CORTICAL & BRAINSTEM

CONTROL OF

MOTOR FUNCTIONS
Voluntary movements
 Organization of Nervous System
• CENTRAL NERVOUS SYSTEM
– Brain and Spinal cord
• PERIPHERAL NERVOUS SYSTEM
– Nerve fibers that carry information between
CNS and periphery
– Afferent division
– Efferent division
 THERE ARE TWO TYPES OF MOTOR OUTPUT
• Reflexive / involuntary ( swallowing, chewing
and walking )
• Voluntary
• To move a limb
– Plan an appropriate motion
– Adjust comparing plan with performance
– Learn by doing it
– Improving by repetition
– synaptic plasticity
• Commands for voluntary movement originate in
cortical association areas.

The movements are planned in the cortex as well as

•
in the basal ganglia and the lateral portions of the
cerebellar hemispheres, as indicated by increased
electrical activity before the movement.

• The basal ganglia and cerebellum funnel information

to the premotor and motor cortex by way of the
thalamus.

Motor commands from the motor cortex are relayed in

•
large part via the corticospinal tracts to the spinal
MOTOR CORTEX
 MOTOR CORTEX
• Primary motor cortex
• Area 4 in brodmann’s classification
• Topographical organization parallels that of somatosensory
cortex represented as motor homunculus
• executes specific / discrete muscle movements
• Premotor area ( brodmann’s area 6)
• Supplementary motor area (brodmann’s area6)
• Premotor area ( lateral portion of B.A 6 )
• More complex patterns of movements
• Creates motor image of total muscle movement
• Sends signal to primary motor cortex directly or via B.G or
thalamus
• Mirror neurons
• Supplementary motor area (medial portion of B.A 6
) plays a preparatory role in Complex, Bilateral /
bimanual muscle contractions
• Excitation provides the background position for the finer
motor control of arms and hands by premotor and motor
cortex
 Specialized areas of motor control
in motor cortex
• Broca’s Area & speech
– Word formation
• Voluntary eye movement field
– prevents involuntary locking of the eyes
• Head rotation area
• Hand skill area
– Damage results in Motor Apraxia
• The proportions of homunculus are
distorted because size of the cortical
sensory area depends on the
number of impulses received from a
particular part of the body. This is
evident as area for sensations from
trunk and back is small and area for
hand and speech is large
LIPS AND MOUTH are represented by the largest area
in cortex in SENSORY HOMUNCULUS
Muscles of VOCALIZATION and muscles of THUMB are
represented by the largest area in MOTOR
HOMUNCULUS
Area for face is represented on both sides but rep. of
rest of the body is one sided i.e. right half of body on
left cerebral motor area & vice versa
1. CORTICAL
The finger areas of thePLASTICITY
contralateral motor
organization
cortex enlarge of
as acortical
patternstructures is not
of rapid finger
fixed
movement is learned with the fingers of one
hand

When a small focal ischemic lesion is produced

2.
in the hand area of the motor cortex of
monkeys, the hand area may reappear, with
return of motor function, in an ADJACENT
UNDAMAGED PART OF CORTEX
representation of the neighboring digits spreads into the
cortical area that was formerly occupied by the amputated
digit.

Conversely, if the cortical area

•
representing a digit is removed, the
somatosensory map of the digit moves to the
surrounding cortex.

Stimulation of the stump or the stimulation of

•
face can lead to feeling of being touched in the
missing limb

•
 How motor cortex functions?
• Receives sensory information and then
operates in association with Basal
Ganglia and Cerebellum to produce an
appropriate motor response`
 DESCENDING MOTOR TRACTS
FROM MOTOR CORTEX TO MUSCLES

DESCENDING MOTOR
PATHWAYS
1. PYRAMIDAL TRACT / PYRAMIDAL SYSTEM
OR CORTICOSPINAL PYRAMIDAL TRACT
Originates from MOTOR CORTEX Terminates in spinal
cord neurons
Discrete movements of hands and fingers
2. CORTICOBULBAR TRACT
fibers pass from motor cortex to motor neurons in
TRIGEMINAL, FACIAL & HPOGLOSSAL NUCLEI in the
brainstem
3. EXTRAPYRAMIDAL TRACT
CORTICOSPINAL TRACT
• ORIGIN/Primary Motor cortex = BETZ CELLS - 30%
Pre motor cortex & Suppl. Motor area- 30% &
Somatosensory cortex- 40%
• Pass through Posterior limb of internal capsule,
Midbrain and basilar PONS
• Emerge as pyramids of medulla(ventral surface)
• 80% Cross over to opposite sides (decussate) & descend as
Lateral Corticospinal Tract
• 20% do not cross & descend as Ventral Corticospinal Tract
• VENTRAL CORTICOSPINAL FIBERS
• Also eventually cross to opposite side of the cord
either in the neck or or upper thoracic region
(bilateral postural movements ) by the
supplementary Motor cortex
TERMINATION OF THE CORTICOSPINL TRACT
• Principally on the interneurons
• Also terminate directly on anterior motor
neurons particularly those controlling finger
muscles which forms the basis for ability to make
fine controlled finger movements
AREA PYRAMIDALIS OF THE PRIM. MOTOR CORTEX
COTAINS BETZ CELLS / GIANT PYRAMIDAL
CELLS---60μmin diameter & are the defining feature
of primary motor cortex ( only 3% 0f total)
Large myelinated fibers -----16μm
• Rate of impulse transmission -70m/sec
• 97% smaller fibers less than 4 μm in
diameter
 CORTICOBULBAR TRACT
• ORIGIN is the same
• Fibers pass from Cerebral cortex to Brain Stem
& synapse either directly or through
interneurons with lower motor neurons of
cranial nerves (trigeminal facial & hypoglossal
nuclei) which supply the muscles of face head
and neck bilaterally
• Their axons descend with corticospinal tract
through pons and medulla
• Corticobulbar tract ends contra laterally in
FACIAL NERVE NUCLEUS that supplies muscles
of the lower part of the face &
• In the HYPOGLOSSAL NERVE NUCLEUS
• Remainder of the cortico bulbar tract
ends bilaterally
EXTRAPYRAMIDAL SYSTEM

ACCESSORY MOTOR PATHWAYS TO

SPINAL CORD
 3. EXTRAPYRAMIDAL TRACT
• Originates from the upper motor neurons from all
portions of brain & brain stem that contribute to
motor control, not part of the direct corticospinal
pyramidal system
• Lower motor neuron is anterior horn motor neuron
• Includes pathways from Basal Ganglia,
Reticular Formation, Vestibular Nuclei & Red
Nuclei
• Regulates axial muscles, muscles of proximal
portion of limbs (coarse movements)
• Head, neck & eye movements
 MORE PATHWAYS FROM CORTEX 🡻
NUCLEI 🡻 SPINAL CORD
1. To Red nucleus 🡻 Rubrospinal tract
2. To Pontine and Medullary Reticular
nuclei / Reticulospinal tract
3. To lateral and medial Vestibular nuclei /
Vestibulospinal tract
4. To sup. colliculus/ Tectospinal tract
5. To Caudate nucleus and Putamen (Basal
Ganglia)
6.To Cerebellum
 FIBER PATHWAYS TO THE MOTOR CORTEX
1.From (Somatosensory) parietal cortex, Frontal cortex
From Visual & Auditory cortex
2.Through Corpus Callosum from opposite cerebral
hemisphere
3.From Thalamus
– Ventrobasal complex (tactile, muscle & joints)
– Ventrolateral and ventroanterior nuclei (Basal Ganglia,
Cerebellum)
– Intralaminar nuclei
 .RED NUCLEUS & RUBROSPINAL TRACT
Located in midbrain
• Input fibers from Pr. Motor Cortex through
corticoruberal tract to magnocellular portion of
red nucleus 🡻 rubrospinal tract
• Decussate(cross over) in lower brain stem and
course along with corticospinal pathway to the
lateral column of spinal cord
• ( LATERAL BRAINSTEM PATHWAYS)
• Mostly terminate on interneurons also on motor
neurons
• Close connections with Cerebellum
 FUNCTIONS OF RED NUCLEUS
• Contains somatographic representation of all
muscles of the body
• Provides an Accessory route for transmission of
signals from motor cortex to spinal cord for discrete
movements
• Can perform discrete movements if corticospinal
fibers are destroyed although fine control of finger
movements is lost
 The corticospinal tract and the rubrospinal
•
tract lie in the dorsal portions of the lateral
white columns.

• Rubrospinal tract affect motor

neurons controlling distal muscles

In the cervical enlargement of the cord (where the

•
hands and fingers are represented), large numbers
of both corticospinal and rubrospinal fibers also
terminate directly on the anterior motor neurons,
 The ventral corticospinal tract and medial
•
descending brain stem pathways
(tectospinal, reticulospinal, and vestibulospinal
tracts) are concerned with adjustments of
proximal muscles and posture,

whereas the lateral corticospinal and

•
rubrospinal tracts are concerned with distal
limb muscles and, particularly in the case of
the lateral corticospinal tract, with skilled
CONVERGENCE OF MOTOR PATHWAYS ON ANTERIOR MOTOR
NEURONS
 FUNCTIONS OF
BRAINSTEM IN CONTROL
OF MOTOR ACTIVITY
MOTOR FUNCTIONS OF BRAIN STEM
• Motor and sensory functions for face and
head regions
• Neck down these functions are
performed by Spinal Cord
• Control of Respiration, CVS, GIT, control
of Equilibrium & body movements,
control of Eye movements
• Way station for command signals
 SUPPORT OF THE BODY
AGAINST GRAVITY
ROLE OF VESTIBULAR & RETICULAR
NUCLEI
 PONTINE RETICULOSPINAL TRACT
EXCITATORY to antigravity muscles ( muscles of
vertebral column & extensor muscles of the limbs)
Receive excitatory input from vestibular nuclei & deep
nuclei of cerebellum
MEDULLARY RETICULOSPINAL TRACT
INHIBITORY To the same antigravity muscles
Receives fibers from Corticospinal Tract & Rubrospinal
tract, counterbalances the pontine excitatory
signals.
• Pontine and Medullary Reticulospinal
Tracts are Involved In maintaining
Posture And Muscle Tone via Input
to γ Motor Neurons
VESTIBULOSPINAL TRACT
Transmit strong excitatory signals to antigravity
muscles in association with Pontine reticular nuclei
MAINTAIN EQUILIBRIUM IN RESPONSE TO SIGNALS FROM
VESTIBULAR APPARATUS
MEDIAL VESTIBULOSPINAL TRACT
• Originates from medial and inferior vestibular nuclei
• Projects bilaterally to cervical spinal neurons
• Controls neck musculature
 LATERAL VESTIBULOSPINAL TRACT
• Originates from lateral vestibular nuclei
• Projects ipsilaterally to neurons at all spinal levels
• Activates antigravity muscles / posture & balance
 BRAINSTEM PATHWAYS
LATERAL MOTOR SYSTEM &
MEDIAL MOTOR SYSTEMS OF THE CORD
LATERAL MOTOR PATHWAYS
• LATERAL CORTICOSPINAL TRACT
• MUCH OF THE RUBROSPINAL TRACT
MEDIAL MOTOR PATHWAYS
• VENTRAL CORTICOSPINAL TRACT
• PONTINE & MEDULLARY RETICULOSPINAL TRACTS
• LATERAL & MEDIAL VESTIBULOSPINAL TRACTS
• TECTOSPINAL TRACT
 MOTOR DEFICITS CAUSED BY
LESIONS OF DESCENDING MOTOR
PATHWAYS
Removal of primary motor cortex & CST
STROKE
• varying degree of paralysis
• Loss of voluntary control of discrete fine
movements of hands and fingers, (gross move
ments can occur)
• Hypotonia and weakness ( loss of tonic stimulatory
effect of motor cortex on spinal cord neurons)
• Spasticity- contralateral / spastic rigidity due to
damage of accessory pathways (B G) that inhibit
vestibular & reticular brain stem motor nuclei
 Lesion of the ventral corticospinal
tract
• produces axial muscle deficits
that cause difficulty with balance,
walking, and climbing.
 MIDCOLLICULAR DECEREBRATION
•
This lesion interrupts all input from the cortex
(corticospinal and corticobulbar tracts) and red
nucleus (rubrospinal tract), primarily to distal muscles
of the extremities. The excitatory and inhibitory
reticulospinal pathways (primarily to postural
extensor muscles) remain intact. The dominance of
drive from ascending sensory pathways to the
excitatory reticulospinal pathway leads to arching of
the body and hyperactivity in extensor muscles in all
four extremities/neck, trunk & extensors of limbs
which is called DECEREBRATE RIGIDITY (γ rigidity)
 MIDCOLLICULAR DECEREBRATION
•
This lesion interrupts all input from the cortex
(corticospinal and corticobulbar tracts) and red
nucleus (rubrospinal tract), primarily to distal
muscles of the extremities. The excitatory and
inhibitory reticulospinal pathways (primarily to
postural extensor muscles) remain intact. The
dominance of drive from ascending sensory
pathways to the excitatory reticulospinal pathway
 DECORTICATION
Removal of the cerebral cortex produces
•
DECORTICATE RIGIDITY which is
characterized by flexion of the upper
extremities at the elbow and extensor
hyperactivity in the lower extremities. The
flexion can be explained by rubrospinal
excitation of flexor muscles in the upper
extremities; the hyperextension of lower
extremities is due to the same changes that
 EXTENSOR RIGIDITY IN ALL FOUR
LIMBS – DECEREBRATE RIGIDITY

FLEXION OF UPPERLIMBS & EXTENSION OF LOWER

LIMBS – DECORTICATE RIGIDITY
ALPHA & GAMMA CO-ACTIVATION/ α-γ LINKAGE

When signals are transmitted from the motor

•
cortex or from any other area of the brain to the
alpha motor neurons, in most instances the
gamma motor neurons are stimulated
simultaneously, an effect called co-activation of
the alpha and gamma motor neurons. This
causes both the extrafusal skeletal muscle
fibers and the muscle spindle intrafusal muscle
 The motor system neurons can be
•
divided into lower and upper motor
neurons.
Lower motor neurons refer to the spinal
•
and cranial motor neurons that directly
innervate skeletal muscles.

Upper motor neurons are those in the

•
cortex and brain stem that activate the
HYPERTONIA
Abnormally high muscle tone, is due to a
greater-than-normal level of alpha motor
neuron activity, which keeps a muscle
contracted despite the individual’s attempt to
relax it. Hypertonia is usually found in disorders
of the descending motor pathways which result
in decreased inhibitory influence exerted by
them on the motor neurons.
• SPASTICITY
is a form of hypertonia in which the muscles do not
develop increased tone until they are stretched a bit,
and after a brief increase in tone, the contraction
subsides for a short time (clasp knife effect )
RIGIDITY
is a form of hypertonia in which the increased muscle
contraction is continual and the resistance to passive
stretch is constant.
UPPER MOTOR NEURON LOWER MOTOR NEURON
LESION LESION
1. Paralysis spastic 1. Flaccid paralysis
2. Muscle wasting 2. In this muscle
absent / minimal wasting is present
3. Fasciculation absent 3. Fasciculation
4. Hyperreflexia / present
clonus present 4. Hyporeflexia
5. Deep tendon 5. Deep tendon
reflexes hyperactive reflexes are absent
6. Babinski sign 6. Babinski sign
present absent
UMNL LMNL

7. MUSCLES AFFECTED 7. INDIVIDUAL MUSCLES

IN GROUPS AFFECTED
8. NO DENERVATION 8. DENERVATION
POTENTIAL IS SEEN POTENTIAL SEEN
9. EMG CHANGES— 9. DECREASED NERVE
NERVE CONDUCTION CONDUCTION
STUDIES SHOW NO
ABNORMALITIES
CLONUS
 CEREBELLUM
• Sits astride the main sensory and motor
systems in brain stem
• More extensively folded than cerebral cortex
• Weighs 10% of the cerebral cortex but
• its surface area is 75% of cerebral cortex
• Topographical representation of different body
parts is present like in motor cortex, basal
ganglia, red nucleus reticular formation & in
cerebellum too
 FUNCTIONS OF CEREBELLUM
1.Timing of motor activities
2. Rapid smooth progression from one muscle
movement to other like running, typing and playing
a piano
3.Contols intensity of muscle contraction by
adjusting the agonist and antagonistic
muscles
4. Helps to sequence the motor activities in
advance
5. Monitors & compares the actual
movement with the movement intended
by motor system and makes corrective
adjustments while they are being
performed
6. Plans the next movement in advance by
a fraction of a second
7. Learns by its mistakes and makes a
stronger or a weaker movement next
time
ANATOMICAL LOBES OF CEREBELLUM
FUNCTIONAL PARTS OF CEREBELLUM
SOMATOSENSORY PROJECTION AREAS IN
CEREBELLAR CORTEX
 INPUT PATHWAYS TO THE CEREBELLUM
1. From other parts of brain
a. Corticopontocerebellar pathway to lat. Div. of
cerebellar hemisphere on opposite side
b. From each side of brainstem
• Olivocerebellar from inferior olive to all parts of
cerebellum, C.C, B.G, R.F & SP.C all excite inferior
olivary nucleus
• Vestibulocerebellar fibers to flocculonodular
lobe of cerebellum
• Reticulocerebellar fibers to vermis
2. From periphery- four tracts
• Dorsal Spinocerebellar tract terminates in vermis &
int.med. zone of cerebellum and receives impulses
from muscle spindles & GTO
• Ventral Spinocerebellar receives less information from
periphery, rather is excited by motor signals which
arrive at the anterior horns from brain and from cord
itself this feedback is called the EFFERENCE COPY of
the anterior horn motor drive.
• Dorsal columns of Spinal cord, Spino-reticular &
Spino-olivary fibers collect and convey information of
movements & position from all parts of body
FUNCTIONAL UNIT OF CEREBELLAR CORTEX
• 30 MILLIONS FUNCTIONAL UNITS
• 3 LAYERS OF CEREBELLAR CORTEX
– EXT. MOLECULAR CELL LAYER
– SINGLE CELL THICK PURKINJE CELL LAYER (the biggest
neurons in the body)
– INT. GRANULE CELL LAYER
5 TYPES OF NEURONS
PURKINJE, GRANULE, BASKET, STELLATE AND GOLGI
CELLS
3 DEEP NUCLEI
DENTATE , INTERPOSITUS & FASTIGIAL
Functional unit of the cerebellar cortex
• IN THE CEREBELLUM EACH INPUT SIGNAL DIVIDES & GOES
TO
(1) directly to the deep cerebellar nuclei
(2) & to the cerebellar cortex overlying the
cerebellar nuclei
FROM THE DEEP NUCLEI OUTPUT SIGNAL leaves
cerebellum & is
distributed to other parts of brain VIA DEEP
CEREBELLAR NUCLEI
FASTIGIAL, INTERPOSED, DENTATE
SO all input signals enter in deep nuclei as
INITIAL EXCITATORY INPUT followed by
INHIBITORY INPUT ( from cerebellar cortex)
• FROM THE NUCLIE FIBERS HAVE ASCENDING
(THALAMUS RED NUCLEUS AND VIA THESE TO
MOTOR CORTEX ) AND
• DESCENDING PROJECTIONS (TO PONTINE
RETICULAR AND INFERIOR OLIVE NUCLEI
 A LARGE PURKINJE CELL AND A DEEP NUCLEAR CELL
FORMS A FUNCTIONAL UNIT
INPUT FIBERS to the deep nuclei are both
excitatory & inhibitory
CLIMBING FIBERS--------------strong excitatory
MOSSY FIBERS ------------------week excitatory
PURKINJE CELLS------------------inhibitory
• OUTPUT from functional unit is from deep
nuclear cell- (always excitatory)
 Direct stimulation of the deep nuclear cells by
•
both the climbing and the mossy fibers excites
them.

By contrast, signals arriving from the Purkinje

•
cells inhibit them------( -ve feed back after a
short delay ) DAMPING

• In performing a rapid motor

movement-DAMPING PREVENTS FROM
 GENERAL PLAN OFEFFERENT PATHWAYS
FROM MIDLINE STRUCTURES ( VERMIS) 🡻 FASTIGIAL N 🡻
BRAINSTEM, Controls equilibrium & posture
FROM INTERMEDIATE ZONE OF CEREBELLUM
🡻 INTERPOSED NUCLEUS 🡻 CEREBRAL CORTEX,
THALAMUS, BASAL GANGLIA, RED N & RETICULAR
FORMATION coordinates agonists and antagonists muscle
contractions of distal muscle
FROM LATERAL ZONE OF CREBELLUM🡻 DENTATE
NUCLEUS 🡻 THALAMUS 🡻 CEREBRAL CORTEX controls
planning & sequence of motor movements
Functional unit of the cerebellar cortex
 CLIMBING FIBERS
• originate from inferior olivary nucleus
which receives proprioceptive input from
all over the body. After sending branches
to deep nuclear cells, continues upwards
to the cerebellar Cortex & synapses
(300) with each purkinje cell –a single
impulse causes a prolonged action
potential---- COMPLEX SPIKE
 MOSSY FIBERS
• provide proprioceptive input from all over the
body + from cerebral cortex, send collaterals
to deep nuclear cells & then synapse with
thousands of granule cells. Their axons divide
into parallel fibers in molecular layer(slowest
conducting fibers) & synapse
(80,000-200,000) with purkinje cells–
• Activation results in a weaker action
potential------- SIMPLE SPIKE
 TURN ON/TURN OFF SIGNALS FROM CEREBELLUM
The typical function of the cerebellum is to RAPID
•
turn-on signals for the agonist muscles and
simultaneous reciprocal turn-off signals for the
antagonist muscles at the onset of a movement.
Parallel signals to pathway(cortico spinal tract )
•
Summation of cortical & cerebellar signals (ESS)
•
Then on approaching termination of the
•
movement, the cerebellum is mainly responsible for
sending turn-off signals to the agonists and
CEREBELLUM COORDINATES OVERALL MOTOR CONTROL THROUGH
1. VESTIBULOCEREBELLUM / FLOCCULONODULAR LOBE
• Provides anticipatory correction for maintaining
equilibrium during rapid motions & rapid changes
in body positions by controlling the balance
between agonist and antagonist muscle
contractions of spine, hip and shoulders
• Receives input from vestibular apparatus, eye and
body periphery and calculates in advance the
probability of different parts from the rates and
directions of the movement
• DAMAGE TO THE FLOCCULONODULAR
LOBE
• results in motor deficits resembling those
produced by a lesion of vestibular
apparatus
• Difficulty in balance, gait ataxia and often
nystagmus
 2.SPINOCEREBELLUM / VERMIS & ADJACENT
PORTIONS OF CEREBELLAR HEMISPHERE
• COMPARES the intended sequential plan of movement
from motor cortex with actual performance of body
• Prevents OVERSHOOT and DAMPS movement by
stopping the movement precisely at the intended point
• Controls BALLISTIC MOVEMENTS (The entire movement
is preplanned & set into motion to go for a specific
distance & then stops)via biphasic function.
LESION,results in dysmetria, ataxia & action/intention tremor
CEREBRAL AND
CEREBELLAR
CONTROL OF
VOLUNTARY
MOVEMENT BY
SPINOCEREBELLUM
 3. CEREBROCEREBELLUM / LATERAL CEREBELLAR HEMISPHERE/
Planning of sequent. mvments with hands, finger & spch
From sensory & premotor areas of cerebral cortex🡻
cerebellum 🡻cerebral cortex ? / distal muscle & speech
Timing of the sequential movement
Appropriate timing for succeeding movement is planned for
smooth progression of movements. CC🡻 CBLM
Extra motor predictive function to time events not mvm
to respond to rapidly changing sensory
information/auditory & visual phenomena/ monkey
bashing into wall
Lesiondecomposition of movements, dysdiadokokinesia
 Destruction of small portions of the lateral
•
cerebellar cortex seldom causes detectable
abnormalities in motor function.

If the deep cerebellar nuclei are not

•
removed along with the cortex, the motor
functions of the animal appear to be almost
normal as long as the animal performs all
movements slowly

To cause serious dysfunction of the

•
 CEREBELLAR LESIONS
• PRODUCE IPSILATERAL DEFECTS
• ROMBERG TEST
• patient who has a problem with
Proprioception (Somatosensory) can still
maintain balance by compensating with
vestibular function and vision. In the
Romberg test, the patient stands upright
and asked to close his eyes. A loss of balance
is interpreted as a positive Romberg sign /
A CEREBELLAR LESION
 CLINICAL ABNORMALITIES OF THE
CEREBELLUM
• Dysmetria and Ataxia
• Past Pointing
• Intention Tremors / action tremor
• Cerebellar Nystagmus / Tremor of Eyeballs
• Dysdiadokokinesia / JUMBLED MOVEMMENTS
• Dysarthria / JUMBLED VOCALIZATION
• Hypotonia
• Decomposition of movements
• Drunken gait
• Movements overshoot the intended mark and
conscious brain overcompensates in opposite
direction
• Failure of progression occurs when motor system
fails to predict and manifests (in advance) as series
of jumbled movements (dysdiadokokinesia,
dysarthria)
• Loss of tonic signals from deep cerebellar nuclei
results in hypotonia
• Scanning speech / jumbled vocalization-due to lack
of coordination
 CEREBELLAR LEARNING
st
• When a person 1 performs a new motor act,
• the degree of motor enhancement by cerebellum at the
onset of contraction,
• the degree of inhibition at the end of contraction
• and their timing are almost incorrect and not precise
• With training the sensitivity levels of the cerebellar
circuits change specially of the climbing fibers from
inferior olive / no more error signals
• The basis of the learning in the cerebellum is
probably the input via the olivary nuclei. each
Purkinje cell receives inputs from 250,000 to 1 million
mossy fibers, but each has only a single climbing fiber
from the inferior olive, and this fiber makes 2000–3000
synapses on the Purkinje cell.

• Climbing fiber activity (large complex spike) is

increased when a new movement is being learned,
and selective lesions of the olivary complex abolish
the ability to produce long-term adjustments in
 BASAL GANGLIA
Accessory motor system that
works in close association with
corticospinal system
Input signals = from cerebral cortex
Output signals = back to the cortex
 COMPONENTS OF BASAL GANGLIA SYSTEM

1. CAUDATE NUCLEUS
2. PUTAMEN (ALSO CALLED STRIATUM COLLECTIVELY)
3. GLOBUS PALLIDUS
4. SUBTHALAMUS
5. SUBSTANTIA NIGRA (PC & PR )---MELANIN
ASSOCIATED WITH BASAL GANGLIA ARE
VA & VL NUCLEI OF THALAMUS
 INTERNAL CAPSULE
• The space between the major masses of
Basal Ganglia
( Caudate nucleus and Putamen),
where lie all the sensory and motor fibers
that connect the cerebral cortex and spinal
cord is known as internal capsule
 MOTOR FUNCTIONS OF BASAL
GANGLIA
PUTAMEN CIRCUIT
1 -To control complex patterns of motor activity/
skilled movements
CAUDATE CIRCUIT
2 -Cognitive control of sequences of motor
functions
3 -To change the timing and to scale the intensity
of movements
THE PUTAMEN CIRCUIT
1. DIRECT PATHWAY
• ENHANCES MOTOR ACTIVITY / EXCITATORY

in the direct pathway, the striatum projects to the

•
internal segment of the globus pallidus.This
projection is inhibitory (GABA). The internal
segment of the globus pallidus projects to the VA
and VL nuclei of the thalamus. These connections
also use GABA and are inhibitory. The VA and VL
nuclei send excitatory connections to PRIMARY
MOTOR CORTEX & to prefrontal, premotor, and
 2. INDIRECT PATHWAY
Reduces the activity of neurons in the motor areas
•
of the cerebral cortex / INHIBITORY
The indirect pathway involves inhibitory connections
from the striatum to the external segment of the
globus pallidus, which in turn sends an inhibitory
projection to the subthalamic nucleus. The
subthalamic nucleus in turn sends an excitatory
projection back to the internal segment of the globus
pallidus. From here fibers via thalamus go back to
prefrontal, premotor & suppl. Motor cortex
 1st & last projections are excitatory and
•
two intervening connections are
inhibitory

The direct (excitatory) and indirect

(inhibitory) pathways of the basal ganglia
 Abnormal movements in the lesions of
putamen circuit
• PUTAMEN
– Flicking, dancing movements of hands & face/Chorea
• GLOBUS PALLIDUS
– Continuous, slow, Writhing movements / Athetosis
• SUBTHALAMUS
– Violent Flailing limb movements / Hemiballismus
• SUBSTANTIA NIGRA
– Parkinson’s Disease (Rigidity, Akinesia & Tremor)
CAUDATE
CIRCUIT
NEURAL PATHWAYS OF CAUDATE CIRCUIT
 ---THE CAUDATE CIRCUIT
1. Cognitive control of sequences of motor functions

• Cognition –thinking process using sensory input and

information already stored in memory
• Caudate Circuit receives large amount of input from
association areas
None of the returning signals pass directly to primary
motor cortex rather go to PFA, PMA & SMA
1. Subconscious & sequential control of pattern of
movement not the individual movement
 2. TIMING AND SCALING THE INTENSITY
•
OF MOVEMENT

(1) to determine how rapidly the movement is

•
to be performed and

(2) to control how large the movement will be.

•
THROUGH CAUDATE CIRCUIT Basal ganglia
•
function in close association with
POSTERIOR PARIETAL CORTEX where
 Lesion of caudate or posterior
parietal cortex
Agnosia. Damage to PPC does not produce
simple sensory deficits but an inability to
accurately perceive objects through normally
functioning sensory system is known as agnosia
• Personal neglect syndrome
In right PPC lesion patient’s perception about
left side of his body is lost
 Or unilateral inattention and
•
neglect.
Individuals with such lesions do not have
•
any apparent primary visual, auditory, or
sensory defects, but they ignore stimuli
from the contralateral portion of their
bodies. This leads to failure to care for
LESIONS OF THE BASAL GANGLIA GIVE
RISE TO CONTRALATERAL DEFICITS
• Because basal ganglia influence
motor cortex , therefore act through
lateral and medial motor pathway
 NEUROTRANSMITTERS IN BASAL
GANGLIA SYSTEM
1. DOPAMINE Pathway (SN 🡻 STRIATUM)
2. GAMMA AMINOBUTYRIC ACID (GABA)
Pathway (STRIATUM 🡻 GP & SN)
3. ACETYL CHOLINE pathway (CX 🡻 STRIATUM)
4. BRAINSTEM PATHWAYS that secrete NE,
SEROTONIN, ENKEPHALIN
5. Multiple GLUTAMATE Pathways
 PARKINSONISM
Loss of neurons of the PARS COMPACTA OF
SUBSTANTIA NIGRA
• Striatum (mainly putamen)suffers from loss of
dopamine
• Dopamine is an inhibitory N.T
• Dopamine has an overall excitatory action on
direct pathway (D1 receptors-GPI )&
an inhibitory action on indirect pathway (D2
receptors-GPE )
 LOSS OF DOPAMINE
DECREASES the activity of DIRECT
PATHWAY & INCREASES the activity
of INDIRECT PATHWAY
Resulting in greater inhibition of
thalamus and decreased activation
of motor cortical areas
 FEATURES OF PARKINSON’S DISEASE
• (BOTH HYPER & HYPOKINETIC FEATURES)
1. Rigidity ( lead pipe / cog wheel)
2. Involuntary tremors / resting tremors
3. Akinesia /bradykinesia
4. Postural instability
5. Other motor dysfunctions – loss of assoc.
movements, facial expressions
dysphagia, speech disorders, gait disturbances
& fatigue
In the absence of inhibitory neurotransmitter
Dopamine,
continuous excitatory output from caudate and
putamen to the corticospinal motor system
results in
LEAD PIPE RIGIDITY/ COGWHEEL RIGIDITY
(motor neuron discharge 🡻es to both agonists
and antagonists)
 -Regular alternating contractions of antagonistic
muscles and/or
- Oscillations of feedback circuits lead to
RESTING TREMORS/INVOLUNTARY TREMORS
1. Decreased dopamine secretion in the
limbic system reduces the psychic drive for
motor activity and results in AKINESIA
 TREATMENT
• L-DOPA / NOT DOPAMINE
– (To restore the normal balance)
• L-DEPRENYL
– (Inhibits monoamine oxidase )
• TRANSPLANT OF FETAL DOPAMINE CELLS INTO
CAUDATE & PUTAMEN NUCLEI
– ( obtained from aborted fetuses )
• BLOCKING THE FEED BACK CIRCUITRY IN THE
BASAL GANGLIA
 CLINICAL SYNDROMES RESULTING
FROM DAMAGE TO BASAL GANGLIA
• (HYPERKINETIC & HYPOKINETIC FEATURES)
• Disturbance in medial motor system results
in tone, posture and balance, gait
• Disturbance in lateral motor system results
in involuntary automatic and purposeless
movements at distal joints –pill rolling
movements and resting tremors of fingers
• Hyperkinetic feature
• Chorea, athetosis and ballism
• Hypokinetic features
• Akinesia = difficulty in initiation of
movement
• Bradykinesia = slowness of movement
 HUNTINGTON’S CHOREA
• Hereditary disorder/trinucleotide repeats CAG
• (HUNTINGTON /toxic to C & P)Loss of GABA
secreting neurons in Caudate & putamen nuclei
which
leads to spontaneous outbursts of GP & SN
activity
Resulting in
• 1. Flicking movements,
• 2.distortional movements &
• 3. dementia ( loss of Ach secreting neurons ).
 FRIEDREICH’S ATAXIA
GAA REPEAT IN AN INTRON GIVES THE CLINICAL
PICTURE OF MOTOR DYSFUNCTION
TARDIVE DYSKINESIA
• IS IATROGENIC IN NATUER CAUSED BY
NEUROLEPTIC DRUGS
WILSON’S DISEASE
• THERE IS HEPATOLENTICULAR DEGENERATION
GIVES RISE TO KEYSER-FLEISHER RINGS
Physiological anatomy of cerebral cortex
• Functional part of cortex is a thin layer of
neurons covering the surface of all
convolutions of cerebrum 2-5 mm thick
• Granular cells
• Interneurons - Excitatory & inhibitory
• Pyramidal & fusiform cells
• All the output fibers
• Layers of cerebral cortex I-VI
• Thalamocortical system
 THALAMOCORTICAL SYSTEM
• Cortex operates in close association with
thalamus / as a functional unit
• When the thalamus is damaged along with
cerebral cortex the loss of function is far
greater than when cortex alone is damaged,
because thalamic excitation of cortex is
necessary for cortical activity
• All sensory pathways pass through thalamus
MOL. LAYER

EXT. GR. LAYE

PYRAMIDAL C

INT. GR. LAYR

LARGE
PYRMIDAL
CELLS LAYER

LAYER OF
FUSIFORM
OR
POLYMORP
HIC CELLS
 Functions of specific cortical areas
Primary motor areas of cortex
Direct connections with specific muscles, for
discrete muscle movements
Primary Sensory areas of cortex
detect specific sensations like visual, auditory or
somatic
Secondary motor & sensory areas of cortex
(PM,SM) Provide patterns of motor activity
Analyze meanings of specific sensory signals
 ASSOCIATION AREAS
They receive and analyze signals simultaneously
from multiple regions of both the motor and
sensory cortices as well as from subcortical
structures.

They are specialized into

A The Parieto-occipitotemporal Association

Area,

B The Prefrontal Association Area

 PARIETO-OCCIPITO-TEMPORAL ASSOCIATION
AREA/GENERAL INTERPRETATIVE AREA
High level of interpretation of signals from all the
surrounding sensory areas
subareas
1. Analysis in time and space/spatial coordination of body
2. Language comprehension /intelligence/WERNICKE’S AREA
3. Visual processing of language/reading ANGULAR GYRUS
AREA / VISUAL ASSOCIATION AREA
4. Area for NAMING OF OBJECTS
 2. PREFRONTAL ASSOCIATION AREA
Receives pre analyzed sensory information
– motor functions /motor planning via motor
control system & basal ganglia /caudate
– Non motor function = Important for elaboration
of thoughts &
– Short term storage of working memories
BROCA’S AREA
Works in close association with Wernicke's area
Neural circuits for word formation where plans & motor
patterns of words to be expressed are decided
• Storage of new language
 C. LIMBIC ASSOCIATION AREA /
LIMBIC CORTEX (ant pole of temp. lobe)
• Along with LIMBIC SYSTEM is Concerned primarily
with behavior, emotion and motivational drive
• AREA FOR RECOGNITION OF FACES
• Medial under surfaces of both occipital & temporal
lobes
Damage to this area results in PROSOPAGNOSIA that
is inability to recognize faces
WERNICKE’S AREA
• WERNICKE’S AREA
• Well developed on left side of brain in right handed
people.
• Plays major role in higher brain functions like higher
comprehension called intelligence
Also known as gnostic area / knowing area / tertiary
association area
• Damage to Wernicke's area
• Person is able to read & hear well but unable to
understand the thought behind them. Electric stimulation
causes auditory &visual hallucination
 ANGULAR GYRUS
• Most inferior portion of post. parietal lobe behind
Wernicke's area
• visual interpretation area
• Damage to angular gyrus
(but intact WERNICKE’S AREA ) results in
DYSLEXIA or WORD BLINDNESS(? Decode at word)
• Because the stream of impulses from visual cortex
to Wernicke's area is blocked
• Can interpret auditory impulses as usual
• SPECIALIZATION OF CEREBRAL
HEMISPHERES

1. DOMINANT OR CATEGORICAL HEMISPHERE

2. NON DOMINANT OR REPRESENTATIONAL
HEMISPHERE
FUNCTIONS/PARIETO OCCIPITO TEMPORAL CORTEX
IN DOMINANT HEMISPHERE / SPECIALIZED H
IN 95% OF PEOPLE WERNICKE’S AREA, ANGULAR
GYRUS, SPEECH & MOTOR CONTROL AREAS ARE
HIGHLY DEVELOPED IN ONE CEREBRAL HEMISPHERE
• Right-handed ness
• Wernicke’s area is 50% larger at birth in the left
cerebral half.
• If left area is damaged or removed in early
childhood then opposite side becomes dominant
• In 95 % of all people left temporal lobe & left
angular gyrus become dominant
• In rest 5 % of the people either both sides
develop simultaneously or right becomes
dominant
• In 90% of the people motor areas controlling
hand muscles are also dominant on left side
resulting in right handedness
 LANGUAGE & COMPREHENSION
• Not the printed words but their conveyed
thoughts are stored as language
• In early life language function develops by
close association of Wernicke’s Area with
prim. & sec. areas of temporal lobe
later in life when reading develops, language
develops from visual information through
angular gyrus
• When we speak of DOMINANT
HEMISPHERE, we primarily speak about
the language based intellectual functions

Lesion of Wernicke’s Area in DOMINANT

HEMISPHERE produces
• Language disorders and capabilities to
perform complex goals are lost
 PARIETOOCCIPITOTEMPORAL CORTEX IN
NONDOMINANT HEMISPHERE/REPRESENT HEMISPH
• This area is important in understanding and
interpreting music and visuospatial relations
LESIONS OF THE Representational /Non Dominant hemisphere

1. Astereognosis—the inability to identify objects by

feeling them—and other

2. Agnosias. Agnosia is the general term used for the

inability to recognize objects by a particular sensory
modality
 FUNCTIONS OF BRAIN IN CUMMUNICATION
LANGUAGE is understanding of written or
spoken words & expressing them in speech and
writing

1. Sensory aspect/ language input via ears & eyes

2. Motor aspect/ language output by vocalization
• Wernicke’s area is concerned with comprehension
of auditory and visual information it projects via
arcuate fasciculus to the broca’s area (area 44) in
the frontal lobe which processes the information
received from the Wernicke's area into a detailed
and coordinated pattern of vocalization(timing ,
sequence and intensity )and projects the pattern to
the concerned muscles in the motor cortex which
initiates the movements of lips, tongue and larynx
to produce speech
• SENSORY ASPECT OF CUMMUNICATION
1. Auditory receptive aphasia/ word deafness
– - inability to understand spoken word/auditory
association area
2. Visual receptive aphasia/ word blindness – inability to
understand written word / visual association area
3. Wernicke’s aphasia/Wernicke's area in D.H / able to
understand but unable to interpret(Spoken&Written)
4. Global aphasia /Wernicke's Area, Angular Gyrus and
Temporal lobe
• Total loss of understanding & communication
MOTOR ASPECTS OF COMMUNICATION
• SPEECH involves
– Comprehension / Wernicke's area
– Expression / Broca’s area
1. LOSS OF BROCA’S AREA causes Motor aphasia
skilled motor patterns of speech and respiratory
muscles are lost
2. DISTURBED ARTICULATION
due to any lesion of facial and laryngeal regions of
motor cortex,
3.LESION OF FEED BACK CIRCUITS of cerebellum
and basal ganglia
 APHASIA
• Are abnormalities of language functions that
are not due to the defect in hearing, vision or
motor paralysis
• Fluent aphasia /
•Wernicke's area
•Arcuate fasciculus / Conduction aphasia
• Nonfluent aphasia /Broca’s area
• Anomia aphasia / angular gyrus / word
blindness
 HIGHER INTELLECTUAL FUNCTIONS OF
PREFRONTAL AREA
speaking ability, elaboration of thought,
prognostication & working memory

The ability of the prefrontal areas to keep

•
track of many bits of information
simultaneously and to recall of this
information as it is needed for subsequent
thoughts is called the brain’s “working
 (1) prognosticate;

(2) plan for the future;

(3) delay action in response to incoming sensory

signals

(4) consider the consequences of motor actions before

they are performed;

(5) solve complicated mathematical, legal, or

philosophical problems;

(6) correlate all avenues of information in diagnosing

rare diseases; and
 Functions of carpus callosum
information stored in the cortex of one hemisphere is made
•
available to corresponding cortical areas of the opposite
hemisphere.
Cutting the corpus callosum
Blocks transfer of information from Wernicke’s area of the
dominant hemisphere to nondominant (the motor cortex on the
other side)
Also blocks transfer of somatic and visual information from the
right hemisphere / non dominant into Wernicke’s area in the
MEMORY
LEARNING is acquisition of the information that makes this possible
and MEMORY is the retention and storage of that information. A

THOUGHT results from a “pattern” of stimulation of many parts of the

nervous system at the same time, probably involving most importantly
the cerebral cortex, thalamus, limbic system, and upper reticular
formation of the brain stem. This is called the

holistic theory of thoughts.

CONSCIOUSNESS can be described as our continuing stream of

awareness of either our surroundings or thoughts.
 Role of synaptic facilitation & synaptic inhibition
The brain has the capability to learn to ignore
•
information that is of no consequence. This results from
inhibition of the synaptic pathways for this type of
information; the resulting effect is called HABITUATION.
This is a type of NEGATIVE MEMORY. For information
that causes pain or pleasure,the brain has a automatic
capability of storing THE MEMORY TRACES. This is
POSITIVE MEMORY. It results from facilitation of the
synaptic pathways, and the process is called MEMORY
EXPLICIT OR DECLARATIVE MEMORY / VERBAL
& SYMBOLIC

( memory of events) is dependent on the

hippocampus for its retention.

IMPLICIT / NONDECLARATIVE / SKILL MEMORY

depends on motor activities such as skills

does not usually involve processing in the
hippocampus
 (1)SHORT-TERM MEMORY,
which lasts for seconds to several minutes, unless they
•
are converted into long term memories

SHORT TERM MEMORY IS BASED ON

1. The nerve signals that travel around and
around a temporary memory trace in a
reverberating neuronal circuit.
2. The secreted neurotransmitter causes
presynaptic facilitation or inhibition for
several minutes
 INTERMEDIATE LONGTERM MEMORIES
• Which last for days to weeks unless memory traces
are activated enough to become more permanent
Can result from temporary chemical and /or physical
changes, in either presynaptic or postsynaptic
membrane known as habituation(negative memory)
or facilitation (positive memory)
neuron
 MOLECULAR MECHANISMS
• HABITUATION results from progressive closure
of calcium channels resulting in decreased
amount of neurotransmitter release from
sensory terminal
• FACILITATION results from blocking of
potassium channels resulting in prolonged
action potential in sensory terminal,
prolonged activation of calcium channels,
increased transmitter release -----facilitation
 LONG TERM MEMORY
One which once stored can be recalled up to years or
even a lifetime later
Results from capacity increasing structural changes at
synapses
– Increase in the no of release sites for N.T.
– Increase in no of vesicles
– Increase in the no of presynaptic terminals
– Changes in dendrites Nerve growth factors/ use
it or lose it
 CONSOLIDATION OF MEMORY
the short-term memory if activated repeatedly will
•
initiate chemical, physical, and anatomical changes in the
synapses that are responsible for the long-term type of
memory. This process requires 5 to 10 minutes for minimal
consolidation and 1 hour or more for strong consolidation.

Rehearsal of the same information enhances the

–
Transference of Short-Term Memory into Long-Term
Memory.

New Memories are codified during consolidation

–
The new memories are not stored randomly in the brain
 Role of specific parts of brain in memory
HIPPOCAMPUS PROMOTES STORAGE OF MEMORIES
The two hippocampi removed for the treatment of
•
epilepsy did not seriously affect the person’s memory
for information stored in the brain before removal of
the hippocampi these people had virtually no
capability thereafter for storing verbal and symbolic
types of memories (declarative types of memory) in
long-term memory.
Hippocampi are not important in acquiring skill
•
ANTEROGRADE AMNESIA OCCURS
FOLLOWING HIPPOCAMPAL &/OR THALAMIC LESION
• Inability to acquire new long term memories of
those types of information that are intelligence
based
HIPPOCAMPI are important output Pathways from
Reward and Punishment centers of limbic system
and along with DMN of thalamus are concerned with
decision making about the retention of good or bad
memories
 RETROGRADE AMNESIA/ hippocampal and
•
specially the THALAMIC LESION
Inability to recall memories from the Past.
The degree of amnesia for recent events is likely to be
much greater than for events of the distant past.
MEMORIES OF DISTANT PAST HAVE BEEN REHEARSED AND
STORED IN WIDESPREAD AREAS OF BRAIN
IN HIPPOCAMPAL LESION ONLY BOTH ANT.AMN. &RET.AMN.
CAN OCCUR . PURE RETROGRADE AMNESIA ONLY IN LESION OF
THALAMUS
 Conditioned reflexes
A CONDITIONED REFLEX is a reflex response to a
•
stimulus that previously elicited little or no response,
acquired by repeatedly pairing the stimulus with another
stimulus that normally does produce the response.

• The meat placed in the mouth was the

UNCONDITIONED STIMULUS (US), the stimulus
that normally produces a particular innate response.

The CONDITIONED STIMULUS (CS) was the bell

•
ringing. After the CS and US had been paired a
LIMBIC SYSTEM
1.Mechanisms that control the levels of activity in
the different parts of brain
◆Directly via ret. excit. Area of brainstem
/directly by stimulating the background
neuronal activity
◆Via neurohormonal systems
2.Motivational control & feelings of pleasure and
punishment
Signals from Pontine brainstem excitatory area to cortex
Signals from periphery to brainstem
cutting the brainstem above the point where fifth cerebral
nerve enters the pons--COMA/cutting below this level, coma
is averted
• Feedback signals passing between the excitatory area and
cerebral cortex in a positive feedback manner result in
AWAKE MIND
• Reticular inhibitory area in lower brainstem
• Thalamus, cortex and long term memory
• CLINICAL STATES FROM REDUCED ALERTNESS
• DROWSINESS
like light sleep ,can be aroused by light touch or
noise
• STUPOR
can be awakened only by strong, vigorous or
painful stimuli
• COMA
can not be aroused by any stimulation
NEURO-HARMONAL SYSTEMS
OF BRAIN
1. LOCUS CERULEUS and norepinephrine system, an
excitatory hormone

2. SUBSTANTIA NIGRA and dopamine system, excitatory

in some areas but inhibitory in others.

3. RAPHE NUCLEI and serotonin system, serotonin

usually is inhibitory
4. RETICULAR EXCITATORY area and acetylcholine
 LIMBIC SYSTEM
on the medial and ventral surface of
the cerebral hemisphere is paleo
cortex, surrounding the deep
structures & associated with overall
behavior and emotions
Border structures around the basal regions of brain /
border system / limbic system performs the function
of

MOTIVATIONAL DRIVES / motivational control

•
of the learning process

FEELINGS OF PLEASURE AND PUNISHMENT.

•
The entire neuronal circuitry of Limbic System
•
controls emotional, behavior and motivational
 BEHAVIORAL & MOTIVATIONAL
CONTROL
• EMOTIONS are subjective feelings or mood
e.g. fear, anger and happiness
• BEHAVIORAL PATTERNS are accompanying
physical responses e.g. attack or defense or
laughing or crying
• MOTIVATION is ability to direct behavior to a
goal
• LIMBIC SYSTEM
consists of the following
• The limbic lobe ( gyrus fornicatus, gyrus
cingulus, isthmus, hippocampal gyrus and
uncus )
• The related subcortical nuclei ( amygdala,
septal nuclei, anterior thalamic nuclei and
hypothalamus )
 PAPEZ CIRCUIT
A circuit that connects the limbic lobe/cortex with the
hypothalamus (the Papez circuit), regulates recent
memory & Emotional behavior. Information passes from
• Cingulate gyrus 🡻Hippocampus then via fornix 🡻
mammillary bodies of hypothalamus 🡻 by
mammillothalamic tract to anterior nuclei of
thalamus which projects back 🡻 cingulate gyrus
• A cortico - hypothalamo – thalamo - cortical
circuit is produced
 HYPOTHALAMUS--- < 1% of brain mass
The hypothalamus is a collection of specific nuclei and associated
fibers that lie beneath the thalamus.
• An integrating center for many important homeostatic
functions
• An important link between the autonomic nervous
system and the endocrine system. HEAD GANGLION
(highest level of ANS ctrl)
• Has two way communicating pathways with all levels of
limbic system-integ/ visc & somatic phenomena assoc.
with behavior
output signals of hypothalamus
are sent in three directions:

(1) to the brain stem,🡻 into the peripheral nerves of the

AUTONOMIC NERVOUS SYSTEM

(2) upward toward to the anterior thalamus and limbic portions

OF THE CEREBRAL CORTEX

(3) into the hypothalamic infundibulum to control most of the

secretory functions of POSTERIOR AND THE ANTERIOR
PITUITARY GLANDS.

• Thus it controls most of the vegetative and endocrine

 VEGETATIVE & ENDOCRINE
FUNCTIONS OF HYPOTHALAMUS
1. Cardiovascular regulation
2. Regulation of body temperature
3. Regulation of body water
4. Regulation of uterine contractility
5. Regulation of milk ejection from breast
6. Gastrointestinal and feeding regulation
7. plays a role in emotional and behavioral patterns
8. participates in the sleep–wake cycle.
Lesions of hypothalamus
 Behavioral functions of
hypothalamus and limbic
system
 Stimulation in the lateral hypothalamus not only causes
1.
thirst and eating, but also sometimes causes overt rage
and fighting.

Stimulation in the ventromedial causes opposite effects

2.
that is, a sense of satiety, decreased eating, and
tranquility.

Stimulation of a thin zone of periventricular nuclei,

3.
usually leads to fear and punishment reactions.

4. Sexual drive can be stimulated from the most anterior

Reward and punishment function of limbic system
• Major reward centers
• Along the course of medial forebrain
bundle in the lateral and ventromedial
nuclei of hypothalamus
• Less potent reward centers
• In septum, amygdala certain areas of
thalamus and basal ganglia
 Punishment centers
The most potent punishment areas
have been found in the central gray area
surrounding the aqueduct of Sylvius and
extending upward into the periventricular zone
of hypothalamus and thalamus.

Less potent punishment areas

are found in some locations in the amygdala
 RAGE PATTERN
Strong stimulation of the punishment centers of the
•
brain, causes the animal to

(1) develop a defense posture, (2) extend its claws,

•
(3) lift its tail, (4) hiss, (5) spit, (6) growl, and (7)
develop piloerection and dilated pupils. Even the
slightest provocation causes an immediate savage
attack.

PLACIDITY AND TAMENESS occurs when reward

 HOW REWARD OR PUNISHMENT
HELPS IN LEARNING AND MEMORY
 a sensory experience that causes neither reward
nor punishment is hardly remembered at all.
Repetition of the stimulus over and over leads to
almost complete extinction of the cerebral
cortical response. That is, the animal becomes
HABITUATED to that specific sensory stimulus
and thereafter ignores it.
If the stimulus does cause either reward or
punishment, the cerebral cortical response
becomes progressively more and more intense
during repeated stimulation, and the response is
said to be REINFORCED (strong memory traces).
 FUNCTIONS OF HIPPOCAMPUS
The hippocampus has numerous connections with
many portions of the cerebral cortex and the limbic
system
An additional channel through which sensory signals
can initiate behavioral reactions.(rage, pleas)
With Stimulation, can become hyperexcitable, (focal
epileptic seizures, auditory and visual hallucinations)
Bilateral removal OF HIPPOCAMPUS can result in anterograde
amnesia (only short term memory is left).
Plays role in consolidation of long term memories
 AMYGDALA
THE AMYGDALA HAS BEEN CALLED THE “WINDOW” THROUGH
•
WHICH THE LIMBIC SYSTEM SEES THE PLACE OF THE PERSON IN THE
WORLD

The amygdala receives neuronal signals from all

•
portions of the limbic cortex, as well as from the neocortex of
the temporal, parietal, and occipital lobes—especially from
the auditory and visual association areas.

The amygdala transmits signals (1) back into these

•
same cortical areas, (2) into the hippocampus, (3) into the
septum, (4) into the thalamus, and (5) especially into the
• Stimulation of amygdala brings about same effects
as direct stimulation of hypothalamus
(BP🡻🡻,HR🡻🡻,GIT pupillary size🡻🡻 ant. Pit. hormones
• Several types of involuntary movements
e.g. tonic, clonic, licking and chewing
• Patterns of rage, pain, punishment and reactions of
reward and pleasure
• Still other areas on stimulation cause sexual
activities, ovulation & ejaculation.
 KLUVER BUCY SYNDROME
RESULTS FROM BILATERAL ABLATION OF THE AMYGDALA

(1) is not afraid of anything,

(2) has extreme curiosity about everything,

(3) forgets rapidly,

(4) has a tendency to place everything in its mouth and

sometimes even tries to eat solid objects, and

(5) often has a strong sex drive

AMYGDALA is a behavior awareness area at subconscious

 Functions of limbic cortex
• As cerebral association area for control of behavior
On stimulation all behavior patterns can be produced
Ablation of ant. Temporal cortex/Kluver Bucy Syndro
Ablation of post. Orbital frontal cortex / insomnia,
restlessness
Ablation of ant. Cingulate gyrus / fits of rage / release
of rage patterns from prefrontal inhibition
• There is definite associations between the specific
cortical regions, limbic system and and behavior
• In the anterior Temporal cortex are olfactory and
gustatory associations
• In para hippocampal gyri are complex auditory &
thought (Wernicke area of post. Temporal lobe)
associations
• In middle and post. Cingulate gyrus are
sensorimotor behavior associations
 RETICULAR FORMATION AND RETICULAR
ACTIVATING SYSTEM

The reticular formation, the

•
phylogenetically old reticular core of the
brain, occupies the midventral portion of
the medulla and midbrain. it contains the
cell bodies and fibers of many of the
serotonergic, noradrenergic, adrenergic,
AFFERENT CONNECTIONS
From a large variety of sources
• afferent pathways to cerebellum and thalamus
(optic, olfactory, auditory, gustatory, trigeminal,
touch, pain, pressure, vibration, proprioception and
visceral stimuli)
EFFERENT CONNECTIONS
• Spinal cord- (descending reticulospinal tracts)
• Cerebrum direct or via thalamus
• cerebellum
• FUNCTIONS
• 1. By acting as an integrating center, is involved in
motor activities ( Reticulospinal tract to extensor
muscles) by
– Pontine excitatory area stimulated by vestibular
nuclei
– Medullary inhibitory area stimulated by cerebral
cortex, basal ganglia and cerebellum
– A mid collicular lesion produces DECEREBRATE
RIGIDITY
– 2.Centers for control of respiration, blood pressure
and heart rate
RETICULAR ACTIVATING SYSTEM
3. The RAS is a complex polysynaptic pathway
arising from the brain stem reticular formation
with projections to the intralaminar and
reticular nuclei of the thalamus which, in turn,
project diffusely and nonspecifically to wide
regions of the cortex

essential for arousal from sleep,

ELECTRICAL ACTIVITY OF BRAIN
BRAIN WAVES

EEG
EVOKED CORTICAL POTENTIALS ( BARBITURATE
ANESTHESIA )
The record of electrical events that occur in the cortex
after stimulation of a sense organ, The first
positive–negative wave sequence is
The 1st response is THE PRIMARY EVOKED POTENTIAL,
•
is highly specific in its location and can be observed only
where the pathways from a particular sense organ end.

The 2nd response is THE DIFFUSE SECONDARY

•
RESPONSE. . not highly localized and is due to activity in
ALPHA WAVES / ALPHA RHYTHM / 8-13 cycles/sec/ 50-100μV
awake but at rest the mind wandering and the eyes closed
(occipital, parietal & frontal region), synchronized
BETA WAVES /β RYTHEM/ ALPFA BLOCK 13-30 c/s When attention
is focused on something / intense mental activity, low voltage
asynchronous, high frequency waves (parietal & frontal),
asynchronous
THETA WAVES / 4-7c/s psychomotor states & infants
Can occur in adults under stress, psychomotor states (parietal and
temporal cx)
DELTA WAVES / 0.5-4 c/s voltage higher than any other type of
brain wave in deep sleep, infancy & organic brain disease
in stupor, surgical anesthesia, and deep sleep;
EFFECT OF VARYING LEVELS OF
CEREBRAL ACTIVITY ON EEG
 During periods of mental activity, the waves
•
usually become asynchronous & the
voltage falls considerably,

CLINICAL USES OF EEG

For diagnosing and localizing conditions as
1. Subdural hematomas / fluid collections
2. lesions of Cerebral Cortex
 PHYSIOLOGY OF SLEEP
defined as unconsciousness from which
the person can be aroused by sensory
stimuli
?nstupor,coma
• CLINICAL STATES FROM REDUCED ALERTNESS
• DROWSINESS
like light sleep ,can be aroused by light touch or
noise
• STUPOR
can be awakened only by strong, vigorous or painful
stimuli
• COMA
can not be aroused by any stimulation
 BASIC THEORIES OF SLEEP
– Fatigue of upper B.ST reticular activating system
– Active inhibition from midpontine level
Neuronal centers (SLEEP CENTERS ) and
neurohumoral substances causing NATURAL SLEEP
– Serotonin secreting Raphe nuclei of the lower half of
the pons and medulla
– Areas in nucleus of tractus solitarious
– Thalamus, hypothalamus
Lesions in a/m areas result in intense wakefulness
Sleep factor / factors ? muramyl peptidase & others
 1.SLOW-WAVE SLEEP / NON REM SLEEP
Deep, restful sleep associated with decrease in
vasomotor tone, respiratory rate, blood pressure and
metabolic rate, is divided into 4 stages
During stage 1 of sleep there is low voltage mix frequency
•
pattern, a theta rhythm & some activity of skeletal muscle.
can be seen

Stage 2 is marked by the appearance of sleep spindles

•
In stage 3, A high amplitude delta rhythm is dominant.
•
In stage 4.Maximum slowing with large waves is seen.
•
SLEEP SPINDLES
REM SLEEP
Occurs in bouts, associated with rapid low voltage activity,
roving movements of eyes, dreaming, bodily movements,
irregular respiratory & heart rate, decreased muscle tone &
EEG shows awake, aroused state---PARADOXICAL SLEEP
Though sensory threshold is elevated yet PGO spikes
A young adult typically passes through stages 1 and 2, and
spends 70–100 min in stages 3 and 4. Sleep then lightens,
and a REM period follows.
This cycle repeats at 90-min intervals throughout the night.
Four to six REM periods /night
 REM SLEEP
Acetylcholine secreting neurons in upper brainstem
reticular formation can activate many portions of brain
which excite both the cerebral cortex and peripheral
nervous system, although the signals can not cause
wakefulness.
SLEEP-WAKE CYCLES
When sleep centers are not activated, upper pontine RAS
is released from inhibition
Positive feedback signals between reticular act. system,
cerebral cortex & peripheral nervous systems followed by
fatigue and sleep
Alert wakefulness
is characterized by high-frequency beta waves,
Quiet wakefulness
is usually associated with alpha waves,
Sleep spindles are bursts of alpha wave activity during
NREM sleep
PGO spikes characteristic of REM sleep
Difficult to tell difference between REM sleep and alert
awake person
Sleep serves for neural maturation, learning &
memory, cognition, clearance of metabolic waste.
PHYSIOLOGICAL EFFECT OF SLEEP
• Effects on functional systems of the body
• Effects on the nervous system
Malfunction of the thought process
Abnormal behaviors like sluggishness, irritability
and can even become psychotic
 SLEEP DISORDERS
• NARCOLEPSY (orexin neurons )
• CATAPLEXY
• RESLESS LEG SYNDROME
• OBSTUCTIVE SLEEP APNOEA
• PARASOMNIAS
– SOMNAMBULISM / sleep walking
– NOCTURNAL ENURESIS /bed wetting
– NIGHT TERROR
 CIRCADIAN RHYTHM
SLEEP-WAKE CYCLES
• Transitions from sleep to wakefulness may involve
alternating reciprocal activity of different groups
of RAS neurons.
• 🡻 activity of norepinephrine and serotonin
containing neurons & 🡻 activity in acetylcholine
containing neurons leads to the appearance of
wakefulness & vice versa
Melatonin release from the richly vascularized
pineal gland also plays a role in sleep mechanisms
 EPILEPSY
is characterized by
uncontrolled, excessive
activity of either part or all of
the central nervous system
• Epilepsy, a syndrome with multiple causes and
shows characteristic EEG patterns during
seizures
• Seizures are divided into
1. PARTIAL / FOCAL SEIZURES
2. GENERALIZED SEIZURES / (GRAND
MAL)
3. ABSENCE SEIZURES (PETIT MAL )
• GRAND MAL EPILEPSY is characterized by
• Tonic seizures
• Tonic-clonic seizures
• Post seizure depression
• High frequency & high voltage EEG
• Initiated by strong emotional stimuli, alkalosis,
drugs, fever & bright lights which activate
reverberating neuronal circuits throughout the
brain
• Stopped by neuronal fatigue
 PETIT MAL EPILEPSY is characterized by
• a few seconds of unconsciousness or 🡻
consciousness
• Twitch like contractions of head or facial muscles
• Blinking of eyes
• Also called ABSENCE SYNDROME
• Results from oscillations between excitatory and
inhibitory cortico thalamic neurons
 FOCAL EPILEPSY
• Lesions involving local part of brain or deeper
structures of brain – a scar or a tumor
When discharge rate increases it spreads to adjacent
cortical regions resulting in
1. March of muscle contractions / Jacksonian
Epilepsy
• Can proceed to Grand Mal Epilepsy
2. Involvement of LIMBIC SYSTEM results in a type of
focal epilepsy called psychomotor seizure
 PSYCHOTIC BEHAVIOR
1. DEPRESSION
Diminished activity of
neurotransmitters-norepinephrine or serotonin or
both which normally drive the limbic area of brain
into feeling of well being, happiness, good appetite &
sex drive
2.MANIC-DEPRESSIVE PSYCHOSIS/ BIPOLAR DISORDER
3. SCHIZOPHRENIA
Prefrontal lobes / excess Dopamine /hippocampus
 Alzheimer disease and dementia
Alzheimer disease is the most common age-related
•
neurodegenerative disorder. Memory declines, initially
manifests as a loss of episodic memory, recollection of
recent events is effected. Loss of short-term memory is
followed by general loss of cognitive and other brain
functions, the need for constant care, and, eventually,
death.

The cytopathologic hallmarks of Alzheimer disease are

•
intracellular neurofibrillary tangles,
 Déjà vu phenomena
Means “already seen”
• In strange surroundings one is alert and on guard, in
familiar surroundings vigilance is relaxed
• An inappropriate feeling of familiarity with new
events or new surroundings is known as
• stimulation of some parts of the temporal lobes in
humans causes a change in interpretation of one’s
surroundings.
 THALAMUS
• A large ovoid mass, part of diencephalon
• Medial surface forms the lateral wall of
3rd ventricle
• There are five major masses of thalamic
nuclei that are intimately connected
MIDLINE & INTRALAMINAR NUCLEI that project diffusely
to wide regions of cortex
SPECIFIC SENSORY NUCLEI that project to specific areas
of cortex and limbic system
1. medial and lateral geniculate bodies/relay
auditory and visual impulses to the respective
cortices
2. VPL & VPM nuclei/ sensory input to post central
gyrus
VA & VL nuclei are concerned with motor functions/from
Basal Ganglia & Cerebellum to motor cortex
 FUNCTIONS OF THALAMUS
1. A RELAY CENTER for sensations, virtually all the
information that reaches cortex is processed in
thalamus so it is called GATEWAY TO CEREBRAL
CORTEX
2. CENTER FOR ALERTNESS & AROUSAL because of
its connections with nuclei of reticular formation via
Thalamocortical System to cortex
3. CENTER FOR INTEGRATION OF MOTOR ACTIVITY
– Motor cortex to Pons to cerebellum to
thalamus back to motor cortex
– Motor cortex to striatum to Globus Pallidus
to thalamus to motor cortex
4. ROLE IN LIMBIC SYSTEM
Anterior nuclei are part of limbic system and
also part of memory consolidation
 THALAMIC SYNDROME
• Thrombosis of the posterolateral branch of
posterior cerebral artery results in
degeneration of VPL nuclei of lateral thalamus
– LOSS OF SENSATION / ANESTHESIA- (contralateral)
– ASTEREOGNOSIS
– SENSORY ATAXIA
– EXCRUCIATING PAIN WITH LIGHT TOUCH
– INVOLUNTARY MOVEMENTS