The Central Nervous System (CNS) - Complete Overview

Fig. 3.2 - Schematic diagram of the CNS (Costanzo Physiology, 7th Ed.)

What is the CNS?

• The skull (for the brain) and vertebral canal (for the spinal cord)
• Three layers of meninges (connective tissue coverings)
• Cerebrospinal fluid (CSF) in the subarachnoid space

Meninges (Protective Coverings)

• Gray's Anatomy for Students, p. 48

Major Divisions of the CNS

1. BRAIN

A. Cerebral Hemispheres (Cerebrum)

• Cerebral cortex - the convoluted (folded) outer surface, divided into four lobes
• Underlying white matter
• Three deep nuclei: basal ganglia, hippocampus, amygdala

The Four Lobes of the Cerebral Cortex:

• Primary - directly receive/send signals (fewest synapses)
• Secondary/Tertiary - more complex processing
• Association areas - integrate diverse information (e.g., limbic association area for motivation, memory, and emotion)

Deep Nuclei:

• Basal ganglia (caudate nucleus + putamen + globus pallidus): receive input from all cortical lobes, project via thalamus to frontal cortex to help regulate movement
• Hippocampus: part of the limbic system; involved in memory formation
• Amygdala: part of the limbic system; involved in emotion; communicates with the autonomic nervous system via the hypothalamus
• Costanzo Physiology 7th Ed., p. 77

B. Diencephalon ("Between Brain")

Thalamus

• Processes almost all sensory information going to the cerebral cortex
• Also processes almost all motor information coming from the cerebral cortex to the brainstem and spinal cord
• Acts as a major relay station for the brain

Hypothalamus

• Lies ventral to the thalamus
• Regulates: body temperature, food intake, water balance
• Controls pituitary hormone secretion (releasing and inhibiting hormones via the hypophysial portal blood)
• Contains cell bodies of neurons that produce ADH (antidiuretic hormone) and oxytocin (secreted by the posterior pituitary)
• Costanzo Physiology 7th Ed., pp. 77-78

C. Brainstem

• Costanzo Physiology 7th Ed., p. 77

D. Cerebellum

• Attached to the brainstem; lies dorsal to the pons and medulla
• Foliated ("leafy") structure
• Functions:
  • Coordination of movement
  • Planning and execution of movement
  • Maintenance of posture
  • Coordination of head and eye movements
• Positioned strategically between the cerebral cortex and spinal cord - integrates:
  • Sensory position information from the spinal cord
  • Motor information from the cerebral cortex
  • Balance information from the vestibular organs of the inner ear

2. SPINAL CORD

Fig. 2.53 - The Spinal Cord (Gray's Anatomy for Students)

• Extends from the foramen magnum to approximately the level of disc L1-L2 in adults
• The distal end is the conus medullaris (cone-shaped); below it, a fine filament called the filum terminale continues inferiorly
• Has 31 pairs of spinal nerves (each with sensory/afferent and motor/efferent components)

Two Enlargements:

Internal Organization:

• Gray matter (central, H-shaped in cross section): rich in nerve cell bodies
• White matter (surrounding the gray matter): rich in nerve fibers/tracts that ascend and descend

Key Pathways:

• Ascending pathways: carry sensory information from periphery to higher CNS levels
• Descending pathways: carry motor information from higher CNS to the motor nerves of the periphery

• Somatic motor - innervate skeletal muscle
• Autonomic motor - innervate cardiac muscle, smooth muscle, glands
• Costanzo Physiology 7th Ed., p. 76; Gray's Anatomy for Students, pp. 119-120

Cells of the CNS

Neurons

Glial Cells (Support Cells)

• Costanzo Physiology 7th Ed., pp. 78-79

Functional Divisions of the CNS

• Gray's Anatomy for Students, p. 48

Quick Summary Table

The Babinski Sign - Complete Guide

1. History & Eponym

• Adams and Victor's Principles of Neurology, 12th Ed., p. 73

2. How to Elicit the Sign

Fig. 3-6 from Adams & Victor's Neurology: A. stroke path, B. normal plantar flexion, C. extensor plantar response (Babinski sign)

• Use a blunt instrument (e.g., tongue depressor, key, or the handle of a reflex hammer)
• Apply a firm but not painful stimulus to the lateral plantar surface of the foot
• Start from the lateral heel, sweep forward toward the small toe, then arc medially toward the big toe
• Observe the movement of the toes

Normal plantar response (A) vs Babinski's sign / extensor plantar response (B) - Neuroanatomy through Clinical Cases, 3rd Ed.

3. Responses - Normal vs Abnormal

"The presence of Babinski's sign in an adult is always abnormal."

• Neuroanatomy through Clinical Cases, 3rd Ed., p. [reflex section]

4. Physiological Basis (Mechanism)

• The corticospinal (pyramidal) tract exerts tonic inhibitory control over the flexion withdrawal reflex
• Plantar stimulation normally produces plantar flexion (a simple spinal reflex suppressed by descending inhibition)

• This inhibitory control is lost ("release phenomenon")
• The primitive flexor/withdrawal reflex is disinhibited
• Plantar stimulation triggers the full withdrawal response: hip flexion + knee flexion + ankle dorsiflexion - and as part of this, the big toe extends (what appears as "upgoing") while other toes fan out
• In physiologic terms, toe extension IS part of the flexor withdrawal response - it's not a true extensor response

• Adams and Victor's Principles of Neurology, 12th Ed., p. 74

5. What It Indicates - UMN Lesion

Classic UMN Syndrome Features:

• Adams and Victor's Principles of Neurology, 12th Ed., Table 3-1, p. 75

Where Along the Corticospinal Tract?

• Cerebral cortex (motor cortex, internal capsule)
• Brainstem (descending corticospinal fibers)
• Spinal cord (lateral corticospinal tract)

6. Common Clinical Conditions Where Babinski Is Positive

"Hyperreflexia, clonus, or a Babinski sign (positive plantar reflex) suggests upper motor neuron pathology, such as cord impingement."

• Rosen's Emergency Medicine

7. Associated UMN Signs (Context of Babinski)

• Spasticity - velocity-dependent increased tone ("clasp-knife" phenomenon)
• Hyperreflexia - exaggerated deep tendon reflexes
• Clonus - rhythmic oscillation (5-7 Hz) at ankle or patella with sustained stretch
• Loss of abdominal reflexes - normally abolished by UMN lesions
• Hemiplegia pattern - arm flexed/pronated, leg extended/adducted

8. Variants of Babinski Sign (Surrogate Signs)

"Several dozen surrogate responses (with numerous eponyms) have been described...all have the same significance as the Babinski response."

• Adams and Victor's Principles of Neurology, 12th Ed., p. 74

9. Grading / Forms of Response

10. Clinical Pearls for Exams

1. Positive Babinski in an adult = always abnormal = UMN/corticospinal tract lesion until proven otherwise
2. Positive Babinski in an infant < 1-2 years = normal (immature myelination)
3. The response is really a disinhibited flexor withdrawal reflex - "toe extension" is physiologically a flexion movement
4. The Babinski sign may be absent early in acute UMN lesions (spinal shock) - do not use its absence to exclude cord injury acutely
5. It cannot be elicited if there is severe weakness of the toe extensors (LMN lesion to the foot)
6. In ALS, you see both Babinski (UMN) and muscle wasting/fasciculations (LMN) - this combination is pathognomonic
7. All Babinski equivalents (Chaddock, Oppenheim, Gordon, etc.) carry the same clinical meaning
8. Babinski sign + spasticity + hyperreflexia + clonus = complete UMN syndrome
9. The abdominal reflexes are lost in UMN lesions (opposite to Babinski, which is gained)

• Adams and Victor's Principles of Neurology, 12th Ed., pp. 73-75 (dedicated section)
• Neuroanatomy through Clinical Cases, 3rd Ed. (plantar response testing)
• Neuroscience: Exploring the Brain, 5th Ed. (UMN vs LMN, Babinski mechanism)
• Tintinalli's Emergency Medicine (clinical context, spinal cord emergencies)
• Rosen's Emergency Medicine (UMN signs)

Babinski Sign - What's Important for First Year Physiology (MBBS)

1. Definition (1 liner - must know)

Babinski sign = dorsiflexion (upward extension) of the great toe + fanning of the other toes when the lateral sole of the foot is stroked from heel to toe.

2. How to Elicit (Technique)

• Use a blunt object (key, tongue depressor, reflex hammer handle)
• Stroke the lateral plantar surface of the foot
• Direction: heel → small toe → arc medially toward big toe
• Force: firm but not painful

3. Responses - The Core Comparison (Most Exam-Asked)

4. Why Is It Positive in UMN Lesions? (The Physiology - Most Important)

The Normal Situation:

• The corticospinal (pyramidal) tract descends from the motor cortex → through brainstem → to anterior horn cells of the spinal cord
• It exerts tonic inhibitory control over spinal reflex circuits
• Plantar stimulation normally produces a simple plantar flexion reflex suppressed by this descending inhibition

When the Corticospinal Tract Is Damaged:

• The inhibitory control is removed (disinhibition / "release phenomenon")
• The primitive flexor withdrawal reflex is released
• Plantar stimulation triggers the full withdrawal (flexor) reflex:
  • Hip flexes → Knee flexes → Ankle dorsiflexes → Big toe extends upward + toes fan
• What looks like "toe extension" is actually part of the protective flexion withdrawal response

"Damage to upper motor neurons initially causes muscles to become weak and flaccid but eventually leads to spasticity, hypertonia, hyperactive stretch reflexes, and abnormal plantar extensor reflex (positive Babinski sign)."

• Ganong's Review of Medical Physiology, 26th Ed.

Key Physiology Concept to Write in Exams:

5. Why Is It Normal in Infants? (Another Favourite Exam Point)

• At birth, the corticospinal tracts are not fully myelinated
• Descending inhibitory control over spinal reflexes has not developed
• So the flexor withdrawal reflex is uninhibited → toe goes up (same as Babinski)
• As myelination completes (around 12-18 months), the response converts to normal plantar flexion
• Persistence after 2 years = abnormal (indicates UMN lesion)

6. UMN vs LMN - The Classic Table (Always in First Year Physiology Exams)

• Neuroanatomy through Clinical Cases, 3rd Ed., Table 6.4 | Ganong's, 26th Ed.

7. The Reflex Arc Background (Physiology Context)

• Costanzo Physiology, 7th Ed., Table 3.5

8. Conditions Causing Positive Babinski (Know for Viva)

9. High-Yield Exam Points - Quick Summary

10. Likely Exam Questions on Babinski Sign

• "What is Babinski sign? How is it elicited? What is its significance?"
• "Differentiate UMN and LMN lesions."
• "Why is Babinski sign positive in infants?"
• "Explain the mechanism of Babinski sign."

• "What is the normal plantar response?"
• "Why does the toe go up in UMN lesion?"
• "At what age does Babinski disappear?"
• "Name two conditions causing positive Babinski."
• "What is the reflex arc involved in Babinski sign?"

Memory: Types & Mechanisms

Overview

Part 1: Classification of Memory

FIGURE 24.1 - Types of declarative and nondeclarative memory with brain structures involved (Neuroscience: Exploring the Brain, 5th Ed.)

A. DECLARATIVE MEMORY (Explicit Memory)

• Memory that can be consciously recalled and expressed
• Requires the medial temporal lobe / hippocampus and diencephalon
• Formed quickly, often from a single exposure; also forgotten more easily
• Subdivided into two types:

"Memory of facts and events is called declarative memory. Declarative memories are accessed for conscious recollection."

• Neuroscience: Exploring the Brain, 5th Ed., p. 2123

B. NONDECLARATIVE MEMORY (Implicit Memory)

• Memory that is expressed through performance, without conscious awareness
• "Knowing how" rather than "knowing that"
• Requires repetition and practice; once learned, very resistant to forgetting
• Several subtypes:

"Procedural memories involve 'knowing how' rather than 'knowing that.' Amnestic patients can learn new motor memories such as mirror drawing, which they can perform once started, although they have no recollection of knowing the task."

• Bradley & Daroff's Neurology in Clinical Practice

C. MEMORY BY DURATION

• Short-term memory = passive holding of information
• Working memory = active manipulation of information while using it (e.g., doing mental arithmetic, following a conversation)
• Working memory relies heavily on the prefrontal cortex

Part 2: Brain Structures for Memory

The Hippocampus - Gateway for Declarative Memory

• Had bilateral temporal lobectomy for epilepsy (removal of hippocampus and surrounding structures)
• Could not form any new declarative memories (profound anterograde amnesia)
• Could still form new procedural memories (e.g., learned mirror drawing, performed it well but had no recollection of having learned it)
• This proved that the hippocampus is required for declarative memory but NOT for procedural memory

Other Key Structures:

Part 3: Memory Consolidation

Two Levels of Consolidation:

• Involves molecular changes at synapses (LTP - see below)
• New protein synthesis stabilizes the memory trace
• This is why protein synthesis inhibitors can block memory formation if given shortly after learning

• Memories initially depend on the hippocampus
• Over time, through repeated reactivation (especially during sleep), memories become transferred to and stored in the neocortex
• This explains why old memories survive hippocampal damage, but recent memories do not (Ribot's Law - temporal gradient of retrograde amnesia)

Sleep and Memory:

• During sleep (especially slow-wave sleep and REM sleep), the hippocampus replays events of the day
• This reactivation transfers memories to the neocortex for long-term storage
• Sleep deprivation impairs memory consolidation

Reconsolidation:

• When a stored memory is retrieved, it temporarily becomes labile again
• The recalled memory must be reconsolidated to remain stable
• This means memories can be modified or even erased at the time of recall (has implications for eyewitness testimony and PTSD treatment)

Part 4: Cellular Mechanism - Long-Term Potentiation (LTP)

"Neurons that fire together, wire together."

• Hebbian principle (Neuroscience: Exploring the Brain, 5th Ed.)

Where Does LTP Occur?

Step-by-Step Mechanism of LTP:

WEAK STIMULUS (normal transmission):
Presynaptic neuron releases glutamate
  → Glutamate binds AMPA receptors → small EPSP
  → NMDA receptors are BLOCKED by Mg²⁺ (voltage-dependent block)
  → No LTP

STRONG STIMULUS (LTP induction):
1. Repeated/strong presynaptic firing releases large amounts of glutamate
2. AMPA receptor activation causes large postsynaptic depolarization
3. Depolarization EXPELS Mg²⁺ from NMDA receptor channel
4. Glutamate + depolarization → NMDA receptor opens → Ca²⁺ floods into postsynaptic cell
5. Ca²⁺ rise activates CaMKII (calcium/calmodulin-dependent protein kinase II) and other kinases
6. CaMKII phosphorylates existing AMPA receptors → increased conductance
7. NEW AMPA receptors are inserted into the postsynaptic membrane ("AMPAfication")
8. Result: same presynaptic stimulus now produces a LARGER EPSP → LTP

Three Properties of LTP (Kandel's - must know):

"Cooperativity ensures that only events of a high degree of significance...will result in memory storage. Associativity allows an event that has little significance in and of itself to be endowed with a higher degree of meaning if that event occurs just before or simultaneously with another more significant event."

• Kandel, Principles of Neural Science, 6th Ed., p. 1397

LTP and Spatial Memory:

• Blocking NMDA receptors in the hippocampus before training in the Morris Water Maze (a spatial memory task) prevents the animal from learning the hidden platform location
• Blocking NMDA receptors after learning does not impair recall
• This confirms NMDA receptors are needed for induction but not maintenance of LTP

Early vs Late LTP:

Part 5: Amnesia (Memory Loss)

• Damages the mammillary bodies and dorsomedial thalamus
• Profound anterograde amnesia + confabulation (making up stories to fill memory gaps)

Summary Diagram

MEMORY
│
├── DECLARATIVE (Explicit) - HIPPOCAMPUS
│   ├── Episodic (Events - "I remember when...")
│   └── Semantic (Facts - "I know that...")
│
└── NONDECLARATIVE (Implicit)
    ├── Procedural/Skills - STRIATUM/BASAL GANGLIA
    ├── Classical conditioning (skeletal) - CEREBELLUM
    ├── Emotional conditioning - AMYGDALA
    └── Priming - NEOCORTEX

Quick Revision Points