortex
A. Precentral cortex
 Precentralcortex is further divided into three
functional areas

1. Primary motor area


2. Premotor area
3. Supplementary motor area
1. Primary motor area
 Thisextends throughout the precentral gyrus and
the adjoining central sulcus. Areas 4 and 4S are
present here

 Specialstructural feature of this layer is the giant


pyramidal cells called Betz cells in ganglionic
layer.
Function of area 4
 Area 4 is the center for movement, as it sends all
efferent (corticospinal) fibers of primary motor
area.
 It activates the lower motor neurons in the spinal
cord: both α-motor neurons and γ-motor neurons
 Activation of α-motor neurons causes contraction
of extrafusal fibers of the muscles.
 Activation of γ-motor neurons causes contraction
of intrafusal fibers leading to increase in muscle
tone.
 stimulation
leads to discrete isolated
movements in the opposite side of the body

 Muscles of various parts of the body are


represented in inverted way from medial to
lateral surface.

 Lowerparts of body are represented in


medial surface and upper parts of the body
are represented in the lateral surface.
Effect of lesion of area 4

 Paralysis
occurs in contralateral side
 Complete paralysis is rare
 More severe if area 6 is also affected
Area 4S

It is called suppressor area.

Itscrutinizes and suppresses the extra


impulses produced by area 4 and inhibits
exaggeration of movements
2. Premotor Area
 Thisincludes areas 6, 8, 44 and 45.
 Giant pyramidal cells are absent in the
ganglionic layer.
 The premotor area is concerned with control of
postural movements by sending motor signals to
axial muscles (muscles near the midline of the
body).
 Functions of area 6:
i. Coordination of movements initiated by area 4.
It helps to make the skilled movements more
accurate and smooth.
ii. The cortical center for extrapyramidal system.
Lesion leads to loss of skilled movement,
grasping reflex
 Function of area 8:
i. Conjugate movement of eyeballs.
ii. It is also responsible for opening and closing
of eyelids, pupillary dilatation and lacrimation.
Lesion leads to the eyes turning to the affected
side. Conjugate movements of eyes are lost
 Broca area:
Broca area is the motor area for speech.
It includes areas 44 and 45
Broca area is present in left hemisphere (dominant
hemisphere) for right-handed people

 Function of Broca area:


Broca area is responsible for movements of
tongue, lips and larynx, which are involved in
speech.
 Lesion leads to aphasia
3. Supplementary Motor Area

 Situated in medial surface of frontal lobe rostral to


primary motor area
 Exact function of this area is not well known
 It is suggested that it is concerned with
coordinated skilled movements
 Lesion in this area leads to the head and eyeballs
turn towards the affected side.
B. PREFRONTAL CORTEX OR ORBITOFRONTAL
CORTEX

 Itis the anterior part of frontal lobe of cerebral


cortex.
 Areas present in prefrontal cortex are 9, 10, 11,
12, 13, 14, 23, 24, 29 and 32.
 Areas 12, 13, 14, 23, 24, 29 and 32 are in medial
surface
 Areas 9, 10 and 11 are in lateral surface.
Functions of prefrontal cortex
1. Short-term memories are registered here.
2. Center for planned actions
3. This area is the seat of intelligence; so, it is also
called the organ of mind
4. It is responsible for the personality of the
individuals
5. Responsible for the various autonomic changes
during emotional conditions, because of its
connections with hypothalamus and brainstem.
 Bilateral
lesion or removal of prefrontal cortex in
human beings does not cause paralysis.

 Itcauses lack of initiation and loss of mental


alertness.
PARIETAL LOBE
 Parietal lobe extends from central sulcus and
merges with occipital lobe behind and
temporal lobe below
 Parietal lobe is divided into three functional
areas:
A. Somesthetic area I
B. Somesthetic area II
C. Somesthetic association area
PARIETAL LOBE
 It is involved in the analysis of:
touch,
pressure,
pain,
knowledge of space position,
the sensation of the environment etc.
SOMESTHETIC AREA I
 Itis also called somatosensory area I or primary
somesthetic or primary sensory area.

 Itis present in the posterior lip of central sulcus, in


the postcentral gyrus

 It has three areas, which are called areas 3, 1 and 2

 Receives sensory fibers from thalamus


Functions of Somesthetic Area I
 Perception and integration of cutaneous and
kinesthetic sensations
Area 1 is concerned with sensory perception. Areas 3
and 2 are involved in the integration of these
sensations.
 Sends sensory feedback to the premotor area
 Concerned with the movements of head and
eyeballs
 Responsible for recognizing the discriminative
features of sensations
Functions of Somesthetic Area II

Receives sensory impulses from


somesthetic area I and from thalamus

Though the exact role of this area is not


clear, it is concerned with perception of
sensation
Functions of Somesthetic Association
Area
 Thisarea is concerned with synthesis of various
sensations perceived by somesthetic area I.

 Thus, it forms the center for combined sensations


like stereognosis

 Lesion of this area causes astereognosis


TEMPORAL LOBE

 Temporal lobe of cerebral cortex includes


three functional areas:
A. Primary auditory area
B. Secondary auditory area or auditopsychic
area
C. Area for equilibrium.
Primary Auditory Area

 Primary auditory area includes:


 1. Area 41
 2. Area 42
 3. Wernicke’s area.
Functions of Primary Auditory Area

 Areas
41 and 42 are concerned only with the
perception of auditory sensation (sound).

 Wernicke’s area is responsible for the


interpretation of auditory sensation and
sending information to Broca area
Functions of Secondary Auditory Area
 This includes area 22

 Itis concerned with interpretation of auditory


sensation along with Wernicke’s area.

 Alsoconcerned with storage of memories of


spoken words
Functions Of Area For Equilibrium

 It
is concerned with the maintenance of
equilibrium of the body.

 Stimulationof this area causes dizziness,


swaying, falling and feeling of rotation
Lesion in Temporal Lobes
1. Aphasia
2. Auditory disturbances e.g. tinnitus, auditory
hallucinations with sounds like buzzing, ringing or
humming.
3. Disturbances in smell and taste sensations
4. Dreamy states: The patients are not aware of their
own activities and have the feeling of unreality
5. Visual hallucinations associated with hemianopia
OCCIPITAL LOBE
 Occipital lobe is called the visual cortex

 Itis divided into three:


1. Primary visual area (area 17)
2. Secondary visual area or visuopsychic area
(area 18)
3. Occipital eye field (area 19).
Functions of Occipital Lobe
1. Primary visual area (area 17) is concerned
with perception of visual sensation

2. Secondary visual area (area 18) is


concerned with interpretation of visual
sensation and storage of memories of visual
symbols

3. Occipital eye field (area 19) is concerned


with reflex movement of eyeballs.
Lesion In The Occipital Lobe

 Lesion in the upper or lower part of visual


cortex results in hemianopia.

 Bilateral lesion leads to total blindness.


HYPOTHALAMUS
Hypothalamus is a diencephalic structure.
It is situated just below thalamus
It is formed by groups of nuclei, scattered in
the walls and floor of third ventricle.
It extends from optic chiasma to mamillary
body.
NUCLEI OF HYPOTHALAMUS
Nuclei of hypothalamus are
divided into three groups:
1. Anterior or preoptic group
2. Middle or tuberal group
3. Posterior or mamillary group.
Anterior or Preoptic group

1. Preoptic nucleus


2. Paraventricular nucleus
3. Anterior nucleus
4. Supraoptic nucleus
5. Suprachiasmatic nucleus
Middle or Tuberal group

1. Dorsomedial nucleus


2. Ventromedial nucleus
3. Lateral nucleus
4. Arcuate (tuberal) nucleus
Posterior or Mamillary group

1. Posterior nucleus


2. Mamillary body
AFFERENT CONNECTIONS TO HYPOTHALAMUS
1. Medial forebrain bundle: From rhinencephalon to
preoptic nucleus, lateral nucleus and mamillary
body
2. Fornix: Hippocampus to mamillary body
3. Stria terminalis: Amygdaloid to preoptic nucleus
4. Corticohypothalamic fibers: Prefrontal area (8)
and precentral area (6) of cerebral cortex to the
supraoptic & paraventricular nuclei of
hypothalamus
5. Pallidohypothalamic fibers: Globus pallidus to
diffused areas of hypothalamus
6. Thalamohypothalamic fibers: Dorsomedial and
midline nuclei of thalamus to diffused areas of
hypothalamus
7. Reticulohypothalamic fibers: Reticular formation of
brainstem to diffused areas of hypothalamus
8. Retinohypothalamic fibers: Fibers from retina to
supraoptic, suprachiasmatic and ventromedial
nuclei of hypothalamus.
EFF. CONNECTIONS FROM HYPOTHALAMUS
1. Mamillothalamic tract: From mamillary
body to anterior thalamic nuclei
2. Mamillotegmental tract: Mamillary
body to the tegmental nuclei of midbrain
3. Hypothalamohypophyseal tract:
Supraoptic and paraventricular nuclei of
hypothalamus to posterior pituitary.
4. Periventricular fibers: Fibers from
posterior, supraoptic and tuberal nuclei
of hypothalamus pass through
periventricular gray matter and reach
the following:
i. Reticular formation in brainstem &
spinal cord
ii. Dorsomedial nucleus of thalamus
iii. Frontal lobe of cerebral cortex
FUNCTIONS OF HYPOTHALAMUS
1. SECRETION OF POSTERIOR PITUITARY
HORMONES: Antidiuretic hormone (ADH) and
oxytocin are secreted by supraoptic and
paraventricular nuclei.

2. CONTROL OF ANTERIOR PITUITARY: By


secreting releasing hormones and inhibitory
hormones.
3. CONTROL OF ADRENAL CORTEX: By
secreting adrenocorticotropic
hormone (ACTH) from paraventricular
nucleus
4. CONTROL OF ADRENAL MEDULLA:
Dorsomedial & posterior hypothamic nuclei
are excited by emotional stimuli. They send
impulses to adrenal medulla thru symp
fibers & cause release of catecholamines.
5. REGULATION OF AUTONOMIC NERVOUS
SYSTEM: Sympathetic division of ANS is
regulated by post & lat nuclei & parasymp
division by ant. group of nuclei.

6. REGULATION OF HEART RATE: Stimulation of


post & lat nuclei of hypothalamus increases
the heart rate. Stimulation of preoptic & ant.
nuclei decreases the HR
7. REGULATION OF BLOOD PRESSURE:
Stimulation of post & lat nuclei increases
arterial BP & stimulation of preoptic area
decreases it.
8. REGULATION OF BODY TEMPERATURE: Two
centers regulates the body temperature:
i. Heat loss center in preoptic nucleus of ant
hypothalamus
ii. Heat gain center in posterior hypothalamic
nucleus
9. REGULATION OF HUNGER & FOOD INTAKE: Regulated
by two centers:
i. Feeding center - in the lat hypothalamic nucleus
ii. Satiety center - in the ventromedial nucleus
These centers are regulated by the following mechs:
i. Glucostatic mechanism
ii. Lipostatic mechanism
iii. Peptide mechanism
iv. Hormonal mechanism
v. Thermostatic mechanism
10.REGULATION OF WATER BALANCE: By two
mechanisms:
i. Thirst mechanism - in the lateral nucleus
ii. ADH mechanism - supraoptic nucleus
11.REGULATION OF SLEEP & WAKEFULNESS:
Mamillary body in the posterior
hypothalamus is for wakefulness and
anterior hypothalamus leads to sleep
12. ROLE IN BEHAVIOR AND EMOTIONAL
CHANGES: There are two centers for
behaviorial and emotional changes. They
are:
i. Reward center - medial forebrain bundle &
ventromedial nucleus of hypothalamus
ii. Punishment center - post & lat nuclei of
hypothalamus
 Rage:Refers to violent & aggressive emotional
expression with extreme anger when the punishment
center is stimulated. Manifested as:-
i. Extension of limbs
ii. Lifting of tail
iii. Hissing and spitting
iv. Piloerection
v. Wide opening of eyeballs
vi. Dilatation of pupil
vii. Severe savage attack even by mild provocation
Arcuate and posterior hypothalamic nuclei

 Sham Rage: Sham rage means false rage.


are involved in the regulation of sexual functions

It is an extreme emotional condition that resembles


rage and occurs in some pathological conditions in
humans.
13.REGULATION OF SEXUAL FUNCTION: Arcuate & post
nuclei are involved in the regulation of sexual
functions
14.ROLE IN RESPONSE TO SMELL: Post hypothalamus,
hippocampus and brainstem nuclei are
responsible for responses of body to olfactory
stimuli
15.ROLEIN CIRCADIAN RHYTHM:
Suprachiasmatic nucleus plays an
important role in setting the biological
clock by its connection with retina via
retinohypothalamic fibers.
DISORDERS OF HYPOTHALAMUS
The lesion of hypothalamus occurs due to tumors,
encephalitis & ischemia. Following features
develop in hypothalamic lesion:
1. Disturbances in CHO & fat metabolisms,
2. Disturbance in sleep
3. Disturbance in symp or parasymp function
4. Emotional manifestations, leading to sham
rage
5. Disturbance in sexual functions
Clinical Manifestations
1. Diabetes insipidus
2. Dystrophia adiposogenitalis
3. Kallmann syndrome
4. Laurence-Moon-Biedl syndrome
5. Narcolepsy
6. Cataplexy.
LIMBIC SYSTEM
 The word "limbic" means "border."
 Originally, the term "limbic" was used to describe
the border structures around the basal regions of
the cerebrum
 But the term limbic system has been expanded to
mean the entire neuronal circuitry that controls
emotional behavior and motivational drives.
 A major part of the limbic system is the
hypothalamus, with its related structures.
Papez Circiut
FUNCTIONS OF LIMBIC SYSTEM
 1. OLFACTION
 2. REGULATION OF ENDOCRINE GLANDS
 3. REGULATION OF AUTONOMIC FUNCTION
 4. REGULATION OF FOOD INTAKE
 5. CONTROL OF CIRCADIAN RHYTHM
 6. REGULATION OF SEXUAL FUNCTIONS
 7. ROLE IN EMOTIONAL STATE
 8. ROLE IN MEMORY
 9. ROLE IN MOTIVATION
RETICULAR FORMATION
Reticular formation is a diffused mass of
neurons and nerve fibers, which form an ill-
defined meshwork of reticulum in central
portion of the brainstem.
It is situated in brainstem & extends
downwards into spinal cord & upwards up to
thalamus and subthalamus
Organization Of Reticular Formation
1. RAPHE GROUP: Situated along the midline of the
brainstem forming a continuous column. They
secrete serotonin (5-hydroxytryptamine), which is an
inhibitory neurotransmitter.
2. PARAMEDIAN GROUP: These includes nucleus
reticularis paramedianus and pontine
reticulotegmental nucleus. They are concerned with
motor functions.
3. LATERAL GROUP: Situated in the lateral one third of the
tegmentum. Nuclei receive sensory signals from the
cranial nerves, cerebellum and spinal cord.
4. MEDIAL GROUP: Nuclei are situated in the
medial two third of the tegmentum. Nuclei
of this group form the major output of the
reticular formation are associated with
motor functions.
5. INTERMEDIATE GROUP: Nuclei are present
only in the medulla. These nuclei are
concerned with autonomic regulation of
respiration, heart rate and blood pressure.
Divisions Of Reticular Formation

Three divisions based on the location in


brainstem:

A. Medullary reticular formation


B. Pontine reticular formation
C. Midbrain reticular formation.
Nuclei Of Medullary Reticular Formation
1. Lateral reticular nucleus
2. Ventral reticular nucleus
3. Dorsal reticular nucleus
4. Gigantocellular reticular nucleus
5. Paragigantocellular reticular nucleus
6. Paramedian reticular nucleus
7. Parvocellular reticular nucleus
8. Magnocellular reticular nucleus
Nuclei Of Pontine Reticular Formation
1. Nucleus reticularis pontis oralis
2. Nucleus reticularis pontis caudalis
3. Locus ceruleus nucleus
4. Subceruleus reticular nucleus
5. Tegmenti pontis reticular nucleus
6. Pedunculopontine reticular nucleus
7. Nucleus reticular cuneiformis.
Nuclei Of Midbrain Reticular Formation

1. Red nucleus
2. Nucleus tegmental pedunculopontis
3. Nucleus reticular subcuneiformis.
Afferent
connections of
reticular
formation
Efferent
connections
of reticular
formation
Functions Of Reticular Formation

Based on functions, reticular formation is


divided into two systems:
A. Ascending reticular activating system
B. Descending reticular system.
Functions of ARAS
1. The ARAS is concerned with arousal, alertness,
maintenance of attention and wakefulness.
Hence, it is called Ascending Reticular Activating
System. Stimulation produces wakefulness by
generalized activation of entire brain
2. The ARAS also causes emotional reactions
3. The ARAS plays an important role in regulating the
learning processes and the development of
conditioned reflexes.
Fxn of Descending Reticular System
Descending reticular system includes
reticular formation in brainstem,
reticulospinal tract and reticular formation in
spiral cord
It is divided into two:
1. Descending facilitatory reticular system
2. Descending inhibitory reticular system.
Descending facilitatory reticular system
i. Facilitation of somatomotor activities
a. Maintains muscle tone by exciting the gamma motor
neurons in spinal cord;
b. It facilitates the movements of the body.
c. It plays a role in wakefulness and alertness by
activating the ARAS.
ii. Facilitation of vegetative functions
It is the center for facilitation of the autonomic functions
such as cardiac function, blood pressure, respiration,
gastrointestinal function and body temperature.
Descending Inhibitory Reticular System
i. Control of somatomotor activities
a. it inhibits the gamma motor neurons
b. It is responsible for smoothness & accuracy
of voluntary movts.
c. It also controls the reflex movements.
ii. Control of vegetative functions.
It is the center for inhibition of several
autonomic functions
ELECTROENCEPHALOGRAM (EEG)
Electroencephalography is the study of
electrical activities of brain.
Electroencephalogram (EEG) is the graphical
recording of electrical activities of brain.
Hans Berger was the first to analyze the EEG
waves systematically and hence the EEG
waves are referred as Berger waves.
Significance Of EEG
1. Epilepsy, which occurs due to excessive
discharge of impulses from cerebral cortex
2. Disorders of midbrain affecting ascending
reticular activating system
3. Subdural hematoma during which there is
collection of blood in subdural space over
the cerebral cortex.
WAVES OF EEG
 EEG may have synchronized or desynchronized
waves.
 Synchronized waves are the regular and invariant
waves, whereas desynchronized waves are
irregular and variant.
 Normally, EEG has three frequency bands
1. Alpha rhythm
2. Beta rhythm
3. Delta rhythm.
 EEG in children shows theta waves
Alpha rhythm
 consistsof rhythmical waves, which appear at a
frequency of 8 to 12 waves/second with the amplitude
of 50 μV.
 They are synchronized waves.
 Obtained in inattentive brain or mind as in drowsiness,
light sleep or narcosis with closed eyes.
 It is abolished by visual stimuli or any other type of
stimuli or by mental effort.
Beta rhythm
Includes high frequency waves of 15 to 60
per second but, the amplitude is low, i.e. 5 to
10 μV.
They are desynchronized waves.
They are recorded during mental activity or
mental tension or arousal state.
It is not affected by opening the eyes.
Delta rhythm
 Includes waves with low frequency & high amplitude.
 These waves have the frequency of 1 to 5 per second
with the amplitude of 20 to 200 μV.
 Its common in early childhood during waking hours.
 In adults, it appears mostly during deep sleep.
 Presence of delta waves in awake adults indicates the
pathologies like tumor, epilepsy, increased intracranial
pressure and mental deficiency or depression.
 Not affected by opening the eyes.
Theta waves
They are obtained generally in children
below 5 yrs.
These waves are of low frequency & low
voltage waves.
Frequency of theta waves is 4 to 8 per sec &
the amplitude is about 10 μV.
PHYSIOLOGY OF SLEEP
 Sleep is defined as state of unconsciousness from
which the person can be aroused by sensory or
other stimuli.
 It is to be distinguished from coma, which is
unconsciousness from which the person cannot
be aroused
 Two Types of Sleep
1. Slow-wave sleep (Non-Rapid eye movement sleep),
2. Rapid eye movement sleep (REM sleep),
Slow-wave sleep
Deep sleep that occurred during the first hour
after going to sleep.
This sleep is exceedingly restful and is
associated with decrease in both peripheral
vascular tone and many other vegetative
functions of the body
Dreams are not likely in this type of sleep and
it occupies about 70% to 80% of total
sleeping period.
REM Sleep (Paradoxical Sleep,
Desynchronized Sleep)
 In
a normal night of sleep, bouts of REM sleep lasting 5 to
30 minutes usually appear on the average every 90
minutes.
 There are several important characteristics of REM sleep:
 Associated with active dreaming & active bodily muscle movts.
 More difficult to arouse by sensory stimuli, & yet people usually
awaken spontaneously in the morning during an episode of REM
sleep.
 Muscle tone throughout the body is exceedingly depressed.
 Heart rate and respiratory rate usually become irregular.
Irregular muscle movements occurs.
Rapid movements of the eyes.
The brain is highly active in REM sleep, and brain
metabolism may be increased as much as 20%
The EEG shows a pattern of brain waves similar
to those that occur during wakefulness.
This type of sleep is also called paradoxical
sleep because it is a paradox that a person can
still be asleep despite marked activity in the
brain.
MECHANISM OF SLEEP
 Sleep occurs due to the activity of some sleep-
inducing centers in brain.
 Stimulation of these centers induces sleep.

SLEEP CENTERS
Two centers which induce sleep are located in
brainstem:
1. Raphe nucleus
2. Locus ceruleus of pons.
1. Role of Raphe Nucleus
 Raphe nucleus is situated in lower pons and
medulla.
 Activation results in non-REM sleep due to release
of serotonin
 Serotonin induces non-REM sleep.

2. Role of Locus Ceruleus of Pons


 Activation of this center produces REM sleep.
 Noradrenaline released by the nerve fibers
Inhibition of Ascending Reticular
Activating System

Ascending reticular activating system (ARAS)


is responsible for wakefulness
Inhibition of ARAS induces sleep.
Lesion of ARAS leads to permanent
somnolence, i.e. coma.
SLEEP DISORDERS
1. INSOMNIA
 It is the inability to sleep or abnormal wakefulness
 It is the most common sleep disorder.
 Itoccurs due to systemic illness or mental conditions
such as psychiatric problems, alcoholic addiction & drug
addiction.
2. HYPERSOMNIA
 It is the excess sleep or excess need to sleep.
 Occurs because of lesion in the floor of the 3rd ventricle,
brain tumors, encephalitis, chronic bronchitis and
disease of muscles
3. NARCOLEPSY AND CATAPLEXY
 Narcolepsy is the sudden attack of uncontrollable
sleep.
 Cataplexy is sudden outburst of emotion.
 Both diseases are due to hypothalamic disorders.
4. SLEEP APNEA SYNDROME
 It is the temporary stoppage of breathing repeatedly
during sleep.
 Apnea is due to decreased stimulation of respiratory
centers, arrest of diaphragmatic movements, airway
obstruction or the combination of all these factors.
5. NIGHTMARE
 It is a condition during sleep that is characterized by a sense of
extreme uneasiness or discomfort or by frightful dreams.
 Discomfort is felt as of some heavy weight on the stomach or chest
or as uncontrolled movement of the body.
 Nightmare occurs due to improper food intake, digestive disorders
or nervous disorders
6. NIGHT TERROR
 Common in children. It is also called pavor nocturnus or sleep
terror.
 The child awakes screaming in a state of fright & semi-
consciousness.
 The child cannot recollect the attack in the morning.
7. SOMNAMBULISM
 Somnambulism is getting up from bed and walking in the
state of sleep (somnus = sleep; ambulare = to walk).
 It
varies from just sitting up in the bed to walking around
with eyes open and performing some major complex task.
 The episode lasts for few minutes to half an hour.
 It occurs during non-REM sleep.
8. NOCTURNAL ENURESIS
 It is the involuntary voiding of urine at bed.
 It is also called or bedwetting.
 It is common in children.
HIGHER INTELLECTUAL FUNCTIONS
Higher intellectual fxns are very essential
to make up the human mind.
These fxns are also called higher brain
fxns or higher cortical fxns.
The extensive outer layer of gray matter
in cerebral cortex is responsible for
higher intellectual fxns.
LEARNING

Learning is defined as the process by which


new information is acquired. It alters the
behavior of a person on the basis of past
experience.
Learning is classified into two types:
1. Non-associative learning
2. Associative learning.
1. Non-associative Learning
 Non-associative learning involves response of a
person to only one type of stimulus. It is based on
two factors:
i. Habituation: means getting used to something, after
constant exposure.
Eventually one starts ignoring the stimulus slowly.
ii. Sensitization: is a process by which the body is
made to become more sensitive to a stimulus.
It is called amplification of response.
2. Associative Learning
Associative learning is a complex
process that involves learning about
relations between two or more stimuli at
a time.
Classic example is the conditioned
reflex
Conditioned Reflex
It is the acquired reflex that requires
learning, memory and recall of previous
experience.
It is acquired after birth and it forms the basis
of learning.
Conditioned reflex is different from
unconditioned reflex.
Unconditioned reflex is the inborn reflex,
which does not need previous experience
Classification Of Conditioned Reflexes
Conditioned reflexes are classified into
two types:
A. Classical conditioned reflexes
B. Instrumental conditioned reflexes.
Classical Conditioned Reflexes
They are those reflexes, which are
established by a conditioned stimulus,
followed by an unconditioned stimulus
Further classified into two, namely
I. Positive or excitatory conditioned reflexes
II. Negative conditioned reflexes.
Method of Study – Pavlov’s Bell-Dog
Experiments
Instrumental Conditioned Reflexes
 They are those reflexes in which the behaviour of
the person is instrumental.
 It is developed by the conditioned stimulus,
followed by a reward or a punishment.
 These reflexes include:
1. Conditioned avoidance reflex
2. Food avoidance reflex
3. Conditioned reward reflex.
MEMORY
Memory is defined as the ability to recall
past experience or information.
It is also defined as retention of learned
materials.
There are various degrees of memory.
Some memories remain only for few
seconds, while others last for hours,
days, months or even years together.
BASIS OF MEMORY
Memory is facilitated by synapses in the brain
Synapse for memory coding is slightly
different from other synapses.
Two separate presynaptic terminals are
present here.
A primary presynaptic terminal called sensory
terminal
A facilitator terminal which end on the primary
presynaptic terminal.
 When, sensory terminal is
stimulated alone without facilitator
terminal, it leads to habituation,
i.e. the firing decreases slowly.
 Ifboth the terminals are
stimulated, facilitation occurs and
the signals remain strong for long
period.
 Memory is stored in brain by the
alteration of synaptic transmission
between the neurons involved in
memory.
Facilitation
 Is the process by which memory storage is
enhanced increasing synaptic transmission and
postsynaptic activity.
 The process is called memory sensitization.
Habituation
 Is the process by which memory storage is
attenuated
 It involves reduction in synaptic transmission and
slow stoppage of postsynaptic activity.
Basis for Short-term Memory
Development of new neuronal circuits
by the formation of new synapses &
facilitation of synaptic transmission.

Number of presynaptic terminals & size


of the terminals are also increased.
Basis for Long-term Memory
 When neuronal circuit is reinforced by constant
activity, memory is consolidated and encoded
into different areas of the brain.
 This encoding makes memory a permanent or a
long-term memory
 Sites of Encoding
Hippocampus and Papez circuit are the main
sites of memory encoding
Frontal and parietal areas are also involved in
memory storage.
Memory
engram

Molecular basis
of memory
Molecular Basis of Habituation:
It is due to passive closure of calcium
channels of terminal membrane.
Release of transmitter decreases, resulting in
decrease in number of action potential in the
postsynaptic neuron.
So, the signals become weak leading to
habituation.
CONSOLIDATION OF MEMORY

The process by which a short-term


memory is crystallized into a long-term
memory.
It causes permanent facilitation of
synapses.
It is possible by rehearsal mechanism
ABNORMALITIES OF MEMORY
1. Amnesia
 Loss of memory is known as amnesia.
 Classified into two types:
i. Anterograde amnesia: Failure to establish new long-
term memories.
It occurs because of lesion in hippocampus.
ii. Retrograde amnesia: Failure to recall past remote
long-term memory.
It occurs in temporal lobe syndrome.
2. Dementia
 It
is the progressive deterioration of intellect, emotional
control, social behaviour & associated with loss of
memory
 It is an age-related disorder (Usually above 65 years).
Causes
 75% of cases, is due Alzheimer disease
 Other causes are hydrocephalus, Parkinson disease,
viral encephalitis, HIV infection, hypothyroidism,
hypoparathyroidism, Cushing syndrome, alcoholic
intoxication, carbon monoxide, heavy metals, etc.
SPEECH

Speech is defined as the expression of


thoughts by production of articulate
sound, bearing a definite meaning.
It is one of the highest functions of brain.
MECHANISM OF SPEECH
It depends on coordinated activities of
central speech apparatus and peripheral
speech apparatus.
Central speech apparatus consists of the
cortical and subcortical centers.
Peripheral speech apparatus includes larynx
or sound box, pharynx, mouth, nasal cavities,
tongue and lips.
Role of Cortical Areas in the Development
of Speech
Development of speech involves
integration of three important areas of
cerebral cortex:
1. Wernicke area
2. Broca area
3. Motor area
Role of Wernicke area – Speech understanding
 It begins in Wernicke area in upper part of
temporal lobe.
 It is responsible for understanding the visual and
auditory information required for the production of
words.
 After understanding the words, it sends the
information to Broca area through arcuate
fasciculus tract.
Role of Broca area – Speech synthesis
Speech is synthesized in the Broca area.
It is situated adjacent to the motor area,
responsible for the movements of tongue, lips
and larynx
It develops the pattern of motor activities
required to verbalize the words.
The pattern of motor activities is sent to motor
area.
Role of motor area – Activation of peripheral speech
apparatus

 By receiving the pattern of activities from Broca


area, motor area activates the peripheral speech
apparatus.

 It
results in initiation of movements of tongue, lips
and larynx required for speech.
 Role
of motor area – Activation of peripheral
speech apparatus – Con’t

 Later,
when the child is taught to read, auditory
speech is associated with visual symbols (area 18).

 Then,there is an association of the auditory and


visual areas with the motor area for the muscles of
hand.
Nervous Control Of Speech
A. Motor Areas
1. Broca area
 It is also called speech center
 It includes areas 44 and 45.
 These areas are situated in lower part of lateral surface of
prefrontal cortex.
 It controls the movements of structures involved in vocalization.
2. Upper frontal motor area
 Upper frontal motor area is situated in paracentral gyrus
 It controls the coordinated movements involved in writing
B. Sensory Areas
1. Secondary auditory area
 It includes area 22.
 Situated in the superior temporal gyrus.
 Concerned with the interpretation of auditory sensation
and storage of memories of spoken words.
2. Secondary visual area
 It includes area 18.
 Present in angular gyrus of the parietal cortex.
Concerned with the interpretation of visual sensation
and storage of memories of the visual symbols.
C.Wernicke Area
It is situated in the upper part of temporal
lobe.
It is responsible for the interpretation of
auditory sensation.
It also plays an important role in speech.
It is responsible for understanding the auditory
information and sending it to Broca area
Disorders Of Speech
It is a communication disorder characterized
by disrupted speech.
It is of four types:
I. Aphasia
II. Anarthria or dysarthria
III. Dysphonia
IV. Stammering.
APHASIA
 Aphasia is defined as the loss or impairment of
speech due to brain damage.
 It is an acquired disorder.
 It is due to damage of speech centers.
 Damage of speech centers impairs the expression
and understanding of spoken words.
 It also affects reading and writing.
 Speech function is localized to left hemisphere in
most of the people.
Causes for Aphasia
 Usually
aphasia occurs due to damage of one or more
speech centers
 Damage of speech centers occurs due to:
1. Stroke
2. Head injury
3. Severe blow to head
4. Cerebral tumors
5. Brain infections
6. Degenerative diseases
DYSARTHRIA OR ANARTHRIA
 Dysarthria refers to disturbed articulation.
 Anarthria means inability to speak.
 They result from paralysis or ataxia of muscles
involved in articulation.

Causes of Dysarthria
 May be due to stroke, brain injury, degenerative
disease like Parkinson disease and Huntington
disease.
DYSPHONIA
 Dysphonia is a voice disorder.
 It is characterized by hoarseness & a sore or a dry throat.
 The voice may be weak, breathy, scratchy or husky.
Causes of Dysphonia
 1. Trauma of vocal cords
 2. Paralysis of vocal cords
 3. Lumps on vocal cords
 4. Inflammation of larynx
 5. Hypothyroidism
 6. Stress (psychological dysphonia).
STAMMERING
 Stammering or shuttering is a speech disorder
characterized by hesitations and involuntary repetitions
of certain syllables or words.
 It
is due to the neurological incoordination of speech
and it is common in children.
 Stammeringis associated with some unusual facial and
body movements.
 Exact cause for stammering is not known.
 It
is thought that it may be due to genetic factors, brain
damage, neurological disorders or anxiety.

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