Physiology - (CNS) Fast Track

CNS
PHYSIOLOGY-cns
SYLLABUS
Introduction to Nervous System: (P. 981)
Organization of the nervous system
The structural and functional unit of nervous system
Neurons (P. 981): Types, morphology, functions, functional components, morphology, types, classification of
nerves
Signal transmission: (P. 982)
Review
Graded potential: Definition, characteristic, physiological significance
Resting membrane potential (P. 982): Ionic basis
Action potential (P. 982): Definition
Ionic basic for electrical, chemical, excitability changes
Propagation (P. 983): Mechanism, factors influencing
Response of Neurons and nerve fibers to injury: (P. 983)
Type of injuries VIII
Type of changes: Wallerian denervation, regeneration, factors influencing regeneration
Microenvironment of the neuron: (P. 984)
Blood brain barrier (P. 984), importance
Synapses: (P. 986)
Ultrastructure, properties, synaptic plasticity, neurotransmitters and mode of transmission
Definition, types, structure and mechanism of transmission
Neurotransmitters (P. 988) and their properties
Sensory receptors: (P. 991)
Definition, classification, properties
Reflexes: (P. 991)
Definition, classification
Reflex arc and stretch reflex
Properties of reflexes, their clinical significance
Higher cortical functions: (P. 993)
Learning, memory, judgment, language, speech
Somato- sensory system: (P. 996)
Classification and characteristics of different sensations
Sensory pathways (P. 996) and regulation at the higher level
Physiology of pain including endogenous pain relief system and referred pain
FAST TRACK BASIC SCIENCE MBBS -979-

Physiology
Control of posture and movement: (P. 1003)

General principles of organization of motor control
Effects of complete transection and hemisection of spinal cord
Descending pathways (P. 1004) involved in motor control
Pyramidal (Corticospinal) system (P. 1005), Extrapyramidal system (vestibulospinal, reticulospinal, tectospinal
and rubrospinal)
Motor Cortical areas (P. 1009)
Basal ganglia (P. 1009)
Cerebellum (P. 1012) and vestibular apparatus in control of motor movements, and their disorders
Thalamus: (P. 1018)
Components, connections, functions
Hypothalamus: (P. 1019)
Components, connections, functions, limbic syndrome
Limbic System: (P. 1021)
Components, connections, functions
Prefrontal lobe: (P. 1023)
Components, connections, functions, effects of lesions
EEG: (P. 1024)
Evoked potentials, their clinical significance
Reticular formation: (P. 1024)
Definition, connections, functions
Physiological basis of consciousness and sleep (P. 1025)
VIII
-980- FAST TRACK BASIC SCIENCE MBBS

CNS
CNS-PHYSIOLOGY
INTRODUCTION OF NERVOUS ii. Based on shape

SYSTEM - Pyramidal
Organization of nervous system - Fusiform
Nervous System - Stellate
- Oval, etc.
Central Nervous System Peripheral Nervous System iii. Based on length of Axon
a. Golgi type I neuron: Having long axon Eg.
Somatic Nervous System Autonomic Nervous System peripheral nerves and long fiber tracts in
CNS.
b. Golgi type II neuron: Having short axon eg.
Enteric Nervous Parasympathetic Sympathetic Basket cell
System Nervous System Nervous System
Morphology of Neuron
Neurons  Parts of neuron are
 Structural and functional unit of Nervous system i. Cell body (Soma)
Types of Neurons - Control centre of a neuron
A. On the basis of function: - Contains cytoplasm with central nucleus,
- Sensory or afferent: Carry input to CNS mitochondria, golgi body, nissl's granules,
VIII
- Motor or efferent: Transmit output of CNS to neurofibrils, centrioles, microtubules.
periphery ii. Processes
- Interneurons or internuncial: Situated in a. Dendrite:
between two neurons and relay information - Short process, usually multiple, may be
with necessary modification. single or even absent, Nissl's granules are
B. On the basis of morphology: present
i. Based on no. of processes - Provide input to the cell body in the form of
a. Apolar: Having no process eg. Chromaffin local potential [not action potential]
cells b. Axon:
b. Unipolar: With 1 process eg. Cells of - Single, arises from axon hillock, contains
mesencephalic nucleus of Trigeminal nerve axoplasm and surrounded by axolemma.
c. Pseudo unipolar: Having 1 axon and cell Nissl's granules are absent.
body attached to axon by a process eg. Cells - Axons carry information away from cell
of Dorsal root ganglion body in the form of action potential.
d. Bipolar: With 2 process eg. Retina, Cochlea, - Action potential are produced in initial
Vestibular ganglia segment i.e. just near the origin of axon. It
e. Multipolar: 1 axon and many dendrites eg. is because initial segment has lowest
Purkinje cells of cerebellum threshold.

Physiology
SIGNAL TRANSMISSION - Due to synaptic transmission, if potential

change i.e. graded potential is towards
Past Question:
hyperpolarization, then it is called inhibitory
1. Describe the difference between EPSP and IPSP postsynaptic potential (IPSP) [KU 2003]
(3 × 2 = 6)[03 Dec]
Resting membrane potential
Graded Potential
 It is the potential difference between inside and
 Electric signals generated due to sub-threshold outside of the membrane of cell during resting
stimuli (electrical, chemical, mechanical) that do condition.
not propagate as action potential is called graded
 It is usually negative and ranging from – 10 mv to
potential.
– 90 mv
 In other words, it is change in membrane potential  It is measured using cathode ray oscilloscope.
due to stimulus below level of firing.
Ionic Basis
Characteristics:
- Sodium potassium pump i.e. Na+-K+-ATPase
1. It is local i.e. changes in membrane potentials
present in cell membrane of cells, continuously
are confined to relatively small region of
pump 3 Na+ ions outward of cell and bring in
plasma membrane.
2K+ ions. This result:
2. It is graded i.e. magnitude of potential change
 Negativity inside the cell as more number of
and signal can be reinforced.
positive ions are pumped out.
3. It is conducted with decrement. (Magnitude
 Increased concentration of K+ and
falls off when conducted from point of origin)
decreased concentration of Na+ ions inside
4. It can be both depolarizing and hyperpolarising the cell.
5. It has no refractory period. - So, for sodium both concentration gradient and
VIII 6. It doesn't follow All or None law. electrical gradient favor for entering inside the
7. It can be summated. cell. But during resting state, the voltage gated
Physiologic Significance sodium channels are closed so the sodium ion
1. Receptor Potential cannot enter inside and membrane potential
due to Na+ is stabilized.
- Graded potential due to stimuli on receptors
(mechano-receptors, thermo-receptors, - But, in case of potassium electrical gradient tries
nociceptors, chemoreceptors) is called to bring in K+ channel available as well. Since,
receptor potential. cells are bag of potassium chemical gradient is
way larger. So, initially heavy K+ efflux occurs.
- If graded potential reached threshold, action
Later, a state will be obtained when rate of K+
potential is generated and sensory information
efflux and K+ influx get equalized and both
is sent to spinal cord of brain.
chemical and electrical gradient will balance each
2. Pacemaker potential
other. As a result, stable membrane potential will
- Graded potential is responsible for cardiac be obtained. This state is called resting state and
automaticity corresponding potential is resting membrane
3. Postsynaptic membrane potential potential.
- Due to synaptic transmission, if potential
Action potential
change i.e. graded potential is towards
 The sequential change of membrane potential
depolarization, then it is called excitatory
postsynaptic potential (EPSP) [KU 2003] after application of a threshold stimulus is called
action potential.

CNS
 Measured by cathode ray oscilloscope

 All or none law is followed. [Law states, "An AP if
produced is produced fully and never partially and +++++–––++++ +++
–––– +++–––––––
the sizes of AP formed in particular nerve fiber is
always same whatever may be strength of
stimulus provided other conditions remain
- Now, charges from adjacent site flow.
constant."]
Ionic Basis of Action potential +++ ––– +++
+++
- During resting state:
 Concentration and electrical gradient of Na+
- Due to movement of charges new area reaches
are directed inwards. So Na+ always has
firing level and action potential is formed here
tendency to rush into cell if channel get
opened. +++–––+++–––+++
 Concentration of K inside is high but as
+ +++–––+++
electric potential inside cell is negative. So,
K+ cannot efflux out heavily. When - Again charges move and other new place reach
membrane potential becomes less negative, firing level and new action potential is formed
its efflux tendency will increase. there again.
- After application of stimulus of threshold - This way action potential is conducted along
intensity, membrane potential gradually membrane in all direction.
becomes less negative and voltage gated Na+
channel open. RESPONSE OF NEURONS AND
- So, Na+ rushes into the cell and depolarizes the NERVE FIBERS TO INJURY
Type of nerve injury VIII
cell.
- For K+, since electrical gradient is now 1. First degree injury
minimized, so chemical gradient dominates - Occurs due to pressure for limited period
which pushes K+ outside causing K+ efflux. - Also called neuropraxia
- This efflux of K+ repolarizes the cell. - Temporary cessation of function
- Efflux of K+ continues due to late closer of Eg: Saturday Night palsy (Neuropraxia of radial
voltage gated K+ channel resulting into nerve)
hyperpolarization.
2. Second degree injury
- Later, membrane potential is restored to
- Injury to axon only, so called axonotemesis
original level by Na+ K+ pump.
- Other structures are intact eg. Phrenic crush
Propagation of Action potential:
3. Third degree injury
- Cells of resting state are negative inside and
- Injury to endoneural tube
positive outside.
++++++++++++ ++++ 4. Fourth degree injury
––––––––––––––– - Injury and disruption of perineurium and
––––––––––––––– nerve fascicles are disorganized.
++++++++++++ ++++
- When AP develops at a site, the outside of the
5. Fifth degree injury
site becomes negative but nearby site are still - Injury up to epineurium such that whole nerve
positive. trunk is disrupted.

Physiology
Note: 3rd, 4th, 5th degree injury are together termed as Regeneration
Neurotmesis.  The proximal segment which survives after
Changes after injury degeneration starts growing and gives out several
fine branches.
 The changes are together termed as
chromatolysis.  These branches grow towards the endoneural
tube of degenerated distal segment.
 Repair begins in 40 days and completed in 80
days.  If by chance, one of fibrils finds the original tube,
1. In cell body it starts growing quickly and other fibrils
disappear.
- Nissl's granules disappear
- Neurofibrils disappear.  Growth continuous rapidly till it reaches the target
structure which the nerve supplied before injury
- Golgi apparatus decrease in number.
 Regrown fiber is thin and unmyelinated which
- Nucleus is pushed to periphery i.e. becomes
eccentric later gets myelinated.
- Cell gets swollen Note: When the regeneration fails, fibers from central
2. In proximal segment [From cell body to site of end interwine and form an expanded mass called
injury] neuroma.
- Retrograde degeneration occurs i.e. from the

MICRO ENVIRONMENT OF NEURONS
site of injury to 1st node of Ranvier.
Past Question:
3. In distal segment [segment distal to site of injury]
- Wallerian degeneration occurs which is 1. Mechanism of circulation of CSF and write down
VIII
orthograde. its important functions. (2 +1 = 3) [05 Dec]
- This occurs in 2 phases:
Blood Brain Barrier (BBB)
a. Early phase (1-7 days): Only functional
changes  It is a partition of demarcation which form barrier
 Changes in activity of enzymes ACh between blood and ventricular cerebrospinal fluid
esterase and choline acetylase existing in reaction to choroid plexus.
 Ultrastructural changes in organelles  Barrier consists of:
 Failure of conduction of nerve impulse
1. Non fenestrated endothelium of the capillaries
b. Late phase (8-32) days: Histochemical and
connected by tight junction between them.
physical changes
 Neurofibrils swell and then disappear 2. A basement membrane of vascular
 Axis cylinder breaks up endothelium
 Macrophages and Schwann cells 3. Perivascular feet and cell bodies of the
increase astrocytes.
 Myelin sheath destroyed by enzymes 4. A network of intercellular spaces between
and removed by macrophage
astrocytes and neurons.
 Endoneural tubes left intact called
5. The cell bodies and processes of neurons.
'Ghost tubes'

CNS
 Is permeable to:  Important normal constituents of CSF are:

- Water, O2, CO2 i. Volumes = 100 ml ( 10 ml)
VIII
- Drugs like sulphadiazine, erythromycin, L-dopa. ii Pressure = 60 - 150 mm of water.
- High lipid soluble substances. iii. Chlorides (NaCl): 120 to 130 mEq/lit. (720 to
- Volatile anaesthetics like N2O, ether. 750 mg/dl)
- H+, Protein, bile salts, catecholamines (only to a iv. Total Base: 157 mEq./lit.
very small extent) v. Glucose: 65 mg/dl.
Note: vi. Total protein (Lumbar): 15 to 45 mg/ dl.
1. Brain-CSF barrier intervenes between the CSF and vii. Cells: 1 to 5 per cubic ml.
the extracellular space and includes:
viii. Na+, K+, HCO-3, Urea, etc.
i. Extra choroidal ependymal cells of the
ventricles having gap junction between them. Formation:
ii. Basement membrane - Formed both by filtration and secretion at the
iii. Sub-ependymal glial membrane choroid plexus of:
2. Brain-CSF barrier is weaker than the BBB.
i. Central part and inferior horn of lateral
Cerebrospinal Fluid (CSF) ventricle
 CSF is a clear, colourless and odourless liquid ii. Third ventricle
which fills the ventricular system and the iii. Fourth ventricle
subarachnoid space.

Physiology
Circulation of CSF [KU 05] Functions of CSF [KU 05]

1. Acts as hydraulic shock absorber to protect the
CNS.
2. Regulates the volume of the cranial cavity by
acting as reservoir.
3. Provide a path for carrying waste products during
neuronal metabolism
4. Convey nutritive material to CNS.
5. Provides proper chemical environment for neuron
activity.
6. Aspiration of CSF from lumbar (i.e. puncture) is
useful in diagnosis of brain disorder.
SYNAPSE
Past Question:
Formed mainly in central part and 1. Describe the difference between EPSP and IPSP.
inferior horn of lateral ventricle
(3 × 2 = 6)[03 Dec]
Inter ventricular foramen
(Foramen of Monro)  It is a physiological junction without anatomical
union between two neurons or between neuron
Third Ventricle and an effector organ.
rd
Choroid plexus of 3 ventricle
VIII also forms CSF Classification
Cerebral aqueduct of Sylvius A. According to parts of neuron involved:
i. Axodendritic: Axon with dendrite (most
Fourth Ventricle
common)
th ii. Axosomatic: Axon with cell body (soma)
Foramina of 4 Ventricles Central canal
of spinal cord iii. Axoaxanic: Axon with axon
1 Medial formen 2 Lateral foramina iv. Dendrodendritic: Dendrite with dendrite (rare).
(Foramen of Magendie (Foramen of Lushka)
B. According to nature of transmission:
Subarachenoid Cisterns 1. Chemical synapse: Through neurotransmitter
Cisterna cerebellomedullaris (cisterna magma) 2. Electrical synapse: Through gap junction
3. Conjoint synapse: Partly electrical and partly
Tentorial Notch Subarachnoid
space around chemical.
Inferior surface of cerebrum spinal cord and C. According to number of neurons involved:
the cauda equina
Superolateral surface of cerebrum i. One to one
Veins of spinal
ii. Many to one
Arachnoid granulation and villi cord
iii. One to many
Absorption into superior sagittal sinus

CNS
Structure of a synapse 
1. Synaptic knob/Terminal boutons/End-feet Neurotransmitter binds to receptor on
- Terminal end of presynaptic axon. It contains: postsynaptic nerve terminal.
a. Synaptic vesicle containing neurotransmitter

b. Mitochondria: For supply of ATP. If neurotransmitter is If neurotransmitter is
c. Microtubules excitatory, ligand gated inhibitory, Cl- channel
Na+ channel open and open and Cl- enters
d. Presynaptic membrane
Na+ enters inside inside
2. Post synaptic membrane: The membrane of neuron
 
which receives information from synaptic knob of
presynaptic neuron is called post synaptic membrane. Excitatory postsynaptic Inhibitory postsynaptic
potential (EPSP) potential (ISPS)
3. Synaptic cleft: Gap of 20-30 nm, separating pre
develops develops
and post synaptic membrane.
 
Impulse transmission at synapse
It triggers action It inhibits action
potential by taking potential as cell
membrane potential to undergoes
threshold hyperpolarization
 
Thus AP is conducted Thus impulse in not
further conducted further
VIII
Properties of Synapse
1. Law of forward conduction
- Conduction of impulse is unidirectional except
electrical synapse
2. Synaptic delay
- The minimal period of time required for impulse
to cross the synapse is called synaptic delay
When action potential arrives to presynaptic nerve - It is about 0.5 milliseconds.
terminal, its depolarization occurs
3. Law of divergence and convergence

- Information from one neuron can pass to many
Voltage gated Ca++ channel open and Ca++ enters
neurons and from many neurons to single neuron.
presynaptic neuron
4. Excitatory postsynaptic potential (EPSP) [KU 03]

- It is a local potential developed on postsynaptic
Ca++ helps to fuse the vesicles with presynaptic
membrane by stimulation of presynaptic fibers
membrane and release of neurotransmitter
causing initial depolarizing response.


Physiology
- It is not sufficient to cause generation of action Occlusion:

potential - The response obtained by stimulating two
- But during this potential, excitability of a nerves together is less than the response
neuron to stimuli is increased. obtained when they are stimulated separately.
- It is generated by: - It is due to the presence of common neuron in
 Opening of ligand gated Na+, Ca++ channels. both groups.
 Agents which close K+ channels - When B and C fire separately, response will be
due to stimulation of X, Y and Y, Z respectively.
 Production of end plate potential in
- But when B and C fire together, response will
neuromuscular junction
be due to stimulation of X, Y, Z i.e. Y will fire
 It can be summated; it is not propagated
only once.
and does not follow All or None Law.
- This phenomenon is called occlusion.
5. Inhibitory post synaptic potential (IPSP) [KU 03]
Subliminal fringe:
- It is a local potential developed on post-
- It is partially excited state
synaptic membrane by stimulation of certain
postsynaptic fibers causing hyperpolarizing - When A and B fire, due to summation X also
response in motor neuron. fires but Y will not fire but remains partially
excited.
- During this potential, excitability of neuron to
other stimuli is decreased. - Any neuron in subliminal fringe has increased
sensitivity than the normal neurons.
- It is generated by inhibitory neurotransmitter
causing high permeability of K+ and Cl- but 7. Synaptic plasticity (Described later)
VIII impermeable to Na+, Ca++ Neurotransmitters
6. Summation, Occlusion and subliminal fringe  The chemical substances liberated at the nerve
ending and help to transfer the message or the nerve
 W
A  impulse in the presynaptic neuron to an adjacent cell
 X like postsynaptic neuron, muscle or gland.
B   Criteria for a chemical to be labeled as

 Y neurotransmitter:
C  i. Chemical must be synthesized in neuron as
 Z neurotransmitter
Summation: ii. Should be stored in the presynaptic endings
- The addition of EPSPs produced by two iii. Should be released at synapse.
separate neurons forming synapse with iv. Should have its specific receptors on
another common neuron is called summation. postsynaptic membrane
- Both A and B produce EPSP on X. Thus addition v. Should be disposed off quickly by a suitable
of EPSP of A and B such that they cause firing system as soon as its action is over.
of X is called summation.

CNS
Some of common neurotransmitters are as follows:

Group Name Site of secretion Action
Amino GABA Cerebral cortex, cerebellum, basal ganglia, retina and spinal cord Inhibitory
acids
Glycine Forebrain, brainstem, spinal cord and retina Inhibitory
Glutamate Cerebral cortex, brainstem and cerebellum Excitatory
Aspartate Cerebellum, spinal cord and retina Excitatory
Amines Noradrenaline Postganglionic adrenergic sympathetic nerve endings, Excitatory and
cerebral cortex, hypothalamus, basal ganglia, brainstem, Inhibitory
locus coeruleus and spinal cord
Adrenaline Hypothalamus, thalamus and spinal cord Excitatory and
Inhibitory
Dopamine Basal ganglia, hypothalamus, limbic system, neocortex, retina Inhibitory
and sympathetic ganglia
Serotonin Hypothalamus, limbic system, cerebellum, spinal cord, retina, Inhibitory
gastrointestinal (GI)tract, lungs and platelets
Histamine Hypothalamus, cerebral cortex, GI tract and mast cells Excitatory
Others Nitric oxide Many parts of CNS, neuromuscular junction and GI tract Excitatory
Acetylcholine Preganglionic parasympathetic nerve endings, Excitatory
Postganglionic parasympathetic nerve endings,
Preganglionic sympathetic nerve endings,
VIII
Postganglionic sympathetic cholinergic nerve endings,
Neuromuscular junction, cerebral cortex, hypothalamus,
basal ganglia, thalamus, hippocampus and amacrine cells of
retina
Neuromodulators Found only in axon Found in all parts of the

 Neuromodulator is the chemical messenger, terminals body
which modifies and regulates activities that take Generally, neuron has Neuron may have one or
place during the synaptic transmission. only one neurotransmitter more neuromodulators
 These peptides do not propagate nerve impulses
Act by changing the
like neurotransmitters.
electric potential-
Have diverse actions
Neurotransmitters Neuromodulators depolarization or
repolarization
Propagate nerve impulse Modify and regulates
through synapse synaptic transmission Chemically,
Chemically,
Packed in small synaptic Packed in large synaptic neurotransmitters are
neuromodulators are
vesicles vesicles amino acids, amine or
peptides
others

Physiology
Some of common neuromodulators are as follows:

Name Site of secretion Action
Opioid Neuromodulators
Enkephalins Many parts of brain, substantia gelatinosa and retina
Dynorphins Hypothalamus, posterior pituitary and duodenum Inhibit pain sensation
 - endorphin Thalamus, hypothalamus, brainstem and retina
Non-opioid Neuromodulators
Bradykinin Blood vessels, kidneys Vasodilator
Substance P Brain, spinal cord, retina, peripheral nerves and intestine Mediates pain, Regulates anxiety,
stress, mood disorders, neurotoxicity,
nausea and vomiting. Causes
vasodilatation
Secretin Cerebral cortex, hypothalamus, thalamus, olfactory bulb, Inhibits gastric secretion and motility
brainstem and small intestine
CCK Cerebral cortex, hypothalamus, retina and small intestine Contracts gall bladder
(Cholecystokinin) Inhibits gastric motility
Increases intestinal motility
Gastrin Hypothalamus, medulla oblongata, posterior pituitary and Increases gastric secretion and motility
gastrointestinal (GI) tract Stimulates Islets in pancreas
VIP (Vasoactive Cerebral cortex, hypothalamus, retina and intestine Causes vasodilation
Intestinal
Polypeptide)
Motilin Cerebral cortex, cerebellum, posterior pituitary and Stimulates intestinal motility
intestine
Neurotensin Hypothalamus and retina Inhibits pain sensation
Decreases food intake
VIII Vasopressin Posterior pituitary, medulla oblongata and spinal cord Causes vasoconstriction
Oxytocin Posterior pituitary, medulla oblongata and spinal cord Stimulates milk ejection and uterine
contraction.
Corticotropin - Hypothalamus Stimulates release of ACTH
releasing
hormone
Growth hormone Hypothalamus Stimulates release of growth hormone
- releasing
hormone
Growth hormone Hypothalamus Stimulates release of growth
- releasing hormone-releasing hormone
polypeptide
Thyrotropin - Hypothalamus, other parts of brain and retina Stimulates release of thyroid
releasing hormones
hormone
Somatostatin Hypothalamus, other parts of brain, substantia gelatinosa Inhibits growth hormone secretion
and retina Decreases food intake
Gonadotropin - Hypothalamus, preganglionic autonomic nerve endings and Stimulates gonadotropin secretion
releasing retina
hormone
Endothelin Posterior pituitary, brainstem and endothelium Causes vasoconstriction
Angiotensin II Hypothalamus, brainstem and spinal cord Causes vasoconstriction
Artrial Hypothalamus, brainstem and heart Causes vasodilation
netriuretic Increases sodium excretion
peptide (ANP)
CNS
C. Based on Nature of stimulus

SENSORY RECEPTORS
1. Mechanoreceptors: For touch, pressure,
Past Question: vibration
1. Classify sensory receptors. (3)[05 Dec] 2. Nociceptors: For pain
 Definition: A biological transducer which can 3. Chemoreceptors: For chemical changes
convert (transduce) various form of energy into 4. Baroreceptors: For pressure changes
action potential in the sensory nerves to which
5. Osmoreceptors: For osmotic changes
they are connected.
Properties of receptors
Classification [KU 05]
i. Specificity of Response
A. Based on sensory modality
ii. Adequate stimulus: Particular form of energy
1. Cutaneous receptors to which a receptor is most sensitive is called
a. Pain receptors: Free nerve endings adequate stimulus.
b. Touch: Pressure receptors iii. Adaptation
- Rapidly adapting: Pacinian corpuscles, iv. Intensity discrimination
Meissner’s corpuscles v. Law of projection
- Slowly adapting: Merkel's disc, Ruffini vi. Doctrine of specific nerve energy
end bulb
vii. Lateral inhibition
c. Temperature receptors: Nerve ending
2. Proprioceptors REFLEXES
a. General proprioception: Muscle receptors, Past Question:
joint receptors 1. Write short notes on Axon reflex. (2)[09 July]
b. Special proprioception: Hair cells of
 Definition: Automatic and reproductive effector VIII
vestibular apparatus
response to a sensory stimulus with the
3. Special sense receptors involvement of central nervous system.
a. Vision: Rods and cones
Classification
b. Hearing: Hair cells
A. Based on development
c. Taste: Taste buds
a. Unconditioned reflex (Inborn) e.g. Knee Jerk
d. Smell: Olfactory receptors
b. Conditioned reflex (Acquired) e.g. Secretion of
4. Receptors for visceral sense:
saliva after seeing a known tasty food
a. Stretch: Baroreceptors in carotid sinus
B. Based on no. of synapse
b. Visceral pain: Free nerve endings
a. Monosynaptic reflex e.g. Knee Jerk
c. Chemical changes: Carotid bodies
b. Polysynaptic reflex e.g. planter reflex
d. Osmotic changes: Osmoreceptors in
hypothalamus C. Based on site of stimulus
B. Based on source of stimulus a. Superficial reflex e.g. Planter reflex
1. Telereceptor e.g. receptors for light, sound b. Deep reflex e.g. Knee joint
2. Exteroceptor e.g. receptors for cutaneous sense D. Based on function
3. Interoceptor e.g. receptors for visceral sense a. Somatic reflex: e.g. knee Jerk
4. Proprioceptor e.g. receptors for proprioception b. Autonomic reflex: e.g. gastrocolic reflex

Physiology
E. Based on segment involved

a. Segmental reflex: Involving only one segment
of spinal cord
b. Intersegmental reflex: Involving more than 1
segment of spinal cord
c. Suprasegmental reflex: Involving brain along
with spinal segments.
Reflex arc
 Intrafusal fibers are of two types:

a. Nuclear bag fiber: Nuclei are aggregated in a
bag-like swollen middle portion of fiber
b. Nuclear chain fiber: Nuclei are arranged in a
single row along long axis of fibers in form of
chain.
Mechanism of stretch reflex
When tendon of muscle is tapped, the muscle is
Stretch Reflex
stretched and along with it, muscle spindles
 Whenever a muscle is stretched suddenly, there is are also stretched and stimulated
VIII reflex contraction of the muscle. This is called
stretch reflex. 
Receptors This stimulation is sent to spinal cord via Group

Ia and Group II sensory fibers
 Muscle spindle
 Muscle consists of two types of fibers: Large 
extrafusal fibers and few small modified fibers Spinal cord processes the stimulation and sends
called intrafusal fibers or muscle spindles. impulse back to muscle via α and  motor
 Muscle spindles are situated in between the neuron.
extrafusal fibers and are connected to them in 
parallel.
 Motor neuron causes contraction of extrafusal
fibers and  motor neuron causes contraction
of intrafusal fibers.
Golgi tendon reflex (Inverse stretch reflex)
 Muscles have 2 types of receptors
i. Muscle spindles: Lying in belly of muscle
ii. Golgi tendon organ: Lying in tendon of muscle
 When a muscle is severely stretched, the tension
of tendons rises.

CNS
 Tension in tendon may reach to that level where  Deep reflex: Knee jerk, bicep jerk
there is risk of detachment of tendon from its  Organic reflex: Swallowing, defecation
bony attachment. ii. Associative learning or conditioning
 In such condition, Golgi tendon organ of tendons - Stimulus which normally doesn't produce
get stimulated. response is combined a number of times
 The stimulation is carried to spinal cord via Group with another stimulus which actually can
Ib sensory fibers. produce response. After continued
 This impulse in spinal cord inhibits α-motor repetition, the original stimulus which
neuron. [KU 13 MCQ] initially couldn't now alone can produce the
 As a result, extrafusal fibers relax and tension on response. Such type of learning is called
tendon is reduced and thus tendon is prevented associative learning.
from detaching from its bony attachment. - E.g. A bell was rung just before meat was
Note: Thus it must be noted that when a muscle is placed in dog's mouth and this was
stretched, it contracts but if it is stretched forcefully repeated a no. of times. Later, even through
then muscle relaxes instead of contracting. no meat was provided, animal salivate
when bell was rung.
Axon reflex
Memory
- Axon reflex is a local neural response and does
not involve CNS connections.  Memory is the ability to solve what is learnt or
- Here, neurotransmitter released is substance P experience and can be recalled in need.
and results in dilation of arterioles and  In other words memory means to retain
capillaries. knowledge for full use.
Classification:
HIGHER CORTICAL FUNCTION VIII
A. On the basis of type of information
Past Questions:
1. Declarative memory:
1. Synaptic plasticity and its relation to learning
- Memory of various details of integrated
memory (3)[10 Jan]
thoughts such as memory of important
2. Short-term and long-term memory (3)[10 Jan]
experience that includes memory of
3. Short term memory (3)[04 Dec]
surroundings, time, relationships, cause of
Learning experience etc.
 It is the process of gathering knowledge or experience.
- It is also called explicit memory.
 It is the ability to alter behavior on the basis of
- It is recalled by conscious effort
past experience.
 There are 2 forms of learning: - It is divided into:
i. Non-associative learning or unconditioning a. Episodic memory (for events)
- Stimulus normally produces particular b. Semantic memory (for facts)
innate response and is not associated with 2. Non-declarative memory/Skill/Habit memory:
any other stimulus.
- Memory frequently associated with motor
- It involves habituation and sensitization.
activity of person’s body such as swimming
E.g.
skill, dancing skill, driving skill, etc.
 Superficial reflex: Planter reflex,
abdominal reflex - It is also called implicit memory.

Physiology
- It is recalled unconsciously. transmission ceases. This phenomenon is

- It is divided into habituation.
i. Priming (recognition of previously Mechanism:
exposed words or objects)  Continuous stimulation causes
ii. Procedural (skills and habits) progressive closure of calcium channel
iii. Associative learning [Reason: Not known]
iv. Non-associative learning  Decreased Ca++ entry in sensory terminal
B. On the basis of duration  Thus, decreased release of neurotransmitter.
1. Short Term Memory [KU 10, 04] ii. Sensitization
- Recalling of events of immediate past i.e. - When a sensory terminal is stimulated
experiences of up-to few minutes to hours along with stimulation of facilitator
or days. terminal, then instead of signal transmission
- It is the period through which the memory becoming progressively weaker, it becomes
is made permanent on consolidated. stronger and will remain strong for long
time without further stimulation of
- It can be easily erased by an electric shock.
facilitator terminal. This phenomenon is
- Regular repetition and rehearsal help to
called sensitization.
make it permanent.
Mechanism:
- The processing is done in hippocampus.
Stimulation of facilitator terminal
2. Long Term Memory [KU 10]

- It is memory of years and sometimes for life
Release of serotonin in surface of Sensory
- Ordinary brain damage or electric shock
terminal
cannot erase it.
VIII 
- Anterior cingulate cortex has role in
Serotonin acts on receptors of sensory
permanent memory.
terminal and activate Adenylyl cyclase
- Physiological and structural changes are

responsible for long term memory.
Increased formation of cAMP
Basis of Learning & Memory or 
Synaptic Plasticity [KU 10] Activation of protein kinase
 After repeated stimulation, many functional and 
anatomical modifications occur on synapse. These Protein kinase phosphorylates and blocks K+
changes are referred as synaptic plasticity. channel
 Functional alterations are mainly responsible for 
+
short term memory and anatomical alterations K cannot efflux outside
are mainly responsible for long term memory. 
A. Functional Alterations Action potential is prolonged
i. Habituation 
- When a sensory terminal is stimulated Prolonged activation of Ca++ channel
repeatedly but without stimulation of 
++
facilitator terminal, signal transmission at Increased Ca entry in sensory terminal
first is great, but it becomes less and less 
intense with repeated simulation until Increased neurotransmitter release

CNS
iii. Potentiation: SPEECH

a. Post-tetanic Potentiation Past Question:
 The production of enhanced 1. Write short notes on Wernicke’s area (3)[04 Dec]
postsynaptic potential in response to
 It is the expression of thoughts and ideas through
stimulation.
production of sound.
 The tetanizing stimulation causes Ca2+ to
accumulate in presynaptic neuron. Physiology of speech
b. Long term potentiation  Area 39 of angular gyrus stores visual images and
recognizes the objects by sight.
 Rapidly developing persistent
enhancement of postsynaptic potential  Area 40 of supramarginal gyrus recognizes familiar
response to presynaptic stimulation objects with the help of touch and proprioception.
after a brief period of rapidly repeated  Area 42 of superior temporal gyrus comprehends
stimulation of presynaptic neurons. language and recognizes familiar sounds and
 It is much more prolonged and can last words.
for days.  These input from hearing, vision, touch and
 Unlike post-tetanic potentiating, it is proprioception are sent to Wernicke's area (Area
initiated by increase in intracellular Ca++ 22) [KU 04]
in postsynaptic neuron rather than  Wernicke's area (Sensory speech area) interprets
presynaptic neuron. the inputs, decides the speech and projects it to
 Involved in long term memory. Broca's area or motor speech area (Area 44, 45).
B. Structural changes  Arcuate fasciculus communicates Wernicke’s area
The important physical structural changes that with Broca's area.
occur are:  After receiving input from sensory speech centers, VIII
1. Increase in vesicle release sites for secretion of 1st plans motor movements of lips and tongue to
transmitter substance produce the desired sound.
2. Increase in number of transmitter vesicles  Broca's area through primary motor area
released stimulates lower motor neuron through primary
3. Increase in number of presynaptic terminals motor area and cause desired movement of
4. Changes in structures of the dendritic spines tongue and lips producing speech.
that permit transmission of stronger signals.
Aphasia
Note: Amnesia: Loss of memory
 It is the disorder of expression of speech.
I. Anterograde amnesia
i. Sensory aphasia
- Memory cannot be stored but the memory
- Affected site: Wernicke's area
already stored remains unaffected.
- Affected person will not remember the events - Patient cannot understand meaning of heard
from the moment after the disease has word or written word.
occurred. - So cannot formulate meaningful speech and
- E.g. In lesion of temporal lobe involving goes on producing speech which are
hippocampus. meaningless.
II. Retrograde amnesia - Also called fluent aphasia.
- Memory created prior to injury is lost while ii. Conduction aphasia
new memories can still be created.
- Affected site: Arcuate fasciculus
- Occurs after brain injury.

Physiology
- Comprehended idea of speech cannot be SOMATO-SENSORY SYSTEM

transmitted to Broca's area (ASCENDING TRACTS)
- Patient can fully understand meaning of Past Questions:
written or heard words.
1. Explain briefly how pain sensation is carried to
- But, patient produces meaningless speech
the centre of the brain from periphery (4)[10 Jan]
- It is another form of fluent aphasia.
2. Write briefly how pain sensation is carried to the
iii. Motor aphasia center from the periphery of the body.
- Affected site: Broca's area (3)[11 July]
- Motor program for speech cannot be made 3. Describe the neural pathways for pain sensation
- Patient understands everything but fails to from the periphery to the cerebral cortex
convert his thought into words, spoken or (4)[08 Jan]
written.
4. Explain the pathways of touch sensations from
iv. Global Aphasia periphery to center. (4)[07 July]
- Affected site: Both Broca's area and 5. Write a note on referred pain. (2)[05 Dec]
Wernicke's area.
6. a. What is meant by fast and slow pain? [3]
- Patient can neither comprehend language nor
b. What is the mechanism of referred pain?
can speak or write.
(2)[06 Dec]
v. Anomic aphasia
7. Referred pain (3, 2)[10 July, 06 June]
- Affected site: Angular gyrus.
8. Neural pathways for touch sensation from
- Patient has no difficulty with speech or periphery to center (3)[08 July]
understanding of auditory information; instead
9. Medial meniscus (3)[03 June]
there is trouble understanding written
VIII language or pictures.
Somato - Sensory System
First order second order Third order
Sensation Receptor Pathways Destination
neutron neuron neuron
Ventral
Posterior Lateral
Pain and Free nerve Substantia posterolateral Posterior
root spinothalamic
temperature endings gelatinosa nucleus of central gyrus
ganglion spinal lemniscus
thalamus
Ventral
Posterior Anterior
Light touch and Substantia posterolateal Posterior
Free nerve ending root spinothalamic,
pressure gelatinosa nucleus of central gyrus
ganglion spinal lemniscus
thalamus
Meissner's
Discriminative
corpuscles, Ventral
touch, vibratory Posterior Fasciculi gracilis
pacinian Nuclei gracilis posterolateral Posterior
sense, conscious root and cuneatus,
corpuscles, and cuneatus nucleus of central gyrus
muscles joint ganglion media lemniscus
muscles spindles, thalamus
sense
tendon organs
Unconscious Muscle spindles, Posterior Anterior and
Nucleus Cerebellar
muscle joint tendon organs, root posterior
dorsalis cortex
sense joint receptors ganglion spinocerebellar

CNS
General consideration A. Receptors:

Ascending pathway consists of 3 neurons - Free nerve endings for both pathways.
arrangement:
Note:
1. First order neuron
i. Adequate stimuli for pain: Noxious tissue
2. Second order neuron
damaging stimuli.
3. Third order neuron
ii. Adequate stimuli for temperature: Change in
Note: temperature either higher or lower than body
- The 3 neuron chain is the most common temperature.
arrangement but some afferent pathway uses
more or fewer neurons. For example: Spino- B. First Order Neuron
cerebellar pathway is 2 neurons chain system. - With cell body in Posterior root ganglion.
Lemniscus 1. Pain fibers:
- Lemniscus or fillet is the prominent bundle of i. A fibers carry fast pain sensation
sensory nerves in brain. (15m/sec.)
- It is four types: ii. C fibers carry slow pain sensation (1
i. Spinal lemniscus: m/sec.)
 Formed by spinothalamic tracts in 2. Temperature fibers:
medulla oblongata
i. A carries cold sensation (10 - 380c)
ii. Lateral lemniscus:
ii. C carries warmth sensation (30 - 450c)
 Formed by the fibers carrying sensation
- These A and C fibers end on the cells of
of hearing from cochlear nuclei to
marginal nucleus and substantia gelatinosa of
inferior colliculus and medial geniculate VIII
body Rolando (SGR) in dorsal horn respectively.
iii. Medial lemniscus: C. Second Order Neuron (LATERAL
 Formed by fibers arising from nucleus SPINOTHALAMIC TRACT)
cuneatus and nucleus gracilis Starts at the substantia gelatinosa of Rolando
iv. Trigeminal lemniscus: (also in lamina IV and VIII)
 Formed by fibers from sensory nuclei of 
trigeminal nerve
Cross to the opposite side in the anterior white
 This lemniscus carries general senses commission just in front of the central canal
from head, neck, face, mouth, eyeballs

and ears.
Ascends in the lateral funiculus as lateral
Note: In the tegmentum of midbrain, Lemnisci are
spinothalamic tract
arranged from medial to lateral side as: Medial,
trigeminal, spinal and lateral. 
Continues as the spinal lemniscus in the brain
1. Pain and Temperature Pathway stem
[KU 11, 10, 08] 
 Pain and temperature is carried by common Ends in ventral posterolateral (VPL) nucleus of
pathway. the thalamus

Physiology
Note:
i. Fibers from the lower segments are
arranged toward the lateral surface of
spinal cord [KU 13 MCQ] while that of upper
segments are towards central canal (i.e. arranged
medially)
ii. Temperature fibers are arranged dorsally while
pain fibers are arranged ventrally.
iii. Spinal Lemniscus:
- A composite bundle of fibers containing:
a. Spinothalamic tracts
b. Spinoreticular tracts
c. Spinomesencephalic (e.g. Spinotectal or
spinal to periaqueductal gray) fibers.
- Formed in brain stem (in Pons)
D. Third order neuron:
Starts at the VPL nucleus of the thalamus

Thalamic radiation via internal capsule

VIII
Reaches the primary sensory cortex
Function of Lateral spinothalamic tract
(Area 3, 1, 2)
- Fibers of lateral spinothalamic tract carry
Note: impulses of pain and temperature sensations.
1. Pain sensation from head and neck region is - Fibers arising from marginal nucleus transmit
carried by the trigeminal nerve. impulses of fast pain sensation.
2. Pain pathway gives following important collaterals - Fibers arising from substantia gelatinosa of
to: Rolando transmit impulses of slow pain and
temperature sensations.
i. Reticular activating system (RAS)
Effect of Lesion on lateral spinothalamic
ii. Periaqueductal grey matter (PAG)
tract:
iii. Reticular formation
- Bilateral lesion of this tract leads to total loss
iv. Hypothalamus of pain and temperature sensations on both
v. Limbic system (Amygdala) sides below the level of lesion
3. The neurotransmitter produced at substantia - Unilateral lesion or sectioning of the lateral
gelatinosa of Rolando by: spinothalamic tract causes loss of pain
i. A fibers is glutamate (analgesia) and temperature
(thermoanesthesia) below the level of lesion in
ii. C fibers is glutamate and substance P.
the opposite side.

CNS
Pain - Elicited by the - Elicited by chemical,

 Pain is defined as an unpleasant and emotional mechanical and mechanical and thermal
thermal types of type (i.e. all types of
experience associated with or without actual
stimuli. stimuli)
tissue damage.
 Pain sensation can be sharp, pricking, electrical, - Carried by - Carried by non-myelinated
myelinated 'A' 'C' fibers
dull ache, shooting, cutting, stabbing, etc.
fibers
Acute and Chronic Pain
- Conduction velocity: - Conduction velocity: 1
Acute Pain Chronic Pain 15m/sec. m/sec.
- Acute pain is a sharp - Chronic pain is the
- Pain is almost - Pain can occur both in the
pain of short duration intermittent or constant
confined to the skin. skin and in almost any
with easily identified pain of longer duration deep tissue or organ.
cause. with different
intensities. - Neurotransmitter - Neurotransmitter involved
involved in primary is substance P.
- It is localized in a small - It widely spreads to sensory neuron is
area before spreading large areas. glutamate.
to neighboring areas.
Referred pain and radiating pain
- Usually it is treated by - It is difficult to treat
medications chronic pain and it  When the pain sensation is felt in a part of the body
needs professional that is fairly remote from the tissue causing the pain,
expert care. this is called referred pain. [KU 10, 06, 05]
Benefits of pain sensation  When the pain is felt both at the site of the viscera
- Pain gives warning signal about the existence
(Local site) and also at referred site, then it is
of a problem to treat.
- It also creates awareness of injury.
called radiating pain. VIII
- Pain prevents further damage by causing reflex Mechanism of referred pain [KU 06]
withdrawal of the body from the source of i. Dermatomal rule: Usually pain is referred to a
injury.
structure that is developed from the same
- Pain forces the person to rest or to minimize
the activities thus enabling rapid healing of embryonic segment or dermatome.
injured part ii. Convergence-projection Theory:
- Pain urges the person to take required
 The basis of referred pain may be
treatment to prevent major damage.
convergence of somatic and visceral pain
Components of pain sensation [KU 06]
fibers on the same second order neurons in
Fast pain Slow pain dorsal horn that project to the thalamus
- Is experienced - Is felt 1.0 sec. or later after and then to the somatosensory cortex.
within about 0.1 sec. the stimulation. iii. Facilitation theory:
after the pain
 The visceral pain produces a subliminal
stimulation is
applied. fringe effect on the cell body (substantia
gelatinosa of Rolando cell) that lowers the
- Pain described by - Pain is described as slow
the patient as sharp burning pain, aching pain, threshold of neurons which receives pain
pain, pricking pain, throbbing pain, nauseous from somatic areas.
acute pain or pain or chronic pain.  Thus, impulse from somatic area is
electric pain. facilitated as a pain.

Physiology
Common examples: - These endogenous opioids inhibit the release

Organs Referred sites of substance P in the posterior gray column by
attaching to opiate receptor of afferent
i. Cardiac pain Inner aspect of the left arm
neuron. Hence, inhibit the pain pathway
and left shoulder
system. This system relieves the pain
ii. Diaphragm Tip of right shoulder endogenously.
iii. Stone in ureter Testicle - Mechanism of pain relief:
iv. Appendix, Ovary Umbilicus Stimulation of A and C fibers, cognitive
v. Stomach Anterior epigastrium processes, anxiety, depression, previous
experiences cause
vi. Gall bladder Epigastric region

vii. Renal Loin
Release of endogenous morphine from
viii. Testis Abdomen periaqueductal gray matter
Pain relief system (-endorphins and enkephalins)
1. The gating theory 
- When pain stimulus is applied on any part of Stimulation of Raphe Magnus Nucleus
body, besides pain receptors, the receptors of 
other sensations such as touch are also
Secretion of Serotonin
stimulated.

- When all these impulses reach the spinal cord
Inhibit the release of substance P from C-
through posterior nerve root, the fibers of
fibers and A-fibers in posterior gray
touch sensation (posterior column fibers) send
VIII collaterals to the neurons of pain pathway, i.e.
column of spinal cord

cells of marginal nucleus and substantia
gelatinosa Blocking of transmission of painful stimulus
i.e. closing of gate
- Impulses of touch sensation passing through
these collaterals inhibit the release of Note:
glutamate and substance P from the pain - Pain itself is an important factor in activating the
fibers. pain-suppression system (negative feedback
- This closes the gate and the pain transmission mechanism)
is blocked. - Area associated with release of endogenous opioid
- Examples: Acupuncture, massage and are:
application of ointment to painful areas can i. Periventricular area of diencephalon
relieve pain. ii. Periaqueductal gray matter of midbrain
2. Endogenous pain relief (Analgesia) System iii. Midline nuclei of the brain stem (Raphe
- Pain is modulated by release of endogenous Magnus Nucleus)
opioid peptides like: - Analgesia: Loss of pain sensation.
i. Endorphins - Hyperalgesia: Increased sensitivity to pain
ii. Enkephalins sensation.
iii. Dynorphins - Paralgesia: Abnormal pain sensation

CNS
2. Doral column tracts [KU 08, 07] First order neurons:

Fasciculus gracilis (tracts of Gall) and fasciculus - Located at all level of spinal cord.
cuneatus (tracts of Burdach) - Fasciculus gracilis: Originates at lumber level
Sensation carried: for lower extremity and is medial to fasciculus
cuneatus.
- Tactile sensation, localization and
discrimination - Fasciculus cuneatus: Originates at thoracic
level for upper extremity and is lateral to
- Vibration, joint sensation, muscle sensation
fasciculus gracilis.
and fine touch.
- The central fibers ascend ipsilaterally upward
- Conscious proprioception (conscious in dorsal column to terminate in respective
kinesthetic sensation) nuclei in medulla i.e. nucleus gracilis and
- Stereognosis (ability to recognize the known cuneatus.
object by touch with closed eyes) Second order neurons:
Receptors: - Originate from nuclei gracilis and cuneatus.
- Receives input from Pacinian's corpuscle, - Axons ascend and decussate forming internal
Meissner's corpuscle, Joint receptors, Muscle arcuate fibers and ascends as compact bundle,
spindles and Golgi tendon organs. the medial lemniscus. [KU 03]
- Ascends through contralateral brainstem.
- Terminates in VPL nucleus of thalamus.
Third order neurons:
- Arises from VPL nucleus of thalamus.
- Project via posterior limb of internal capsule to
the postcentral gyrus in somatosensory cortex VIII
(area 3, 1, 2)
Effect of Lesion
- Loss of fine tactile sensation; however, crude
touch sensation is normal
- Loss of tactile localization
- Loss of two point discrimination
- Loss of sensation of vibration
- Astereognosis (inability to recognize known
objects by touch while closing the eyes)
- Lack of ability of differentiate the weight of
different objects
- Loss of proprioception (inability to appreciate
the position and movement of different parts
of the body)
- Sensory ataxia or posterior column ataxia
(condition characterized by uncoordinated,
slow and clumsy voluntary movements
because of the loss of proprioception).

Physiology
3. Spino-cerebellar tracts - Enters the cerebellum contralaterally through

superior cerebellar peduncle.
A. Posterior spino-cerebellar Tract:
- Cells of origin (first order neuron) are located - Termination: Those fibers that crossed over to
at the base of posterior gray column in nucleus the opposite side in the spinal cord cross back
dorsalis /Clark's column (Lamina VII) which within the cerebellum and terminate into
extends from T1-L2. lower limb area of cerebellar cortex.
- Afferents: Collaterals of ascending tracts of Sensation carried:

posterior funiculi and transmit impulses of i. Unconscious proprioceptive and exteroceptive
various proprioceptive endings (Group Ia, Ib, information (i.e. subconscious kinesthetic
and II) as well as touch and pressure receptors. sensation) of lower extremity and lower part of
- Second order neurons: Ascends ipsilaterally as body
posterior spino-cerebellar tract. ii. Concerned with general status of posture and
- Enters the cerebellum ipsilaterally through the movements of entire lower limb.
inferior cerebellar peduncle. Note: For upper extremity and upper half of body:
- Termination: Lower limb areas of anterior and Rostral cerebellar tract.
posterior lobes of cerebellum. Effect of lesion:
Sensation carried: - Lesion of this tract leads to loss of subconscious
i. Unconscious proprioceptive touch and kinesthetic sensation in the oppotise side.
pressure sensations i.e. sub conscious 4. Spinotectal tact
kinesthetic sensation from lower extremity and
Situation:
lower half of body to cerebellum.
- Occupies the lateral side of lateral white
ii. Fine co-ordination of lower limb muscles
column, anterior to lateral spinothalamic tract,
VIII during posture and movement.
Origin:
Note: For upper extremity and upper half of body: - Originate from chief sensory nucleus (like
Cueno-cerebellar tract (posterior external arcuate anterior spinothalamic tract)
fibers) Course:
Effect of Lesion - After taking origin, the fibers cross to opposite
- Unilateral loss of the subconscious kinesthetic side through anterior white commissure to the
sensation occurs in lesion of this tract on the lateral column
same side, as this tract has uncrossed fibers. - Then, these fibers ascend to the midbrain
along with anterior spinothalamic tract.
B. Anterior spino-cerebellar tract: Termination:
- Origin (First order neuron): From the wide - Fibers of spinotectal tract end in the superior
receptive fields of Golgi tendon organs in lower colliculus of tectum in midbrain
half of body and lower extremities. Sensation carried:
- The axons entering the spinal cord from the - Concerned with spinovisual reflex
posterior root ganglion terminate by synapsing
with second order neurons in the nucleus
5. Spinoreticular Tract
dorsalis at the base of posterior gray column. Situation:
- Second order neurons: Cross to the opposite - Situated in anterolateral white column
side and ascends as the anterior spino- Origin:
cerebellar tract in contralateral white column. - Fibers of this tract arise from intermediolateral
nucleus.
CNS
Course: CONTROL OF POSTURE AND

- After taking origin, some of the fibers cross the MOVEMENT
midline and then ascend upwards Past Questions:
- Remaining fibers ascend up in the same side
1. State briefly the features of upper motor neuron
without crossing.
lesion (UMNL) and lower motor neuron lesion
Termination:
(LMNL) (2 + 2= 4)[04 Dec]
- All the fibers terminate in the reticular
2. How do you differentiate upper motor neuron
formation of brainstem by three ways:
lesion from lower motor neuron lesion?
i. Some fibers terminate in nucleus reticularis
(4)[03 June]
gigantocellularis and lateral reticular
nucleus of medulla in the same side. Some 3. Briefly describe Tabes Dorsalis (2)[05 Dec]
fibers terminate in the nuclei present in the 4. Describe the difference between: Upper motor
opposite side. and lower motor neuron paralysis
ii. Some fibers terminate in nucleus reticularis (3 × 2 = 6) [03 Dec]
points caudalis of the pons in the same side 5. Describe with the help of a diagram the effects of
or opposite side hemisection of spinal cord at the level of C5,6,7.
iii. Very few fibers terminate in midbrain. (2 + 3 = 5) [03 Dec]
Sensation carried: 6. Tabes dorsalis (2)[06 June]
- Concerned with consciousness and awareness 7. Myasthenia gravis (2)[09 July]
6. Tract of Lissauer (Fasciculus 8. Brown-sequard syndrome
Dorsolateralis) (3)[09 July, 07 July, 04 Dec]
 It is constituted by the fibers of first order neurons 9. Babiniski’s sign [2][09 July]
VIII
Situation: 10.Upper motor neuron paralysis
- Situated in the lateral white column between (3, 2)[10 July, 04 Dec]
the periphery of spinal cord and tip of 11.Spinal shock (3)[08 July, 06 Dec]
posterior gray horn
12.Alzheimers diseases (3)[11July,07 July]
Origin:
Upper Motor Neuron (UMN) and Lower
- Formed by fibers arising from the cells of
posterior root ganglia and enters the spinal Motor Neuron (LMN)
cord through lateral division of posterior nerve 1. LMN: Those neurons which come out of CNS
root (Brain-stem or spinal cord) and connected to the
Course: neuromuscular system are lower motor neurons.
- After entering spinal cord, the fibers pass Note:

upwards or downwards for few segments on i. Preganglionic, sympathetic and parasympathetic
the same side and synapse with cells of fibers are not LMN.
substantia gelatinosa of Rolando ii. Cranial nerves originated from brainstem are
Note: Axons from these cells (second order neurons) LMN.
join the lateral spinothalamic tract. 2. UMN: Group of all those neurons that originate in
Sensation carried: higher level and connecting to the lower motor
neuron directly or indirectly and altering the
- Pain and thermal sensations
activity of LMN are upper motor neurons.

Physiology
UMN
Pyramidal system Extrapyramidal system
Cortical origin Subcortical origin - Cortical in origin - Subcortical in origin.

(Pyramidal Tract) (Extrapyramidal Tract)
- Myelination starts - Myelination starts before
at birth and birth.
Corticospinal Corticonuclear nd rd
completes by 2 -3
Tract (Corticobulbar) year.
Fibers
- Slower rate of - Faster rate of conduction
Tecto Rubro Reticulo Vestibulo Olivo conduction.
Spinal Spinal Spinal Spinal Spinal
- Mainly control the - Mainly control the
Pyramidal Tract movements of movements of lower
 Those tracts which pass through pyramid are upper limbs. limbs
called pyramidal tract.
- Function: fine - Function: Maintain
For example: Corticospinal Tract
voluntary posture and tone of body
 Pyramidal tracts of spinal cord are the descending
movements and certain tone reflexes.
tracts concerned with voluntary motor activities of
the body - For example: - For example: Tectospinal,
Note: Corticonuclear tract does not pass through Corticospinal and Rubrospinal,
pyramid but is functionally similar with corticospinal corticonuclear reticulospinal,
tract. Thus, these two tracts are collectively called tracts vestibulospinal, etc.
pyramidal system.
VIII
Descending pathways involved in motor control
Pathway Function Origin Site of crossover Destination Effect of Lesion
Most cross at Upper motor neuron type
Internuncial
Primary decussation of lesion:
neurons or alpha
Rapid, skilled, motor cortex pyramids and - Voluntary movements
motor neurons
voluntary (area 4), descend as lateral are affected
(Branches to:
Corticospinal movements, secondary corticospinal tracts; - Muscle tone is increased
Cerebral cortex,
tracts especially motor cortex some continue as leading to spasticity
basal nuclei, red
distal ends of (area 6), anterior - All superficial reflexes
nucleus, olivary
limbs parietal lobe corticospinal tracts are lost and the deep
nuclei, reticular
(areas 3,1,2) and cross over at reflexes are exaggerated
formation)
level to destination - Babinski sign positive
Inhibit or - Disturbances in
facilitate respiration, blood
voluntary pressure, movements of
movement; body and muscle tone
Reticulospinal Reticular some cross at Alpha and gamma
hypothalamus
tracts formation various levels motor neurons
controls
sympathetic-
parasympathe
tic outflows

CNS
Pathway Function Origin Site of crossover Destination Effect of Lesion

Reflex - Loss of movement of
postural hand in response to
Tectospinal Superior alpha and gamma
movements soon after origin visual and auditory
tract colliculus motor neurons
concerning stimuli
sight
Facilitates - Disturbances in activity
activity of of flexor muscles
flexor muscles
Rubrospinal Alpha and gamma
and inhibits Red nucleus Immediately
tract motor neurons
activity of
extensor
muscles
Facilitates - Difficulty in adjustment
activity of of hand and body during
Vestibulospinal extensor Vestibular Alpha and gamma acceleration
uncrossed
tract muscle and nuclei motor neurons
inhibits flexor
muscles
General Consideration: v. In the medulla:
Descending pathway consists of 2 neurons. - All the fibers reunite again to form a compact
i. Upper motor neurons (UMN) and band to produce the medullary pyramids
ii. Lower motor neurons (LMN) (Upper part of pyramid)
Note: UMN forms the tracts. - Lower medulla: Great motor decussation
(Pyramidal decussation): About 90% of
Corticospinal Tracts
the fibers cross to the opposite side while
Origin: 10% remains uncrossed. VIII
i. 1/3 fibers from area 4 (2% giant pyramidal
cells of Betz)
ii. 1/3 from area 6. 90% crossed 10% uncrossed
iii. Rest 1/3 from area 3,1,2 and other areas.  
Lateral corticospinal tract Anterior corticospinal
Course:
- Descends in the lateral tract
i. In the cerebral Hemispheres :
funiculus of the spinal - Descends in the
- Corona radiata: Fan shaped arrangement of the
cord (below C2 segment) anterior funiculus
fibers while coming down from the cortex.
 along sides of

- Termination: Anterior anterior median
ii. In the internal capsule:
gray column of all fissure upto
- In the anterior 2/3rd of the posterior limb.
spinal segments: midthoracic level
 i. 55% cervical 
iii. In the mid brain: segment. Cross the midline
- Occupy the middle 3/5th of the crus cerebri ii. 20% Thoracic and terminate in
(Cerebral peduncles) segment. the anterior gray
 iii. 25% Lumbo-sacral column of spinal
iv. In the pons: segment cord.
- Pass through the basilar part of the pons LMN:
- Tract is broken into small bundles by the - Synapse with internuncial neurons.
intervening pontine nuclei. 
- Synapse with  motor neurons (+ some 
 motor neurons)

Physiology
Note: Babinski sign (Extensor Planter

i. Standing position (Extensor group of muscles): response) [KU 09]
regulated by:  Cause: Lesion of corticospinal tracts (Pyramidal
- Vestibulospinal and pontine reticulospinal tracts)
tracts.  The great toe becomes dorsally flexed and the
ii. Sitting position (Flexor group of muscles): other toes fan outward in response to stretching
regulated by: the skin along the lateral aspect of the sole of the
- Rubrospinal and medullary reticulospinal tracts. foot.
iii. Visual reflex: Tectospinal tract.
Note:
i. Normal response is plantar flexion of all the toes.
ii. Remember that the Babinski sign (extensor reflex)
is normally present during the first year of life
because the corticospinal tract is not myelinated
until the end of first year of life.
iii. In normal adults, the original reflex (extensor) is
suppressed by the pyramidal tract.
iv. Planter flexor response is initiated by the touch
with the ground  help in walking.
v. Babinski sign is also present in deep sleep and
coma.
UMNL v/s LMNL [KU 10, 04, 03]
VIII UMN lesion LMN lesion

i. Muscle tone increased i. Muscle tone decreased
ii. Spastic paralysis. ii. Flaccid paralysis.
iii. Paralysis of a group of iii. Paralysis of individual
muscles. muscles.
iv. Babinski sign present. iv. Babinski sign absent.
v. Muscle wasting absent v. Muscle wasting
present.
vi. Deep reflexes become vi. Deep reflexes are
hyperactive absent (areflexia) or
hyporeflexia.
Function of Corticospinal tract vii. Electrical reactions are vii. Electrical reactions are
- Pyramidal tracts are concerned with voluntary normal abnormal
movements of the body
viii. Clonus present viii. Clonus absent
- Fibers of the pyramidal tracts transmit motor
impulses from motor area of cerebral cortex to ix. Fascicular twitch ix. Fascicular twitch
the anterior motor neurons of the spinal cord. absent present
- This tract is responsible for fine, skilled For examples: Rabies For examples: Polio
movements.

CNS
Types of Paralysis
Paralysis Parts of the body affected Causes
Monoplegia Paralysis of one limb Isolated damage of central nervous system or
peripheral
Diplegia Paralysis of both the upper limbs or both the Isolated damage of brain
lower limbs
Hemiplegia Paralysis of upper limb and lower limb of one Lesion in motor cortex and corticospinal tracts in
side of the body posterior limb of internal capsule on the side
opposite to the paralysis
Paraplegia Paralysis of lower half of the body Injury to lower part of spinal cord
Quadriplegia Paralysis of all the four limbs Injury to upper part of spinal cord (shoulder level
or tetraplegia or above), at which the motor nerves of upper
limbs leave the spinal cord
Note: v. Paralysis of bladder and rectum (Sphincters
Crossed hemiplegia or Crossed paralysis: also paralyzed)
- If there is paralysis of the inferior and superior vi. Vasomotor tone lost.
extremities of one side and involvement of some vii. Severe fall in BP (up to 40mm Hg.)
cranial nerves of the opposite side, the conditions - Persists for 3 to 4 weeks in human.
is called crossed hemiplegia. 2. Stages of reflex activity
- Cause: It is produced due to a lesion in brainstem, - Activities of the affected tissues gradually
and involvement of vertebrobasilar artery reappear:
I. Resumption of activities of the
- Involves the cranial nerves of that side (LMNL
preganglionic sympathetic neurons and VIII
type) and the corticospinal tract for the opposite return of vasomotor tone.
side (UMNL type) before the pyramidal
i. Internal urethral sphincter regain its
decussation. tone (earliest to appear)  lead to
Spinal cord injuries retention of urine.
ii. Gradual rise of BP (up to normal)
A. Complete transection of spinal cord:
iii. Segmental vascular reflexes also
 Features in different stages are: reappear.
1. Stage of flaccidity (Spinal shock) [KU 08, 06] II. Muscle tone returns gradually.
- When the spinal cord is suddenly transected, - Flexor tone returns first resulting in
all cord functions including the cord reflexes paraplegia in flexion
are lost below the transaction due to sudden III. Tendon Jerks reappear
removal of facilitation from higher centers; IV. Reflexes like mass reflex, withdrawal reflex
called spinal shock. are seen.
- Features are: 3. Stage of reflex failure
i. Threshold for all reflexes gradually increases
i. All the muscles are completely paralyzed.
ii. Failure of reflex and death.
ii. Loss of all type of reflexes.
Note:
iii. Loss of all types of sensation
i. Remembers that injuries above C5 spinal level
iv. Complete loss of muscle tone. results in death due to respiratory muscle
paralysis.

Physiology
ii. Complete cord transaction is due to: i. Same side: Loss of all sensation except pain
- Gunshot and temperature.
- Wounds  May be a band of Hyperesthesia
- Dislocation of spine ii. Opposite side: Loss of pain and temperature
- Occlusion of blood vessels 3. Below the level of Lesion: Features of UMN
- Transverse myelitis, etc. lesion on same side.
i. Same side: Loss of fine touch and
B. Brown-Sequard Syndrome/ Incomplete Proprioception (due to damage of tracts of Gall
Transaction of Spinal Cord and Burdach)
(Hemisection) [KU 09, 07, 04, 03]  UMN type of Paralysis
Due to hemisection of the spinal cord (by a bullet ii. Opposite side: Slight motor paralysis (due
or stab wound, or by expanding tumor), there is: to damage of anterior corticospinal tract)
1. Above the lesion: Normal  Extensive sensory Loss i.e. Pain,
2. At the level Lesion: Features of LMN lesion on temperature and crude touch (Due to
same side and normal motor functions on the damage of anterolateral system)
opposite side.
Brown-Sequard Syndrome [KU 09, 07, 04]
Level Same side Opposite side
Sensory changes Motor changes Sensory changes Motor changes
Lower motor neuron lesion Sensations lost: Sensations
type: carried by crossed tracts:
1. Loss of muscle tone 1. Crude touch
At the level of lesion
2. Flaccid paralysis 2. Pain

3. Loss of all reflexes 3. Temperature
4. Wastage of muscle Sensations retained: Sensations
5. Loss of vasomotor tone carried by uncrossed tracts:
VIII Complete anesthesia
1. Fine touch
2. Tactile localization
3. Tactile discrimination
4. Vibration sense
5. Conscious kinesthetic
No paralysis
sensation
If it occurs:
6. Stereognosis
1. Very mild
Sensations lost: Upper motor neuron lesion Sensations lost: Sensations
2. Resembles
Sensations carried by type: carried by crossed tracts:
lower motor
uncrossed tracts: 1. Increased tone 1. Crude touch
neuron type
Below the level of lesion
1. Fine touch 2. Spastic paralysis 2. Pain

2. Tactile localization 3. Loss of superficial 3. Temperature
3. Tactile discrimination reflexes Sensations retained: Sensations
4. Vibration sense 4. Exaggeration of deep carried by uncrossed tracts:
5. Conscious kinesthetic reflex 1. Fine touch
sensation 5. Babinski positive sign 2. Tactile localization
6. Stereognosis 6. Rigidity in limbs 3. Tactile discrimination
Sensations retained: 7. No muscular wastage 4. Vibration sense
Sensations carried by 5. Conscious kinesthetic
crossed tracts: sensation
1. Crude touch 6. Stereognosis
2. Pain
3. Temperature
CNS
Syringomyelia Motor Cortical Areas

- Syringomyelia is spinal cord disorder 1. Primary motor area (area 4):
characterized by cavitation and gliosis in the - Situated in the precentral gyrus.
central region of the neuroaxis.
- There is representation of the whole body in
- Syringomyelia is due to developmental the motor cortex  Motor Homunculus.
abnormality in the formation of the central
 For detail refer anatomy CNS (Telencephalon)
canal
- Fine and skillful voluntary movements are
- Common affected sites: Brain stem and
controlled.
cervical region of spinal cord.
2. Premotor area (area 6):
- Sensory disturbances are more pronounced
- Situated in posterior parts of superior, middle
than motor disturbances.
and inferior frontal gyri.
- Signs and symptoms:
- Controls extra-pyramidal fiber system.
 Pain and temperature sensations are lost
3. Supplementary motor area (area 6):
bilaterally
- Situated on the medial surface of the
 Touch persists (Reason: Mostly ascending
hemisphere anterior to the paracentral lobule
tracts in posterior funiculus is unaffected).
- Produces bilateral movements
 Lower motor neuron weakness is present in
- Helps the primary motor area in planning
the small muscles of the hand
complex movements.
 Bilateral spastic paralysis of both legs may
4. Posterior partial cortex
occur
- Involved in performing complex movements
Tabes Dorsalis [KU 06, 05]
which are learned by individual.
- In neurosyphilis, organism causes a selective
- Contribute fibers to pyramidal system,
destruction of nerve fibers at the point of VIII
somatosensory area and premotor area.
entrance of dorsal root into the spinal cord (up
to dorsal root ganglion) BASAL GANGLIA
- Common affected sites: Lower thoracic and
Past Questions:
Lumbosacral region of spinal cord.
1. Parkinson's disease
- It affects both sensory and motor function of
spinal cord. (2, 3)[10 July, 08 Jan, 04 Dec, 06 Dec]
- Signs and symptoms: 2. Functions of basal ganglia (3)[03 June]
 During the onset of degenerative changes, Parts:
there is stabbing pain in lower limbs (which a. Corpus striatum
may be very severe) b. Claustrum
 Then, there is impairment and loss of all c. Amygdaloid body
sensations:
 Loss of pain sensation (typical feature)
 Loss of position sense, vibration sense
 Hypersensitivity of skin to touch, heat
and cold
 Sensory ataxia is seen
 Both superficial and deep reflexes are lost
 Hypotonic urinary bladder with loss of
micturition reflexes.
Physiology
Connection:
VIII
Direct (Stimulatory) pathway

- It is stimulatory pathway to motor cortex.
- It stimulates fiber concerned with agonistic muscle.
- Dopamine excites direct pathway whereas acetylcholine inhibits it.
Excitation
Cerebral cortex [Neocortex]
Glutamate (+) Glutamate (+)
Corpus striatum GABA () Globus pallidus GABA () Thalamus

[Putamen D1] internus [VA, VL, DM]
Dopamine (+)
Substantia nigra [Pars compacta]

CNS
Indirect (Inhibitory) pathway

- It is inhibitory pathway to cortex.
- It inhibits fibers concerned with antagonistic muscles.
- Dopamine inhibits indirect pathway whereas acetylcholine stimulates it.
Inhibition
Cerebral cortex [Neocortex]
Glutamate(+) Glutamate (+)
Globus Globus
Corpus striatum GABA () pallidus pallidus GABA () Thalamus
[Putamen D2] externus internus [VA, VL, DM]
Dopamine () GABA ()

Glutamate (+)
Substantia nigra Subthalamus
[Pars compacta] nucleus
Mechanism of motor control - So when there is any defect in two pathways,

- For any movement to occur, two types of unnecessary motor plans get stimulated and
motor plan are necessary inappropriate body movement occurs without
- One plan is concerned with stimulation of intension of person.
agonistic muscle and other is concerned with - Such inappropriate movement without
inhibition of antagonistic muscle intension of person is called resting tremor.
- For example, if intended movement is flexion Functions of basal ganglia [KU 03]
of knee, one plan should be how to stimulate 1. Control of muscle tone: VIII
flexors of leg and other plan should be how to
- Basal ganglia decrease the muscle tone by
inhibit the extensors
inhibiting gamma motor neurons through
- For this, 2 pathways operate in basal ganglia. descending inhibitory reticular system in
Direct pathway will stimulate the cortical fiber brainstem.
concerned with flexors and indirect pathway
2. Control of motor activity (Anticipation,
will inhibit fibers concerned with extensors
preparation and Execution of movements)
In case of lesion
i. Regulation of voluntary movements: Whole
- Since birth, many motor plans are created to system of basal ganglia is involved in integrated
perform various movement and they are way.
stored in basal ganglia.
ii. Regulation of conscious movements (cognitive
- When similar actions are to be performed, control of activity): Fiber between cerebral
specific previously formed motor plan operate cortex and caudate nucleus are concerned with
and other plan get inhibited i.e. to perform a regulation of conscious movements.
certain action, only motor plan to the task
iii. Regulation of subconscious movements:
operate and other get inhibited.
Cortical fibers reaching putamen are directly
- This inhibition of other plan is also done by concerned with regulation of subconscious
inhibitory pathway of basal ganglia. movements.

Physiology
3. Control of motor reflexes:  Environmental toxins

- Basal ganglia are responsible for coordination  Dopamine antagonist like (neuroleptic,
and integration of visual and labyrinthine chlorpromazine, metoclopramide)
reflexes as these reflexes are important in
 Mutation in the gene coding for the protein
maintaining posture.
involved in synapse called -synuclein.
4. Control of automatic associated movements:
Signs and symptoms:
- For examples: Swinging of arms while walking,
i. Static tremor or resting tremor
facial expression while talking, etc.
ii. Rigidity (Stiffness of muscles)
5. Timing and scaling of motor activity
iii. Bradykinesis/Hypokinesia (Slowness of
6. Role in arousal:
movements)
- Globus pallidus is involved
iv. Fastinant gait (Patient walks quickly in short
Basal Ganglia disorder: steps by bending forward)
1. Degeneration of corpus striatum: v. Speech problems (Speech becomes slurred and
a. Hyperkinetic disorders: Tremors, chorea, they hesitate to speak)
Hemiballismus. Treatment:
b. Hypokinetic disorder: Athetosis - Levodopa is first line of drug for Parkinsonism
2. Degeneration of Substantia nigra (Parkinsonism) but it must be provided with peripheral
decarboxylase inhibitor (Carbidopa,
[KU 10, 08, 06, 04]
Benserazide) to prolong it action.
- Parkinson disease is a slowly progressive
VIII [Levodopa (250mg) + Carbidopa (25mg)]
degenerative disease of nervous system
associated with destruction of dopamine secreting
neurons of substantianigra and locus ceruleus. CEREBELLUM
- Degeneration of dopaminergic pathway cause Past Questions:
imbalance between dopaminergic (inhibitory) and
1. Describe in brief the connections and functions of
cholinergic (excitatory) pathway giving rise to
cerebellum. (2 +3 = 5)[08 Jan]
motor defect.
2. Describe the connections and functions of
Causes:
cerebellum. (2+3=5)[07 June]
- The major cause for Parkinsonism is
3. What is vertigo? (2)[04 June]
degeneration of dopamine secreting neurons
4. Tremor (3)[06 June]
in nigrostriatal (dopaminergic) pathway.
5. Righting reflex (3)[06 June]
- It is also due to:

CNS
1. Connections [KU 08, 04]
Cerebellar Peduncle Afferent tracts Efferent tracts
- Dentothalamic
Superior cerebellar - Anterior spinocerebellar
- Globose-emboliform-
Peduncle - Tectocerebellar
rubral.
Middle Cerebellar - Pontocerebellar (forming Part of cerebro-ponto-cerebellar

----
peduncle circuit)
- Posterior spino-cerebellar tract - Fastigial vestibular

- Cuneo-cerebellar tract (Posterior external arcuate fibers) - Fastigial reticular
- Anterior external arcuate fibers - Cerebello-olivary
Inferior cerebellar
- Vestibulo-cerebellar tract
peduncle
- Olivo-cerebellar tract
- Parolivo-cerebellar tract
- Reticulo-cerebellar fibers
Note:
- No efferent fiber passes through middle cerebellar peduncle.
aspartate) Purkinje cells, stellate cells and VIII
Neuronal Activity in Cerebellar Cortex
basket cells through the parallel fibers.
- Climbing fibers (from inferior olivary nucleus)
- Stellate cells and basket cells, which are
and Mossy fibers (remaining input fibers) are
activated by granule cells, inhibit the Purkinje
afferent fibers to cerebellar cortex which
cells by releasing GABA (Feed forward
controls the discharge from deep cerebellar
inhibition)
nuclei via the fibers of Purkinje cells.
- Golgi cell that is activated by mossy fibers, in
- Climbing fibers excite (by releasing aspartate):
turn, inhibits the transmission of impulse from
i. Purkinje cells directly (very strong mossy fiber to granule cells by releasing GABA
excitatory effect) (Feedback inhibition)
ii. Deep cerebellar nuclei via collaterals - Deep cerebellar nuclei, which are activated by
- Mossy fibers excite (by releasing glutamate): collaterals from climbing and mossy fibers,
i. Purkinje cells indirectly via granule cells send excitatory impulses to thalamus and
(weak excitatory effect) different nuclei in brainstem.
ii. Granule cells and Golgi cells in the glomeruli - However, signals discharged from Purkinje cells
inhibit the activities of deep cerebellar nuclei
iii. Deep cerebellar nuclei via collaterals
and vestibular nuclei (by releasing GABA).
- Granule cells, which are activated by mossy
fibers in turn, excite (by releasing glutamate or
Physiology
VIII
Neuron Action on Action Neurotransmitter released

Climbing fibers - Purkinje cells Excitation Aspartate
- Deep cerebellar nuclei
Mossy fibers - Granule cells Excitation Glutamate
- Golgi cells
- Deep cerebellar nuclei
Granule cells - Purkinje cells Excitation Glutamate /Aspartate
- Stellate cells
- Basket cells
Stellate cells - Purkinje cells Inhibition GABA
Basket cells - Purkinje cells Inhibition GABA
Golgi cells - Granule cells Inhibition GABA
Purkinje cells - Deep cerebellar nuclei Inhibition GABA
- Vestibular nuclei

CNS
How cerebellum regulates motor activity? - So type of output that cerebellum gives
- Deep Nuclear cells and Purkinje cells are the depends upon degree of stimulation of deep
functional unit of cerebellum. nuclear cell, relative to degree of its inhibition.
- Output of cerebellum is given by Deep - Usually stimulation is much stronger than
Cerebellar nuclei. inhibition, so deep nuclei fire and Purkinje cell
For rapid and short movements: regulate the output.
- Motor cortex via its collaterals stimulates Reason of tremor during Cerebellar defect:
cerebellum when movement begins. - Almost all movements of body are "pendular"
- Signal comes to cerebellum either via climbing - When some movement is done, momentum
fiberor via mossy fiber. develops and because of momentum, all
- Both of these fibers excite deep nuclei and pendular movements have tendency to
deep nuclei fires. overshoot.
- Within fraction of second after stimulation of - Person with intact cerebellum can overcome
deep nuclei, these fibers also stimulate this momentum via inhibitory signal of Purkinje
Purkinje cells (directly by climbing fiber, cell to Deep nuclei.
indirectly by mossy fiber via granule cell). - So normal person can stop the movement
- Stimulated Purkinje cells within next fraction of precisely at intended point, thereby preventing
second inhibit deep nuclei. overshoot and tremor.
- Thus, signal to deep nuclei is initially excitatory - But in case of cerebellar deficit, momentum is
and within a fraction of second turns not managed and overshoot occurs.
inhibitory. - When overshoot occurs, conscious centre of
- Initial excitatory signal to deep nuclei causes cerebellum recognizes this and initiate a
firing of deep nuclei. movement in reverse direction attempting to VIII
bring arm to its intended position.
- When deep nuclei fire, the generated impulse
is carried to motor cortex. This signal of - But the arm, by virtue of its momentum,
cerebellum supports motor cortex and helps in overshoots once more in opposite direction.
muscle contraction. - Again to correct this overshoot, cerebellum
- In next fraction of second, inhibition of deep initiate movement in initial direction and again
nuclei results in no output of cerebellum. overshoot occurs.
- So signal from cerebellum to motor cortex - Thus arm oscillates back and forth to its
ceases. Motor cortex in absence of supporting intended point for several cycles before it
impulse from cerebellum stops the on-going finally fixes on its mark.
movement. - Such abnormal movement is called action
- Thus, movement doesn't go beyond the tremor or intention tremor.
intended mark i.e. movement dampens and 2. Cerebellar disorders [KU 06]
overshoot is prevented. A. Cerebellar syndrome:
For prolonged movement: - Lesion in one cerebellar hemisphere gives rise
- Mossy fiber and climbing fiber continuously to signs and symptoms that are limited to the
stimulate deep nuclei. same side of the body.
- Purkinje cells are also continuously stimulated i. Muscular hypotonia.
by these fibers. ii. Postural changes and alteration of gait.

Physiology
iii. Disturbances of voluntary movement Red Nucleus

(Ataxia) Connections:
iv. Intention tremors Afferent from Efferent to
v. Dysdiadochokinesia (Inability to perform a. Cerebral cortex a. Spinal cord through
alternating movements regularly and through corticospinal rubrospinal tract
rapidly) fibers. b. Reticular formation
b. Cerebellum through through rubroreticular
vii. Disturbances of ocular movement
superior cerebellar tract.
(Nystagmus) peduncle. c. Thalamus
viii. Disorders of speech (Dysarthria) c. Lentiform nucleus. d. Substantia nigra
d. Subthalamic and
B. Gait:
hypothalamic nuclei
- Gait is the pattern of movement of limbs of e. Substantia nigra
animals, including human, during locomotion f. Spinal cord.
over a solid substrate Functions:
- Different types of gait: - Relay center for motor system
i. Hemiplegic gait (unilateral upper motor - Facilitate the flexor muscle tone
neurone lesion) - Control of complex muscular movements
ii. Scissor-like gait (spasticity due to bilateral - Control of righting reflexes
upper motor neurone damage) - Control of movements of eyeball
- Control of skilled movements.
iii. Ataxic gait (cerebellar dysfunction)
Muscle Tone (Tonus)
VIII iv. Festinant gait (basal ganglia
 Muscle tone is resistance offered by a muscle
lesion/Parkinson's disease)
against stretch in resting condition due to a state
v. Waddling gait (proximal muscle weakness) of partial contraction of extrafusal fibers resulting
vi. Bizarre/unusual gait (Huntington's disease) from asynchronous discharge of motor neurons.
 The state of Partial contraction in a muscle at rest
3. Functions [KU 08, 04]
is called muscle tone.
i. Maintenance of equilibrium with the help of
 The resting length of muscle is maintained due to
vestibular apparatus muscle tone.
ii. Regulation of muscle tone Importance of Muscle Tone:
iii. Regulation of Posture - Muscle tone plays important role in
maintenance of posture.
iv. Fine, skilled and smooth performance by
- Muscle tone is like a background activity over
coordination of movements
which muscle contraction (i.e. increased tone)
v. To help the motor cortex in planning and becomes easier.
programming of movements. - Muscles with normal tone can act more
vi. Involved in motor learning efficiently than a muscle with abnormal tone.
vii. Timing calculation and scaling of motor - Tone is more in antigravity muscles such as
extensor of lower limb, trunk muscles and neck
activity.
muscles.

CNS
Development of Muscle Tone: Applied Aspects:

- Gamma motor neurons and muscle spindles Hypertonia:
are responsible for the development and
- It is a muscular disease characterized by increased
maintenance of muscle tone.
muscle tone and inability of the muscle to stretch.
- Muscle tone is purely a reflex process.
- Spasticity is a motor disorder characterized by
- Sequence of events:
stiffness of the certain muscles due to continuous
Impulses from gamma motor neuron contraction.
 - Paralysis (complete loss of function) of the muscle
Activation of intrafusal fibers and due to hypertonicity is called spastic paralysis.
generation of impulses
Hypotonia:

- It is the muscular disease characterized by
Transmission of impulses to spinal cord via
decreased muscle tone.
primary sensory nerve fibers (afferent
fibers) - Flaccidity: Muscle during hypotonia offers very
 little resistance to stretch. Thus, muscle becomes
Stimulation of alpha motor neurons flaccid (lack of firmness) and condition is called
 flaccidity.
Transmission of impulses via alpha motor - The paralysis of muscle with hypotonicity is called
neuron fibers (efferent fibers) flaccid paralysis and it results in wastage of
 muscles.
Stimulation of extrafusal fibers Atonia:
 - Total loss of muscle tone.
VIII
Partial contraction of muscle

Muscle tone Conceptual Part:
Regulation of muscle tone: Total motor control system
- Supraspinal facilitatory centers (Which Suppose a football player intends to kick a football,
increases the muscle tone) following series of events that take place in his brain:
 First prefrontal cortex (judgement area) decides whether it
i. Motor area 4 in cerebral cortex
is appropriate to hit the football or not, if he should hit
ii. Cerebellum
then, in which direction and with what power he should
iii. Descending facilitatory reticular system hit the ball.
iv. Red nucleus  After making decision, prefrontal cortex sends its impulse
v. Vestibular nucleus to pre-motor and supplementary motor cortex. Now, these
cortical areas start to make motor program based on
- Supraspinal inhibitory centers (Which
decision made.
decreases the muscle tone)
 Pre-motor cortex makes plan of advanced movements (i.e.
i. Suppressor areas of cerebral cortex
appendicular movement) whereas supplementary motor
ii. Basal ganglia cortex makes plan for primitive movement (i.e. axial
iii. Descending inhibitory reticular system movement)

Physiology
 For planning, 1st these cortical areas need to know the Thalamic nuclei and functions [KU 10]
present position of structures (i.e. whether hip, knee, foot
Thalamic Nucleus Function
are flexed or extended, how far is the ball from foot).
These information are achieved from cerebellum via Anterior - Emotional tone
cerebello-thalamo-cortical fibers. - Mechanisms of recent
memory.
 Once initial position is determined, further planning
starts. To kick football, knee should be extended so Dorsomedial - Integration of somatic,
extensors must be stimulated and flexors must be visceral and olfactory
inhibited. information.
 Basal ganglia via direct pathway stimulate corticospinal - Relation to emotional
fibers concerned for extension and via indirect pathway feeling and subjective
inhibit corticospinal fiber concerned for flexion. states.
 Maintenance of tone of hip, vertebral spine, tone in next Ventral anterior - Influences activity of
leg, head movement, hand movements, facial expression, Ventral lateral motor cortex
etc. is done subconsciously by basal ganglia. Ventral posterior:
 Motor planning is done on basis of previous experience. 1. Ventral
Previously made motor plans are stored in basal ganglia, - Relays common sensations
Posteromedial (VPM)
pre-motor cortex. to consciousness.
2. Ventral
 Now, pre-motor and supplementary motor are ascompile Postrolateral (VPL)
all the planning done by consulting cerebellum and basal
Intralaminar - Influences levels of
ganglia.
consciousness & alertness.
 After all planning is done, pre-motor and supplementary
Reticular - Cerebral cortex regulates
VIII motor areas stimulate primary motor cortex. thalamus
 Now, primary motor area, via corticospinal tract,
stimulates the lower motor neuron and movement for Medial geniculate body - Hearing
desired action (kicking ball) starts. Lateral geniculate - Visual information from
 Cerebellum constantly gets updated about the movement, body opposite field of vision.
it judges whether direction and velocity of movement is Note:
matching to reach the intended position. It corrects if
- Thalamus is relay station of all sensory inputs to
movement is not appropriate.
the specific areas of cortex (except olfaction)
 Thus, desired action is accomplished. through its VPL and VPM nuclei along with lateral
geniculate body and medial geniculate body
Thalamic Syndrome [KU 10]
THALAMUS  Results due to damage of the Posterior thalamic

nuclei due to blockage of thalamogenicute
Past Question:
artery.
1. State the functions of thalamus. What is thalamic  Features:
syndrome? (3+1=4)[10 July]
i. All modalities of somatic sensation may be
diminished on the contralateral side of the body.
 Refer Anatomy CNS for details ii. Threshold for touch, pain and temperature is
usually rises on the opposite side.

CNS
iii. Hemiplegia, hemiparesis, Hyperesthesia and 1. Connections:

severe spontaneous pain.
iv. Thalamic phantom limb: Sometimes patient Afferent (From) Efferent (to)
may develop an illusion that the limb is lost. i. Medial and spinal lemnisci i. Descending fibers in
v. Sensory ataxia occurs due to sensory ii. Tractus Solitarius reticular formation
incoordination. to brainstem and
iii. Reticular formation
vi. Atypical over reaction to pain occurs. spinal cord.
iv. Visual fibers
vii. Visual field defect can also occur.
ii. Mammillothalamic
v. Medial forebrain bundle
HYPOTHALAMUS vi. Auditory fibers
tract
iiii. Mammillotegmental
Past Questions: vii. Corticohypothalamic fibers
tract.
1. Name the nuclei of hypothalamus and describe viii.Hippocampohypothalamic
their function. (2+3=5)[04 June] iv. Hypothalamo-
fibers (part of limbic
2. Describe the functions of hypothalamus. hypophyseal tract.
system)
(4)[03 Dec] v. Tubero-infundibular
ix. Thalamohypothalamic
3. Satiety and feeding centers (3)[07 July] tract.
fibers
4. Role of Hypothalamus in water balance in body
x. Tegmental fibers
(3)[08 July]
2. Main Hypothalamic Nuclei and their Function [KU 04, 03]

Region Area Nucleus Function
Medial preoptic nucleus i. Regulates the release of gonadotropic hormones from the
adenohypophysis
VIII
ii. Contains the sexually dimorphic nucleus, which releases
GnRH, differential development between sexes is based
upon in utero testosterone levels
Supraoptic nucleus Vasopressin release
Paraventricular nucleus i. Oxytocin release
Medial
ii. Thyrotropin-releasing hormone release
iii. Corticotropin-releasing hormone release
Anterior Anterior hypothalamic i. Controls parasympathetic system
nucleus ii. Thermoregulation (Response to heat i.e. Anti-rise centre)
iii. Sweating
iv. Thyrotropin inhibition
Suprachiasmatic nucleus Control Circadian rhythms
Lateral preoptic nucleus Same as medial preoptic nucleus
Lateral nucleus i. Increase water intake (thirst center)
Lateral
ii. Initiate eating and increase food intake (Hunger center)
Part of supraoptic nucleus Vasopressin release

Physiology
Region Area Nucleus Function

Dorsomedial hypothalamic Controls parasympathetic system
nucleus - Decrease blood Pressure
- Decrease heart Rate
- GI stimulation, etc.
Medial Ventromedial nucleus i. Inhibit eating and reduce food intake (satiety center)
Tuberal ii. Neuroendocrine control
Arcuate (infundibular) i. Growth hormone-releasing hormone (GHRH)
nucleus ii. Feeding
iii. Dopamine release
Lateral nucleus Thirst and hunger centres
Lateral
Lateral tuberal nuclei -----
Mammillary nuclei (part of i. Feeding reflexes
mammillary bodies) ii. Memory
Posterior nucleus i. Controls sympathetic system:
- Increase blood pressure
Medial
- Pupillary dilation
Posterior - Shivering
- Vasopressin release, etc
ii. Thermoregulation (Response to cold i.e. Antifall centre)
VIII Lateral nucleus Thirst and hunger centres
Lateral Mammillary nuclei i. Feeding reflexes
ii. Memory
Role of hypothalamus in regulation of - Now the person feels thirsty and drinks water.
body water [KU 08] - Water intake increases the ECF volume and
 Hypothalamus regulates body water in 2 ways: decreases the osmolality
i. By creating the sensation of thirst Decrease in ECF volume
ii. By controlling excretion of water into the 
urine. Increase in osmolality of ECF

1. Thirst Center:
Stimulation of osmoreceptors in hypothalamus
- Located in the lateral hypothalamic nuclei

- There are some osmoreceptors in the areas Activation of thirst center
adjacent of thirst center.

- When the extracellular fluid (ECF) volume Feeling of thirst
decreases, the osmolality of ECF is increased. 
- If the osmolarity increases by 1% to 2%, the Water intake
osmoreceptors are stimulated. 
- Osmoreceptros in turn, activate the thirst Increase in volume of ECF and decrease in
center and thirst sensation is initiated. osmolality of ECF

CNS
2. Control of renal excretion of water: - Destruction of satiety center leads to

- Supra optic nucleus is involved hyperphagia and the animal becomes obese.
This type of obesity is called hypothalamic
Supraoptic nucleus is stimulated by
obesity.
concentrated fluid electrolyte

Regulation of food intake by glucostatic
Secretion of Antidiuretic hormone (ADH) or
mechanism:
Vasopressin - Cells of satiety center function as glucostats or
glucose receptors, which are stimulated by

increased blood glucose level.
Transported to kidneys and acts on collecting
ducts Increase in appetite  Food intake
  
a. Increased reabsorption of water Activation of Increases in
b. Decreases loss of water into the urine feeding center blood glucose
(i.e cause retention of water)  level
 No more inhibition 
Return of electrolyte concentration to normal. of feeding center Stimulation of
 satiety center
Satiety and Feeding Centers [KU 07]
No more 
1. Feeding center (Hunger center): Lateral
stimulation of Inhibition of
hypothalamic nuclei satiety center feeding center
After about
- Stimulation of Lateral hypothalamic nuclei in  
3 hours
an animal leads to experience extreme hunger,
Decrease in blood  Stoppage of
a voracious appetite and an intense desire to glucose level food intake
search for food (hyperphagia) VIII
- Glucostats do not give response to very high
- Inhibited by satiety center
level of glucose in blood (hyperglycemia). So,
- Destruction of feeding center leads to loss of in conditions like diabetes, hyperglycemia fails
appetite (anorexia) and the animal refuses to to stimulate the satiety center. The satiety
take food. center does not inhibit the feeding center, so
2. Satiety Center: Medial hypothalamic nuclei the frequency of food intake increases
- Stimulation of Medial hypothalamic nuclei (polyphagia).
results an animal (that is eating food) suddenly
stop eating
- Inhibits lateral hypothalamic nuclei when LIMBIC SYSTEM
stimulated Past Questions:
1. What are the components of limbic system?
Insulin Inhibits Briefly describe the functions of limbic system.
Glucose MHN LHN Hunger
(–) (2 +3 = 5) [08 July]
2. Reward and punishment center (3)[11 July]
Medial Lateral
hypothalamic hypothalamic 3. Role of limbic system in reward and punishment
nuclei (satiety nuclei (Hunger (3)[06 June]
center) center) 4. Neural basis of fear and rage (2)[04 Dec]
5. Papez circuit (3)[11 July]

Physiology
1. Components [KU 08] - It has a more significant role in memory

a. Olfactory Pathway functions than in emotions.
b. Pyriform lobe Role of Limbic System in Reward and
c. Amygdaloid body: Evokes anxiety and rage. Punishment [KU 11, 06]
d. Hippocampal formation
 Limbic system is concern with the affective nature
e. Limbic lobe
of sensory sensations – that is:
f. Hypothalamus
Pleasant Unpleasant
 
Reward Punishment
 
Satisfaction Aversion
Greatly affect the behavior of the

animal
Reward centers (Pleasure centers)
 Located along the course of medial forebrain
bundle especially in lateral and ventromedial
nuclei of Hypothalamus
 Electrical stimulation of these areas pleases or
2. Functions [KU 08]
satisfies the animal
i. Homeostatic responses against fluctuating
VIII  Inhibited by stimulation of punishment centers
environment.
ii. Emotional behavior or mood. Punishment Centers (Fear centers)
iii. Recent memory (through the reverberating [KU 04]
Papez circuit)
 Located in:
iv. Role in reward and Punishment.
1. Central gray matter surrounding the aqueduct
Papez neuronal circuit [KU 11]
of Sylvius in the mesencephalon
- Papez circuit begins and ends with the
hippocampus (or the hippocampal formation) 2. Periventricular zones of the hypothalamus and
- Papez circuit goes through the following neural thalamus
pathway: 3. Amygdala and hippocampus (less potent)
Hippocampal Fimbria and  Stimulation of these areas causes an animal to
formation (subiculum) fornix shows all the signs of displeasure, fear, terror,
pain, punishment and even sickness.
Mammillary  Stimulation in punishment centers can frequently
bodies inhibit the reward and pleasure centers.
Entorhinal cortex
Note:
Mammillo- i. Punishment and fear can take precedence over
thalamic tract
pleasure and reward.
Cingulate gyrus Anterior nucleus ii. - Weaker stimuli give a sense of reward
of thalamus - Stronger stimuli cause rage

CNS
Rage [KU 04] iv. Has a tendency to place everything in its

 This is approximately the behavior that one would mouth
expect from an animal being severely punished v. Often has a sex drive so strong
and it is a pattern of behavior that is called rage. (hypersexuality) that it attempt to copulate
 Strong stimulation of the punishment centers of with immature animals, of wrong sex or of
the brain specially: different species.
1. Periventricular Zone of the hypothalamus vi. Visual agnosia
2. Lateral hypothalamus
PREFRONTAL CORTEX
Causes the animal to (ORBITOFRONTAL AREA)
i. Develop a defense posture
Past Question:
ii. Extend its claws
8. Describe the functions of prefrontal cortex.
iii. Lift its tail
(4)[04 Dec]
iv. Hiss
- Large areas on frontal lobe are also called
v. Spit
silent area of brain which is associated with
vi. Growl higher functions called prefrontal cortex.
vii. Develop Piloerection, wide-open eyes and - Includes Brodmann’s area number : 9-14, 23,
dilated pupils. 24, 32 and 44-47.
Note: In the normal animal, the rage phenomenon is Connections
held in check mainly by inhibitory signals from the
Afferents (From) Efferents (to)
ventromedial nuclei of the hypothalamus,
hippocampi, anterior limbic cortex (especially in 1. Dorsomedial nucleus of 1. Caudate nucleus
anterior cingulated gyri and subcallosal gyri) thalamus 2. Frontopontine tract
2. Anterior nucleus of 3. Mid brain via
VIII
Function of Amygdala thalamus (part of Papez corticotegmental fibers
 Relate environmental stimuli to coordinated circuit) 4. Ventral and medial
behavioral autonomic and endocrine responses 3. Frontal and other areas thalamic nuclei
(i.e. 2, 4, 8, 24 etc) 5. Reticular formation
 Responses include:
6. Hypothalamus via fornix
- Intense emotion, such as aggression or fear
- Feeding and drinking Functions [KU 04]
- Agnostic (fighting) behavior 1. Controls behavior like aggression via limbic system
- Mating and maternal care 2. Controls sympathetic and parasympathetic
activities (ANS) via hypothalamus.
- Responses to physical or emotional stresses.
3. Controls higher intellectual activities like learning,
Kluver–Bucy Syndrome memory and judgment.
 When the anterior part of both temporal lobes are 4. Involved in recent memory
destroyed (in a monkey) along with amygdala. 5. Personality maintenance
This causes changes in behavior called Kluver – 6. Controls of emotional effects
Bucy syndrome. Frontal lobe Syndrome
 Features shown by animals: 1. Inability to perform two works at a time
i. Is not afraid of anything 2. Inability to follow the proper sequence to achieve
ii. Has extreme curiosity about everything a task E.g. Cooking which requires sequential
iii. Forgets rapidly steps.
Physiology
3. Lack of initiative. - Found during sleep, after over breathing,

4. Inability to store a programme intracranial tumors.
5. Incontinence Importance of EEG
6. Anosmia i. For the diagnosis of brain diseases like
7. Impairment of moral sense epilepsy, brain tumors, cerebral hemorrhage
8. Failure to realize the gravity of a situation. ii. To study the different stages of sleep.
iii. To find different states of consciousness i.e. full
ELECTROENCEPHALOGRAM (EEG) alertness to coma.
 EEG is the recording of spontaneous cerebral
iv. Also used to indicate the brain death.
cortex activities.
 If the sensory pathway is stimulated then typical RETICULAR ACTIVATING SYSTEM
potential changes can be recorded from the scalp
(RETICULAR FORMATION)
or cortical surface but not from the deeper layers.
These are evoked potentials. Past Questions:
 These are 4 types of EEG waves: , , ,  1. RAS and sleep (3)[04 Dec]
i. -waves: 2. Reticular activating system (3)[05 Dec]
- 8-13 Hz frequency, 50 µV amplitude  Reticular formation is the diffuse network of the
- Found in awake when mind is wandering. neurons and nerve fibers that extends from spinal
cord through the medulla, the pons, the mid
ii. -wave:
brain, the subthalamus, the hypothalamus and
- 14-30 Hz frequency, 5-10 µV amplitude thalamus.
- Found in normal alert individual, during mental  It is divided into 3 longitudinal columns:
tension and generalized activation of CNS.
i. Median column
iii. -wave:
ii. Medial column
- 4-7 Hz frequency 10µV amplitude
iii. Lateral column
VIII - Found normally in children, during emotional stress
 Consists of various nuclei arranged in pontine,
in adults, during disappointment & frustrating.
medullary and mid-brain level
iv. -wave:
 Also contains vital centers like vasomotor centre,
- 1-3 Hz frequency, 20-200 µV amplitude respiratory centre, etc.
Connections:
Afferent Efferent
Cerebellum
Cerebellum
Thalamus
Cerebral cortex Cerebral cortex
Substantia nigra
Corpus striatum Reticular
Formation Red nucleus
Thalamus Tectum
Spinal cord ascending Spinal cord motor tracts
tracts
Special sensory pathways Hypothalamus
(Optic, auditory, olfactory, taste)

CNS
Ascending Reticular formation (Reticular SLEEP

activating system) [KU 05, 04] Past Questions:
- Polysynaptic pathway extending from lower
1. Describe the difference between: REM and Non
pons to level of thalamus. It receives collaterals REM sleep [3 × 2 = 6][03 Dec]
from all sensory pathways. 2. REM sleep [2][04 Dec]
- As all the sensory pathways sends collateral to 3. REM and NREM sleep [2, 3][08 Jan, 06 Dec]
ARAS, impulse reaches almost to all areas of 4. Comparison of REM and non-REM sleep[3][10 Jan]
brain which is responsible for arousal, alertness 5. RAS and sleep [3][04 Dec]
and wakefulness.
 Sleep is a naturally recurring states of reduced/
- An impulse reaches cerebral cortex via: absent consciousness and suspended sensory
i. Classical pathway activity from which person can be aroused by
ii. Ascending reticular system sensory or other stimuli.
- Perception of stimulus is by classical pathway Physiological changes during Sleep
when ARAS is responsible for activation of all
1. Plasma volume: Decreases by 10% during sleep
areas of cerebral cortex leading to wakefulness.
2. CVS:
Function of ARAS:
- Heart rate reduces (45 - 60 beats per minute)
- Produces consciousness, maintenance of
- Blood pressure falls (90 - 110 mm of Hg)
alertness
3. Rate and force of respiration decreases,
- Influence learning and memory
respiration becomes irregular
- Maintenance of circadian rhythm
4. Salivary secretion decreases but gastric secretion
- Responsible for electrical activity of cerebral
is not altered (may be increased); activity of GI
cortex
tract increases.
Descending Reticular System VIII
5. Formation of urine decreases and specific gravity
- It includes reticulospinal tracts and influence of urine increases
both motor and sensory pathways.
6. Sweet secretion increases but lacrimal secretion
- Can be inhibitory or facilitatory decreases
i. Inhibitory DRS 7. Muscle tone decreases except ocular muscle tone
a. Somatosensory control (sleep paralysis)
- For accurate voluntary movement 8. Babinski sign becomes positive during deep sleep
- Regulates reflex movements 9. Threshold for most of the reflexes increases
- Regulates muscle tone and posture. 10.Pupil are constricted, eyeball move up and down
b. Control of vegetative function and light reflex is retained
- Inhibition of various autonomic functions 11.Brain is not inactive during sleep i.e. associated
ii. Facilitatory DRS with dreaming, etc.
- Facilitates movement and muscle tone i. Slow wave sleep (Non-Rapid eye
- Facilitates all autonomic function movement sleep or NREM sleep)
- Activates ARAS and helps maintaining alertness [KU 10, 08, 03]
- Integrating role in emotions and pain It is divided into 4 stages
transmission a. Stage 1
- It influences neuroendocrine secretions and their - This is light sleep and individuals can be
functions through hypothalamic connections. easily aroused.

Physiology
- -waves (during eye opening) are converted - REM sleep is associated with memory
into -waves. consolidation.
- Muscles are active and eye roll slowly. - Babinski’s sign is positive during sleep.
b. Stage 2 Mechanism of Sleep
- EEG shows sleep spindles (high frequency,
 Sleep occurs due to the activity of some sleep -
high amplitude waves of short duration),
inducing centers in brain.
superimposed on θ-wave.
 Complex pathways between the reticular
- Arousal becomes slightly difficult
formation of brainstem, diencephalon and
c. Stage 3 cerebral cortex are involved in the onset and
- Sleep spindles superimposed on -waves maintenance of sleep.
- Threshold for arousal increases  It is believed that reduction of RAS activity i.e.
d. Stage 4 cutting of sensory stimuli produces sleep.
- EEG shows synchronization and -waves  Supraoptic region of hypothalamus ensures that
dominate. sleep occurs at night.
Note:  Activation of Raphe nucleus results in Non-REM
Cycle of NREM sleep  state I  II  III  IV  sleep. It is due to release of serotonin by the
III  II  I then REM sleep starts. nerve fibers arising from this nucleus.
 Nor-adrenaline released by the nerve fibers
ii. Rapid Eye movement (REM) sleep
arising from locus cereleus of pons induces REM
[KU 10, 08, 06, 04, 03] sleep.
- In this sleep there is rapid movement of
Note: Lesion of ascending reticular activating system
eyeballs due to phasic contraction of extra-
(ARAS) leads to permanent somnolence, i.e. coma.
VIII ocular muscles.
- Also called Paradoxical sleep NREM Sleep v/s REM Sleep [10, 08, 06, 04, 03]
- Characters: NREM Sleep REM Sleep
 It is active form of sleep usually associated - No rapid eye movement - Rapid eye movement
with dreaming and active bodily muscle - Dreaming is absent - Dream is present
movements
- Neurotransmitter: - Nor-adrenaline
 Heart rate and respiratory rate becomes
Serotonin
irregular
 Person is difficult to arouse by sensory - BP, pulse, respiration are - All are irregular
stimuli than during deep slow wave sleep regular
 Eye movement, some body movements are - Arousal threshold – - Threshold is much
present increase more increased
 Muscle tone is depressed throughout the
- Brain activity less - Brain activity more
body
- EEG shows slow high - EEG shows ‘’ wave
Note:
voltage ‘’ wave
- Secretion of growth hormone from pituitary gland
increases during NREM sleep.

CNS
SPECIAL POINTS FOR MCQs

1. Structural and functional unit of the nervous system is nerve cell.
2. Brain stem comprise of medulla, Pons and midbrain.
3. Rhombencephalon comprise of medulla, Pons and cerebellum.
4. Area concerned with regulation of heart rate, B.P and respiration are located in brain stem
(Reticular formation).
5. Intermediolateral horn of the spinal cord contains sympathetic cell bodies that extend only
between T1 and L2 segment of the spinal cord.
6. Sub-synaptic membrane is the surface of the cell membrane involved in the synapse. It is a part of
post-synaptic neuron.
7. Axo-dendritic is most common and dendodendritic is rarest of all the synapses in the nervous
system.
8. Axo-dendritic, Axo-somatic and Axo-axonal are commonly located in spinal cord while dendo-
dendritic is commonly located in olfactory bulb.
9. Most synapses in the nervous system are chemical.
10. When summation occurs, activity in one nerve fiber is said to facilitate activity in another to
approach the firing level. VIII
11. Opening of sodium channel and closing of Potassium channel produce EPSP.
12. Opening of chloride and potassium channel produce IPSP.
13. Electrical event that occurs in neuronal inhibition is hyperpolarization.
14. The part of a motor neuron that has the lowest threshold for a propagated action potential is
dendrite.
15. Reflex contraction of a skeletal muscle in response to its stretching is an example of afferent, direct
and post synaptic inhibition.
16. Golgi bottle neuron is an inhibitory interneuron in the anterior horn of spinal cord. [KU 2013,
MCQ]
17. Golgi neuron when activated liberates glycine at its ending. i.e. glycine is inhibitory
neurotransmitter.
18. Renshaw cells (Short axon neurons lying in the grey matter) are inhibitory.
19. GABA is a major inhibitory transmitter in the CNS.
20. GABA acts by increasing the permeability of neuron to Cl- and K+.
21. Post-tetanic potentiation is increased post-synaptic potentials in response to stimulation.

Physiology
22. The receptors of touch, pain, pressure and thermal are located in skin, therefore, also called
cutaneous or superficial senses.
23. Information from special senses is carried by cranial nerves while that from superficial sense is
carried by spinal nerves.
24. Receptors for vision are telereceptors.
25. We do not feel our clothes once they are put on because they activate the tactile receptors which
are rapidly adapting receptors.
26. Meissner’s corpuscles are sensitive to mechanical deformation. Thus, they respond specifically to
light touch.
27. Pacinian corpuscles are major receptors for Pressure.
28. Ruffini end organ is mainly associated with sensation of cold.
29. Nociceptive stimuli are transmitted by naked nerve endings (pain receptors).
30. Kinaesthetic sensation (sensation of joint movements) are detected by joint receptors which
include Pacinian corpuscles, Golgi tendon organs and Ruffini’s end organs.
31. Stimulation of touch receptors causes a sensation of touch and not of warmth because of specific
pathway involved and specific part of the brain the sensation ultimately activates.
32. The intensity of sensory stimuli is determined by frequency of action potential.
33. Reflex are consists of receptor, effector organ, afferent and efferent neurons.
VIII 34. Knee reflex, biceps reflex and Ankle reflex are monosynaptic reflexes while corneal reflex,
abdominal reflex, Babinski reflex, Golgi tendon reflex are polysynaptic (superficial ) reflexes.
35. Antigravity muscles have high density of muscles spindles receptors for stretch reflex.
36. Main function of nuclear bag fiber is to maintain muscles length.
37. The brain area that facilitates the stretch reflex is vestibular nucleus.
38. Mass reflex is an autonomic reflex characterized by urination, defecation, sweating, Fluctuation in
BP.
39. Perception refers to understanding of sensation’s meaning.
40. Somatosensory vibratory information reaches the brain through dorsal columns of spinal cord.
41. The somasthetic sensations relay in ventro-posterior nucleus of the thalamus.
42. Sexual sensation ascends to the brain through the spinothalamic tract.
43. Gross (crude) touch sensations are carried by ventral (anterior) spinothalamic tract.
44. First synapse of fibers conducting pain takes place at the level of gray matter of dorsal horn of
spinal cord.
45. Substantia gelatinosa of spinal cord corresponds to lamina II and III.
46. First relay station of pain is spinal cord not thalamus.

CNS
47. Somatosensory area I of the cerebral cortex respond maximum to tactile discrimination and two
point discrimination.
48. All sensations relay in sensory cortex except olfaction.
49. Lesion in posterior column leads to sensory ataxia.
50. Pain sensation is associated with withdrawal reflex, emotion and autonomic changes.
51. Pain producing substance is substance P.
52. Perception of pain alone does not require the cerebral cortex and it can occur at subcortical level
(thalamus).
53. Painful stimuli are conveyed by A-delta and C fibers.
54. True visceral pain arises from distension.
55. When pain seems to spread from the local area to the distant site, this is called radiating pain.
56. When pain is experienced at the site other than the injured diseased part, it is called referred pain.
57. Analgesia system of brain consists of Periaqueductal grey matter (midbrain), Raphe magnus
nucleus (medulla) and substantia nigra of basal ganglia.
58. β-endorphin is analogue of morphine found in high concentration in substantia gelatinosa.
59. Acupuncture exerts its analgesic effect by causing release of opioid peptide.
60. Giant betz cells in brain are found in motor cortex.
61. Sensorimotor cortex includes premotor, motor and somatosensory cortex.
62. Pyramidal tracts originate in sensorimotor cortex.
VIII
63. The pyramidal cells and tracts constitute the upper motor neurons, whereas spinal and cranial
neurons, which directly innervate the muscles, constitute the lower motor neurons.
64. Most common site of lesion to the pyramidal tracts is internal capsule.
65. Pre-central sulcus and corticospinal tracts are required for voluntary movement.
66. Body posture and complex course movements are controlled mostly by extrapyramidal system.
67. Vestibular nuclei of brain help supporting the body against gravity.
68. Fastest conducting descending tract is lateral corticospinal tract.
69. Babinski sign is seen in upper motor neuron lesion.
70. If once Babinski becomes positive, it will remain positive for the rest to the life thereafter.
71. An individual with positive Babinski sign neither can run faster nor can travel long distance.
72. A unilateral upper neuron lesion in the internal capsule is best characterized by diminished use
of contralateral muscles below the lesion.
73. The cause of spinal shock is functional depression of the nervous system.
74. As the stage of spinal shock passes off, functional activity first appears in sphincter vesicae
(internal urethral sphincter).
Physiology
75. Following hemiplegia, reflex activity returns after 2-3weeks.

76. After spinal cord transaction, reflex movement that appears quite early is flexor reflex.
77. In Brown-Sequard syndrome, sensation lost on same side is proprioception.
78. Dissociated anesthesia is usually seen in case of intramedullary tumour.
79. Skeletal muscle activity depends upon pattern and rate of discharge of motor neutrons.
80. Anterior descending pathways are concerned with control of muscles of trunk and proximal
limbs.
81. Distal limb muscles are concerned with fine and skilled movements.
82. Highest level of motor control system comprises of cerebral cortex, limbic cortex and association
cortex area.
83. The subcortical centers that control body movements include cerebellum, Basal ganglia and brain
stem nucleus.
84. Learning of motor skill is mainly carried out at subcortical level of motor control system.
85. Midbrain is the centre for integration of righting reflexes which consists of sequential chain of
reactions to maintain normal standing position and keep the head upright.
86. Part of the brain which is absolutely essential for life is reticular formation.
87. For arousal response, important ascending pathway is reticulocortical.
88. RAS produces the conscious state, maintains a state of alertness and responsible for electrical
VIII activity of cerebral cortex.
89. Anesthetics produce unconsciousness by depressing condition in ascending reticular system.
90. Oldest lobe of cerebellum is flocculonodular lobe.
91. Control of axial and limb muscles and postural reflexes is a function of spinal cerebellum.
92. Skilled voluntary movements are controlled by neocerebellum.
93. Purkinje cells (the biggest neurons in the body) axons form the only output of the whole
cerebellar cortex to the deep cerebellar nuclei.
94. In cerebellar cortex, afferents from inferior ollivary nucleus ascends as the climbing fibers.
95. Output of granule cell is always excitatory while that of Purkinje, Golgi and basket cells are
always inhibitory.
96. The major afferent input to cerebellum from motor cortex is via middle cerebellar peduncle.
97. Part of the brain serving as a great sensory relay station is thalamus.
98. Almost all of the cerebral cortex has direct 2-way communication with thalamus.
99. The posterolateral nucleus of thalamus relays cerebellar impulses to motor cortex (areas 4 and 6).
100. Blockage of thalamogeniculate branch of posterior cerebral artery leads to thalamic syndrome
[involve damage to posteroventral and posterolateral nuclei]

CNS
101. Largest fiber system of hypothalamus that connects it with limbic system is fornix.
102. Hypothalamus is connected to anterior pituitary via hypothalamohypophyseal portal blood
vessels and not by the nerve fibers.
103. The mammillo-tegmental tract is route through which hypothalamus influences ANS.
104. Circadian rhythm is controlled by suprachiasmatic nuclei of hypothalamus.
105. The hypothalamus is called the head ganglia of the ANS. Its stimulation produces autonomic
reflexes.
106. Satiety centre is located in ventromedial nucleus of hypothalamus (Medial hypothalamic nucleus)
Thirst and Hunger Centres are located in lateral hypothalamic nucleus.
107. Satiety centre is regulated by blood glucose level because the cells in satiety centre functions as
glucoreceptors.
108. Drinking can be induced by injection of hypertonic saline into preoptic nucleus of hypothalamus.
109. Alcohol produces diuresis by inhibiting release of ADH from the hypothalamus [supraoptic
nucleus]
110. Limbic cortex is the oldest part of cerebral cortex made up of allocortex.
111. Limbic system plays important role in emotions of rage and fear, autonomic control, concerned
with olfaction and memory.
112. Sex behaviour in an individual is determined by coordinated activity of limbic system,
hypothalamus and neocortex.
VIII
113. Broca’s area of speech lies at inferior frontal gyrus (area 44, 45).
114. Fluent aphasia is characterized by lesion in the Wernicke’s area (area 22).
115. Inborn reflex are unconditioned reflexes
116. In conditioned reflex, there is formation of new functional connections within the nervous system.
117. The part of the brain principally stores memory is hippocampus.
118. Best explanation for long term memory is due to RNA synthesis inside the neuron.
119. Damaging of hippocampus is likely to cause anterograde amnesia.
120. Memory failure in old age is called senile dementia.
121. In cerebrum, parietal lobe  sensory function; Occipital  vision; Temporal  hearing;
Prefrontal organ of mind.
122. The cells in cerebral and cerebellar cortex are organized in 6 and 3 layers respectively.
123. The prefrontal lobe receives the major projection from thalamus.
124. Higher intellectual functions are linked to prefrontal cortex.
125. Commonest feature of prefrontal lobe lesion is distractibility.
126. The major afferent input to basal ganglia is from motor cortex.

Physiology
127. Substantia nigra contains bodies having dopamine and its axons terminate in the neostriatum i.e.
putamen & caudate nucleus. This forms nigrostrial pathway.
128. Blood brain barrier is not present in Area posterma in fourth ventricle. (Also absent in
hypophysis cerebri, pineal body and choroid plexus)
129. Out of all nucleus present in basal ganglia, corpus striatum plays greatest role in regulating gross
movement of body.
130. Hyperkinetic syndromes such as chorea and athetosis are usually associated with physiological
changes in basal ganglia complex.
131. Chorea is frequently seen in children as a complication of rheumatic fever mainly due to
involvement of the caudate nucleus.
132. Kernicterus is a hemolytic disease of newborn where globus pallidus is damaged.
133. Wilson disease (muscular rigidity + tremors + cirrhosis liver) is due to deposition of copper in
substantia nigra.
134. Athetoid movements are found in basal ganglia lesions.
135. The frequency of EEG wave decrease in the following order
β > α > θ >  [@Mnemonic: BAT - Dance]
136. EEG wave in hippocampus is θ wave.
137. -wave is seen in Deep sleep. [Stage-III NREM sleep]
VIII 138. In an awake, relaxed person, EEG shows predominance of β-wave.

139. Source of EEG is EPSPs and IPSPs of cortical cells which behave like dipoles.
140. Epileptic foci generate high voltage, localized waves in the EEG.
141. True sleep is stage-II NREM sleep [β dominance stage].
142. Rapid eye movement, dreaming and penil erection are related to REM or paradoxical sleep.
143. NREM sleep is produced by stoppage of serotonergic neurons of raphe nuclei.
144. Discharge of nor-epinephrine from neurons in pontine reticular formation produces REM sleep.
145. Discharge of cholinergic neurons is necessary for shifting NERM sleep to REM sleep.
146. Raphe nucleus, locus ceruleus and preoptic area of hypothalamus produces sleep.
147. The main difference between REM sleep and wakefulness is decreased muscle tone.
148. Cushing’s triad includes hypertension, Bradycardia and irregular respiration.
153. Most sensitive part of axon is axon hillock.
154. CSF has pH slightly less than plasma but iso-osmolar with plasma and exerts pressure of 10–12
cm of H2O.
155. Apolar neurons are present in chromatin cells of Adrenal medulla.
156. The basic spinal reflex of posture is stretch reflex.

CNS
157. Nissil’s granules are equivalent to ribosome and Endoplasmic reticulum.

158. Myelin sheath in CNS is formed by oligodendrocytes but is formed by Schwann cells in
Peripheral Nervous System.
159. Microglia are derived from blood, phagocytic in function and are motile.
160. Myelination starts at 8th week of intrauterine life and completed within few years after birth.
161. Aδ and C group of nerve fibers transmits pain.
162. Destruction of thalamus leads loss of all sensation except smell.
162. Sensation of Itching is carried by C fibers.
163. Hemiplegia occurs due to lesion of internal capsule of opposite sides.
164. Quadriplegia occurs due to lesion of spinal cord below level of C5.
165. The receptors for pain, touch & temperature are free nerve endings.
167. Hair cells of vestibular apparatus are receptors for special proprioception.
168. The dynamic γ-motor fiber supplies bag fibers whereas γ-static supplies chain fiber of muscle
spindle.
169. Reciprocal innervations causes contraction of one group of muscle while relaxation of next group
of muscle.
170. The pain of appendicitis is referred to periumblical region; cardiac pain to tip of right shoulder.
171. The major tracts of extrapyramidal system include Reticulospinal, Vestibulospinal, Rubrospinal
and Tectospinal tracts. VIII
172. Extrapyramidal system regulates skeletal muscle tone by influencing both &  motor neurons.
173. Pyramidal system is responsible for fine & skilled movements whereas extrapyramidal helps in
gross movement.
174. There are no any outgoing fibers from middle cerebellar peduncles.
175. Most of the output signals leave the cerebral cortex from cell layer V.
176. Spinal shock is due to functional depression of nervous system.
177. Edinger-Westphal Nucleus sends it preganglionic fibers to ciliary ganglion which in turn sends
the postganglionic fibers to sphincter pupillae.
178. Thermoregulatory center is present in hypothalamus and temperature is maintained by PGE2
action.
179. In hypothermia and hypoglycemia the ECG becomes of low frequency.
180. Global aphasia occurs if both Broca's and Wernicke's area are involved.
181. In anterograde amnesia – new memory can't be stored but the past memory is intact but vice -
versa occurs in retrograde amnesia.

Physiology
182. Alzheimer's disease is due to degeneration of cholinergic nerve terminals in the cerebral cortex
and hippocampus.
183. Lymphatics are absent in brain as CSF acts as lymph in brain.
184. Babinski sign is positive in child below 18 months, in pyramidal tract lesion and in deep sleep.
185. The receptor of deep reflex = muscle spindle.
186. Wallerian degeneration is a retrograde degeneration.
187. Usually pyramidal tracts are lesioned at internal capsule.
188. Cerebral cortex is concerned with conditioned reflex.
189. Hippocampus is principle site of memory storage.
190. Hippocampus is not required for implicit or non-declarative memory.
191. Kluver–Bucy syndrome is characterized by Hypersexuality, altered feeding habit.
192. Circadian rhythm is controlled by supra chiasmatic nucleus of hypothalamus.
193. Bilateral lesion in lateral hypothalamic area produces anorexia.
194. Dysarthric aphasia is due to lesion of caudate nucleus.
195. Hyperkinetic (tremors) features of Parkinson’s disease are due to Dopaminergic activity and
Cholinergic activity.
196. Parkinson’s disease is due to degeneration of nigrostriate pathway (Substantia nigra)
197. Tremors can be seen in Thyrotoxicosis, chronic alcoholism, Parkinsonism & Wilson's disease.
VIII
198. Electrical activities in cerebral cortex are mainly due to RAS and basal ganglia.
199. Sleep can be induced by Acetylcholine, serotonin and nor-epinephrine.

Physiology - (CNS) Fast Track

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Physiology - (CNS) Fast Track

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CNS

FAST TRACK BASIC SCIENCE MBBS -979-

Control of posture and movement: (P. 1003)

-980- FAST TRACK BASIC SCIENCE MBBS

INTRODUCTION OF NERVOUS ii. Based on shape

FAST TRACK BASIC SCIENCE MBBS -981-

SIGNAL TRANSMISSION - Due to synaptic transmission, if potential

-982- FAST TRACK BASIC SCIENCE MBBS

 Measured by cathode ray oscilloscope

FAST TRACK BASIC SCIENCE MBBS -983-

- Retrograde degeneration occurs i.e. from the

-984- FAST TRACK BASIC SCIENCE MBBS

 Is permeable to:  Important normal constituents of CSF are:

FAST TRACK BASIC SCIENCE MBBS -985-

Circulation of CSF [KU 05] Functions of CSF [KU 05]

-986- FAST TRACK BASIC SCIENCE MBBS

a. Synaptic vesicle containing neurotransmitter

FAST TRACK BASIC SCIENCE MBBS -987-

- It is not sufficient to cause generation of action Occlusion:

B   Criteria for a chemical to be labeled as

-988- FAST TRACK BASIC SCIENCE MBBS

Some of common neurotransmitters are as follows:

Neuromodulators Found only in axon Found in all parts of the

FAST TRACK BASIC SCIENCE MBBS -989-

Some of common neuromodulators are as follows:

C. Based on Nature of stimulus

FAST TRACK BASIC SCIENCE MBBS -991-

E. Based on segment involved

 Intrafusal fibers are of two types:

Receptors This stimulation is sent to spinal cord via Group

-992- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -993-

- It is recalled unconsciously. transmission ceases. This phenomenon is

-994- FAST TRACK BASIC SCIENCE MBBS

iii. Potentiation: SPEECH

FAST TRACK BASIC SCIENCE MBBS -995-

- Comprehended idea of speech cannot be SOMATO-SENSORY SYSTEM

-996- FAST TRACK BASIC SCIENCE MBBS

General consideration A. Receptors:

FAST TRACK BASIC SCIENCE MBBS -997-

-998- FAST TRACK BASIC SCIENCE MBBS

Pain - Elicited by the - Elicited by chemical,

FAST TRACK BASIC SCIENCE MBBS -999-

Common examples: - These endogenous opioids inhibit the release

-1000- FAST TRACK BASIC SCIENCE MBBS

2. Doral column tracts [KU 08, 07] First order neurons:

FAST TRACK BASIC SCIENCE MBBS -1001-

3. Spino-cerebellar tracts - Enters the cerebellum contralaterally through

- Afferents: Collaterals of ascending tracts of Sensation carried:

Course: CONTROL OF POSTURE AND

- After entering spinal cord, the fibers pass Note:

FAST TRACK BASIC SCIENCE MBBS -1003-

Cortical origin Subcortical origin - Cortical in origin - Subcortical in origin.

-1004- FAST TRACK BASIC SCIENCE MBBS

Pathway Function Origin Site of crossover Destination Effect of Lesion

FAST TRACK BASIC SCIENCE MBBS -1005-

Note: Babinski sign (Extensor Planter

VIII UMN lesion LMN lesion

-1006- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -1007-

2. Flaccid paralysis 2. Pain

1. Fine touch 2. Spastic paralysis 2. Pain

Syringomyelia Motor Cortical Areas