Long answer type question for cns, Schemes and Mind Maps of Anatomy

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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

2. CEREBELLUM

Functional divisions:

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

Connections:

Peduncles Afferent fibers Efferent fibers

Superior Cerebellar Peduncle Ventral spinocerebellar tract Tectocerebellar Trigemino cerebellar fibers Dentato thalamocortical fibers Dentatorubral fibers Middle Cerebellar Peduncle Cerebro ponto cerebellar ----------------------

Inferior Cerebellar

Peduncle

Dorsal spinocerebellar

Cuneo cerebellar

Reticulo cerebellar

Vestibulo cerebellar

Olivo cerebellar

Cerebello reticular

Cerebello vestibular

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

1. Substantia nigra

5. Subthalamic Body

Connections:

Direct pathway:

• Cortex
• Glutamine Striatum Dopamine Substantia nigra

• GABA Globus pallidus Interna

Thalamus

D 1

5 marks

1. PAIN PATHWAY

Pain is carried by two pathways: i) Neospinothalamic pathway ii) Paleospinothalamic pathway

Neospinothalamic tract: ( carries fast pain)

1 st^ order neuron: Aδ fibers from receptors to spinal cord 2 nd^ 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. 3 rd^ order neuron : From thalamus to somatosensory cortex (areas 3, 2 &1)

Paleospinothalamic tract: ( carries slow pain)

1 st^ order neuron: ‘C’fibers from receptors to spinal cord 2 nd^ 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 3 rd^ 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

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

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

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

↑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 horn cell 1. Damage to the anterior horn cell and below
2. Spastic paralysis 2. Flaccid paralysis
3. Exaggeration of deep reflexes & loss of superficial reflexes 3. Loss of both superficial and deep 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: Damage of dorsal column tracts

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

3. PARKINSONISM/ PARKINSON’S DISEASE

• a disease caused by lesion in basal ganglia

Causes

Degeneration of nigrostriatal fibers

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

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