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10 marks
1. Pyramidal tract
Origin :
• Primary motor Cortex (Area 4) - 30 %
• Premotor Cortex (area 6) - 30%
• Somatosensory cortex (Areas 3,1, 2, 5 & 7) - 40%
Course:
• Corona radiata: a radiating pattern in the subcortical areas
• Internal Capsule: through the genu and anterior 2/3rd of posterior limb of internal
capsule
• Mid brain: Fibers occupy middle 1/5th of cerebral peduncles
• Pons: The tract is split into a number of bundles by the presence of pontine nuclei
• Medulla:
Upper part:
forms a bulge called pyramid
Lower part:
80% of the fibers cross to the opposite side & 20% of the fibers descend on the same side
(The crossing of fibers is called motor decussaation)
• Spinal cord:
The crossed fibers form the lateral corticospinal tract
The uncrossed fibers form the anterior corticospinal tract
Termination:
lateral corticospinal tract – synapse with anterior horn cells directly and supply to
the distal limb muscles
anterior corticospinal tract – synapse with the anterior horn cells through internuncial neurons and
supply the axial and proximal limb muscles
Functions:
• Control of voluntary fine and skilled movements (lateral corticospinal tract)
• Control of gross voluntary movements (anterior corticospinal tract)
• Facilitates muscle tone
• Facilitates superficial reflexes
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2. CEREBELLUM

Functional divisions:
• Vestibulocerebellum (Flocculonodular lobe)
• Spinocerebellum (Vermis & intermediate zone)
• Neocerebellum (cerebrocerebellum)

Connections:

Peduncles Afferent fibers Efferent fibers

Superior Cerebellar Ventral spinocerebellar tract Dentato thalamocortical fibers
Peduncle Tectocerebellar Dentatorubral fibers
Trigemino cerebellar fibers

Middle Cerebellar Cerebro ponto cerebellar ----------------------

Peduncle

Inferior Cerebellar Dorsal spinocerebellar Cerebello reticular

Peduncle Cuneo cerebellar Cerebello vestibular
Reticulo cerebellar
Vestibulo cerebellar
Olivo cerebellar
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Functions:
1. Control of body posture & equilibrium (Vestibulocerebellum & Spinocerebellum)
• Influences antigravity muscles and maintains posture
• Maintains equilibrium during standing, walking etc.,
2. Control of Gaze (Movements of eyeballs) – Vestibulocerebellum
• Controls eye movements and coordinates with head
3. Control of muscle tone & Stretch reflex (Spinocerebellum)
• Facilitates γ motor neurons in the spinal cord
• Forms an important site of α – γ linkage
4. Control of voluntary movements (Neocerebellum)
• Planning and programming of voluntary movements
• Controls coordination of movements
• Correction of purposeful movements (comparator of a servo-mecanism)
• Regulates time, rate, range, force and direction of muscular activity
• Learning of motor skills
• Influences the activity of agonists, antagonists & synergistic muscles
• Smooth transition of movements
• Cognition
• Mental rehearsal of complex action
3. BASAL GANGLIA / BASAL NUCLEI-

Components:
1. Caudate nucleus Corpus striatum
2. Putamen
3. Globus pallidus
- Externa
- Interna
4. Substantia nigra
5. Subthalamic Body
Connections:
Direct pathway:
+ Cortex

+ Glutamine

Striatum Dopamine Substantia nigra

D1

- GABA
Globus pallidus Interna

+
Thalamus
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- Excitatory pathway
- Facilitates the intended movement

Indirect pathway:
-
Cortex

+ Glutamine

Globus pallidus Externa Striatum Dopamine Substantia nigra

D2
- GABA
Subthalamic nucleus + Globus pallidus Interna

PPN -
Brain stem & Spinal cord Thalamus

- Inhibitory pathway
- Inhibits the unwanted movement

Basal Ganglia functions

• Control of motor activity
• Initiation of voluntary movements
• Suppression of unwanted movements
• Planning and Programming of a voluntary movement
• Execution of automatic associated movement
- Swinging of arms during walking
- Gestures during speech
• Cognitive control of motor activity
• Inhibits muscle tone – inhibits γ motor neuron discharge
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5 marks
1. PAIN PATHWAY
Pain is carried by two pathways:
i) Neospinothalamic pathway
ii) Paleospinothalamic pathway
Neospinothalamic tract: (carries fast pain)
1st order neuron: Aδ fibers from receptors to spinal cord
2nd order neuron: From dorsal horn of spinal cord → cross to opposite side → ascend in the lateral
white column → end in the ventral postero lateral (VPL) & ventral postero
medial (VPM) nuclei of thalamus.
3rd order neuron: From thalamus to somatosensory cortex (areas 3, 2 &1)
Paleospinothalamic tract: (carries slow pain)
1st order neuron: ‘C’fibers from receptors to spinal cord
2nd order neuron: From dorsal horn of spinal cord → cross to opposite side → ascend in the lateral
white column → end in intralaminar & midline nuclei of thalamus
3rd order neuron: From thalamus to entire cerebral Cortex
Special features:
Neospinothalamic tract: concerned with localization and interpretation of quality of pain
Paleospinothalamic tract: concerned with perception of pain, arousal and alertness
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2. Modulation of Pain/ Endogenous Pain Relief System

Gate control theory of pain
- Large myelinated A fibers interact with small unmyelinated C fibers via inhibitory cells of the
Substatia gelatinosa of the spinal cord
- Stimulation of C fibers inhibits SG cells & favours passage of pain
- Stimulation of large ‘A’ fibers increases SG activity & block pain transmission by presynaptic
inhibition
Endogenous pain relief from PAG/central pain suppressing mechanism
- Descending pathways arise from Periaqueductal gray matter →release Encephalin → Descend &
connect with Nucleus raphe magnus of medulla →release of Serotonin → posterior horn cells of
spinal cord → inhibits the release of substance “P” from the pain fibers
Opioid peptides:
Enkephalins & Endorphins-
Two sites of action:
-Block the pain receptors
-At spinal level – binds to opioid receptors & decreases the pain transmission
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3. REFERRED PAIN
Visceral pain felt at the somatic structures is called referred pain
Eg: Appendicitis pain at the umbilicus
Cardiac pain at the inner aspect of left arm
Theories of referred pain: (mechanism of referred pain)
1. Convergence theory: Fibers carrying pain from the viscera & the corresponding dermatome
(somatic structures) converge on the same pathway to the cortex
2. Facilitation theory: The visceral pain facilitates Substantia Gelatinosa Rolando [SGR] cells
which receive somatic pain nerves

CONVERGENCE THEORY

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4.Withdrawl reflex
Refers to the withdrawal of body parts by flexion of limbs when a painful (noxious) stimulus is applied.
-It is a polysynaptic reflex
Receptors: Nociceptors
Afferent Limb: Type III & IV somatic afferents
Center: Spinal Cord
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Efferent fibers: Somatomotor neuron supplying the flexor muscles of same side and
extensor muscles of opposite side.
Response:
Mild stimulus- flexion of limb of same side and extension of limb of opposite side.
Stronger stimulus - response in all four limbs.
(Reason: a) Irradiation of impulse, b) Recruitment of more motor units)
Special features:
Withdrawl reflex is a protective reflex (protects the tissue from damage)
Pre potent (stops all other spinal reflexes temporarily)
Shows local sign ie., response depends upon the location of the stimulus
Stronger stimulus causes wide spread and prolonged response

3 MARKS
Functions of Hypothalamus
a) Regulation of food intake

Ventromedial Nucleus Lateral Nucleus

(Satiety center) (Feeding Center)

Inhibits feeding center Hunger

↑Food intake ↓food intake

b) Regulation of water intake
Tonicity of body fluid ECF volume

Osmoreceptors Baroreceptors

Thirst center Thirst center Angiotensin II

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↑Water intake ↑Water intake Subfornical organ

Thirst center
c) Regulation of body Temperature
Pre optic nucleus of anterior hypothalamus (heat loss center) → Sweating and vasodilatation
Posterior hypothalamus (heat gain center) → Shivering & vasoconstriction

APPLIED

1. Differentiate UMN & LMN lesion

UMN Lesion LMN lesion

1. Damage to the motor tracts above the anterior 1. Damage to the anterior horn cell and
horn cell below
2. Spastic paralysis 2. Flaccid paralysis
3. Exaggeration of deep reflexes & loss of 3. Loss of both superficial and deep
superficial reflexes reflexes
4. Babinski Sign positive 4. Babinski sign negative
5. No muscular atrophy 5. Atrophy of paralysis
(E.g) Hemiplegia (E.g) Poliomyelitis

2. Hemisection of spinal cord (Brown – sequard syndrome)

Refers to lesion in one lateral half of the spinal cord

Level of spinal cord Same side Opposite side

Below the level of section Sensory: Sensory:
Damage of dorsal column -Loss of pain
tracts Temperature and crude touch
-Loss of fine touch, tactile
discrimination, pressure, Motor : Normal
vibration, kinaesthetics and
stereognosis Vasomotor: Normal
Motor: UMN paralysis
Vasomotor: Temporary loss
of vasomotor tone
(vasodilatation)
At the level of lesion Sensory Sensory: Not affected
-Anaesthesia (complete loss
of sensation) Motor: Not affected
Motor: LMN paralysis
Vasomotor: Loss of Vasomotor: Not affected
vasomotor tone

3. PARKINSONISM/ PARKINSON’S DISEASE

-a disease caused by lesion in basal ganglia
Causes
Degeneration of nigrostriatal fibers
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Clinical Features
Akinesia / Bradykinesia
-Lack of initiation of movements
-retardation of movements
- loss of automatic, associated movements (statue like appearance, mask like face)
-Defect in speech
-loss of timing & scaling of movements (micrographia)
Rigidity
• Hypertonia in the agonistic and antagonistic muscle
• Caused by increased discharge of gamma motor neuron
• 2 types of rigidity
Cog wheel – intermittent resistance in passive movement
Lead pipe – continuous resistance to passive movement
Tremor
• Occurs at rest
• Pill rolling tremor
o Alternate contraction & relaxation of agonists and antagonist of hands and fingers at a
frequency of 6-8 hertz/second
• Absent in sleep
Festinant gait
• body is bent forward
• moves forward with short quick shuffling steps as if to catch center of gravity
TREATMENT
Levo Dopa --- can cross the blood brain barrier, but dopamine cannot cross

4. CEREBELLAR LESION
Features: (4 A, 4 D & SIN)

Ataxia Dysmetria Scanning speech

Atonia Decomposition Intention tremor
Asynergia Dysdiadochokinesia Nystagmus
Asthenia Drunken gait

Physiological Basis:
Ataxia - In co-ordination of movements
Atonia/ Hypotonia - Cerebellum has got a excitatory influence over muscle tone. So lesion of
cerebellum leads to loss of this excitation and there by hypotonia occurs
Asynergia – Lack of coordination
Asthenia – Slow movements (muscles get tired easily)

Dysmetria - errors in the rate, range, force and direction of movements (This leads to
decomposition of movement, overshooting & undershooting the targets (intention
tremor), Rebound phenomenon etc.,)
Dysdiadochokinesia - Inability to perform rapid, alternate movements(supination & pronation of
hands)
Decomposition of movement – movement occurring in stages
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Drunken gait – Walking in a clumsy manner with a wide base (walks in a zig zag line)

Scanning speech – Slow and lalling (Like a baby)

Intention tremors - Oscillatory movements of hands during movements/ tremor that develops during
movement
Nystagmus - Jerky movements of eyes when trying to fix the eyes on a subject
Other Features:
Posture – Head rotated to normal side. The trunk is bent with the concavity towards the
affected side.
Equilibrium – Loss of equilibrium
Rebound phenomenon – failure of termination of movement
5. Effect of lesion of pyramidal tract At Various Levels
Motor cortex – monoplegia
Corona radiata – monoplegia
Internal capsule – contralateral hemiplegia
Brain stem – contralateral hemiplegia.
Above C5 – both upper & lower limbs (Quadriplegia)
Below T1 – only lower limbs (Paraplegia)
APPLIED QUESTIONS
1. A 65 year old patient complains to the doctor that his muscles are stiff and can initiate
movements with difficulty. On examination it is found that there is rigidity, rest tremor, absence
of automatic associated movements
a) What is your diagnosis? a) Parkinsonism
b) How will you treat? b) With L-Dopa
2. A patient was admitted to the hospital with the following complaints:
inability to perform alternate movements rapidly and oscillatory movements of hand during a
voluntary movement but not at rest.
a) What is medical terminology used for the above symptoms?
b) Where is the probable site of lesion?
a) Inability to perform alternate movements – Adiadocokinesia
Oscillatory movements of hands during movements – intention tremors
b) Cerebellar lesion
3. A patient was admitted to hospital with involuntary rhythmic movements of his hands which
disappear on voluntary movements. On examination he showed rigidity throughout passive
movement
a) What is the lesion? Where is it located?
b) What is the possible cause of this disease?
a) Lesion of nigrostriatal fibres in the basal ganglia
b) Deficiency of dopamine
4. A sixty year old man has expressionless face and tremor of hands even at rest. Name the condition
and the physiological basis for the use of L- Dopa in his treatment
The condition is called Parkinsonism. As L- Dopa can cross the blood brain barrier, it is used for
treatment.
5. A 65 years old man came to the doctor with the complaint that his movements were slow with no
appreciated swinging of arms while walking, difficulty in standing up, tremors in the hand at rest.
O/E, there was muscular rigidity, mask- like face, “ pill- rolling” movements in the fingers and the
speech was slurred and monotonous. No sensory loss was seen and the stretch reflexes were
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normal.
a) What is your diagnosis? a) Parkinsonism
b) Which part of the CNS is affected? b) Basal ganglia
c) What is the treatment? c) L- Dopa (a derivative of dopamine)
6. A patient complaints of incordination of movement and instability in maintaining posture. O/E, he
Was found to have intention tremor and inability to perform rapid alternate movement. Which
structure of the CNS is most likely involved in this dysfunction? What will be the state of muscle
tone in this disease and what is the physiological basis of change of the muscle tone?
Structure involved – Cerebellum
Muscle tone status – Hypotonia
7.Name the disease that results after destruction of the dopamine secreting fibers of thesubstantia
nigra. Mention two important clinical features of the condition
Parkinsonism. Clinical features – Rigidity & tremor at rest
8. A 5 year old boy complains of pain in the back & neck. He had a body temperature of 102®F. The
following morning, there was complete paralysis of the right leg. On examination, the muscle tone
was greatly reduced, tendon reflexes were abolished in affected limb. After a month, the muscles of
the affected limb showed marked atrophy. There was no sensory loss.
1. What is your diagnosis? Poliomyelitis
2. What is the type of lesion? LMN lesion