Notes On CNS Physiology by Medical Study Center

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Notes On CNS Physiology

Gray Matter of Spinal Cord: in the spinal cord gray matter is in the form of H shaped pillars which can be
divided into three types of columns i.e. anterior horn or ventral horn, posterior horn or dorsal horn and
in segments from T1 to L2 there is lateral horn.
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Neurons in these horns are
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Ventral Horn: Two groups of neurons
Dorsal Horn: there are 4 groups of neurons
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Alpha motor neurons which are large multi polar neurons and their nerve fibers are alpha efferents
which innervate skeletal muscle. Gamma neurons present in ventral horn are small and multi polar
neurons and there nerve fibers are gamma efferents which innervate the intrafusal fibers of the muscle
spindles. Both these alpha and gamma efferents come out of the spinal cord through ventral root of
spinal nerves.
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1. Substantia gelatinosa: this group of neurons is present at the apex of the posterior gray column.
These neurons receive afferent nerve fibers carrying impulses of pain, temperature and crude
touch.
2. Nucleus Proprius: this group is located anterior to the first group. These neurons receive
afferent nerve fibers carrying impulses of proprioception and two point tactile discrimination.
3. Clarkes column or nucleus dorsalis: this group is present at the base of the posterior gray
column. These neurons are present in segments from T1 to L3, 4. These neurons are part of
spinocerebellar tract and these receive afferent nerve fibers from spinocerebellar tract.
4. Visceral Afferent Nucleus: Present at the base of the posterior horn lateral to the clarkes
column. It is also present in segments only from T1 to L3, 4. It receives afferent nerve fibers
carrying impulses from various viscera.
Lateral Horn: in this horn, there are Autonomic preganglionic neurons. Preganglionic sympathetic in T1
to L2. Similar neurons are also present in sacral segments which are parasympathetic preganglionic.
Nowadays we divide the gray matter of spinal cord into 9 laminae and in the sensory tract we use these
laminae to describe the synapses.
Shared By: Ussama Maqbool(N61)
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FUNCTIONS OF SPINAL CORD:
1. It is a part of central nervous system and it contains ascending and descending tracts.
2. In the spinal cord there are neuronal circuits and centers for various reflexes and these reflexes
are involved in posture maintenance, movements, and withdrawal of parts, local regulation of
blood flow, regulation of GIT motility and secretions, micturition, defecation and other reflexes.
3. Initial integration of various sensory informations.
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For the reflex action a specific organization is required known as reflex arc.
REFLEX ACTION: an automatic response to a stimulus without involvement of will or consciousness. The
purpose of this is to have quick response and to save time because this action has a protective value.
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The reflex arc consists of 5 subcomponents.
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1. Receptor: it responds to the stimulus and generates impulses

2. Sensory or afferent neuron: it carries impulses from the receptor to the centre.
3. Centre: it is always present in CNS and this is integrating station. In the centre there is one or
more synapse between the afferent and efferent neuron.
4. Efferent neuron or motor neuron: it carries impulses from the centre to the effector or target
tissue.
5. Effector or target tissue: it is a responding tissue. These include skeletal muscle, smooth muscle,
cardiac muscle and glands.
For the reflex action, it is essential to have integrity of reflex arc. We can classify reflexes in different
ways.
Depending upon the number of synapse in the centre i.e. monosynaptic, disynaptic and multi or poly
synaptic.
The other way of classifying is unconditioned or inborn reflexes and acquired or conditioned reflexes
Unconditioned Reflexes: Salivation, micturition, light reflex etc
Conditioned reflex: these are acquired in response to condition stimuli with the help of unconditioned
stimulus. Pavlovs experiment and salivary secretion.
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Reflexes can be clinically classified into four types i.e.
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1. Superficial: receptors are present in skin or mucus membrane like conjunctival, corneal, plantar,
cremesteric etc
2. Deep: receptors are present in deep tissues i.e. muscles or tendons like biceps, triceps jerk.
3. Visceral: receptors are present in the viscera i.e. light reflex, baro receptor, bain bridge reflex
4. Pathological: present in diseased state i.e. babinskis sign and clonus
PROPERTIES OF REFLEX ACTION:
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In reflex arc there is one or more than one synapse, so most of the properties of reflex arc are properties
of synapses.-
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1. Central Delay: delay in the centre of reflex arc. If it is monosynaptic reflex arc then delay is 0.5
milli sec that is the time taken by one synapse to conduct impulse. By finding out central delay
we can say that the reflex arc is monosynaptic, disynaptic or polysynaptic.
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Central delay can be calculated by
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Central Delay = Reaction time (time in which the response occurs after application of stimulus)
peripheral time (Time taken by the impulses to be conducted by afferent and efferent neurons)
2. Summation: adding up of the effect of stimuli especially if the stimuli are subthreshhold. It is of
two types i.e.
a. Spatial Summation: Impulses are conducted along increased number of synaptic knobs
or afferent nerve fibers to the post synaptic neurons simultaneously.
b. Temporal Summation: impulses are conducted along the same number of presynaptic
knobs or afferent nerve fibers repeatedly to the post synaptic neurons and this result
into the adding up of the effect of repeated stimuli leading to excitation of postsynaptic
neuron. The rate of repetition of stimuli should be such that the effects of previous
stimulus is there when the second stimulus comes.
3. Facilitation: when response of post synaptic neuron or motor neuron is more than expected.
Suppose there are two afferent nerve fibers i.e. A and B. Afferent A and B makes synapse with
two types of motor neurons or post synaptic neurons i.e. subliminal fringe and discharge zone or
excited zone neurons. In facilitation the affect of subliminal fringe neurons is added to the affect
of discharge zone neurons when both A and B neurons are stimulated simultaneously.
When each motor neuron is excited in the muscle one G tension is produced.
4. Occlusion: Response of the post synaptic or motor neurons is less than expected. Mechanism is
partial sharing of motor neurons by both the afferents.
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5. Recruitment and after discharge: Recruitment means more and more motor neurons become
excited upon continuous repeated stimulation in same muscle. After discharge is that the
response of postsynaptic neurons continues after the stoppage of stimulus. After discharge is
shown by the poly synaptic reflexes only. After discharge is because of two mechanisms i.e.
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a. Long or Delayed Path: because of presence of more inter neurons.

b. Presence of Reverberating Circuits
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6. Irradiation: Excitation spreads from motor neurons of one muscle to the motor neurons of the
other muscles. Example is that of flexor withdrawal reflex. With stronger stimulus there is more
stimulation.
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7. Reciprocal Inhibition: For a smooth reflex action, when there is contraction of agonist there
must be relaxation of antagonist. This is because of reciprocal innervations.
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8. Fatigue: if a reflex is elicited repeatedly, after sometimes the response decreases which is
because of fatigue of synaptic transmission.
9. RENSHAW CELLS: these are the inhibitory inter neurons
MONOSYNAPTIC REFLEXES
STRETCH REFLEX: Most vastly studied reflex.
Whenever a skeletal muscle is stretched, it contracts. Example is that of knee jerk.
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Receptors for the stretch reflex are muscle spindles. Stretch reflex controls the increase in the length.
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Muscle Spindles are present in between the muscle fibers.
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Length is 3-10 mm. it is along the long axis of muscle. Ends are fused with the sides of the muscle fiber.
So whenever there is change in the length of muscle, same change occurs in muscle spindle. Each
muscle spindle is encapsulated and contains modified muscle fibers which are called intrafusal muscle
fibers. Number of muscle spindles in the muscle varies. There is greater number of muscle spindles in
the muscles concerned with fine skilled movements like those of hand. There are 4-12 intrafusal fusal
fibers in each muscle spindle. There are 2 types of intrafusal fibers i.e. Nuclear bag fibers and nuclear
chain fibers.
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1. Nuclear Bag fibers: number is 1-3. it has a central dilated portion which contains the nuclei.
2. Nuclear Chain fibers : shorter, number 3-9 and these contain nuclei in the form of a chain
throughout the length of fiber. Ends are attached to the sides of nuclear bag fibers.
These fibers has got two portions i.e. end portion which is contractile and contains actin myosin
filaments. The central portion is without actin myosin filaments and this is the receptor portion. Muscle
spindles are excited whenever the central portion of intrafusal fibers are stretched.
Nerve Supply of Muscle Spindle: There are two types of nerve endings present along the intrafusal fibers
1. Primary or annulospiral: these are wrapped around the central portion of both nuclear bag and
chain fibers. These are class 1a having diameter of 17 micrometer and velocity of conduction 70120 m/sec.
2. Secondary Or Flower Spray: these are present only around nuclear chain fibers. these are class 2
having diameter of 8 micrometer and velocity of 30-70 m/sec.
Motor nerve supply is through the gamma efferent which supply the end portion of intrafusal fibers in
muscle spindle which is contractile. The diameter is 3-6 micrometer and velocity of conduction is 15-30
m/sec. gamma efferents come out through ventral root and forms 30% of nerve fibers in ventral root.
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Muscles Spindles are stimulated by:
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1. Stretching of Muscle spindles i.e. Lengthening of Muscle Spindles.

2. Internal stretching which means the spindle can be stimulated without the stretching of muscle.
It is involved in muscle tone. Whenever impulses comes through the gamma efferents to the
end portion of the intrafusal fibers, end portion contracts and central portion is stretched
leading to stimulation of muscle spindle.
There are two types of stretch i.e.

1. Steady or static stretch
2. Dynamic or quick stretch.
When muscle is subjected to steady or continuous stretch, discharge of impulses from both primary and
secondary nerve endings increases and this discharge remains increased as long as the muscle remains
stretched. So nuclear chain fibers are involved in the response to the static stretch. When a dynamic
stretch is applied to the muscle, there is tremendous increase in the discharge of impulses from only
primary nerve endings which remains as long as the muscle is rapidly stretched.
Primary nerve endings respond to both increase in the length of the muscle and also rapid increase or
rate of increase in the length of muscle. Secondary nerve endings respond only to the increase in the
length of the muscle and not the rate.
Whenever muscle contracts there is shortening of muscle and along with that there is shortening of
muscle spindle so discharge of impulses from the muscle spindle decreases and this results into
relaxation of muscle.
FUNCTIONS OF MUSCLE SPINDLE:
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Regulate the length of muscle and prevent the length to go beyond limits.
Involved in the muscle tone mechanism.
There are the receptors for the clinically tested reflexes.
To have smooth voluntary movements, there is coactivation of alpha and gamma motor
neurons. For voluntary movements, impulses are initiated from motor cortex and comes to the
alpha motor neurons for contraction of muscle. At the same time impulses also come to the
gamma motor neurons.
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1.
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Gamma efferents to the intrafusal fibers are of two types i.e. static and dynamic.
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It is involved in the muscle tone mechanism and so it is also called as myotatic reflex.
It is also involved in the maintenance of posture.
Helps in lifting of weight and load.
It also prevents the unsteady and jerky movements and this is the dampening function of the
stretch reflex.
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FUNCTIONS OF THE STRETCH REFLEX:
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Gamma efferents facilitates the response of muscle spindle to two types of responses i.e. dynamic and
static.
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MUSCLE TONE: Continuous state of partial muscle contraction is called muscle tone. It involves the
muscle spindle and the stretch reflex.
There is some continuous gamma efferent discharge to the end portion of the intrafusal fibers of the
muscle spindle and this leads to the contraction of end portion resulting into the stretching of central
portion of intrafusal fibers leading to internal stretching. So there is discharge of impulses to the spinal
cord where these excite the alpha motor neurons and from there impulses come to the muscles to
cause their contraction.
Gamma efferent discharge is controlled basically by a bulboreticular facilitatory area in the brain stem.
In the reticular formation of the brain stem, in the upper pons. From this area, impulses come along the
reticulo spinal tract to facilitate the gamma motor neurons.
The normal influence of the cerebral cortex and basal ganglia on the muscle tone is inhibitory. That is
why in their lesions there is hypertonia. The normal influence of cerebellum on the muscle tone is
faciliatatory. The effect of cerebellum is through both alpha and gamma motor neurons. In lower motor
neuron lesion there is atonia or hypotonia.
DISYNAPTIC REFLEX: example is Inverse Stretch reflex also called the golgi tendon organ reflex also
called lengthening reaction. It is also called autogenic inhibition. Receptors are golgi tendon organs.
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When a strong stretch is applied to a muscle, it undergoes relaxation. With increased intensity of
stretch, muscle contracts with more force. So at extremes muscle damage can occur however this is
prevented by the relaxation of muscle at high muscle tension caused by stimulation of golgi tendon
organs. These receptors are encapsulated, their size is 0.5 to 1mm. these are located at the junction of
the muscle fibers and tendons. 10 -15 muscle fibers are connected to each tendon organ. From these
tendon organs, impulses are carried along 1 b nerve fibers. Velocity of conduction is 70 m/sec. these 1b
fibers go to the spinal cord first synapse with inter neuron which in turn synapse with the motor
neurons. Through these inter neurons there is inhibition of motor neurons. So the synaptic delay will be
1 milli/sec. this is a protective reflex. It prevents tearing of the muscle and detachment of the tendons
from the bones. Golgi tendon organs are involved in the regulation of muscle tension. Inverse stretch
reflex helps to regulate muscle tension.
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CLASP KNIFE RIGIDITY: in a patient of upper motor neuron lesion, due to involvement of extra pyramidal
tracts, there is clasp knife rigidity.
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Both of the monosynaptic and disynaptic reflexes dont show recruitment and after discharge.
POLYSYNAPTIC REFLEX: Superficial Reflexes & flexor withdrawl reflex.
FLEXER WITHDRAWL REFLEX: whenever a noxious stimulus is applied to a part of the body, the part
becomes flexed and withdrawn away from the source of stimulus. In this reflex, receptors are
nociceptors which are free nerve endings and stimuli are noxious which are of different types i.e.
mechanical like pin prick, chemical or thermal.
In this reflex, response depends upon the intensity of stimulus and it is a graded reflex.
In this reflex when one leg is flexed, the other leg becomes extended and it is crossed extensor reflex
and it is a part of withdrawl reflex. Purpose of this reflex is to support the body.
A number of interneurons are involved in the centre of this reflex some of which may be inhibitory and
other may be excitatory. Central delay is more than 1.5 seconds.
This reflex involves reciprocal inhibition because of reciprocal innervation. Motor neurons supplying the
flexers on the same side are excited and motor neurons supplying the extensors on the same side are
inhibited. This is opposite on the other side.
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Recruitment, after discharge and irradiation are present in this reflex.
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SENSORY RECEPTORS: these are specialized cells or nerve endings in the body which responds to various
stimuli. Receptors generate impulses which inform the CNS about the changes in the external and
internal environments. These are transducers which convert different forms of energy into electrical
energy that is nerve impulse or action potential.
Becoming aware of presence of a particular stimulus is called sensation.
Stimulus is the change in environment.
Sensory receptors are classified in different ways.
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1. Exteroreceptors: these are present in the superficial surface of body i.e. skin and mucus
membranes and respond to changes in external environment.
2. Interoreceptors: present inside the body and respond to changes in internal environment like
baroreceptors, osmoreceptors, chemoreceptors.
3. Teloreceptors: these respond to stimuli at a distance like receptors for hearing and vision.
4. Proprioceptors: these receptors respond to changes in position and movement.
Other classification
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1. Mechanoreceptors: respond to mechanical deformation of receptor membrane or of the

membrane of the cells adjacent to the receptors. These include a large number of receptors i.e.
free nerve endings, merkels discs, meisners corpuscles, pacinian corpuscles, hair follicle
receptos, ruffinis nerve endings, muscle spindle, golgi tendon organs, receptors in the vestibular
apparatus and cochlea, baroreceptors.
2. Thermoreceptors: these respond to temperature changes i.e. cold receptors and warmth
receptors.
3. Nociceptors: these respond to noxious stimuli. These detect tissue damage.
4. Chemoreceptors: respond to chemical changes include chemoreceptors in the carotid and aortic
bodies. Receptors in the chemosensitive area in the medulla oblongata. Olfactory receptors in
the olfactory membrane. Taste receptors. Osmoreceptors in the hypothalamus. Glucostat cells
in the satienty center of the hypothalamus.
5. Electromagnetic Receptors: respond to electromagnetic rays and these include rods and cones.
Other classification
1. Non encapsulated
2. Encapsulated
FREE NERVE ENDINGS: non encapsulated, widely distributed in different tissues of the body i.e.
epidermis and dermis of skin, mucus membrane of GIT, EPITHELIUM OF RESPIRATORY TRACT, fascia,
cornea, periosteum, perichondrium, tympanic membrane dental pulp etc.
Impulses are carried by both myelinated and unmyelinated nerve fibers. These are involved in the
sensation of crude touch, tickle, itch, pressure, pain, cold and warmth. These undergo slow adaptation.
MERKELS Discs: Non encapsulated, present in the form of clusters in the deeper part of the epidermis of
skin. Respond to continuous touch like holding a pen. Under go slow adaptation.
HAIR FOLLICLE RECEP TORS: non encapsulated, these along with their nerve fibers are wrapped around
the hair follicles and these are stimulated by bending of hair. These undergo rapid adaptation.
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MEISNERs CORPUSCLES: Encapsulated. Present in dermal papillae of skin of palm, sole, nipple and
external genitalia. Each corpuscle has a capsule and in the capsule there are flattened cells arranged
transversely along the long axis of corpuscle. Endoneurium of nerve fibers which enter the corpuscle
becomes fused with the capsule of the receptor. Number of meisners corpuscles decreases with age.
These are involved in fine touch, two point tactile discrimination and also low frequency vibration i.e.
frequency upto 80 Hz. These undergo rapid adaptation.
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PACINIAN CORPUSCLES: these are ovoid shape receptors. Size is 2 mm long and 0.5 mm thick and are
visible to naked eye. These are present in deeper part of skin, fascia, ligaments, joint capsules,
periosteum, peritoneum and many other tissues. These have a thick capsule. On cut section, capsule has
got onion like appearance. The capsule consists of concentric compressed lamellae of flattened cells.
These may be modified schwan cells. In the core of the corpuscle, there are the nerve endings. These
receptors respond to touch and also high frequency vibrations. These undergo rapid adaptation.
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RUFFINIs END ORGANS: these are present in the dermis of skin. Encapsulated. Inside there is a bundle
of collagen fibers along with the nerve endings. These respond to heavy pressure or stretching of the
skin. These undergo slow adaptation.
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KRAUSEs END BULB: Encapsulated and are present in the skin of nipple and external genitalia. There
structure resembles that of meisners corpuscles. They respond to two point tactile stimulation.
Undergo rapid adaptation.
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PROPERTIES OF SENSORY RECEPTORS:
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1. SPECIFITY: each receptor responds to specific stimulus or specific type of energy. Stimulus which
is specific for each type of receptor is called adequate stimulus. Receptors may respond to
stimuli other than adequate if the intensity is much greater than that of adequate stimulus.
Example: light rays are the specific stimulus for photo receptors. But when we apply deep
pressure over the eye balls, light halos are perceived.
2. Specific pathways carry impulses from specific type of receptors and these pathways terminate
into a specific part of the cerebral cortex e.g. visual pathway starts from the photoreceptors and
terminate in visual cortex. This is called labeled line principle.
3. The sensation evoked is that for which the receptor is specialized no matter how or where along
the pathway the activity is initiated. This principle, first enunciated by Mller in 1835, has been
given the rather cumbersome name of the law of specific nerve energies. For example, if the
sensory nerve from a Pacinian corpuscle in the hand is stimulated by pressure at the elbow or by
irritation from a tumor in the brachial plexus, the sensation evoked is touch. Similarly, if a fine
enough electrode could be inserted into the appropriate fibers of the dorsal columns of the
spinal cord, the thalamus, or the postcentral gyrus of the cerebral cortex, the sensation
produced by stimulation would be touch. The general principle of specific nerve energies
remains one of the cornerstones of sensory physiology.
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4. No matter where a particular sensory pathway is stimulated along its course to the cortex,
the conscious sensation produced is referred to the location of the receptor. This principle
is called the law of projection. Cortical stimulation experiments during neurosurgical
procedures on conscious patients illustrate this phenomenon. For example, when the
cortical receiving area for impulses from the left hand is stimulated, the patient reports
sensation in the left hand, not in the head.
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Phantom limb: patient complains of pain and proprioceptive sensation in the limb which is
amputated. Reason being in the stump of amputated limb, cut end of nerve fibers for the
mentioned receptors are stimulated by the pressure.
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5. Receptor Potential or Generator Potential: Whenever a stimulus is applied to a receptor a

localized change which is hypo polarization occurs in the membrane of receptor. This is because
of influx of sodium. This generator potential resembles EPSP. When receptor generator
potential reaches the threshold of excitation, then there is generation of action potential. So the
purpose of this generator potential is to bring the membrane potential to the threshold of
excitation.
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Amplitude of receptor potential depends upon the intensity of stimulus.

Rate of discharge of impulses from the receptor along the sensory nerve fibers depends upon
the amplitude of receptor potential. So we can say that greater the intensity of stimulus more
will be the amplitude of receptor potential and greater will be the rate of discharge of impulses
from the sensory fibers arising from the receptor.
Opening of sodium channels occurs due to different types of stimuli.
6. ADAPTTAION: When a stimulus of constant intensity is applied to a receptor continuously,
discharge of impulses along a sensory nerve fibers, decreases after some time. Depending upon
the degree of adaptation we can divide the receptors into0 two types
a. Phasic Receptors: these undergo rapid adaptation. These include the touch receptors
like meisners corpuscles, hair follicle receptors and pacinian corpuscles.
b. Tonic Receptors: Slow and incomplete adaptation. These include pain receptors, barro
receptors, muscle spindles, receptors for the cold.
These both types of adaptations are physiologically important. Rapid adaptation enables us to
perceive new stimuli or new events, also to perceive change in the intensity of stimuli. E.g. in the
morning when we take bath and wear clothes, we feel the presence of clothes for a very short
period of time and then we dont feel it. However if an insect crawls on the skin we can feel that
also. The slow and incomplete adaptation of certain receptors is also physiologically beneficial.
Pain sensation is a warning or protective sensation. As long as a damaging stimulus is there, we
can perceive the stimulus and so we can seek treatment. Muscle spindles which undergo slow
adaptation are involved in tone and postural regulation.
Mechanism of adaptation of receptors: Suppose a pacinian corpuscle is to be adapted. Suppose
a touch stimulus is applied to a part of the pacinian corpuscle. This slight pressure causes the
indentation of the receptor membrane. Under this indentation the pressure increases. This
increased pressure will be exerted on the core where there are nerve endings and so these
nerve endings will be stimulated and there will be discharge of impulses along the nerve fibers.
After sometimes, the increased pressure under the area of indentation becomes dispersed. So
this will lead to less discharge of impulses after some time.
Other mechanism involved is accommodation. After some time there is inactivation of sodium
channels.
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7. Intensity Discrimination: Brain is able to discriminate the intensity of stimuli. Two types of
feedbacks go to the brain, to have intensity discrimination. First feedback is the rate of
discharge of impulses from the receptors. Other feedback is the number of receptors
stimulated.
8. Sensory Unit: A sensory unit consists of single sensory nerve fiber and all its peripheral nerve
branches. The number of peripheral branches varies. Receptive field of a sensory unit is the area
from where sensory impulses are carried by the sensory unit. Receptive fields of different
sensory units also vary in size. E.g. receptive field of sensory unit in the cornea and sclera is 5200 square mm.
SENSATIONS:
There are two types of sensations i.e. somatic sensations and special sensations.
SOMATIC SENSATIONS: we divide the somatic sensations into three main types i.e.
1. Mechanoreceptive: these can be further divided into
a. Tactile: these include
i. Touch
ii. Pressure
iii. Tickle
iv. Itch
v. vibration
b. Position
2. Pain
3. Thermal
TACTILE SENSATIONS:
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Receptors involved are: Free nerve endings, merkels disks, meisners corpuscles, pacinian corpuslces,
hair follicle receptors, ruffinis end prgans and krauses end bulbs. From the tactile receptors, 3 types of
sensory nerve fibers carry impulses i.e.
A beta nerve fibers carry impulses from the encapsulated receptors and velocity is 30-70 m/sec
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A delta nerve fibers carry impulses from both encapsulated and non encapsulated receptors and velocity
is 5-30 m/sec.
C type fibers which are unmyelinated and they carry impulses from non encapsulated and the velocity of
conduction is 0.5 2 m/sec.
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Tip of tongue
Finger tips
Lip
Palm
Forhead
Back of hand
Neck
Back
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4.
5.
6.
7.
8.
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Touch Sensation: it is a light pressure when applied produces indentation of the receptor membrane or
membrane of the cell adjacent to the cell and this indentation may be upto 10 micrometer. Sensitivity to
touch varies in different parts of the body and it depends upon the number of toch receptors present.
So the part which are more sensitive carry greater number of receptors. In descending order of
sensitivity
Two point tactile discrimination is the ability to distinguish two very near stimuli of touch. Minimum
distance varies in different parts of the body. This distance is least in most sensitive parts and i.e. 1-3
mm and greatest in least sensitive parts i.e. back 20-50 mm.
Touch sensation can be checked by asthesio meter which consists of metallic handle to which metallic
hair can be attached. These metallic hair or brisles are of different thicknesses.
One aspect of touch sensation is stereognosis which is the ability to identify the object by touching with
hands and eyes closed. This property is highly developed in blind people.
Pressure Sensation: it is perceived when there is deformation of deeper tissue. Almost the same
receptors carry the pressure sensation i.e. free nerve endings and ruffinis nerve endings.
Tickle and Itch: these are perceived when there is light local repetitive mechanical stimulation. Tickle
gives pleasure. Itch is annoying. Receptors involved are C Mechanoreceptors which are free nerve
endings and impulses are carried by C type of Nerve fibers. Itching is also produced by the chemical
stimuli such as histamine and bradykinin. When there is itching it leads to scratch reflex. Scratching
results into relief of itching by two ways 1) by scratching irritant is removed. 2) when there is severe
scratching, it results into pain and pain impulses suppress itch impulses by inhibition in the spinal cord.
Itching can occur in skin or certain mucus membranes like that of eye. Impulses of tickle and itch are
carried by ventral spinothalamic tract.
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Light touch, two point tactile stimulation ad Phasic pressure are carried by dorsal column medial
lamniscal system.
Crude touch and pressure are carried by ventral spinothallamic tract.
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Vibration: it is a thrill or buzzing sensation perceived, when a vibrating tuning fork is placed over a part
of body especially bony part. Repetitive rhythmic pressure stimuli are perceived as vibration. There are
two types of vibrations i.e. Low frequency vibrations (80 hz) which stimulates the meisners corpuscles.
High frequency vibrations (500 Hz or More) stimulates pacinican corpuslces. Impulses of vibration are
carried by dorsal column medial laminiscal system
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Position Sensation: divided into two
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1. Static Position: conscious perception of different parts of body with respect to each other
2. Kinesthetic: conscious perception of rate of movement of different parts of body.
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In these sensations the receptors involved are proprioceptors. These receptors are present in deeper
parts of skin, ligaments, joint capsules, muscles and tendons. Proprioceptors include muscle spindles,
golgi tendon organs, pacinian corpuscles and ruffinis end organs. Impulses of proprioception are carried
by dorsal column medial laminiscal system.
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PAIN SENSATION:
It is a protective sensation. It is a warning for a disease or something damaging in the body.
Whenever a noxious stimulus is applied to a body, there is pain and the part is flexed and withdrawn
from the source of noxious stimulus. If the pain is in viscera, it draws attention of the individual to seek
treatment. Pain receptors are nociceptors and these are free nerve endings. These are widely
distributed in different parts of the body. Two types of nerve fibers carry pain impulses i.e.
A Delta and C nerve fibers carry pain. A delta having velocity of conduction 5-30 m/sec and these carry
fast pain impulses. C fibers are un myelinated and these conduct slow pain impulses and velocity of
conduction is 0.5 to 2 m/sec. there are two types of pain i.e.
1. First / Fast pain: it is sharp, short and pricking pain. It is more localized.
2. Second/ Slow pain: it is diffuse, dull and burning pain. It occurs after the first pain and it is
associated with tissue damage.
Pain impulses are carried by lateral spinothalamic tracts. Pain occurs when there is application of
noxious stimulus which could be mechanical, chemical and thermal.
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Thermal: Extremes of temperature, freezing cold and burning hot.
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Mechanical: it can be pin prick, or cut with a sharp object, in viscera distension or increased pressure,
raised intracranial pressure.
Chemical: these include histamine, bradykinin, serotonin, substance p and insect bites.
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Some tissues are without pain receptors. In compact pain receptors are in periosteum. In bone diseases
unless it involves periosteum, there is no pain. In the brain receptors are in meninges. So in brain tumor
there is no pain unless meninges are involved. Similarly in lungs pain receptors are in pleura. In
intestines it is in peritoneum. In liver and spleen pain receptors are only in their capsules. In the muscles
tissue itself, there are no pain receptors but in the connective tissue covering.
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Pain sensation has got two aspects i.e. pain perception and reaction to pain or emotional aspect of the
pain. Reaction to the pain varies with the individuals. In severe pain there is vocalization, clenching of
hands, contraction of facial muscles, narrowing of palpebral fissure, change in blood pressure and heart
rate. There may be skin flushing or pallor. There may be violent movements of the body. Pain sensitivity
varies with different individuals and in different races. Pain receptors undergo very slow and incomplete
adaptation.
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Pain can also be classified into superficial pain and deep pain.
Superficial pain: involves superficial viscera and localized.

Deep pain: also known as visceral pain involves viscera and is not so localized but diffuse in nature. It is
colicky in nature. Visceral pain is felt in the area of the viscera and is also referred to different distant
structures. E.g cardiac pain refers to the left shoulder, left arm neck. Ureteric colic radiates to testicles.
Basis of referred pain is dermatomal rule. Structure where pain originates and the structure to which the
pain radiates receive the sensory nerve supply from same segment of spinal cord.
Pain sensitivity can be tested by pinching of skin. Pin prick by measured pressure. Application of heat
above 45 degree centigrade.
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THERMAL SENSATION: Human beings can perceive different grades of thermal sensation.
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In thermal sensation three types of receptors are involved i.e. cold receptors, warmth receptors and
pain receptors. Pain receptors are stimulated at the extremes of temperature i.e. freezing cold and
burning hot. Thermal receptors are located beneath the skin and mucus membrane. These thermal
receptors are in the form of aggregations or clusters called spots i.e. cold spots and warm spots. Cold
spots are much more. There is 4-10 times greater number of cold spots than warmth spots. From the
cold receptors impulses are carried by A delta fibers but some also from C type. From the warmth
receptors impulses are carried by C type of fibers. Temperature receptors are non encapsulated.
Discharge of impulses from different receptors at different temperatures is mentioned in above
diagram.
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Thermoreceptors undergo adaptation to some degree in neutral or indifferent zone of 29-36 degree
centigrade and above and below this there is not so much adaptation.
Mucus membrane of the mouth is relatively insensitive to high temperature. We can take hot drinks like
tea and coffee. Exposed areas of the body are relatively less sensitive to temperature changes as
compared to covered areas. The covered areas can detect a temperature change of 0.2 degree
centigrade. While the exposed areas can detect change of 0.5 to 1 degree centigrade.
Thermoreceptors can respond to change in the temperature and also respond to changing temperature.
Response is much more to changing temperature.
Thermoreceptors are stimulated by change in the rate of metabolism.
ASCENDING TRACTS OR SENSORY TRACTS:

These tracts are divided into different groups i.e.
DORSAL COLUMN MEDIAL LAMINISCAL SYSTEM
ANTEROLATERAL SYSTEM / SPINOTHALAMIC TRACT
SPINOCEREBELLAR TRACTS
MISCELLANEOUS
SPINOTACTAL
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VISCERAL SENSORY TRACTS.
DORSAL COLUMN MEDIAL LAMINISCAL SYSTEM: This dorsal column has got certain features
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1. It consists of rapidly conducting myelinated nerve fibers and velocity of conduction may be upto
110 m/sec
2. Sensations carried by this tract requires perception of fine grades of intensity like sensation
carried are light touch, tactile discrimination.
3. Sensations carried by this tract require accurate and precise localization like in two point tactile
discrimination.
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Sensation carried by this tract include fine touch, tactile discrimination Phasic pressure, vibration,
proprioception.
First order nerve fibers carrying impulses enter the spinal cord through the dorsal nerve root. Without
synapse they enter the posterior white column to ascend as dorsal column medial leminiscal system. As
the tract ascends, fibers from the upper part of the body are added laterally. From the 6th thoracic
vertebra a septum appears in the tract to divide it into two fasciculi i.e. medial fasciuls gracilus and
lateral one is fasciulus cuneatus. These two fascicule ascend to enter the medulla oblongata where they
synapse with the second order neuron in the nucleus gracillis and nucleus cuneatus. Second order nerve
fibers arise from these two nuclei and these are called internal arcuate fibers. Internal arcuate fibers
cross over to the opposite side to form medial laminiscus. This crossing over in the medulla oblongata is
called sensory decussation in the lower part. Medial laminiscus ascends through the brain stem. In the
brain stem medial laminiscus is joined by trigeminal pathway carrying same sensations and then the
medial laminiscus synapse in the thalamus with the VPL. the fibers coming from trigeminal pathway
synapse in the VPM.
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From the VPL third order nerve fibers arise which pass through the internal capsule to terminate in the
somatosensory area in the poscentral gyrus.
Some fibers arising from the cuneate nucleus go to the cerebellum through the internal cerebellar
peduncle. These are also called cuneocerebellar fibers. These fibers carry proprioceptive impulses to the
cerebellum.
If the lesion of this tract is in spinal cord, effect will be ipsilateral and if the lesion is above upper part of
medulla then the effect will be on the contralateral side.
25 August, 2010
ANTEROLATERAL SYSTEM / SPINOTHALAMIC TRACT
There are 3 features of this tract
1. Small myelinated nerve fibers and relatively slow conducting. The velocity is 40 m/sec.
2. Sensations carried by these tracts do not require perception of fine grades of intensity. These
sensations are crude.
3. Sensations carried by these tracts do not require spatial orientation and accurate localization.
There are two types of spinothalamic tract i.e.
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1. anterior or ventral spinothalamic tract: these carry sensations of crude touch, pressure, tickle
itch and sexual sensations. First order fibers enter the spinal cord through the dorsal nerve root
and these synapse with the neurons in the lamina V and VI. From these laminae 2nd order
neurons arise and from here they cross over to the opposite side through the anterior gre and
white commisure and from the opposite side ventral spinothalamic tract forms. This tract forms
in the lower part of the body and as the fibers ascend the fibers from the upper part of the
body are aggregated medially to the lower fibers. Tract enters the medulla and reaches spinal
laminiscus which is made up of three tracts i.e ventral spinthalamic tract, lateral spinothalam ic
and spinotactal tract. From here fibers ascend through the pons, midbrain and then it synapse in
the neurons in the ventrobasal complex of thalamus i.e. VPL. from here 3rd order nerve fibers
arise and from here fibers pass through the posterior limb of internal capsule to terminate into
the post central gyrus of the somatosensory area.
2. Lateral Spinothalamic tract: this tract carries impulses of pain and temperature. First order
nerve fibers enter the spinal cord through the dorsal nerve root and these synapse with the
neurons in the lamina I, II and III including substantia gelatinosa. From these neurons 2nd order
nerve fibers arise which cross over obliquely to the opposite side through anterior grey and
white commisure. After crossing over they form the lateral column of the tract on the opposite
side. As the tract ascends fibers from the upper part of the body are added on the anteromedial
aspect. Fibers from the lower part are on the posterolateral aspect of the tract. The tract
ascends through the spinal cord to enter the medulla oblongata where it joins the spinal
laminiscus which ascends through the brain stem. Temperature and fast pain fibers synapse
with the neurons in the ventro basal complex of thalamic nuclei. From here 3rd order nerve
fibers arise which pass through the posterior limb of internal capsule to terminate into the
postcentral gyrus in the somatosensory area. Most of the Slow pain fibers do not go to the
ventrobasal complex of thalamic nuclei. They go to other areas including reticular formation,
tactum of midbrain and periaqueductal grey matter. Some fibers also go to the intra laminar and
midline nuclei of the thalamus. From here 3rd order neurons arise which go to the sensory
cortex. In some books pathway of fast pain fibers is discussed as neospinothalamic tract and
that of slow pain fibers is discussed as paleospinothalamic tract. In the neospinothalamic tract
the neurotransmitter between the 1st order A delta fibers and 2nd order neuron in lamina I, II
and III is Glutamate. In paleospinothalamic tract the neurotransmitter between the 1st order C
fibers and 2nd order neurons is substance P.
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The effect of lesion of these tracts is on the contralateral side.
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SPINOCEREBELLAR TRACTS:
Spinocerebellar tracts consists of fast fibers having velocity of conduction 120m/sec.

These are of two types
1. Posterior spinocerebllear tracts.: first order neurons enter the spinal cord through the dorsal
nerve root and synapse with the second order neurons in the clarkes nucleus or nucleus
dorsalis present in the segment T1 to L3 and L4 at the base of posterior grey column. 2nd order
nerve fibers arise which without crossing over enter the lateral white column to form the tract.
The tract ascends in the spinal cord to enter the medulla oblongata. And from here it passes
through the inferior cerebellar peduncle to go the cerebellum where they terminate in the
vermis and intermediate zone on the same side. Fibers from the lumbar and sacral segment
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ascend to join the clarkes column in the L3 and L4. So in this tract fibers come from trunk and
lower limbs, not from the upper limb. This tract carry impulses from the proprioceptors about
the change in the length, muscle tension, position and movements. These impulses are used by
cerebellum to coordinate movements of lower limbs and to also maintain the posture.
2. Ventral/Anterior Spinocerebellar tract: 1st order nerve fibers enter the spinal cord through the
dorsal nerve root and synapse with the 2nd order neurons located near the clarkes column.
From these neurons second order nerve fibers arise which cross over to the opposite side to
enter the lateral white column on the opposite side. The tract ascends in the spinal cord to enter
the medulla oblongata and passes through the pons and in the midbrain it passes through the
superior cerebellar peduncle to enter the cerebellum. In the cerebellum the fibers cross back to
terminate into the vermis and intermediate zones of both sides. Here Some fibers may remain
uncrossed but mostly they cross in cerebellum. This tract also carries impulses from the
proprioceptors to the cerebellum and are used for coordination of movements. This tract
provides information to the cerebellum about the motor impulses which have reached the
ventral horn of spinal cord along the cortico spinal and rubrospinal tracts.
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MISCELLANEOUS GROUP OF TRACTS:
SPINOTACTAL TRACTS: First order nerve fibers enter the spinal cord through the dorsal nerve root, these
synapse with 2nd order neurons in the posterior grey column of the spinal cord. 2nd order nerve fibers
arise which cross over to the opposite side to enter the lateral white column of the opposite side. The
tract ascends through the spinal cord to enter the medulla oblongata. Here it joins the spinal laminiscus.
The tract fibers terminate into the superior colliculus in the tactum of the midbrain. This tract provides
afferent pathway for spinovisual reflexes which are involved in the control of movement of head and
eyes towards the source of stimulation. Superior colliculus is also involved in the reflex pathway upon
stimulation by light.
SPINORETICULAR TRACT: 1st order nerve fibers enter the spinal cord through the dorsal nerve root.
These synapse with the second order neuron in the posterior grey column in spinal cord. 2nd order nerve
fibers arise which without crossing over ascends and form the tract on the same side. It ascends to
eneter the medulla oblongata and terminate into the reticular formation in the midbrain, pons and
medulla. This tract provides afferent impulses to the reticular formation and is involved in the control of
level of consciousness. The sensory input to the reticular formation maintains excitation in the reticular
activating system.
SPINOOLIVARY TRACT: 1st order nerve fibers enter the spinal cord through the dorsal nerve root and
synapse with the 2nd order neurons in the posterior grey column from where 2nd order nerve fibers arise.
Most of the fibers cross over to the opposite side to enter the lateral white column to form this tract.
The tract ascends through the spinal cord to enter the medulla oblongata. Here the tract fibers synapse
with the neurons in the inferior olivary nucleus. From this nucleus 3rd order nerve fibers arise which
cross over to the opposite side to enter the inferior cerebellar peduncle to go to the cerebellum. This
tract carries impulses from proprioceptors to the cerebellum.
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SENSORY VISCERAL TRACTS: in the viscera mostly the receptors present are stretch receptors and pain
receptors. Impulses from the viscera of the thorax and abdomen enter the spinal cord through dorsal
nerve root and then these fibers join the spinothalamic tract to be carried to the sensory cortex.
Impulses about fullness of urinarty bladder before micturition and impulses about the fullness of rectum
before defecation are carried by dorsal column medial laminiscal system.
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Dorsal column carries conscious proprioception and rest of the tracts carry unconcsiouc propriocetion
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ANALGESIA SYSTEM
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It is pain control system in CNS. Pain sensitivity in different individuals vary which is partly due to this
system.
Components of Analgesia system are:

1. Periventricular nuclei surrounding the third ventricle in the hypothalamus
2. Periaqueductal grey matter present in the midbrain and upper pons and is the grey matter
surrounding the aqueduct of sylvius
3. Raphe magnus nucleus in the lower pons and upper medulla oblongata. It is a thin midline
nucleus.
4. Pain inhibitory complex in the dorsal horn of the spinal cord. Incoming pain fibers i.e. A delta
and C fibers synapse here.
Some authors also include a group of nuclei in pons and medulla known a reticularis para giganto
cellularis.
Neurotransmitters in analgesia system are
1. Enkephalin is the main neurotransmitter in the analgesia nucleus. Both fibers of 1 and 2 secrete
enkaphalin.
2. Fibers from 3 secrete serotonin in the dorsal horn.
3. Enkephalin is secreted from 4.
When any component of analgesia system is stimulated it leads to suppression of pain sensation.
Analgesia system when stimulated suppresses both fast and slow pain. This system also inhibits the
reflexes initiated by pain like fexor withdrawal reflex.
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In the brain there are receptors with which morphine bind to produce analgesia. And these receptors
are called opiate receptors. Enkephalin binds with opiate receptors to produce analgesia. There are
different types of enkephalin like endorphins, dynorphins, met enkephelin and leuenkephelin.
How the analgesia system get stimulated, it is not clear. In acupuncture there is evidence of release of
endorphins.
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The enkephelin secreted in the dorsal horn can cause inhibition of the pain carrying fibers in the spinal
cord through pre synaptic inhibition.
CEREBRAL CORTEX:
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It is composed of grey matter and forms complete covering of the cerebral hemispheres. It is about 2 -5
mm thick. It is thickest at the crest of the gyrus and thinnest at the bottom of sulcus. The total surface
area of the cerebral cortex is about one quarter meter.
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Cerebral cortex has got 6 layers
1. Outermost is molecular layer composed of dense network of nerve fibers and these nerve fibers
are dendrites and axons which come from the deeper layers.
2. External granular layer which is composed of pyramidal cells and stellate cells and dendrites
from these go to the molecular layer and axons go to the deeper layer.
3. External pyramidal layer which consists of small pyramidal cells. There dendrites pass to the
molecular layer and axons to the white matter.
4. Internal granular layer which contain stellate cells, small pyramidal cells. In this layer there is a
horizontal band of nerve fibers which is called the band of Baillarger.
5. Internal pyramidal layer also called the ganglionic cell layer which consists of large and medium
sized pyramidal cells. There axons pass into the white matter. In the precentral gyrus this layer
contains very large or giant pyramidal cells called Betz cells which give rise to nerve fibers which
constitute 3 percent of the total nerve fibers in the corticospinal tracts. And these terminate
directly on to the alpha motor neurons in the ventral horn of the spinal cord. In this layer there
is also inner band of Baillarger.
6. Multiform or polymorphic layer which conisits of cells of different morphology.
Incoming sensory fibers to the cerebral cortex first go to the layer number 4. From here the spread can
be to the outer layers or to the inner layers.
In the somatic sensory area, neurons are arranged in the form of vertical columns and each vertical
column has a diameter of 0.3 to 0.5 mm and each column contains about 10,000 neurons and each
vertical column of sensory neurons is concerned with one modality of sensation.
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I f all the six layers are distinct and developed then the cerebral cortex is called homotypical. If all the six
layers are not distinct and not well developed then it is called heterotypical cerebral cortex which is
again of two types i.e. granular and agranular.
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In granular type of heterotypical cerebral cortex the granular layers i.e. 2 and 4 are well developed while
the pyramidal layers i.e. 3 and 5 are not well developed. This type of cortex is present in postcentral
gyrus, superior temporal gyrus and hippocampal gyrus. Most of these areas are sensory areas.
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In agranualr type pyramidal layers i.e. 3 and 5 are well developed and distinct while the granular layers
are not well developed. This type of cortex is present in the precentral gyrus and other parts of frontal
lobe which are mainly motor areas.
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FUNCTIONAL AREAS IN THE CEREBRAL CORTEX:
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SENSORY AREAS:
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The functional areas in the cerebral cortex have been numbered after broadman. These areas can be
divided into two types i.e. sensory and motor.
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Methods to study or invesitigate sensory areas:
1. Ablation method: in this method a part of cerebral cortex is damaged and the sensory deficit
produced is studied,
2. Evoked potential method: stimuli are applied on different parts of the body and potentials from
cerebral cortex are recorded.
3. Clinicopathological study: the patient is having sensory deficit and after death of patient
different parts of cerebral cortex are studied.
Different sensory areas in the cerebral cortex include
1. Somatic sensory area S1: it is located in the post central gyrus on the lateral surface of cerebral
hemisphere. It also extends to the medial surface into the paracentral lobule. It is brodmans
area 1,2 and 3. In this area there is contralateral representation of different parts of the body
and body is represented upside down. By point to point sensory stimulation of different parts of
body a figure of body can be formed in this area and this is called sensory homunculus or
sensory figuring in the area S1. Different parts of the body in the sensory homunculus are not
represented according to size but according to their sensory function. Parts of the body having
greater number of sensory receptors have greater representation in sensory homunculus like
jaw, lips tongue and fingers. Thorax thigh and limbs occupy smaller area. The genital organs are
on the medial surface of the cerebral hemisphere. Face has got some bilateral representation.
The S1 area recives fibers from the VPL and VPM nucleus of thalamus.
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Functions: this area is involved in the perception of all the somatic sensations from the contra
lateral side of the body. This area is also concerned with the perception of fine grades of
intensity. It is also involved in stereognosis. When there is lesion of this area, the sensation of
fine touch, propriocepteion, tactile discrimination and vibration is mostly affected while pain is
least affected. Thalamus is subcortical centre for pain.
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WERNICKES AREA: Also called general interpretive area, sensory speech area located in the
posterior part of the superior temporal gyrus behind the auditory cortex. It is brodmans area
22. This area is highly developed in the dominant hemisphere so well developed in left
hemisphere. This area receives impulses or signals from the visual association area and also
from the auditory area. In this area visual and auditory informations are completely understood.
Thoughts are formulated. What to be expressed or answered is decided. Words are chosen.
Words are arranged into sentences. Signals are sent to the brocas area i.e. motor speech area
along the arcuate fasciculus. This area is concerned with high intellectual functions. This is also
called sensory speech area. When this area is damaged there is sensory aphaisa or fluent
aphasia.
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VISUAL AREAS:
1. Primary visual area: it is located around the calcarine fissure. It is brodmans area 17. It
receives impulses from the visual pathway. Secondary visual area or visual association area
which is located anterior and superior to primary visual area.
2. ANGULAR GYRUS: It is located between wenickes area and visual area. It is brodmans area
39. There is involved in language, mathematics and cognition.
Primary auditory area: located in superior temporal gyrus. Brodmans area 41. It receives impulses from
auditory pathway and there is interpretation of auditory impulses.
TASTE AREA: located at the inferior end of post central gyrus, superior wall of brodmans area 43.
OLFACTORY AREA. Divided into two parts medial and lateral. Medial consints of septal nusclei anterior
to hypottahlams. Pyriform cortex, prepyriform cortex and cortical portion of amygdila.
MOTOR AREAS OF CEREBRAL CORTEX:
METHODS OF INVESTIGATION OF MOTOR AREAS:
1. ABLATION METHIOD: part of cerebral cortex is damaged and loss of motor activity is noted.
2. POINT TO POINT electrical stimulation of motor areas is carried out and movement
produced is noted.
3. CLINICOPATHOLOGICAL STUDY: the patient having paralysis when he dies, his brain is
inspected for damage.
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Motor area can be divided into four types:
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1. PRIMARY MOTOR AREA: Located in the precentral gyrus on the lateral surface of cerebral
hemisphere. It also extends to the medial surface into the paracentral lobule. It is brodmans
area 4. It is composed of agranular type of cerebral cortex. In this area there is also
topographical representation of various parts of the body and there is motor homunculus in
the primary motor area and there is contralateral and upside down representation. Motor
homunculus is the mirror image of sensory homunculus. The area of representation in the
motor homunculus is according to functional importance and not on anatomical size. Parts
of the body involved in fine skilled movements occupy the much larger portion of
homunculus. Generally there is contralateral representation but Face has some bilateral
representation. Blood flow to different parts of the motor area depends upon the activity of
the body part.
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Connections of primary motor area:
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i. It receives afferent from the premotor area, supplementary area and primary
motor area of opposite side.
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ii. Afferents from the somatosensory area, visual area and also from auditory area.
iii. Afferents from basal ganglia, thalamus and cerebellum also red nucleus.
iv. Efferents to the primary motor area of opposite side.

v. Efferents to the spinal cord as corticospinal or pyramidal tracts.
vi. Cortico bulbar fibers. Cortico striate fibers which go to basal ganglia. Cortico
thalamic fibers going to thalamus. Corticoponto cerebellar fibers going to
pontine nuclei and then to cerebellum
Electrical stimulation of this area leads to coordinated movements involving contralateral
side of the body. Movements are initiated in the primary motor area.
2. PREMOTOR AREA: it is located anterior to the primary motor area on the lateral surface of
hemisphere. It is brodmans area 6. It is broad at the top and narrow below. It occupies
superior, m idle and inferior frontal gyri. There is also topographical representation of
various body parts and this resembles that in the primary motor area.
When this area is stimulated there is movement involving groups of muscles. Gross rotation
of head eyes and trunk to the opposite side. This area stores programs of motor activity in
the light of the past experience or past information. It programmes the activity of primary
motor area. It is connected to the primary motor area directly or through basal gangli and
then through thalamic nuclei to the primary motor area.
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3. SUPPLEMENTARY MOTOR AREA: it is located anterior and superior to the premotor area on
the medial surface of the cerebral hemispheres. It occupies the medial frontal gyrus. It
extends upto the cingulate sulcus on the medial surface of hemisphere. In this area different
parts of body are also topographically represented and the pattern is that the face is
anterior, feet are posterior and trunk is towards the cingulated sulcus. This area has
connections with the primary motor area and also with both sides of the body. When this
area is stimulated, there are movements involving both sides of the body. This area is
involved in the control of positional or attitudinal movements.
4. SPECIAL MOTOR AREAS:
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a. Motor speech area or brocas area: located in inferior frontal gyrus, anterior to face
representation in the primary motor area. It is brodmans area 44. It receives signals
from the Wernickes area along the arcuate fasciullus. This area forms detailed
motor pattern for the contraction of muscles involved in phonation and articulation.
Signals are sent to the primary motor area to initiate muscle contraction for
phonation and articulation. When there is damage to the brocas area there is
motor aphasia or non fluent aphasia. This patient has difficulty in uttering words.
Speech is limited to only few words.
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b. Frontal Eye Field: it is located anterior to the premotor area in the middle frontal
gyrus. It is brodmans area 8. When this area is electrically stimulated, there is
conjugate deviation of eyes to the opposite side. This area also controls eyelid
movements or blinking. It also controls voluntary fixation. We are able to fixate eyes
on different objects. When this area is damaged there is inability to fixate eyes from
one object to the other.
c. Area for head rotation: it controls the head rotation, number is not given but it is
present above frontal eyefield.
d. Area for hand skills which controls the hand skills. When there is damage to this
area, it leads to motor apraxia. In motor apraxia movements become incoordinate
and non purposeful.
DESCENDING TRACTS:
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CORTICOSPINAL TRACT: Originates from cerebral cortex. Contains about 1 million neurons and contains
only about 3% of betz cells. 30 % fibers orginates from the primary motor area and another 30% from
premotor and supplementary motor areas. 40% of fibers originate from somatic sensory area. After
origin from cerebral cortex, these fibers pass through corona radiate. Then they converge towards the
genu and anterior 2/3rd of the posterior limb of internal capsule. Fibers for the upper parts of the body
are in genu and fibers for the lower part are lateral. After this the fibers enter the midbrain. Here the
fibers occupy the middle 3/5th of the cerebral peduncle or crus cerebri. Here fibers for the upper parts
are medial and for lower parts are lateral. From the midbrain tract fibers enter the pons. In the pons,
tract is broken into bundles due to transverse ponto cerebellar fibers. After this the tract enters the
medulla oblongata. In the upper part the bundle of fibers again group together to form pyramidal
shaped swelling on the anterior aspect of medulla oblongata. This name pyramidal is given because of
these pyramids formed in the upper part of medulla. In the lower part of the medulla oblongata, 80% of
fibers cross over to the opposite side to form motor decussation. After crossing over the crossed fibers
enter the lateral white column to form lateral corticospinal tract. Remaining uncrossed 20 % enter the
anterior white column to form anterior cortico spinal tracts. Fibers of the anterior cortico spinal tract
cross over in the spinal cord to terminate on to the motor neurons in the cervical and upper thoracic
segments of spinal cord. These fibers are thought to be from the supplementary motor areas. Fibers of
the corticospinal tract, when they terminate in the spinal cord, they first synapse with interneurons and
which in turn synapse with the motor neurons in the ventral horn of the spinal cord. Only fibers from
from the betz cells have direct termination with the motor neurons of spinal cord. Fibers of the lateral
corticospinal tract terminate onto the motor neurons in the ventral horn of spinal cord at various levels.
The termination is indirect. If we take the tract overall, 45% fibers of this tract terminate into in the
cervical segments, 20 % into thoracic segments and remaining 35% terminate into the lumbar segments
of spinal cord. There are certain collateral branches which go to different parts of brain i.e. caudate
nucleus, lentiform nucleus, red nucleus, olivary nuclei and also reticular formation.
FUNCTIONS OF CORTICOSPINAL TRACT:
It controls fine skilled movements of limbs particularly the distal parts of limbs.
CORTICO BULBUR TRACT: it has got same pathway as the corticospinal tract but the tract fibers cross
over in the brain stem to terminate on to the motor neurons in the nuclei of cranial nerves.
EXTRACORTICOSPINAL OR EXTRAPYRAMIDAL TRACTS:
RUBROSPINAL TRACT: it originates from the red nucleus which is present in the tegmentum of mid
brain. Then these cross over to the opposite side and descend through the pons, medulla oblongata to
enter the lateral white column of spinal cord and it terminates onto the motor neurons in the ventral
horn of spinal cord at various level of spinal cord. Termaintion is indirect through interneurons. Red
nucleus has connections with cerebral cortex and cerebellum. Rubrospinal tract forms an alternate or
accessory pathway through which cerebral cortex and cerebellum can control the motor activity.
Rubrospinal tract is fascillitatory for flexers and inhibitory for extensors or antigravity muscles.
TACTOSPINAL TRACT:
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It originates from the superior colliculus in the tactum of mid brain. Then it descends without crossing
over, descend through the pons and medulla oblongata to reach spinal cord where it terminates on to
the motor neurons in the ventral horn in the upper cervical segments of the spinal cord. In the brain
stem, this tract is near the medial longitudinal bundle and in the spinal cord it is near the anterior
column. This tract is involved in the control of reflex postural movement of head and neck in response to
visual stimulation. Here from superior colliculus impulses also go to the extraocular muscles to control
the movement of eyes.
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RETICULOSPINAL TRACT: it arises from reticular formation. Reticular formation consists of groups of
scattered neurons along with nerve fibers. It is present in midbrain, pons and medulla. Superiorly
reticular formation is connected to cerebral cortex and inferiorly to the spinal cord. One component of
reticular formation is called reticular activating system.
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Two components of reticulospinal tract
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1. Pontine reticulo spinal tract: arise from the reticular formation of pons. Most of the fibers
remain uncrossed. Tract enters the anterior white column of spinal cord. Then it terminates
onto the motor neurons in the ventral horn at various levels. This tract is fascillitatry to the
extensors or the antigravity muscles. It controls the activity of both alpha and gamma motor
neurons. In the control of muscle tone it plays an important role.
2. Medullary reticulospinal tract: it originates from the reticular formation of medulla oblongata.
Most of the fibers cross over to the opposite side and these descend to enter the lateral white
column of spinal cord. This tract is inhibitory to the extensors.
VESTIBULOSPINAL TRACT: vestibular nuclei are present in the floor of 4trh ventricle in the lower pons
and upper medulla oblongata. Vestibular nuclei receive fibers from the inner ear and also cerebellum.
There are two components of this tract. The major component is lateral vestibulospinal tract and minor
component is medial vestibulospinal tract.
LATERAL PART: remains uncrossed and terminate on the motor neurons of spinal cord. Facilliatatory to
the extensors of the body.
Medial part: it arises from the medial vestibular nucleus. This nucleus, receives fibers mainly from the
semicircular canals. After the origin, the tract fibers remain uncrossed and they terminate onto the
motor neurons in the cervical segments of the spinal cord. This tract is also facilitatory to the extensors.
OLIVOSPINAL TRACT: it originates from the inferior olivary nucleus in the medulla oblongata. After the
origin, it crosses over to the opposite side and descends into the lateral white column of spinal cord.
This tract is also involved in the control of motor activity. Inferior olivary nuclei receive fibers from the
motor cortex, corpus striatum, red nucleus and spinal cord.
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DESCENDING AUTONOMIC PATHWAYS: These pathway arise from the higher centres which control the
autonomic nervous system and these include, cerebral cortex, hypothalamus, amygdala and reticular
formation. These fibers cross over to the opposite side and join the reticulospinal tracts to enter the
spinal cord in the lateral white column. The tract fibers terminate onto the preganglionic sympathetic
neurons in the spinal cord segments from T1 to L2 and also to the preganglionic parasympathetic
neurons in the sacral segments mainly S2-4.
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Motor system consists of two types of neurons
02 September, 2010
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1. Lower motor neurons: neurons which innerveate skeletal muscles. These form final common
pathway to skeletal muscles. If any impulse has to pass to the sk. Muscle, it has to pass through
LMN. These are located in the anterior grey column of spinal cord. These are alpha motor
neurons. The motor neurons in the nuclei of cranial nerves in the brain stem are also LMN.
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2. Upper Motor Neurons: these are located above the level of lower motor neurons. These are
supraspinal neurons. These are located in the cerebral cortex and brain stem. These neurons
along with their pathways are the UMN. These include the corticospinal and the
extracorticospinal system which control the motor activity through separate pathways.
LMN LESIONS:
Causes: Injury or trauma to the alpha motor neurons or motor fibers in the ventral root of spinal cord.
Infection as in polio mellitus. Vascular like thrombosis, hemerrohage. Degeneration like in motor neuron
disease. Tumor involving the LMN.
Features:
1. Only few muscles are affected.
2. In the affected part there is flaccid paralysis. Loss of voluntary movements along with loss of
muscle tone.
3. Loss of all superficial and deep reflexes.
4. Muscle tone is because of myotatic reflex so there is Atonia or Hypotonia.
5. Muscle atrophy due to loss of trophic action of motor nerves supplying the muscles.
6. Intact motor nerve supply maintains the growth and structure of the muscle.
7. There are fasciulations and fibrillations. Fsiculations are spontaneous contractions of group of
muscles fibers and fibrillations are contractions of individual muscle fibers. These appear when
there is slow degeneration of LMN.
8. Contractures of paralysed muscles (Shortening)
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9. Reaction to degeneration.
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10. Response to faradic electrical stimulation stops after 7 days while the response to galvanic
stimulation stops after ten days of lower motor neuron lesion. Normal muscle can respond to
both type of stimulation. Faradic stimulation is interrupted current stimulation and galvanic is
direct current stimulation
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11. Babinskis sign is not present in LMN.
UPPER MOTOR NEURON LESION:
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Causes: Trauma, vascular lesions like thrombosis hemerrhoge in brain, brain tumor or abscess.
In the UMN there are two types of tracts i.e. Cortico Spinal and Extra cortico spinal tract.
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Features of Cortico Spinal tract lesions:
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1. Loss of fine skilled voluntary movements especially of the distil parts of limbs.
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2. Babinskis sign is Positive i.e. abnormal plantar reflex. It is also present in other conditions like in
infants (because of incomplete myelination of tract), during sleep and intoxication.
3. Loss of superficial abdominal reflex. T7 T12. This reflex is lost due to facillitatry effect of the
corticospinal tract on the interneurons involved in reflex arc.
4. Loss of cremesteric reflex. L1 Again the same reason.
Features due to lesions of Extracortico Spinal Tract:
1. There is spastic paralysis. Loss of voluntary movements along with hypertonia.
2. There is involvement of large number of muscles i.e. there may be hemiplegia.
3. Deep reflexes become exaggerated or brisk.
4. There may be ankle or knee clonus.
5. Clasp knife rigidity.
6. There are no fasciulations and no fibrillations.
7. There is slight muscle atrophy and this is due to disuse.
In clinical practice we always find the mixture of lesions of Corticospinal and Extracorticospinal tracts.
Rigidity involves both agonists and antagonists
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LESIONS of SPINAL CORD:
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1. Lesion of Posterior Nerve root:
a. if only one posterior nerve root is damaged, there is no significant sensory loss, because
of overlapping of adjacent dermatomes. To produce significant sensory loss, atleast
three posterior nerve roots should be damaged.
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b. Loss of all superficial and deep reflexes as reflex arc is not completed.
c. Loss of muscle tone in the affected part.
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d. Movement of affected part is also difficult because of loss of proprioceptive input to the
brain.
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2. LESION OF Ventral root: it contains both somatic motor nerve fibers and autonomic fibers.
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a. There is flaccid paralysis.
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b. All the superficial and deep reflexes are lost.
c. If the lesion of ventral root is in segment from T1to L2 then there is inhibition of
sympathetic outflow and this leads to vasodilation, fall in peripheral resistance and
blood pressure and also there is loss of sweating.
3. Hemi Section of Spinal Cord: one half is damaged and other is intact. Cause is fracture
dislocation of vertebral column due to stab wound, bullet wound or expanding tumor.
a. First there is stage of spinal shock, then there is stage of reflex activity.
b. At the Level of Hemisection:
i. There is Ipsilateral LMN type of paralysis. No motor loss on the opposite side.
ii. Complete anesthesia (Complete loss of Sensations) at the level of hemisection
which is ipsilateral. On the contralateral side there is no significant sensory loss
c. Below the Level of Hemisection:
i. There is Ipsilateral UMN type of Paralyis. No motor loss on contralateral side.
ii. Ipsilateral loss of sensations carried by Dorsal column medial Laminiscal System
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iii. Loss of sensations carried by spinothalamic tract on the contraletral side i.e.
crude touch, tickle, itch, pressure, pain and temperature. Sensory loss on the
contralateral side 1 to 2 segments below the section because of oblique
crossing.
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d. Above the Level of Hemisection:
i. Hyperasthesia because of stimulation of cut section of nerves.
If the hemisection involves the segments T1 to L2, then there is disturbance of Sympathetic outflow with
fall in the peripheral resistance and blood pressure and loss of sweating Ipsilateral.
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Brown Sequard Syndrome: Ipsilaterally there is predominant motor loss and contralaterally there is
predominantly sensory loss. Features are same as that of the Hemisection.
COMPLETE TRANSECTION OF SPINAL CORD:
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Cause is fracture dislocation of vertebral column, stab wound, bullet wound or expanding tumor.
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If transaction is above C3 level, life is not possible without artificial respiration.
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If transaction is in the lower cervical segments then there is quadriplegia.

If transaction is in lower thoracic level, then there is paraplegia.
The effects of spinal cord transaction can be discussed in three stages

1. Stage of Spinal Shock or Stage of Flacidity: Immediately after transaction, there is complete
flaccid paralysis, loss of all sensations below the level of transaction. All superficial and deep
refelexes are lost. Loss of muscle tone in smooth muscle and skeletal muscle. Even the sphincter
tone is lost. There is urinary and fecal incontinence. If the transaction is in the segments of T1 to
L2 then there is disturbance in sympathetic outflow i.e. loss of peripheral resistance and fall of
BP. Legs become cold and blue. The cause of this stage is loss of tonic faciliatatry impulses from
higher centers to neurons. This stage remains for 2 to3 weeks.
2. Stage of Reflex Activity: this stage starts after 2 to 3 weeks. Muscle tone begins to return 1ST in
the smooth muscle. Sphincters regain their tone which leads to urinary and fecal retention. Tone
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also returns to the smooth muscles of the blood vessels which improves the blood pressure. The
spinal cord sympathetic neurons learn to function independently without facilitatory impulses
from the higher centers. This improves the blood pressure. Tone also begins to return in the
skeletal muscle. First it returns in the flexors of the body. They become less flabby. This return is
reflex in nature but tone as not as much as normal because the myotatic reflex is weak in the
absence of facilitatory impulses from higher centers. As tone returns first in the flexors so legs
become flexed. So there is paraplegia in flexion. Muscles start contraction during reflex activity
but not for voluntary movements. Spontaneous muscle contractions appear especially in the
flexors. Flexor reflex appears. Initially the response is weak but gradually it increases. A Mass
reflex or Mass response appears which is when skin over the legs or anterior abdominal wall is
scratched, there is contraction of flexors of both legs and anterior abdominal wall muscles along
with evacuation of urine from bladder even if it is less in amount which may be partly due to
contraction of muscles of anterior abdominal wall. There is profuse sweating below the level of
transaction especially if the segments involved are below T1,2. In males erection can can occur
when there is mechanical stimulation of skin of glans penis or inner side of thigh. After 3 6
months of recovery, below the transection there is upper motor neuron type of lesion.
Sensations dont recover at all. There is automatic bladder and there is automatic defecation
reflex. The patients learn how to elicit defecation and micturition by scratching the skin of
perianal area or inner side of thigh. This stage of reflex activity continues if the patient has good
nursing care.
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3. Failure of Reflex Activity: If the patient dosent have good nursing care then the patient goes in
to this stage. This stage starts if there is general infection or toxemia. Response during reflexes
decreases, wasting of muscles. Bed sores appear.
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INCOMPLETE TRANSECTION OF SPIN AL CORD: there is severe damage to the spinal cord but not
complete transaction. In it first there is spinal shock and then the stage of reflex activity. Stage of reflex
activity has certain peculiar features.
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1. Muscle tone first appears in extensors leading to paraplegia in extension. Reason is in

incomplete transaction, reticulospinal and vestibulospinal tract which are faciliatatory to
extensors escape the damage.
2. Extensor thrust reflex: the patient is on his back and his one leg is flexed at hip and knee and
foot is resting on the bed. The examiner with the palm of hand exert upward pressure on the
sole of foot of flexed leg. This results into contraction of triceps and posterior calf muscles,
resulting into extension of legs.
3. When flexor reflex is elicited, there is more strong crossed extensor reflex.
4. Phillipsons reflex: when one leg of the patient is flexed passively, the other leg becomes
extended and after some time, the flexed leg become extended and extended leg becomes
flexed. So there are steppage movements. This means in this type of transection locmotory
movements can occur but walking is not possible.
5.
After the recovery in these patients there will be UMN type of paralysis below the level of
transection.
6. At the level of transection, there will be LMN type of paralysis.

7. Sensations dont recover.
8. There are disturbances of micturition and defecation.
LESIONS OF SPINAL CORD:
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SYRINGOMYELIA: Excessive over growth of neuroglia with cavity formation in the grey matter around
the central canal of spinal cord. If this disease affects the brain stem, then this disease is called
syringobulbea. There is dissociated anesthesia. Sensations carried by lateral spinothalamic tract are lost
while those carried by ventral spinothalamic tract and dorsal column tract remains intact. There is loss
of pain and temperature with intact touch sensation. As there is loss of pain and temperature so the
reflexes which can be elicited due to pain and temperature are also lost. If this disease affects smokers
then they have burned finger tips. When the disease progresses, there is LMN type of weakness in the
hands and arms and there is UMN type of weakness in legs.
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TABES DORSALIS: it is present is patients suffering from syphilis. The syphilis organism causes selective
destruction of sensory nerve fibers in the dorsal nerve root at the entry point in spinal cord. The disease
affects mainly the lower thoracic and lumbar segments of spinal cord. There is severe stabbing pain in
the legs and other parts of the body because of stimulation or irritation of sensory nerve fibers. There is
increased sensitivity to touch, cold and warmth. There is paresthesias. Then there is loss of pain
sensation in parts of legs and other parts of body., due to loss of proprioceptive impulses there is ataxia
in the dark or when the eyes are closed. There is hypotonia. There is loss of tendon jerks. Knee and ankle
jerks are lost initially. There is atonic bladder and overflow dribbling because of loss of sensory nerve
fibers. There is argyl Robertson pupil. Pupil constricts during accommodation but fails to constrict during
light reflex.
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CEREBELLUM
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The Largest part of Hind Brain and it is posterior to pons and medulla oblongata, located in posterior
cranial fossa, covered by a layer of dura matter i.e. tentorium cerebelli.
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Cerebellum consists of 2 cerebellar hemispheres with narrow middle vermis.

Can be divided into 3 lobes i.e. anterior, middle or posterior lobe, floculonodular lobe.
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Two fissures divide the cerebellum in to these lobes i.e. primary fissure separates the Anterior lobe from
middle lobe. Uvulonodular fissure separates the posterior lobe from floculonodular lobe.
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Developmentally cerebellum is divided into three parts i.e. paleo, neo and archi cerebellum.
Paleo cerebellum is the old part and consists of anterior lobe and uvula and pyramid of vermis.
Neo cerebellum is middle or posterior cerebellum minus uvula and vermis.

Archi cerebellum is the oldest part and consists of floculo nodular lobe.
On the surface of cerebellum there is grey matter known as cotrtex and core is white matter. Cortex is
thrown in folds known as folea which has fissures and gyri. In cut section there is branched appearance.
This appearance is called Arbor Vitae.
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Each cerebellar hemisphere is divided into two parts i.e. intermediate zone and lateral zone.
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In the vermis and in the intermediate zone, there is topographical representation of different parts of
body. In the vermis axial parts of body are represented while in the intermediate zone limbs and facial
parts are represented. In lateral zone there is no topographical representation. This representation
receives afferent fibers from the respective parts of motor cortex. Similarly it receives afferent fibers
from the respective parts of body and also from motor nuclei of brain stem.
Efferents go to respective parts in motor cortex, red nucleus and reticular formation.
There are 10 primary lobules in the vermis.
1st lingula
2nd and 3rd central lobule
4th culmen
5th declive
6th folium
7th tubre
8th pyramil
9th uvula
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10th nodule
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STRUCTURE OF CEREBELLAR CORTEX: it is composed of three layers of grey matter.
1. Molecular layer: outer most. It consists of outer stellate and inner basket cells. In addition it
contains dendrites and nerve fibers which come from the deeper layers.
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2. Purkinge cell layer: consists of single layer of purkinge cells. These are flask shaped. From the
top of these cells dendrites arise and pass into the molecular layer, where these give rise to
primary secondary and tertiary branches. A primary and secondary branches are smooth while
the tertiary branches are covered with dendritic spines. From the base of these cells axons arise
which pass to the deeper layers and then these axons enter the white matter and become
myelinated. Most of the axons from purkinge cells synapse with the neurons in the deep
cerebellar nuclei or intra cerebellar nuclei. Some of the axons bypass the deep cerebllar nuclei
to go to the vestibular nuclei and these axons which bypass are perhaps from vermis or
floculonodular lobe.
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3. Granular layer: it is composed of granule cells. These are small cells with deeply staining nuclei
and scanty cytoplasm. There axons pass into the molecular layer where these end into T shaped
terminals or endings which synapse with the dendrites of purkinge cells. Incoming Mossi fibers
synapse with the dendrites of granule cells. Golgi cells are also present in the granular layer.
Dendrites of golgi cells pass to the molecular layer while their axons synapse with the dendrites
of the granule cells.
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White matter of cerebellum consists of three types of nerve fibers i.e.
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1. Intrinsic fibers: These are the nerve fibers which pass from the cerebellar cortex to vermis and
also from one cerebellar hemisphere to the other. So these remain within the cerebellum.
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2. Climbing Fibers: these come from the inferior olivary nuclei. These fibers give collaterals to
synapse with neurons in the deep cerebellar nuclei. Then these fibers go to the molecular layer
to synapse with the dendrites of purkinge cells. One climbing fiber synapses with the dendrites
of about ten purkinge cells.
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3. Mossi Fibers: these are all the other afferent nerve fibers other than climbing fibers. These also
give collateral to synapse with neurons in the deep cerebellar nuclei and then these pass into
the granular layer where these synapse with dendrites of granule cells. One mossi fiber gives a
number of branches with dendrites of hundreds of granule cells.
Afferent nerve fibers mainly enter the cerebellum throum anterior and middle cerebellar peduncles.
Efferent fibers from the cerebellum begin as the axons of purkinge cells. Most of these synapse with
deep cerebellar nuclei. Then axons from the deep cerebellar nuclei arise and these form the efferents
from the cerebellum.
DEEP CEREBELLAR NUCLEI: There are four nuclei on each side. From lateral to medial side these are
1. Dentate
2. Emboliform
3. Globos
4. Festigial
Emboliform and Globos are collectively called as nucleus interpositus.
Efferent fibers from 1st three come out of the cerebellum from superior cerebellar peduncle.
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Efferent from the last one come out through the inferior cerebellar peduncle.
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NEURONAL CIRCUIT OF CEREBELLUM: in the cerebellum there are 30 million functional units and each of
these functional unit consists of a purkinge cell and a deep nuclear cell. (see figure 56-7). Deep nuclear
cells are excited through direct collaterals from climbing fibers and mossi fibers. Deep nuclear cells can
be inhibited only through purkinge cells. Stellate cells, basket cells and golgi cells are also inhibitory in
nature and these are inhibitory to purkinge cells.
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Purkinge cells even at rest discharge at rate of 50-100 impulses/ second. Similarly deep nuclear cells also
discharge impulses even at rest.
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FUNCTION OF CEREBELLUM:
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Basic function of cerebellum is synergism i.e. activity of agonists and antagonists is coordinated. It
controls the timing of turn on signals to agonists and simultaneous turn off signal to the antagonists at
the start of movement and then to control the timing of turn off signal to agonists and simultaneous
turn on signal to antagonists at the end of movement.
CONNECTIONS OF CEREBELLUM:
Cerebellum is connected to brain stem through three peduncles i.e.
Superior to the midbrain
Middle to the pons
Inferior to the medulla oblongata
These peduncles contain both afferent and efferent fibers.
1. INFERIOR CEREBELLAR PEDUNCLE:
a. Afferents: these include
i. posterior spino cerebellar tract
ii.
cuneo cerebellar tract which are also called as posterior external arcuate fibers
iii. vestibule cerebellar tracts which are from the vestibular nuclei
iv. olivocerebeallar from olivary nuclei
v. reticulo cerebellar fibers which arise from reticular formation
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b. Efferents:
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i. Cerebello vestibular
ii. Cerebello reticular
2. MIDDLE CEREBELLAR PEDUNCLE: Largest of the three peduncles.
3. SUPERIOR CEREBELLAR PEDUNCLE:
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a. Afferent:
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a. Pontocerebellar fibers: main fibers and form part of corticoponto cerebellar pathway.
i. Anterior spino cerebellar tract
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ii. Rubro cerebellar tract from red nucleus
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iii. Tacto cerebellar tract from tactum of mid brain
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b. Efferents: these go to the
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Ventroanterior and ventrolateral nuclei of thalamus and then these go to the

cerebral cortex.
ii. Some go to the red nucleus from where they go to the thalamic nuclei and then
to cerebral cortex.
iii. Some also go to the basal ganglia.

So cerebellum has got the reciprocal connections with the cerebral cortex, red nucleus, vestibular nuclei,
reticular formation. So these connections indicate the basis of functions of cerebellum.
FUNCTIONS OF CEREBELLUM:
Lateral Zone:
1. It has connections with motor cortex. It also called as cerebrocerebellum. It is concerned with
palnning and programming of movements. Cerebellum does not initiate movement but controls
sequence and timing of successive movements that lead to smooth progression from one
movement to next.
2. Lateral zone has extra motor function. Predictive Function: it helps individual to predict how
rapidly movement will occur.
Intermediate Zone:
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1. Inaddition to motor cortex and red nucleus, it has connections with the spinal cord. This part
receives impulses from the proprioceptors. It compares the intended plan of movement with
actually performed movement, especially of distal parts of limbs. So it acts as a comparator. If
there is any discrepancy from the intended plan of movement, corrective signals are sent to
motor cortex to correct it. Cerebellum gets the intended plan of movement through impulses
from motor cortex and red nucleus.
2. It also controls the rate, range, direction and force of movement.
3. It has a damping function that it prevents the pendular movements and tremors.
4. It also controls the ballistic movements such as movements of fingers during typing and
movements of eyes during reading. Similarly movements of eyes of person sitting in moving
vehicle looking outside.
5. This intermediate zone has got connections with spinal cord, it ias also called spinocerebellum.
Vermis and Floculonodular Lobe:
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1. It has got connections with the vestibular system. This is also known as vestebulocerebellum.
This part is concerned with the control of posture, equilibrium and also eye movements.
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2. It is also related to the motion sickness. In animals it has been seen that if the uvula and nodule
is damaged then the animal becomes less sensitive to motion sickness.
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3. It also controls the stretch reflex and muscle tone through the bulboreticular facilitatory area in
the reticular formation.
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CEREBELLAR DISEASE:
It occurs when the lesion involves cerebellar cortex and one or more deep cerebellar nuclei. In
cerebellar disease there is no muscle paralysis and no sensory loss.
1. Ataxia: incoordinated movements due to errors in the control of rate, range, force and direction
of movements.
2.
Asynergia: normally there is synergism between agonists and antagonists. This is lost in
cerebellar disease.
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3. Dysmetria and Past pointing: dysmetria is inability to control range of movement. Past pointing
is a manifestation of dysmetria. In it the hand overshoots the intended mark.
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4. Dysdiadokokinesia or Adiadokokinesia: inability to perform rapid opposite, alternate

movements like rapid suppination and pronation.
5. Gait and Posture: there is staggering or drunken gait. The patient walks on a wide base. The
head of the patient is rotated and flexed towards the affected side. Shoulder on the affected
side is lower as compared to the other side.
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6. Action or Intention Tremors: Tremors are absent at rest and these appear when the patient
performs voluntary actions.
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7. There is Slurred or Scanned Speech due to dysarthria which is incoordinate contractions of

muscles involved in phonation and articulation.
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8. Rebound phenomenon: the patient is unable to stop a movement promptly which is due to loss
of influence over the stretch reflex.
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9. Decomposition of movements: the patient is unable to perform actions involving simultaneous

movements at more than one joint. Movements are broken into components.
10. Nystagmus: rhythmic osscilatory movements of eye especially when eyes are fixed to one side.
11. Hypotonia: because of loss of facilitatory affect on stretch reflex.
12. There is pendular knee jerk.
CEREBELLAR FUNCTION TESTS:
1. Finger nose test
2. Finger finger test
3. Rapid Suppination and pronation of hand
4. Ask the patient to walk in stratight line.
VESTIBULAR APPARATUS:
In the Petrous part of the temporal bone, there is system of tubes and chambers which is called
Labyrinth. There is a bony labyrinth inside the membranous labyrinth. Lab yrinth cocnsists of two parts
i.e. Cocchlea and Vestibular Apparatus. Cochlea is concerned with hearing and Vestibular apparatus is
concerned with equilibrium
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Vestibular apparatus on each side consists of three semi circular canals and two chambers i.e. the utricle
and saccule. These three semi circular canals on each side are anterior or superior, horizontal and
posterior. The semi circular canals are oriented in such a way that each is oriented at right angle to the
other two. When head is bent 30 degrees forward, the lateral canals are horizontal with the surface of
earth. The anterior canals are in a vertical planes which is projected forwards and 45 degrees outwards.
The posterior canals are also in a vertical plane that projects backwords and 45 degrees outword. The
plane of anterior canal on one side is parallel with the plane of posterior canal on the other side and are
called matched pair.
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Each semicircular canal opens in the utricle. Each canal has two ends, one end is ampullated (dilated)
and the other is non ampullated. Ampullated ends of all three canals have sepearte openings in the
utricle while the non ampullated ends of anterior and posterior canal have common opening in the
utricle called crus commune. Non ampullated end of horizontal canal also opens via separate opening.
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Semicircular canals are filled with endolymph. In the ampullated end of each canal there is a receptor
organ called crista ampularis. This crista ampularis consists of thousands of hair cells and in between the
hair cells there are supporting cells called the sustenticular cells. From top of hair cells cilia arise which
are embedded into a gelatinous material on the top called cupula. Vestibular nerve endings synapse
with the basis and sides of the hair cells.
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Each hair cell has 50 to 70 stereocillia and these cilia at one end are short and the height increases
towards the other side and at one side of hair cell there is very large cilium called kinocilium. Minute
filaments connect the tip of short stereocillium with the longer stereocillium till it is connected with the
kinocillium. The advantage of this arrangement is that the cilia can bent as a group. When there is
bending of stereocillia towards the kymocillium, there is depolarization. Even at rest the impulses are
discharged from hair cells at a rate of about 100 impulses/cell. During depolarization there is marked
increase in discharge of impulses. When there is bending of cilia away from kinocillium results into
hyperpolarization or inhbition. The discharge of impulses decreases below the resting state. The
kinociliium in all the hair cells is towards the same side.
Mechanism of Excitation of Hair Cells: Bending of stereocillium towards kinocillium causes stretch of
membrane of hair cells. This results into opening of cation channels. There is calcium influx (some books
say potassium) which causes depolarization. Resting membrane potential is -60 mV and the threshold is
-40 mV. When there is bending of stereocillium away from kinocillium there is more closure of cation
channels. So membrane potential becomes more negative i.e. -65 mV which results in hyperpolarization.
Semicircular canals are filled with endolymph. It is the movement of endolymph in the semicircular
canals which result in the excitation or inhibition of hair cells in the crista ampullaris. In the horizontal
canal kinocillium is towards the utricle. In anterior and posterior canals, the kinocillium is towards the
canal. Movement of endolymph towards the utricle stimulates the hair cells in the crista ampullaris of
horizontal canal and it inhibits the hair cells in the anterior and posterior canal. Opposite happens in the
movement of endolymph away from the utricle.
FUNCTIONS OF SEMICIRCULAR CANALS:
1. Semicircular canals detect rotation or angular acceleration and maintains equilibrium.
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When there is start of rotation, the semicircular canals begin to rotate but endolymph because
of inertia remains stationary and this leads to excitation of hair cells in the crista ampularis and
discharge of hair cells increases upto many hundred impulses per second. After some seconds,
endolymph also starts moving. So discharge of impulses from hair cells decreases and it
decreases towards the basal level of impulses and then as long as the person is rotated, the rate
of discharge of impulses remain at resting or basal level. At the end of rotation the semicircular
canals stop the rotation but endolymph because of momentum continues to move in the
direction of rotation. So there is bending of stereocilia in the opposite direction. So the
discharge of impulses from the hair cells decreases even below the resting level. Then after
some seconds the discharge of impulses increases back to the resting level. We can say
semicircular canals give signals of one polarity at the start of rotation and of the opposite
polarity towards the end of rotation.
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2. Semicircular canals can also detect velocity of rotation or angular acceleration. The degree of
rotation required to stimulate semicircular canals is one degree per second per second.
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3. Semicircular canals also have a predictive function. These can predict before time that a
disturbance of equilibrium is going to occur so that corrective signals are sent to produce
readjustments to prevent occurrence of the disturbance of equilibrium.
4. The semicircular canals help to maintain stable image of objects on the retina during rotation or
head movement and this is carried out by compensatory eye movements which are called
nystagmus or vestibulo ocular reflex. Nystagmus is observed at the start of rotation and at the
end of rotation.
Nystagmus is rhythmic osccilatory eye movement. Nystagmus has got two components i.e. slow
component and a quick component. Slow component is in the direction which is opposite to
that of rotation while the quick component is in the direction of rotation. When the person is
rotated to left side then there is slow movement of eye towards the right side to maintain stable
image of the objects on the retina. This is upto certain limit after which the eye snaps back to
the left side on the new fixation point and then it again moves slowly to the right side. Slow
component is initiated by impulses from the semicircular canals while the quick component is
controlled by impulses from the brain stem. Nystagmus is not initiated by visual impulses so it is
also present in the blind people. Nystagmus is generally horizontal which means the eyes move
in horizontal plane. Nystagmus may be vertical when head is bent to one side during rotation.
Nystagmus may be rotatory when head is bend forward during rotation.
5. The semicircular canals along with other parts of vestibular system are involved in the conscious
perception of gravity and motion.
6. Semicircular canals for their normal fucntionaning require normally functioning cerebellum
specially vermis and floculonodular disease. In cerebellar disease the semicircular canals can not
operate normally.
UTRICLE AND SACCULE:
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In the utricle and saccule, the receptor organs are macula. Size of the macula is about 1-2 mm and
macula is present on the inferior surface of utricle and saccule. In the utricle, the macula is oriented in
the horizontal plane. So utricle helps to maintain equilibrium during upright position. Macula in the
saccule is oriented in the vertical plane so saccule helps to maintain equilibrium in the lying position.
Macula consists of thousands of hair cells and inbetween the hair cells there are supporting cells and
sustenticular hair cells. Vestibular nerve endings synapse with the base and size of the hair cells. From
the top of each hair cells, 50-70 cillia project out. At one end or side there is shortes cilium and their
length increase progressively till at the other end there is very long cilium. Minute filaments connect
shorter cilium to longer till the kinocilium. On the top of cilia there is gelatinous material containing
otoliths which are composed of calcium carbonate crystals. Even at rest these cause the bending of
cilium. So even at rest hair cells in the macula discharge at rate of about 100 impulses per second.
Because of the presence of these otoliths the macula is also called otolith organ. Hair cells in the macula
are oriented in different directions. Some hair cells are stimulated when the head is bent forward. Some
hair cells are stimulated when the head is bent backward. So this means bending of head in one
direction excites specific hair cells or we can say bending of head in one direction leads to a specific
pattern of excitation which gives information to the brain centre about the position of head. Macula are
most effective to detect head position and to maintain equilibrium when head is in the vertical or near
vertical position.
FUNCTIONS OF MACULA IN THE UTRICLE AND SACCULE:

1. The macula detects position of the head with respect to the upright position and help to
maintain equilibrium when the head is away from the vertical or upright position.
2.
The macula detects linear acceleration and helps to maintain equilibrium during linear
acceleration. The macula in the utricle are involved in the horizontal acceleration while the
macula in the saccule are involved in the vertical acceleration. Suppose a person is standing in a
bus and bus moves suddenly, the person prevents his falling by bending his body forwards. This
is through the macula in the utricle. When the person is in moving bus and then the bus stops
suddenly, the otolith in the macula tends to fall forward and the person bends himself backward
to prevent the forward fall.
3. The macula cannot detect the velocity of linear acceleration.
4. The macula does not have predictive function.
VESTIBULAR FUNCTION TESTS:
1. Rotation Test: a person is rotated in a reveloving chair and the effects of rotation are observed
and we compare the effects with the normal person. We cant separate both ears.
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VESTIBULAR PATHWAY AND CONNECTIONS OF VETIBULAR APPARATUS:
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2. Caloric Test: we can test the each side separately. Water having temperature aboue or below
the body temperature is introduced in the external auditory meatus. It produces convection
currents in the endolymph of inner ear resulting in the excitation of hair cells and there is
nystagmus which is then compared with the normal response.
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Vestibular nerve carries afferent nerve fibers from the vestibular apparatus and the 1st order neurons
are located in vestibular ganglion. There are 18500 nerve fibers in vestibular nerve. Out of these 98% are
afferent or sensory and just 2 % are efferent in the vestibular nerve. Efferent nerve fibers come from the
ipsilateral lateral vestibular nucleus and bilaterally from the reticular formation near the 6th nerve
nucleus. The efferent fibers secrete acetyl choline from their nerve endings. Their functions is not clear.
These fibers are inhibitory in nature.
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Most of the vestibular nerve fibers synapse into the vestibular nuclei. Vestibular nusclei are located at
the junction of pons and medulla oblongata. There are 4 vestibiular nuclei i.e. superior, medial, lateral or
Deiters Nucleus and inferior nucleus. some of the vestibular nerve fibers bypass to go to the festigial
nucleus, uvula and floculonodular lobe of cerebellum and brain stem reticular formation. 2nd order nerve
fibers which arise from vestibular nuclei go into the vestibulospinal tract to the brain stem reticular
nuclei into the medial longitudinal bundle and festigial nucleus, uvula, floculonodular lobe and cortex of
cerebellum. Superior and medial vestibular nuclei receive afferent nerve fibers mainly from semicircular
canals. From these nuclei nerve fibers arise which go into the medial longitudinal bundle and into the
medial vestibulospinal tract. Fibers which go into the medial longitudinal bundle go to the motor nuclei
of 3rd, 4th and 6th cranial nerves to control corrective eye movements in order to fixate image of objects
on retina during movement of head. Fibers which go into the medial vestibulospinal tract goes to the
upper cervical segments of spinal cord to control appropriate movements of head and neck during
rotation. Lateral vestibular nucleus receive nerve fibers mainly from the utricle and saccule. From this
nucleus nerve fibers arise to form the lateral vestibulospinal tract which controls the movements of
body. Inferior or descending vestibular nucleus receives nerve fibers from both semicircular canals,
utricle and saccule. From this nucleus nerve fibers arise which go to the cerebellum and reticular nuclei
of brain stem. The hcnages in body like that of bp, nausea, vomiting and heart rate changes are
mediated through these connections. Vestibular pathway also passes through the thalamic nuclei to the
cerebral cortex. These connections with the cerebral cortex are involved in the conscious perception of
motion and also orientation in space.
FEATURES OF VESTIBULAR DISEASE:
1. The basic symptom is vertigo which is feeling of rotation in the absence of actual rotation. The
patient may feel that the external world is rotating or the patients own body is moving or there
may be unsteadiness of the legs.
2. Nausea, vomiting, sweating, changes in heart rate and blood pressure, skin pallor, nystagmus,
diplopia nd actual falling.
MENIERES DISEASE: There are attacks of vertigo and progressive impairment of hearing. Exact cause in
not known. One finding on postmartum is that the endolymph filled channels in the inner ear are
enlarged.
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MOTION SICKNESS: there is nausea, vomiting during travelling. There is abnormal overstimulation of
vestibular system in this condition.
BASAL GANGLIA:
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These are masses of grey matter in the white matter of each cerebral hemispheres. There are 5
components in the basal ganglia.
1. Caudate
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2. Putamen
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4. Substantia nigra
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3. Globus pallidus
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5. Subthalamic nucleus.
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Caudate and putamen are collectively clled as corpus striatum
Putamen and globus pallidus are collectively called as letiform or lenticular nucleus.
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Caudate is separated from putamen by the internal capsule.
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Basal ganglia have got extensive connections and these can be discussed in the form of two main circuits
i.e.
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1. Putamen circuit: fibers from the premotor, supplementary motor and somatic sensory area
pass to the putamen. And from the putamen these pass to the globus pallidus. From the
external part of globus pallidus fibers arise which go to the ventroanterior and ventrolateral
nuclei of thalamus. From these thalamic nuclei fibers arise which go to the primary motor,
premotor and supplementary motor areas. There are some additional connections of this
circuit which are
a. From the external globus pallidus fibers go to the substantia nigra then to the
thalamic nuclei and then to the cerebral cortex.
b. From globus pallidus to subthalamic nucleus and from her to thalamic nuclei and
then to cerebral cortex.
c. From globus pallidus to subthalamic nucleus and then back to the globus pallidus
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2. CAUDATE CIRCUIT: Fibers from the premotor, supplementary motor and somatic sensory
area fibers pass to the caudate nucleus and from the caudate to the globus pallidus internal
part and then from external part fibers go to the ventro anterior and ventrolateral nuclei of
thalamus. From here fibers go to the premotor, prefrontal and supplementary motor areas.
So in the caudate circuit there is no connection with the primary motor area.
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NEUROTRANSMITTERS IN BASAL GANGLIA:
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1. Corticostriate fibers which pass from the cerebral cortex to corpus striatum are cholinergic.
They release acetyl choline which is excitatory.
2. Nigrostriate fibers which pass from substantia nigra to corpus striatum are dopaminergic and
they release dopamine at their nerve endings.
3. Fibers which pass from caudate and putamen to substantia nigra and globus pallidus release
GABA.
4. Fibers which pass from the brain stem to the basal ganglia release nor epinephrine, serotonin
and enkaphelin.
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FUNCTIONS OF BASAL GANGLIA:
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Basal ganglia do not function independently. These function in association with the cerebral cortex and
the cortico spinal system.
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1. Basal ganglia with the help of cortico spinal system control complex and skilled motor activity
especially of distal parts of limbs. Like playing basketball, hammer a nail e.t.c. there is role of
putamen circuit in this function
2. Cognitive control of the motor activity. Basal ganglia re involved in the control of sequence of
motor activity in order to achieve a specific goal. In this function, there is also involvement of
the sensory input and information already stored in the brain. For example a person is walking
on the road and suddenly he sees a wild animal and that person immediately start running and
try to hide in a safe place. This sequence of motor activity in order to achieve a specific goal
which in this case is saving life is controlled by basal ganglia. Sensory input is important in this
case. There is involvement of caudate circuit in this function.
3. Control of timing and intensity or extent of movement. Basal ganglia helps to decide and control
how rapidly the movement will be and how large the movement will be. Caudate circuit is
involved in this function. There is also involvement of posterior periatal complex.
LESIONS OF BASAL GANGLIA:
1. Athetosis: continuous slow writhing movement involving hand, arm, face or neck. This is due to
lesion of globus pallidus.
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2. Parkinsons Disease: also called paralysis agitans. This disease was first described by james
Parkinson. This disease is due to degeneration in the pars compacta of substantia nigra which
results into the dopamine deficiency in the caudate and putamen. Dopamine content of the
caudate and putamen is reduced to 50% or even less than that. On the caudate and putamen
there is a balance between the excitatory influence of acetyl choline and inhibitory influence of
dopamine. When there is deficiency of dopamine there is imbalance which leads to the features
of parkinsons disease. Causes of parkinsons disease are:
a. Idiopathic seen in old people
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b. Trauma or head injury
c. Complication of influenza
d. Complication of treatment with phenothiazine derivatives.
1.
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Features of this disease include
akinesia, hypokinesia which is difficulty in initiating movements.
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2. Lead pipe or cogwheel rigidity. This rigidity is due to increased motor neuron discharge
both to agonists and antagonists.
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3. Static tremors which are present at rest. These disappear during sleep and decrease
during voluntary action. These become worse when patient is conscious that somebody
is watching. Tremors may involve fingers, hands, lips or tongue. If hands are involved
then there are pill rolling movements.
4. Because of rigidity the patient appears like a statue. Back is flexed, arms are adducted
and flexed, knees are bent, patient walks with short steps. When the patient starts
walking he is difficult to stop.
5. Mask like face due to loss of expression on the face.
6. Loss of associated movements such as unconscious arm swinging during walking.
7. Babinskis sign is not present
8. No loss of superficial reflexes.
9. Tendon jerks are difficult to be elicited because of rigidity otherwise they are present.
10. No sensory loss and paralysis.
Treatment of Parkinsons Disease: L Dopa is given which passes through blood brain barrier and it
converts into dopamine in brain. Dopamine as such cannot be given because it doesnt pass through the
blood brain barrier. Synthetic dopamine agonists such as bromochriptine is beneficial in these patients.
Anticholinergic drugs are also used which inhibit the excitatory effects of acetylcholine. Monoamine
oxidase inhibitors are also used and these inhibitors inhibit the breakdown of dopamine. L deprenyl is
one of the MAOI. In addition in some patients who dont respond to drugs, electrocoagulation of ventro
anterior and ventrolateral thalamic nuclei. Now a days, transplanataion of fetal dopamine cells in the
caudate and putamen is carried out and this is successful in some cases.
3. CHOREA: involuntary rapid flicking or dancing movements affecting hands, arms, face or may be
other parts of the body. Lesion is in the caudate and putamen. There are two types of chorea i.e.
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a. Huntingtons Chorea: Inherited disorder, manifested in 3rd of 4th decade of life. There
are flicking or distortion movements affecting hands arms face and may be other parts
of the body. There are nerve fibers in the pathway of basal ganglia which secrete GABA
which is inhibitory in nature. When these neurons in the caudate and putamen are
damged, the inhibitory influence of caudate and putamen over the sub stantia nigra and
globus pallidus is gone and this leads to outbursts of signals from substantia nigra and
globus pallidus to the cerebral cortex and result is the chorea. There is also dementia in
many patients. Dementia is not due to the GABA neurons in the caudate and putamen
but it is due to the damage to the cholinergic neurons in the cerebral cortex.
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b. Sydenhams or Rheumatic chorea: it is a complication of rheumatic fever.
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4. Heibalismus: Sudden violent movement involving one limb or one side of body. It is due to lesion
in the subthalamic nucleus.
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5. Wilsons Disease: it is also called hepatolenticular degeneration. It is genetic, autosomal

recessive disorder of the copper metabolism. In this disease, plasma concentration of
ceruloplasmin is low. There is deposition of copper in different parts of the body including the
lenticular nucleus and the liver. This results into degeneration in the liver and also in the
lenticular nucleus.
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THE LIMBIC SYSTEM: this system consists of limbic cortex and associated deep structures. Limbic means
extra or border. The limbic cortex consists of a ring of cortical tissue around the hilus of cerebral
hemisphere. The libic cortex consists of orbitofrontal cortex, subcalossal gyrus, singulate gyrus,
parahippocampal gyrus and uncus. Associated deep structures included nin the limbic system are are
shown in diagram.
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Limbic system is connected to the reticular formation through the medial forebrain bundle. This bundle
contains both the afferent and efferent fibers. Fibers arise from septum and paraolfactory area and then
these fibers pass through the hypothalamus to the reticular formation. Phylogenetically, limbic cortex is
the oldest part of the cerebral cortex.
Functions of Limbic System:
1. Inlvolvement in the control of olfaction specially amygdala.
2. Control of sexual functions.
3. Control of emotion and behavior.
4. Control of food intake
5. Involvement in memory specially in recent memory.
HYPOTHALAUMS: it is the part of diencephalon which is below the hypothalamic sulcus. It forms the
anteroinferior wall and the floor of the third ventricle. We can divide hypothalamus into four parts i.e.
preoptic, supraoptic, tuberal and mammillary. The nuclei in these four parts of the hypothalamus are as
follows:
1. Preoptic: lateral and medial preoptic nuclei.
2. Supraoptic: suproptic nucleus, suprachiasmatic nucleus, paraventricular nucleus and anterior
nucleus.
3. Tuberal: Ventromedial, dorsomedial, arcuate, posterior and lateral nuclei.
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4. Mammillary: supramammillary, premammillary, medial and lateral mammillary nuclei.
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Hypothalamus can also be divided into three parts. Anterior, posterior and lateral hypothalamus.
CONNECTIONS OF HYPOTHALLMUS:
AFFERENTS TO THE HYPOTHALAMUS ARE FROM
1. Amygdala
4. Nucleus of tractus solitaries
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3. Reticular formation of midbrain
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2. Hippocampus
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5. Locus ceruleus: these secrete norepinehrine at the nerve endings
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6. Raphe magnus nucleus: these secrete serotonin at their nerve endings
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7. Afferents from the sensory pathways

8. Optic chiasma
9. Thalamic nuclei
10. Lentiform nucleus

EFFERENTS FROM THE HYPOTHALAMUS GO TO
1. Amygdala
2. Hippocampus
3. Nucleus of tractus solitarius
4. Reticular formation of mid brain
5. Spinal cord
6. Nervous connections with posterior pituitary and vascular connections with the anterior
pituiatory. Supraoptic and paraventricular nuclei of hypothalamus secrete ADH and oxytocin.
These hormones are transported along with their carrier proteins along the nerve fibers to the
posterior pituitary where they are stored. These are the hormones of
hypothalamoneurohypophyseal system. In the median eminence and infundibulum of the
hypothalamus, there are sinusoids. Blood from these sinusoids pass through the hypophyseal
portal blood vessels and these pass through the or communicate with the capillary plexus in the
anterior pituitary.
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FUNCTIONS OF HYPOTHALAMUS:
It has got a number of functions.
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1. Control of autonomic nervous system: stimulation of posterior and lateral hypothalamus results
into sympathetic responses sucha s increase in the heart rate and blood pressure, papillary
dilatation, piloerection, secretion of catecholamines from adrenal medulla and hyperglycemia.
Stimulation of anterior hypothalamus results into parasympathetic responses such as slowing of
heart rate and fall in blood pressure, papillary constriction, contraction of urinary bladder, GIT
motility and secretions. in addition hypothalamus is also a relay station in the pathway of
sympathetic cholinergic nerves which produce vasodilatation in skeletal muscle and sweating.
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2. Control of water balance of the body: water balance is maintained through the control of intake
water and excretion through the kidney. When the thirst centre in lateral hypothalamus is
stimulated, there is conscious desire to take water and fluids. Thirst centre is stimulated when
there is increased osmolarity of ECF, Hypovolemia and also by angiotensin II. In the anterior
hypothalamus, there are osmoreceptors which are specialized neurons which respond to
changes in osmolarity. Water excretion is controlled by ADH. Stimuli which secrete ADH may be
osmotic or volume. If there is hyperosmolarity or Hypovolemia, there is secretion of ADH. These
stimuli will act on hypothalamus and ADH is released which acts on the distal parts of renal
tubules to reabsorb water.
3. Control of uterine contraction and milk ejection: oxytocin is synthesized in hypothalamus,
mainly the paraventricular nuclei. Oxytocin causes uterine contraction to help in the child birth.
In the second stage of labor there are high levels of oxytocin. In milk ejection of milk letdown
there is role of oxytocin. The baby suckles breast of the mother, impulses from the receptor
around nipples go to the hypothalamus and then there is release of oxytocin from anterior
pituitary. Oxytocin causes contraction of myoepithelial cells as a result of which milk is ejected
from the breast. This is a neuroendocrinal reflex. Afferent part is nervous and efferent is
endocrine.
4. Control of food intake or hunger: in the lateral hypothalamus, there is a feeding centre or
hunger centre. When this centre is stimulated there is desire to take food and there is hunger.
Activity of the feeding centre is controlled by a satiety centre in the ventromedial nucleus of the
hypothalamus. When satiety centre is active, feeding centre is inhibited. When satiety centre is
inactive, feeding centre is activated. In the satiety centre, neurons are called glucostat cells.
Glucose uptake in the glucostat cells depends upon the presence of adequate concentration of
insulin. In almost all brain cells glucose uptake dont require insulin except glucostat cells in
satiety centre. In uncontrolled diabetes mellitus, there is poly phagia and increased apetite
because of inactivity of satiety centre because there is less insulin as result of which there is
overactivity of feeding centre resulting in polyphagia. Mammillary bodies in the hypothalamus
control feeding reflexes such as swallowing and licking of the lips.
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5. Regulation of body temperature: in the preoptic area of hypothalamus there is a centre which
regulate the temperature. When temperature of the body increases with respect to thermostat
in the hypothalamus, various temperature decreasing mechanisms are initiated which include
cutaneous vasodilatation and sweating. When body temperature decreases with respect to
thermostat, various temperature increasing mechanisms are initiated and these include
cutaneous vasoconstriction, shivering and later on there is chemical thermogenesis. Shivering
centre is located in posterior hypothalamus.
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CSF is present in the subarachinoid space, ventricles and central canal and in subarachanoid space in
cisterns around the brain and spinal cord. Cisterns are the dilated spaces around the brain stem.
Important cisterns are the Cisterna magna, cistern pontine and lumber cistern.
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Total amount of CSF in the subarrachanoid space is 150 ml and the rate of formation is about 500 ml per
day. (20 ml/hour). CSF is formed mainly from the choroid plexus of the ventricles especially the lateral
ventricle. It is also formed from the ependymal cells lining the ventricles. Some CSF comes from the
brain tissue through the perivascular spaces. The blood vessels supplying the brain first travel for some
distance on the surface of the brain and then these penetrate into the brain tissue and they carry a layer
of pia matter around them. So a space is formed between the blood vessel and pia matter. Perivascular
spaces are present around the blood vessels upto arterioles and venules but not around the capillaries.
These spaces communicate with the subarachanoid space. In the brain there are no lymphatics.
Perivascular spaces function as lymphatics.
Flow of CSF: CSF is formed in lateral ventricles. From here it goes in third ventricle through foramen of
monro. From third ventricle CSF flows into the aqueduct of sylvius which opens in the 4th ventricle. Here
additional quantity of CSF is added. From 4th ventricle CSF passes through 3 foramina i.e. 2 lateral
foramina of luschka and foramen of megandie into cistern megna which is a part of subarachanoid
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space. From here it flows into venous sinuses especially the sagital sinus. The flow of CSF from
subarachanoid space to venous sinuses is through arachanoid villi. These arachanoid villi are microscopic
finger like projections. The macroscopic aggregations of these villi are called arachanoid granulations.
These arachanoid villi are covered with epithelial cells which contain large holes. Through these holes
CSF along with proteins and even RBCs c can pass. Valves are present at the arachanoid villi. These villi
allow the passage of CSF from subarachanoid space into venous sinuses only. This flow is because of
pressure difference and the pressure is always 1.5 mm of Hg higher in the subarachanoid space as
compared to venous sinuses.
In certain conditions CSF pressure increases. Normally the quantity of CSF in the subarachanoid space
remains normal. Causes of increased CSF pressure includes
1. Large brain tumor or space occupying lesion in skull
2. Hydrocephalus
3. Hemerrhoge or infection in brain. A large number of RBCs or pus cell present in CSF can cause
blockage of arachanoid villi.
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Normal CSF pressure range is 7-18 cm of water and on the average it is 12 cm of water in lying position.
Cushings reflex is initiated at around 45 cm of water. When there is high intracranial pressure there is
papiledema. Lumbar puncture is performed in space between L3 and L4.
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Secretion or Formation of CSF: 50-70 % of CSF is formed from choroid plexus. Choroid plexus is
cauliflower like growth of blood vessels covered by ependymal cells. Choroid plexus project into lateral
horn , third ventricle and the roof of 4th ventricle. Formation of CSF mainly involves active transport.
There may be facilitated or simple diffusion. Formation of CSF starts with the active transport of sodium.
There is NaK Atpase pump in the lining of choroid plexus. When sodium is trqansported actively there is
secondary active transport of chloride followed by osmosis of water. Glucose if transported by carrier
mediated diffusion. Blood brain barrier is permeable to CO2. Co2 binds with water to form carbonic acid
which dissociates into bicarbonate and hydrogen ions. this reaction is catalyzed by carbonic anhydrase.
Secretion of CSF is inhibited by carbonic anhydrase inhibitors. When metabolic inhibitors like aubain or
DNP are given there is decreased formation of CSF. This confirms that the formation of CSF involves
active transport. We can also say that the formation of CSF involves ultrafiltration because proteins are
not filtered. Composition of CSF resembles that of plasma or ECF. pH of CSF is 7.35. specific gravity is
1.005 and it is transparent colorless fluid.
Comparison of different constituents in the CSF and Plasma
Plasma
CSF
Proteins:
7500 mg/dL
25 mg/dL
Glucose:
100 mg/dL
60 mg/dL
Sodium
142 mEq/L
150mEq/L
Chloride
100 mEq/L
115mEq/L
Potassium:
4 mEq/L
3 mEq/L
Urea:
25-30 mg/dL
20 mg/dL
Bicarbonate:
24 mEq/L
25 mEq/L
Calcium
10 mEq/L
5.5 mEq/L
This composition confirms that the formation of CSF involves Active transport.
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1. It supports and protects the delicate tissue of brain and spinal cord.
FUNCTIONS OF CSF:
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2. It acts as a fluid cushion or shock absorber against the damage to the brain tissue which may be
caused by rapid changes in the position of the body and acceleration or deacceleartion.
3. CSF regulates the intracranial pressure. Normally the pressure is maintained by the balance
between formation and secretion.
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4. It acts a route of excretion from brain and spinal cord.
5. CSF keeps the surface of brain and spinal cord moist and may provide nutrition.
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6. CSF has a role in the regulation of water balance of the body. Because osmolarity changes in the
CSF affects osmorecptors in anterior hypothalamus and the thirst centre in the lateral
hypothalamus.
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7. CSF is also involved in the control of respiration. CO2 can cross both the blood brain barrier and
blood CSF barrier and in the brain interstitium and also CSF there is formation of hydrogen ions.
these act on the central chemosensitive area to stimulate respiration. Hydrogen ions formed in
the CSF are more rapid and effective to stimulate the central chemosensitive area as compared
to hydrogen ions formed in brain.
8. CSF has got a diagnostic value. Lumbar puncture.
9. It can also act as a therapeutic route. Spinal anesthesia and antibiotic administration.
HYDROCEPHALUS: it is excess of water in the cranial vault or skull. There are two tupes i.e.
1. External or communicating: CSF flows out of ventricular system into the subarachanoid space
easily. Blockage is either in the subarachanoid space due to large tumor or blockage may be at
the level of arachanoid villi like in hemerrhoge or infection. In this type CSF accumulates in the
subarachanoid space and in the ventricles. If it occurs in new borns there marked swelling and
enlargement of head and there is also brain damage.
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2. Internal or non communicating: CSF cannot flow out of the ventricular system into the
subarachanoid space. There may be blockage at the interventricular formaen or the blockage
may be at the aqueduct of sylvius or the blockage may be at the foramina of megandie or
luschka. There is marked enlargement of ventricles and brain tissue is compressed into shell like
structure.
AUTONOMIC NERVOUS SYSTEM
Autonomic nervous system is also called visceral or vegetative nervous system because it controls the
activity of different viscera like those of heart, intestines, bladder e.t.c. this system was given name
autonomic because it was thought that this system acts independent of CNS. This is not true because it
is controlled by various centres in brain stem, hypothalamus, other parts of limbic system, some parts of
cerebral cortex and spinal cord.
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This system is organized on the basis of reflex arc. This means impulses originate from visceral receptors
and these are carried by autonomic afferents to the CNS where these are interrelated and from here
impulses come along the autonomic efferents to the visceral effectors. Autonomic afferents are not well
defined but the autonomic efferents are well defined. Autonomic efferent pathway originates from CNS
and then becomes part of the PNS. The peripheral part of autonomic efferents consists of preganglionic
neurons and post ganglionic neurons. Cell bodies of preganglionic neurons are located in CNS and their
axons come out of the CNS as autonomic outflow. Anatomically there are three types of autonomic
outflow i.e. cranial, thoracolumbar and sacral.
Cranial: 4 of the 12 cranial nerves containing parasympathetic fibers which are preganglionic. These are
3, 7, 9 and `10th cranial nerves.
Sacral outflow: it is from sacral segments.
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Thoracolumbar Outflow: this outflow is from T1 to L2.
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There are two components of autonomic nervous system
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2. Parasympatehtic
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1. Sympathetic
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Craniosacral outflow constitutes parasympathetic while thoracolumabr outflow is sympathetic.
Preganglionic autonomic nerve fibers come out of the spinal cord through the ventral route. These are
myelinated and belong to B type of nerve fibers. Each nerve fiber diverges to synapse with 8-10
postganglionic neurons which are located outside the CNS in the form of aggregations and these
aggregations of neurons are called autonomic ganglia.
Postganglionic nerve fibers arise from Autonomic ganglia. These are unmyelinated and C type of nerve
fibers.
Preganglionic sympathetic nerve fibers are much shorter than the post ganglionic sympathetic.
Postganglionic parasympathetic fibers are musch shorter than preganglionic parasympathetic.
TYPES OF AUTONOMIC GANGLIA:
1. Paravertebral: These are in the form of chain or trunk called sympathetic trunk on the
anterolateral surface of vertebral column on both sides. This chain consists of number of
autonomic ganglia which are interconnected. In the sympathetic chain neurons are
postganglionic sympathetic. A total of about 23 or 24 ganglia are present in this chain. Three
are cervical, 10-12 thoracic, 4 lumbar, 4 sacral and 1 coccegeal. The cervical ganglia are
superior, middle and inferior cervical ganglia.
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2. Prevertebral: these are associated with certain large blood vessels. These are three in
number i.e. celiac along with abdominal aorta, superior mesenteric along with superior
mesenteric artery and inferior mesenteric along with inferior mesenteric artery. These
ganglia contain postganglionic sympathetic neurons.
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3. Terminal or outlying: these are present near the viscera to be supplied. These contain
neurons which are parasympathetic postganglionic.
SYMPATHETIC NERVOUS SYSTEM:
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It consists of thoracolumbar outflow. In the spinal cord there is lateral horn from T1 to L2. Cell bodies of
preganglionic sympathetic neurons are present in the lateral horn. Their axons come out through the
ventral root of spinal cord. These nerve fibers are sympathetic preganglionic. These nerve fibers leave
the ventral root to pass toward sympathetic trunk as white rami communicantes. In sympathetic trunk
some of nerve fibers synapse with the neurons at the same level or at a higher or lower level. Remaining
nerve fibers by pass sympathetic trunk which are called splanchnic nerve fibers which are again of three
types i.e. greater, lesser and least. These go towards the prevertebral group of autonomic ganglia and
also towards the adrenal medulla. From the sympathetic trunk, nerve fibers which are sympathetic
postganglionic arise and these join the spinal nerve as grey rami communicantes. These are
unmyelinated nerve fibers and belong to group C.
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1. HEAD AND NECK REGION: Sympathetics from T1 to T2 supply the head and neck region. They go
to cervical ganglia particularly superior cervical ganglion synapse there and postganglionic
sympathetic fibers arising from there supply the head and neck region. On sympathetic
stimulation following effects occurs:
a. Pupillary dilatation or mydriasis.
b. Contraction of smooth muscle in eye lid WIDENING OF PALPEBRAL FISSURE.
c. VASOCNSTRICTION, PILOERECTION AND SWEATING OF skin.
d. Slight cerebral vasoconstriction.
Horners syndrome: there is destruction or damage to the cervical sympathetic or superior cervical
ganglion. Features include ptosis, miosis and anhydrosis.
2. THORACIC REGION: Sympathetics from T3 T6 supply the thoracic region. The preganglionic
goes to the cervical ganglia particularly to middle and inferior cervical ganglia from where
postganglionic sympathetic fibers arise. On stimulation following effects occurs:
a. On heart positive chronotropic, ionotropic, bathmotropic effects occurs. Stroke volume
increases. On coronary blood flow the direct effect is coronary vasoconstriction but
indirect effect is more powerful which is through the release of vasodilators as a result
of increased metabolism which increases the blood flow.
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c. On skin there is vasoconstriction, piloerection and sweating.
b. There is relaxation of bronchial smooth muscle and this leads to bronchodilatation.
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3. ABDOMINAL REGION: sympathetic from T6-T11 supply the thoracic region. Some will synapse in
trunk and some preganglionic fibers by pass the sympathetic trunk and goes to prevertebral
ganglia from where postganglionic fibers arise. Following effects occurs on stimulation:
a. GIT sphincters are contracted. Generally there is decreased GIT MOTILITY.
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b. Relaxation of gall bladder.
c. Contraction of smooth muscle in the capsule of spleen and liver.
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d. There is renin secretion from juxtaglomerular cells.
There is also splanchnic vasoconstriction.
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f.
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e. There is renal vasoconstriction
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g. Secretion of catecholamines from adrenal medulla. Adrenal medulla is supplied by

preganglionic sympathetic fibers which comes through least nerve. Pheochromocytes in
adrenal medulla are embryologically postganglionic which have lost their nerve fibers to
become secretory and secrete catecholamines. So adrenal medulla is a part of
sympathetic nervous system.
4. LOWER LIMBS: T11-T12 and L1-L2.

a. Through the sympathetic cholinergic vasodilator nerves there is vasodilation just at the
onset of activity. There is increased glycolysis, force of skeletal muscle contraction and
increased lipolysis.
5. PELVIC VISCERA: Sympathetic from L1-L2
a. Relaxation of detrusor muscle and also the trigone and internal urinary sphincter.
b. Contraction of vas deferens, prostate leading to ejaculation.
6. GENERAL EFFECTS OF SYMPATHETIC NERVOUS SYSTEM
a. Mental alertness
b. BMR increases
c. In liver lipogenesis and in adipose tissue there is lipolysis.
PARASYMPATHETIC NERVOUS SYSTEM:
It consists of craniosacral outflow:
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CRANIAL OUTFLOW:
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3rd nerve: from edinger westphal nucleus parasympathetic preganglionic fibers arise which go to third
nerve nucleus. these fibers synapse in the cilliary ganglion and from the cilliary ganglion fibers arise
which are parasympathetic postganglionic. These fibers as short cilliary nerve supply the cilliary muscle
and sphincter papillae.
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7th nerve: parasympathetic preganglionic fibers arise from superior salivary nucleus. these synapse with
the neurons in the sphenopalatine and submandibular ganglia. From here post ganglionic fibers arise
which supply the nasal, lacrimal glands, submandibular and sublingual salivary gland.
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9th nerve: parasympathetic preganglionic fibers arise from inferior salivary nucleus. these fibers synapse
with neurons in the ottic ganglion and from this ganglion nerve fibers arise to supply the parotid gland.
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10th nerve: parasympathetic preganglionic fibers arise from dorsal nucleus of vagus. These fibers
synapse with the neurons located in the walls of the viscera to be supplied. Vagus nerve contains about
75% of the total parasympathetic nerve fibers. Vagus is from vagabond because it has got extensive
nerve supply
Effects of vagal stimulation are
1. Negative chronotropic, negative ionotropic, negative dromotropic and negative bathotropic

effect on heart.
2. Stroke volume decreases.
3. On coronary blood vessel there is slight vasoconstriction through indirect effect however direct
effect is vasodilatation.
4. Bronchoconstriction
5. Bronchospasm
6. Mucus secretion from bronchi
7. Vagi supply the intestine upto the proximal half of colon. The effects on git include increased GIT
secretion and motility. GIT sphincters are relaxed.
SACRAL OUTFLOW: From S2, 3, 4,5 parasympathertic preganglionic fibers arise which go to pelvic viscera
through pelvic nerves or nervi erigentes. Effects of stimulation are:
1. Increased stimulation and motility of distal half of colon.
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2. Relaxation of internal anal sphincter and this results into defecation. So in defecation there is
involvement of sacral parasympathetics. When feces accumulate in rectum and there is
stretching of rectum there is activation of intrinsic myenteric reflex but this reflex is not
powerful to cause defecation so it will need sacral parasympathetic reflex.
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3. Effects of stimulation on urinary bladder is that there is contraction of detrusor muscle and
relaxation of trigone area. So there is micturition. So we can say that this nervous system helps
in throwing out of excreta from the body.
4. There is vasodilatation of erectile tissue of penis and clitoris and this results into erection.
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Sympathetic which supply the sweat gland are cholinergic similarly sympathetic vasodilator nerves
which supply some vasodilator vessels are also cholinergic. Also the adrenal medulla supplied by the
preganglionic sympathetic fibers are also cholinergic.
OVERALLA CTIONS OF BOTH SYMPATHETIC AND PARASYMPATHETIC NERVOUS SYSTEM
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SYMPATHETIC NERVOUS SYSTEM:
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1. Sympathetic nervous system is widely stimulated in emergency so this is called fight and flight
reaction i.e. it enables the individual to stay and fight against emergency or to run away. There
is requirement of vigorous muscular activity during fight and flight.
2. This nervous system is stimulated also during exercise

3. Stimulated during emotional stress such as during rage.
4. Stimulated on exposure to severe pain, cold and when there is hypoglycemia.
5. When this nervous system is stimulated, capability of individual to perform vigorous nervous
activity is increased.
6. It is catabolic nervous system and require energy.
7. In the eyes there is papillary dilatation which means more light can enter the eyes
8. Mental alertness.
9. Bronchodilatation which means more air can enter the lungs.
10. Increased cardiac output.
11. More blood flow to active muscles. Increased glycolysis.
12. Increased lipolysis and increased free fatty acids level in blood.
13. Increased secretion of catecholamines from adrenal medulla
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All these effects are designed to increase the capability of individual to perform vigorous muscular
activity.
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In animals if there is sympathectomy, the animal will not be able to fight against the stress. If the animal
is kept in a cage to have restricted life then the animal can survive.
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1. this nervous system is protective in nature
PARASYMPATHETIC NERVOUS SYSTEM:
2. it is anabolic. It generates energy and conserves energy.
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3. In the eye the pupil is constricted and there is decreased amount of light falling on the retina to
prevent its damage.
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4. On the heart, there is slowing of heart and decreased force of contraction so it conserves
energy.
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5. On the GIT it increases the GIT motility and secretion.

6. So it helps in the digestion and absorption of nutrients.
7. This nervous system helps in the removal of excreta from the body.
8. This nervous system also helps to preserve species because erection involves this nervous
system.
NEUROTRANSMITTERS AND RECEPTORS IN THE AUTONOMIC NERVOUS SYSTEM:
In the autonomic nervous system there are 2 neurotransmitters i.e. acetyl choline and norepinephrine.
So two types of nerve fibers i.e. cholinergic secreting acetyl choline and adrenergic releasing nor
epinephrine.
All the autonomic preganglionic nerve fibers whether sympathetic or parasympathetic are cholinergic.
All the parasympathetic postganglionic fibers are cholinergic.
Sympathetic postganglionic fibers supplying the sweat glands and some blood vessels of skeletal
muscles are cholinergic.
Most of the post ganglionic sympathetic fibers are adrenergic except the one mentioned above.
RECEPTORS:
In the ANS there are two types of receptors on the effector cells i.e. cholinergic receptors and
adrenergic receptors.
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Cholinergic are again of types i.e. muscuranic and nicotinic

Muscuranic receptors: Muscariune is a poisonous substance present in the stool of poisonous tode.
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Located in the effector cells stimulated by parasympathetic fibers which are postganglionic and fibers
which are sympathetic postganglionic cholinergic .
Nicotinic receptors: Activated by nicotine.
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Located at the synapses between preganglionic and postganglionic nerve fibers. These are also present
in muscle membrane in the neuromuscular junction.
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Acetyl choline activates both of these receptors.
ADRENERGIC RECEPTORS: present in the effector cells supplied by sympathetic postganglionic fibers.
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These are further divided into alpha and beta receptors. Alpha further into alpha 1 and alpha 2 and beta
are further divided into beta 1 and beta 2.
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Norepinephrine mainly activates alpha and epinephrine activates both alpha and beta.
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Effect of catecholamines depecnds upon the type of receptors present in the effector organ.
Sympathetic responses which are mediated through alpha receptors include the responses which
involve smooth muscle contraction i.e. pupillary dilatation, widening of palpebral fissure, contraction of
GIT sphincters., Contraction of internal urinary sphincter, vasoconstriction and piloerection.
Sympathetic responses which are mediated through beta receptors include the responses which involve
smooth muscle relaxation i.e. bronchodilatation, vasodilatation, relaxation in the GIT wall, relaxation
detrusor muscle. Actions on heart i.e. cardioacceleration. Metabolic actions of sympathetic such as
glycogenolysis, lipolysis increased glycolysis are through beta receptors.
In different viscera there is sympathetic tone or parasympathetic tone. The continuous state of basal
activity of these nervous systems in viscera is called sympathetic tone or parasympathetic tone.
Importance of this nervous system is that the functi.. forexample in the blood veseels
there is sympatethic tone or vaso motor tone which means the blood vessel wall remains partially
contracted. On sympathetic stimulation there is vasoconstriction and on sympathetic inhibition there is
vasodilatation. Heart is under the effect of vagal tone when there is vagal stimulation heart rate
decreases and when the vagus is inhibited heart rate increases. GIT has got parasympathetic tone and
when Parasympathetic stim ulation to GIT is increased there is increased parastalsis.
Autonomic nervous system regulates visceral functions through autonomic reflexes.

EYE: Light reflex, accommodation reflex, dark reflex
Cardiovascular reflexes: Baroreceptor reflex, Bainbridge reflex, left atrial reflex, volume reflex.
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GIT Reflexes: there is reflex secretion of saliva and other juices on the sight and smell of food. Salivation
when something is introduced into the mouth. Reflex contraction of gall bladder. entero gastric reflexes.
Gastrocolic reflex. Mass reflex, defecation reflex.
Control of Urinary bladder: reflex for micturtion, reflex for sexual function i.e. ejaculation and erection.
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Temperature regulation i.e. sweating.
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There is drop of pressure whenever something moves with high velocity.
Sound has got three properties

1. Pitch: it depends upon the frequency of vibrations. It depends upon the length and tension of
vocal cords and also thickness of edges of vocal cords. In males, vocal cords are longer and their
edges are thick so male voice is of low frequency. In the females, the vocal cords are shorter and
their edges are thinner so female voice has got high pitch.
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2. Loudness: it depends upon the amplitude of vibration of sound. Greater the force of expired air,
greater will be the amplitude of vibration of vocal cords so louder will be sounds.
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3. Quality of sound called as timber
ARTICULATION: formation of words from the sound produced in the larynx. The main muscles of
articulation are soft palate, tongue and lips. Teeth also help in articulation. Speech consonents are
associated with certain anatomical structures.
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P and B are labial
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D and T are dental. There is apposition of top of tongue on the back of teeth.
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N is nasal.
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RESSONANCE: it refers to quality or timber of the sound. From the resonance we can infer about the
source of so und. Resonance depend s upon overtones. In human body, there are certain resonating
chambers which include nasal cavity, paranasal sinuses, pharynx, mouth cavity and thoracic cavity. So
these chambers give resonance to the sound. Change in the quality of sound occurs when there is nasal
obstruction and that is called as nasal twang.
CONTROL OF SPEECH: In the dominant cerebral hemisphere, there are speech areas in the cerebral
cortex. Most of us are right handed so left hemisphere is dominant however in the person who are left
handed, still left hemisphere is dominant. So in left hemisphere there are motor speech areas.
1. Brocas Speech area: it is located in anterior frontal gyrus, anterior to the face representation in
the face area in te primary motor cortex. It receives impulses. . in this area, there is
formation of detailed motor patterns for the contraction of muscles involved in phonation and
articulation. From this area impulses go to primary motor area to initiate muscle contractions
for phonation and articulation.
2. Wernickes Area: also called as sensory speech area. This area is located in the posterior part of
superior temporal gyrus behind the primary auditory area. It is brodmanns area 22. This area
receives impulses from visual association areas and auditory areas. The visual and heard
informations are completely understood. Thoughts are formulated. What to be spoken or
expressed is decided. Words are chosen to express the thoughts. Words are arranged into
sentences. Signals from this area go to the brocas area along the arcuate fasicullus. This area is
involved in high intellectual functions.
3. Angular Gyrus: located in the lower part of the parietal lobe behind the wernickes area and
anterior to the visual associateion area. It is brodmanns area 39. In angular gyrus there is
interpretation of visual information.
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4. Area for the naming of objects: located at the junction of posterior temporal lobe and anterior
occipital lobe. It is not numbered. Names of the objects originate with the help of the auditory
input. While the details of objects are stored in the brain due to visual inputs.
In addition to these speech areas in the dominant hemisphere, respiratory centre, the respiratory
centre, motor cortex, sensory cortex, cerebellum and basal ganglia are also involved in the control of
speech mechanism.
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PATHWAY FOR SPEAKING OUT HEARD WORD OR PATHWAY FOR ANSWERING TO A VERBAL QUESTION
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When a question is asked, the question is heard or received through the auditory pathway to the
auditory cortex. From here signals go to the wernickes area. The question is understood and what to be
answered is decided here. From wernickes area impulses go along the arcuate fasciulus to the brocas
area. Where formation of detailed motor patterns. From here these go to the primary motor area to
cuase contraction of muscles of speech.
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PATHWAY FOR SPEAKING OUT WRITTEN WORD OR PATHWAY FOR ANSWERING TO A WRITTEN
QUESTION
When a question is asked, the question is received in the primary visual area and then to the secondary
visual area and then to angular gyrus. From there impulses go to the wernickes area. The question is
understood and what to be answered is decided here. From wernickes area impulses go along the
arcuate fasciulus to the brocas area. Where formation of detailed motor patterns. From here these go
to the primary motor area to cuase contraction of muscles of speech.
WRITTEN SPEECH: the thoughts are formulated in werncikes area. From here impulses go to the brocas
area where detailed motor patterns of muscles involved in writing are formed which then goes to the
primary motor area.
Both for verbal and written speech, there are feedback mechanisms to the brain whether the thoughts
are being expressed correctly or not. For spoken speech there are two feed backs i.e.
1. Auditory feedback: when we speak we also here.
2. Proprioceptive feedback: impulses from the proprioceptors go to the brain.
For written speech, the two feedbacks are
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1. Visual feedback
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2. Proprioceptive feed back
DISORDERS OF SPEECH:
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1. Aphasia: speech disorder which are not due to defect of hearing or vision and not due to muscle
paralysis. These are due to lesion in the speech areas in the dominant cerebral hemispheres.
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a. Motor Aphasia: also called as non fluent aphasia. The patient has difficulty in emitting or
uttering words. Speech is slow and limited to few words. In some cases words retained
are those which were being spoken at the time of injury or CVA which caused the
aphasia. This is due to damage to the brocas area.
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b. Sensory Aphasia: also called as fluent aphasia. The speech of the patient appears to be
normal. Rather patient talks excessively and apparently speech appears to be normal.
But the talk carries little sense. Written and heard words are not correctly understood.
Thoughts are not correctly formed. Sentences are not correctly made. There is damage
in werncikes area.
c. Word Blindness or Dyslexia: in this disorder the patient can see but cannot interpret
written words. This is called word blindness. Reading is not normal. And lesion is in
angular gyrus or visual association area.
d. Global Aphasia: this is severe form of aphasia in which patient is totally demented and
the cause is widespread lesion involving wernickes area, angular gyrus, part of tempral
lobe and superior border of sylvian fissure.

Notes On CNS Physiology by Medical Study Center

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Notes On CNS Physiology

Neurons in these horns are

Ventral Horn: Two groups of neurons

Dorsal Horn: there are 4 groups of neurons

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The reflex arc consists of 5 subcomponents.

1. Receptor: it responds to the stimulus and generates impulses

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Reflexes can be clinically classified into four types i.e.

PROPERTIES OF REFLEX ACTION:

Central delay can be calculated by

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a. Long or Delayed Path: because of presence of more inter neurons.

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9. RENSHAW CELLS: these are the inhibitory inter neurons

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Muscle Spindles are present in between the muscle fibers.

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Muscles Spindles are stimulated by:

1. Stretching of Muscle spindles i.e. Lengthening of Muscle Spindles.

There are two types of stretch i.e.

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FUNCTIONS OF THE STRETCH REFLEX:

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POLYSYNAPTIC REFLEX: Superficial Reflexes & flexor withdrawl reflex.

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Recruitment, after discharge and irradiation are present in this reflex.

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1. Mechanoreceptors: respond to mechanical deformation of receptor membrane or of the

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5. Receptor Potential or Generator Potential: Whenever a stimulus is applied to a receptor a

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Amplitude of receptor potential depends upon the intensity of stimulus.

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Position Sensation: divided into two

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Thermal: Extremes of temperature, freezing cold and burning hot.

Superficial pain: involves superficial viscera and localized.

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ASCENDING TRACTS OR SENSORY TRACTS:

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VISCERAL SENSORY TRACTS.

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The effect of lesion of these tracts is on the contralateral side.

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Spinocerebellar tracts consists of fast fibers having velocity of conduction 120m/sec.

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