BIOMEDICAL SCIENCE

PSYCHOLOGY/PSYCHOPHYSIOLOGY

HET227 Neurophysiology

SOMATOSENSORY SYSTEM

LECTURES
 BIOMEDICAL SCIENCE
PSYCHOLOGY/PSYCHOPHYSIOLOGY

HET227 Neurophysiology

SOMATOSENSORY SYSTEM LECTURES

CONTENTS

INTRODUCTION TO SOMATOSENSORY SYSTEM _____________________________________________1

NERVOUS SYSTEM OVERVIEW______________________________________________________________1
STRUCTURE OF NEURONS________________________________________________________________1
THE SYNAPSE ____________________________________________________________________________2
CLASSIFICTION OF NEURONS ____________________________________________________________2
INTRODUCTION TO NEUROGLIA _________________________________________________________3
MEMBRANE PROPERTIES OF NEURONS___________________________________________________3
RECEPTORS & RECEPTIVE FIELDS__________________________________________________________6
INTRODUCTION TO REFLEXES _____________________________________________________________7
CLASSIFICATION OF REFLEXES ____________________________________________________________7
REVIEW OF CLASSIFICATION OF NEURONS _________________________________________________8
EMBRYOLOGICAL DEVELOPMENT _________________________________________________________9
EMBRYOLOGICAL DEVELOPMENT OF NERVOUS TISSUE ___________________________________11
SPINAL CORD _____________________________________________________________________________12
DIVISIONS OF THE SPINAL CORD __________________________________________________________12
PERIPHERAL NERVE ORGANISATION ______________________________________________________14
DORSAL ROOT ORGANISATION ____________________________________________________________14
SPINAL CORD ORGANISATION _____________________________________________________________14
ORGANISATION OF SECONDARY SPINAL CORD NEURONS __________________________________15
ASCENDING PATHWAYS ___________________________________________________________________16
DORSAL (POSTERIOR) COLUMN PATHWAY ______________________________________________16
DORSAL-MEDIAL LEMNISCUS PATHWAY ________________________________________________16
SPINOTHALAMIC TRACTS_______________________________________________________________17
LOCALISATION OF SENSATION ____________________________________________________________17
DETERMINATION OF PAIN _________________________________________________________________18
THALAMIC NUCLEI _______________________________________________________________________18
SOMATOSENSORY CORTEX________________________________________________________________19
POSITION SENSES _________________________________________________________________________22
CLINICAL CONSIDERATIONS ______________________________________________________________23
STIMULUS INTENSITY _____________________________________________________________________25

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 INTRODUCTION TO SOMATOSENSORY SYSTEM

Our sensory responses rely on our perception (both conscious & unconscious) of sensory information.
• Afferent information below conscious awareness = (mainly) visceral information - essential for
determining the appropriate efferent output to maintain the body’s homeostasis
• Afferent information above conscious awareness = perception information:
• Somatic sensation - arising from body surface.
o “soma” = body
o “somatic” = of the body
• Special senses - including vision, hearing, taste & smell, balance.

Perception is the conscious interpretation of the external world created by the brain from a pattern of nerve
impulses delivered to it from sensory receptors.
Afferent neurons have receptors at their peripheral endings which respond to stimuli in both the internal and
external world.
• What we perceive is different to what is really there.
• Receptors detect only a limited number of existing forms.
• There are between- & within individual differences in sensory responses.
• In types of receptors & sensitivities.
• In neural processing of /stimulus/responses.

Pathology of the senses results in deprivation or excessive stimulation.

Appropriate neurological treatment depends on specific diagnosis.
Diagnosis can include simple tests using direct stimuli or electrical stimuli.
Evoked potentials – visual, auditory, somatosensory…
Automated and semi-automated EP testing equipment….

NERVOUS SYSTEM OVERVIEW

Includes all the neural tissue in the body.

Neurons - Basic functional units.
Neuroglia or glial cells - Connective tissue of the nervous system.
Basic support cells (separate & protect neurons)
Outnumber neurons (~ half volume of whole nervous system)
But number about ~90% of cells within CNS (less branching  smaller volume)
Central Nervous System (CNS):
• Spinal cord and brain.
• Responsible for integrating, processing, coordinating sensory data and motor commands.
• Sensory information about conditions inside and outside body.
• Motor commands to control or adjust activities of peripheral organs (eg skeletal muscles).
• Brain is also seat of higher cortical function (memory, learning, emotion etc).

Peripheral nervous system (PNS):

• All neural tissue outside the CNS.
• Carries information between the CNS and other parts of the body.
o TO the CNS = sensory information  afferent “ad” = to, “ferre” = carry.
o FROM the CNS = motor commands  efferent “effero” = to bring about.

STRUCTURE OF NEURONS

Neurons have a variety of shapes.

Most common type in CNS: multipolar neuron.
(Large cell body or soma, connected to single, elongated axon, several short, branched dendrites).

Cell body:
• Relatively large, round nucleus.
• Perikaryon: the cytoplasm surrounding the nucleus
o Contains organelles to provide energy & synthesize organic materials.
Dendrites:
• Variable number, extending from cell body.
• Typically highly branched

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 • Each branch with dendritic spines
o carry information from other neurons
o represent 80-90 % neuron’s total surface.
Axon:
• Long, cytoplasm process – capable of propagating electrical signals (action potentials)
• Base or initial segment of the axon is attached to the cell body at a thickened region or axon hillock.
• Telodendria: fine extensions at the end of the axon trunk which end at synaptic terminals.
THE SYNAPSE
Synapses are junctions between 2 neurons.
Axon terminal of presynaptic neuron  sends the message
Dendrites or cell body of postsynaptic neuron  receives the message.
• Action potentials trigger the release of neurotransmitters by the synaptic terminal.
o Neurotransmitters are packaged in the synaptic vesicles.
o Released at the presynaptic membrane
o Received by receptors in the postsynaptic membrane.
• Presynaptic cell is usually a neuron.
• Postsynaptic cell can be either a neuron or another type of cell.
o Synapse between a neuron & a neuron – can occur on a dendrite, on a cell body, or along the axon
of the receiving cell.
o Synapse between a neuron & muscle: neuromuscular junction.
o Synapse between a neuron & gland: neuroglandular junction.
Structure of the synaptic terminal varies with the type of postsynaptic cell.
• A synaptic knob occurs when the postsynaptic cell is a neuron.
Synaptic cleft - Narrow cleft between pre- & postsynaptic cells which the neurotransmitter diffuses across to bind to
postsynaptic membrane receptors.
CLASSIFICTION OF NEURONS
Neurons can be grouped by structure or by function.
Structural classification:
Classification based on of the relationship of the dendrites to the cell body and the axon.
1. Anaxonic neurons. - Small, no distinguishing features that distinguish dendrites from axons.
• Located in brain & special sense organs.
2. Bipolar neurons. - Smaller than uni- and multipolar neurons
• 2 distinct processes: dendritic process – branching extensively at its distal tip – and axonal process, with cell
body between. Rare, occur in special sense organs.
3. Unipolar neurons. - Most common sensory neurons of PNS; End at synapses in the CNS
• Dendrites and axons are continuous, with cell body lying off to one side.
o axons may be 1 m or more; longest from tips of toes to spinal cord.
4. Multipolar neurons. - ,Most common neuron in CNS
• 2 or more dendrites and single axon

Functional classification:
1. Sensory neurons or afferent neurons.
• About 10 million in the body.
• Somatic sensory neurons =- monitor outside world & our position within it.
• Exteroreceptors: eg touch, temperature, pressure sensations, & more complex senses of sight, smell,
hearing.
• Proprioceptors – monitor position & movement of muscles & joints.
• Visceral sensory neurons – monitor internal conditions & status of other organ systems.
• Interoceptors – monitor internal systems (digestive, respiratory, cardiovascular, urinary, reproductive)
and sensations of taste, deep pressure & pain.
2. Motor neurons or efferent neurons.
• About 1/2 million in the body.
• Somatic motor neurons =- innervate skeletal muscles.
• You can have conscious control over this activity.
• Visceral motor neurons = innervate all peripheral effectors other than skeletal muscles (smooth muscle,
cardiac muscle, glands, adipose tissue). Monitor internal conditions & status of other organ systems.
3. Interneurons or association neurons.
• 20 billion (most within brain & spinal cord).
• Responsible for distribution of sensory information & coordination of motor activity.

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 INTRODUCTION TO NEUROGLIA

Neuroglia or glial cells make up about 90% if the cells within the CNS.
• Connective tissue of the CNS.
• They do not initiate or conduct nerve impulses.
• They physically support the interneurons, metabolically and functionally.
Major types of glial cell s in the CNS:
1. Astrocytes - Star shaped, most abundant. Important functions:
• Main “glue” of CNS – ie create a 3D framework for CNS to hold neurons together in proper spatial
relationships.
• Form scaffold to guide neurons to correct destination during fetal brain development.
• Help maintain the blood-brain barrier.
• Help repair damage neural tissues to stabilise the tissue and prevent further injury.
• Help control the interstitial environment (volume of blood flow through capillaries; transport
nutrients/ions/dissolved gases between capillaries & neurons; regulate concentration of sodium &
potassium ions & CO2)
• Enhance synaptic formation & transmission, & play a role in neurotransmitter activity (absorb &
recycle some neurotransmitters; release chemicals to enhance or suppress communication across
synaptic terminals).
2. Oligodendrocytes - Form insulative myelin sheaths around axons in CNS; Provide structural framework.
• Myelin insulation increases the nerve conduction velocity.
• Effectively tie clusters of axons together in same sheath segment (or internodes).
• Appear glossy white (lipids present)
•  white matter in CNS = dominated by myelinated axons.
•  grey matter = dominated by unmyelinated axons.
3. Microglia
• Immune defence cells of the CNS (“cousins” of monocytes – white blood cells).
• Smallest and least numerous.
• Capable of migrating through neural tissue – move to affected areas to remove foreign invaders or tissue debris.
• Remain stationary until activated by infection or injury.
4. Ependymal cells - Line internal cavities of the CNS.
• Contribute to formation of cerebrospinal fluid (have cilia which contribute to the flow of the fluid through the
ventricles).
• Serve as neural stem cells with the potential to form new neurons & glial cells.
Major types of glial cells in the PNS:
Cell bodies of PNS clustered in ganglia.
Neuronal cells in PNS are insulated from their surroundings by two types of neuroglia:
1. Satellite cells
• Surround the neuron cell bodies in ganglia.
• Similar to astrocytes  Regulate internal environment
2. Schwann cells
• Forms a segment of myelin sheath around one segment of a single peripheral axon.
• Series of Schwann cells needed to form a sheath along entire length of axon.

MEMBRANE PROPERTIES OF NEURONS

The important membrane processes:

o Resting potential – the transmembrane potential of a resting cell.
o All neural activities begin with a change in the resting potential.
o Graded potential – a temporary localised change in the resting potential.
o Decreases with distance from the stimulus.
o Action potential – occurs if the graded potential is sufficiently large.
o Propagates across the surface of the membrane.
o Does NOT decrease with distance from the stimulus.
o Synaptic activity – produces the graded potentials in the postsynaptic cell membrane.
o Involves release of neurotransmitters (eg Ach) that bind to receptors on postsynaptic cell membrane

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o Information processing – in its simplest form, integrates stimuli at the individual cell level.

TRANSMEMBRANE or RESTING POTENTIAL

Membrane potential = a separation of charges across the membrane or to a difference in the relative number of
cations and anions in the intra- and extra-cellular fluid. Measured in mV.
Transmembrane potential = membrane potential of a resting or undisturbed cell.
• At the resting potential, ion movement occurs through passive and active mechanisms.
• Passive forces: Uses chemical and electrical forces.
o Chemical gradients:
 Potassium ions move OUT, driven by concentration gradient.
 Sodium ions move IN, driven by concentration gradient.
o Electrical gradients:
 Cell membrane more permeable to potassium than to sodium.
  potassium leaves more rapidly than sodium enters.
  results in excess of negatively charged proteins inside & greater positive charge
outside near the outer surface of the cell.
• Active forces:
o The sodium-Potassium Exchange pump.
o The cell must expend energy (ATP) to “bail out” sodium ions that leak in and to recapture
potassium ions that leak out (passive forces).
o ATP is used by an ion exchange pump – balances the passive forces of diffusion
o  resting potential remains stable.

CHANGES IN THE TRANSMEMBRANE POTENTIAL:

MEMBRANE CHANNELS
The transmembrane potential is dynamic, rising & falling in response to temporary changes in membrane
permeability.  changes result from opening or closing of specific channels.
OPENING of gated channels alters the rate of ion movement across the cell membrane  changes transmembrane
potential.
Chemically-regulated channels
• open or close when they bind specific chemicals.
• eg receptors that bind ACh at the neuromuscular junction.
Voltage-regulated channels
• open or close in response to changes in the transmembrane potential.
• characteristic of areas of excitable membrane (capable of generating and conducting an action potential).
• Sodium, potassium & calcium channels.
o Sodium channels have an activation gate (opens on stimulation to let sodium ions in) & an
inactivation gate (closes to stop the entry of sodium ions).
Mechanically-regulated channels
• open or close in response to physical distortion of the membrane surface.
• Important in sensory receptors (touch, pressure, vibration).
At the resting potential – most gates are CLOSED.

GRADED or LOCAL POTENTIALS

o A temporary localised change in the resting potential.

o Decreases with distance from the stimulus.
 Changes in the transmembrane potential that CANNOT SPREAD far from the area surrounding the site of
stimulation.
o Any stimulus that opens a gated channel will produce a graded potential.
o STEP 1: Arrival & spreading of additional positive charge which shifts the transmembrane potential toward 0 mV.
o Increase in positivity of resting potential (-70 mV) toward 0 mV == depolarisation
o Includes smaller negative values (-65 mV, -10 mV) or above 0 mV (+10mV etc).
o STEP 2: LOCAL current – the movement of positive charges parallel to the inner & outer surfaces of a
membrane.
o Sodium ions are released from its outer surface.
o They move toward open channels replacing ions that have already entered the cell.
o STEP 3: The degree of polarisation decreases with distance. At some distance from the entry point, the effects
of the transmembrane potential are undetectable.

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Repolarisaiton = the process of restoring the normal resting potential after depolarisation.
Involves both ion movement through membrane channels + activities of ion pumps.
Hyperpolarisation = loss of positive ions resulting in an increase in negativity of resting potential from –70 mV to
–80 mV or more.
o Opening a gated potassium channel  potassium rate of outflow increases == interior loses positive ions.

ACTION POTENTIALS

o Initiation of an action potential requires a depolarisation large enough to open voltage-gated channels.
o Opening occurs at the threshold for the axon,
o THRESHOLDS: typically between –60 mV & -55 mV
==depolarisation of 10-15 mV.
o Below threshold – eg a shift to –62 mV  graded potential.
o Above threshold – eg a shift to –60 mV  action potential.
o The properties of an action potential are independent of the relative strength of the depolarising stimulus, as
long as that stimulus exceeds threshold
 the ALL-OR-NONE principle.
 Depolarisation to threshold
 Activation of sodium channels & rapid depolarisation
 Inactivation of sodium & activation of potassium channels
 Return to normal permeability
Refractory periods
o Absolute refractory period– (0.4-1.0 sec) the period from when an actin potential begins until the normal
resting potential has stabilised during which the membrane will not respond at all to additional depolarising
stimuli.
o The smaller the axon diameter, the longer the period.
o Relative refractory period– begins when the sodium channels regain their normal resting potential and
continues until the transmembrane potential stabilises at resting levels. –
o Will only respond if the membrane is sufficiently depolarised.
o Usually requires larger than normal stimulus.

Propagation of Action Potentials

Continuous Propagation of unmyelinated axons:
• Continuous chain reaction along axon.
• Action potential in initial segment results in depolarisation.
• Local current depolarises adjacent portion.
• Action potential develops in this segment, & previous segment enters refractory period.
• Cycle is repeated along length of axon.
• Action potentia always proceeds AWAY from site of generation – cannot reverse.
• Occurs at approx 1 m/sec
Saltatory Propagation of myelinated axons:
• Complete myelin sheath  increases resistance to flow of ions across the membrane
o  prevents continuous propagation
o Ions can only cross the cell membrane at the nodes  only nodes depolarise
• Action potential jumps from node to node
 saltatory propagation (saltare == leaping)
• Less surface area is involved & fewer sodium ions need to be pumped out (uses less energy)
 More rapid – about 50 x faster than unmyelinated fibres of comparable size.

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 RECEPTORS & RECEPTIVE FIELDS

Receptors for general senses scattered throughout the body.

Classification system divides into four types of receptors by nature of the exciting stimulus:
Nociceptors Pain (JP TO DISCUSS LATER)
Chemoreceptors Chemical concentration (CO TO DISCUSS NEXT SEMESTER)
Thermoreceptors Temperature
Mechanoreceptors Touch, pressure, proprioception

Thermoreceptors free nerve endings located in dermis of skin, in skeletal muscles, in liver, in hypothalamus.
Cold receptors: 3 – 4 times more numerous than Warm receptors
No structural differences identified between Cold and warm receptors.
Use same pathways that carry pain sensations.
Phasic receptors: very active when temperature is changing, but quickly adapt to stable temperature.

Mechanoreceptors sensitive to stimuli that distort their cell membranes.

Tactile receptors: Closely related sensations of touch, pressure, vibration.
Baroreceptors: Detect pressure changes in walls of blood vessels, portions of digestive, reproductive, and
urinary tracts.
Proprioreceptors: Monitor positions of joints and muscles. Most structurally and functionally complex of
general sensory receptors.

Tactile receptors:
Free nerve endings – sensitive to touch & pressure. Situated between epidermal cells. Tonic receptors with small
receptive fields.
Root hair plexus – nerve endings of hairs, monitoring distortions and movements across the body surface. Adapt
rapidly.
Merkel’s discs – fine touch and pressure receptors. Extremely sensitive tonic receptors, with very small receptive
fields.
Meissner’s corpuscles – perceive sensations of fine touch and pressure and low-frequency vibration. Adapt to
stimulation within a second of contact. Most abundant in eyelid, lips, fingertips, nipples, external genitalia.
Pacinian corpuscle – sensitive to deep pressure. Fast-adapting, most sensitive to pulsing or high frequency
vibration.
Ruffinian corpuscles – sensitive to pressure and distortion of the skin, located in reticular (deep) dermis. Tonic,
show little adaptation.

Detection of stimuli

Receptor specificity: Each receptor has a characteristic sensitivity. Eg touch receptor sensitive to pressure but
relatively insensitive to chemical stimuli
May result form structure of receptor cell or from presence of accessory cells or structures that shield the
receptor cell from other stimuli.
Receptors may be quite localised – eg in muscle spindles and tendon organs – or may be more diffuse – eg bare
nerve endings in the skin.
Free nerve endings extend through the tissue the way plant roots extend through the soil. Can be stimulated
by different stimuli, and exhibit little receptor specificity. Eg responding to tissue damage by providing
pain sensation – may be stimulated by chemical stimuli, pressure, temperature changes or trauma.
Knowledge of the location of a stimulus is termed topognosis.

RECEPTIVE FIELD: The spatial region throughout which stimulation causes an afferent neuron to respond
That is: The area monitored by a single receptor cell.
The centre of a receptive field is generally the most sensitive to stimuli
Response decreases as the stimulus is moved outward to the periphery of the field.
With some receptors, particularly skin pain, temperature and mechanoreceptors, as stimulus intensity increases it
may then start to stimulate an adjacent receptive field producing overlap.

ACUITY The precision with which a stimulus is located.

Different sensory modalities and different regions of the body vary in the level of acuity.
The larger the receptive field – the poorer your ability to localize a stimulus.

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 Touch on tongue or fingertips – Highly localised touch. receptive fields less than a millimetre. Very acute.
Touch on general body surface – receptive field of 7 cm diameter. Less acute
Heart pain is even less acute and tends to be widespread and diffuse.

TWO-POINT DISCRIMINATION or TWO-POINT THRESHOLD is one way of determining the acuity for a given
stimulus in various parts of the skin.
Over the whole body, two-point discrimination varies from less than 10 mm to as much s 65 mm.

Acuity is dependent on several aspects;

• Receptive field size
• Innervation density: relates to spacing or density of the receptors
• Central convergence: relates to the possibility of several signals form various receptive fields all
eventually converging on one central neurone; this will decrease acuity.
• Lateral inhibition: occurs when stimulation of the periphery of the receptive field causes inhibition in higher
order neurones.
o This can increase acuity by sharpening up the edges of the perceived fields and reducing overlap.

INTRODUCTION TO REFLEXES

Reflexes are built-in, automatic responses triggered by stimuli in the skin/joints.

• Simple or basic reflexes are unlearned responses (knee jerk).
• Acquired or conditioned reflexes are the result of learning/practice (somersault).
Reflexes are usually controlled by the spinal cord, but most reflexes do not travel up to the brain to be processed –
which is why they occur so quickly.
• The reflex response is predictable - they always travel the same pathway.
• Reflex arc - the very simple nervous pathway involved in the reflex action, typically involving 5 basic
components:
• Receptor which responds to a stimulus.
• Afferent or sensory pathway.
• Integrating centre – CNS (particularly spinal cord &/or brain).
• Efferent or motor pathway.
• Effector – muscle or gland which carries out the response.
• Excite the muscle to respond (shorten) & inhibit the antagonist muscle.
CLASSIFICATION OF REFLEXES

Classified based on the basis of:

1. Their development:
• Innate reflexes
• Acquired reflexes – learned, enhanced by repetition.
• MAY be modified over time or suppressed through conscious effort.
2. The site of information processing
• Spinal reflexes – processing in the spinal cord.
• Monosynaptic reflexes: simplest, little delay (with a latency to response onset of 15-25 msec);
• Polysynaptic reflexes: more complicated responses. Can involve several muscle groups.
• Cranial reflexes – processed in the brain eg reflex movements in response to loud noises.
3. The nature of the resulting motor response
• Somatic reflexes – provide mechanism for involuntary control of muscle system
• Superficial reflexes – triggered by stimuli at the skin or mucous membrane.
• Stretch reflexes – (deep tendon reflexes or myotactic reflexes) triggered by sudden elongation of
a tendon.
• Visceral reflexes – automatic reflexes – control activities of other systems.
4. The complexity of the neural circuit involved.
• Monosynaptic reflexes - simple
• Polysynaptic reflexes - complex

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These are NOT mutually exclusive categories (different ways of describing a simple reflex).

Monosynaptic reflexes: simplest, little delay (with a latency to response onset of 15-25 msec);
• Stretch reflex – automatic regulation of skeletal muscle length. Eg ‘knee jerk’ reflex.
• Action potentials carried to & from spine along large myelinated Type A fibres;
• Complete reflex takes 20-40 msec.
• Include postural reflexes – to help maintain normal upright posture.
• Muscle spindles are the sensory receptors involved in the stretch reflex.
• When a skeletal muscle is stretched, the muscle spindles elongate  muscle tone increases  provides
automatic resistance  reduces chance of damage due to overstretching.

Polysynaptic reflexes: more complicated responses. Can involve interneurons which control several muscle groups.
• Tendon reflex: - Monitors external tension produced during a muscular contraction, prevents tearing or breaking
of tendons.
• Separate receptors from muscle spindles & proprioceptors in tendons.
• Withdrawal reflex: - moves affected parts of the body away form a source of stimulation.
• Strongest withdrawal reflexes are triggered by pain. Eg.
• Flexor reflex – affects muscles of a limb.
o Involves reciprocal inhibition – one set of motor neurons are stimulated, those controlling
antagonistic muscles are inhibited.
• Crossed extensor reflex: - the motor response occurs ON THE OTHER SIDE OF THE BODY.
• Complements the flexor reflex – they happen simultaneously.
ALL polysynaptic reflexes share the same characteristics:
1. Involve pools of interneurons.
2. Are intersegmental in distribution (extend across spinal segments, may activate muscles in different parts
of body).
3. Involve reciprocal inhibition.
4. Have reverberating circuits to prolong the reflexive motor response.
5. Several reflexes may cooperate to produce a coordinated controlled response.

DIAGNOSTIC TESTING

Many somatic reflexes can be tested for assessment of neurological function.

Superficial reflex: Babinski response or plantar reflex.
Stretch reflexes: patellar, biceps, triceps & Achilles reflexes.

REVIEW OF CLASSIFICATION OF NEURONS

Unmyelinated fibres – impulse conduction is continuous (uninterrupted).

Maximum speed is 15 m/s.
Myelinated fibres – excitable membrane is confined to nodes of Ranvier (myelin is electrical insulator)
Impulse conduction is saltatory (interrupted or jumping) – jumping from node to node.
Greater speed of conduction, with maximum of 120 m/s.

Larger myelinated fibre = more rapid conduction.

Larger fibres have longer internodal segments and the nerve impulses take a longer stride between nodes.
A ‘rule of six’ to express the ratio between size and speed:
10µm external diameter = conduct at 60 m/s
15 µm diameter = conduct at 90 m/s

Peripheral nerve fibres are classified in accordance with conduction velocities and other criteria.
Motor fibres are classified into Groups A, B, C, in descending order.
Sensory fibres classified into Types I – IV.
BUT there is some interchange in practice:
Unmyelinated sensory fibres are usually called C fibres rather than Type IV.

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 EMBRYOLOGICAL DEVELOPMENT

During first 2-3 weeks of development

• amnion,
• yolk sac,
• allantois
• chorion.
Amnion
• surrounds the developing embryo/fetus.
• Sac becomes filled with amniotic fluid (initially derived from maternal blood)
• Eventually extends all the way around the embryo.
• Buoyant environment; protects against physical trauma, helps maintain constant homeostatic temperature
• Helps prevent growing embryonic parts from adhering and fusing together
• Allows the embryo freedom of movement, aiding musculoskeletal development.
Yolk Sac
• Inner layer of endoderm and outer layer of mesoderm.
• Hangs from the ventral surface of the embryo.
• Forms part of the gut (digestive tract)
• Produces the earliest blood cells
• Source of primordial germ cells that migrate into the embryo’s body to seed the gonads.

Allantois
• Essential to placenta formation.
• Forms as a small out-pocketing at the caudal end of the yolk sac
• Structural base for constructing the umbilical cord that links the embryo to the placenta, and becomes part of the
urinary bladder.
• When fully formed, the umbilical cord contains a core of embryonic connective tissue (Wharton’s jelly), the
umbilical arteries and vein, and is covered externally by amniotic membrane.
Chorion
• helps form the placenta
• Encloses the embryonic body and all other membranes.

Gastrulation: Germ Layer Formation

Lays down the basic structural framework of the embryo
• The transformation of the 2-layered embryonic disc into the 3-layered embryo in which the primary germ layers
are present.
• cellular rearrangement and widespread cell migrations.
• Shortly after the amnion forms
• Embryonic disc elongates and broadens anteriorly (becomes a pear-shaped plate of cells)
• Primitive streak (a raised groove) appears on its dorsal surface and establishes the longitudinal axis of the
embryo
• Cell migration follows, resulting in the division of the cells into the 3 primary germ layers.
• The embryonic tissues from which all tissues and organs of the body develop.
• Ectoderm forms from the top layer of cell mass
• separates to form the amniotic cavity.
• Endoderm forms from another layer
• also separates to form the yolk-sac.
• Mesoderm The 3rd layer forming between these 2 layers
• The 3 layers attached to the trophoblast (now called the chorion) by a structure formed by the mesoderm called
the body stalk (future umbilical cord).
• Early in embryonic life the yolk sac merges with the body stalk and becomes non-functional.

Ectoderm “outer skin” develops into

• All nervous tissue
• Epidermis of skin
• Cornea, lens of eye and internal eye muscles
• Internal and external ear
• Neuroepithelium of sense organs
• Epithelium of pineal gland, pituitary gland, and adrenal medulla
• Epithelium of oral and nasal cavities, paranasal sinuses, salivary glands, and anal cavity.

Endoderm “inner skin” becomes epithelial lining of

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• gastrointestinal tract (except oral and anal cavities) and epithelium of its glands
• urinary bladder, gallbladder and liver
• pharynx, auditory (Eustachian) tubes, tonsils, larynx, trachea, bronchi and lungs
• thyroid, parathyroid, pancreas, thymus gland
• a number of other organs including the vestibular and lesser vestibular glands, prostate, vagina

Mesoderm “middle skin” forms

• All skeletal, most smooth and all cardiac muscle;
• Cartilage, bone and other connective tissue;
• Blood, bone marrow, lymphatic tissue;
• Endothelium of blood vessels and lymphatic vessels;
• Dermis of skin
• Middle ear
• Epithelium of kidneys and ureters, adrenal cortex, gonads and genital ducts.

Organogenesis: Differentiation of the Germ Layers

Formation of body organs and organ systems.
Cells of the embryo continue to rearrange themselves, forming clusters, rods, or membranes that differentiate into
definitive tissues and organs.
Each of the primary tissues formed during gastrulation proceed to undergo growth, differentiation and
morphogenesis

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 EMBRYOLOGICAL DEVELOPMENT OF NERVOUS TISSUE

NEURULATION: formation of the neural tube

The entire nervous system originates from the neural plate, an ectodermal thickening in the form of the amniotic sac.
• During the 3rd week after fertilisation, the plate forms paired neural folds, which unite to create the neural
tube and neural canal.
• Union of the folds commences in the future neck region and proceeds rostrally (towards the head) and
caudally (towards the tail) from there.
• Neuropores - the open ends of the tube – are closed off before the end of the 4th week.
• Cells at each edge of each neural fold escape from the line of union and form the neural crest alongside the
tube. Cell types derived from the neural crest include spinal and autonomic ganglion cells and the Schwann
cells of peripheral nerves.
• Anterior end of the neural tube becomes the brain
• The rest becomes the spinal cord.
• By end of 1st month of development, 3 primary brain vesicles are obvious: fore-, mid- and hindbrain
• By end of 2nd month, all brain flexures are evident, cerebral hemispheres cover the top of the brain stem and
brain waves can be recorded.
SPINAL NERVES
The dorsal (posterior) part of the tube is called the alar plate;
Neurons developing in the alar plate are predominantly sensory in function and receive dorsal nerve roots
growing in from the spinal ganglia.
The ventral (anterior) part of the tube is the basal plate:
Neurons in the basal plate are predominantly motor and give rise to ventral nerve roots.
At appropriate levels of the spinal cord the ventral roots also contain autonomic fibres.
Dorsal and ventral roots unite to form the spinal nerves.
The spinal nerves emerge from the vertebral canal in the interval between the neural arches being formed
by the mesenchymal vertebrae.
BRAIN VESICLES
Rostrally, the closed neural tube expands in the form of three brain vesicles:
the prosencephalon, (forebrain) –
the mesencephalon (midbrain)
the rhombencephalon (hindbrain).
Alar plate expands on each side to form the telencephalon (cerebral hemispheres)
Basal plate remains in place as the diencephalon
An optic outgrowth from the diencephalon is the forerunner of the retina and optic nerve.
Embryonic brainstem: the diencephalon, mesencephalon, and rhombencephalon.
The brainstem buckles as development proceeds.
Results in the mesencephalon being carried to the summit of the brain.
The rhombencephalon folds upon itself, causing the alar plates to flare and creating the rhomboid (diamond
shaped) fourth ventricle of the brain.

DEVELOPMENT OF THE SPINAL CORD AND PERIPHERAL NERVES

Enlargement of the intermediate zone of the alar plate creates the dorsal horn of grey matter.
The dorsal horn receives the central processes of dorsal root ganglion cells which are derived from the neural crest.
Partial occlusion of the neural canal by the developing dorsal grey horn gives rise to the dorsal median septum and
to the definitive central canal of the cord.
Enlargement of the intermediate zone of the basal plate creates the ventral grey horn and the ventral median fissure.
Axons emerge from the ventral horn and form the ventral nerve roots.
NEURAL ARCHES
During the 5th week, the mesenchymal vertebrae surrounding the notochord give rise to neural arches to protect the
spinal cord.
Initially bifid (split), later fusing around the midline to form the vertebral spines.
Spina bifida – when the two halves of the neural arches fail to unite.
Spinal nerves develop as the muscle/skin etc develop.
Dermatomes are the strips of skin and muscles supplied by an individual spinal nerve.
Dermatomes are orderly in the embryo, but as the body develops the dermatome is distorted by the continuing growth.
Dermatomes are clinically important, because damage or infection or a spinal nerve or dorsal root ganglion will
produce characteristic loss of sensation in the skin.
EG shingles – a virus infects dorsal root ganglia, causing a painful rash whose distribution corresponds to that of the
affected sensory nerve.

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 SPINAL CORD

Spinal cord in man is bout 45 cm long and weighs about 30 g.

The spinal cord and nerve roots are sheathed by pia mater and float in cerebrospinal fluid contained in the sub-
arachnoid space.
Cord is partially divided by ventral (anterior) sulcus.
Central canal.
Small dorsal (posterior) sulcus.
Spinal cord terminates approximately at the lower end of the second lumbar vertebra.
• During growth of the fetus and young child, the spinal cord does not continue to lengthen as the vertebral
column lengthens, so the cord becomes located progressively more superiorly in the vertebral canal.
• The lumbar and sacral nerves arise from higher up the vertebral canal and then course downward through the
lower canal as a large bundle of nerves until they emerge at the appropriate lumbar or sacral region.
Like the brain, the spinal cord is composed of grey (deep) and white (surface) matter.

White matter:
• Mainly tracts of axonal processes coursing up and down the cord

GREY MATTER
• Contains the nerve cell bodies, along with many short nerve fibres, and can be the site of very extensive
synaptic exchanges.
• Has appearance of multiple horns.
• Arranged in two halves.
• Central region around the central canal.
• Two ventral (anterior) horns project from the central area.
• Location of anterior motor neurons – efferent
• Stops some distance from the perimeter.
• Two dorsal (posterior) horns project from the central area.
• Location of sensory neurons – afferent
• Project almost tot eh perimeter
• Two lateral horns - small projections of grey matter lateral to the central region in some regions of spinal cord.

Proportions of grey and white matter vary in different regions of the cord
Cord overall size varies in different regions
• largest in cervical region (lower half of the neck)
• most white matter in the upper reaches of the cord (sensory and motor pathways serving all four limbs)
• most grey in the lumbar region (lower end of the spinal cord).
Over the dorsal limit of the column is the dorso-lateral sulcus.

DIVISIONS OF THE SPINAL CORD

• Between the dorso-lateral (postero-lateral) sulcus and the small dorso (posterior) sulcus is the dorso-
intermediate sulcus (postero-intermediate sulcus).
• Dorsal (posterior) funiculus – the white matter between the dorsal column and dorso-lateral sulcus.
• Ventral (anterior) funiculus – the white matter between the ventral column and the ventral sulcus.
• Grey commissure – the grey matter between the dorsal and ventral columns.
• Substantia gelatinosa – the tip of the dorsal grey column.
• Dorsolateral tract – between the substantia gelatinosa and the perimeter of the cord.

The dorsal grey column can be divided into:

• Substantia gelatinosa
• Nucleus proprius
• Nucleus tertius (ventral and medial)
• Visceral grey (lateral)
• Intermediomedial
• Intermediolateral

In the thick sections of the spinal cord, the nerve cells exhibit a laminar or layered arrangement.
True lamination is confined to the posterior horn.
10 laminae of Rexed have been defined in the grey matter.

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WHITE MATTER – ASCENDING AND DESCENDING TRACTS
The white matter can also be divided into columns:
• Two dorsal (posterior) white columns lying between dorsal grey horns
• Two lateral white columns lying on each side of the cord lateral to the grey matter
• Two ventral (or anterior) white columns lying between and anterior to the ventral grey horns.
All these contain fibre tracts that run lengthwise along the cord.
• Propriospinal tracts – travel for only a few segments of the cord
• Connect separate cord segments of grey matter with one another to help in performance of cord reflexes
(“segment” is portion of cord that corresponds to a single pair of spinal nerves).
• Remainder of white matter contains:
• Ascending tracts - carry sensory information to the brain
• Descending tracts – carry motor signals from the brain to the cord.

NOTE: Text books usually illustrate ascending and descending tracts on opposite sides of the spinal cord. This is for
ease of illustration only.

ASCENDING (SENSORY) TRACTS

• Fasciculus gracilis and fasciculus cuneatus
• Both medial to the dorsal grey column
• Together make up most of the dorsal white columns
• carrying signals directly from spinal sensory roots all the way to the gracile and cuneate nuclei in the
lower end of the medulla
• Mainly fine, discriminatory touch
• Allows recognition of surface locations of sensory stimuli on the skin or the positions of the different
parts of the body.
• Ventral and dorsal spinocerebellar tracts
• lateral margin of cord
• relay signals from the posterior grey horns upward to the cerebellum
• Spino-olivary tract
• Lateral margin of the cord and ventral to ventral spinocerebellar tract
• from the posterior grey horns of the cord to the inferior olive of the medulla.
• Sensory signals transmitted in spinocerebellar tracts and also in spino-olivary tract
• signals from muscles and joints that appraise the cerebellum at all times about the movements and positions of
different body parts.
• Ventral and lateral spinothalamic tracts
• Carrying signals relayed to posterior grey horn, then through the anterior white commissure and finally upward
through these tracts on the opposite side of the cord to the brain stem and thalamus.
• crude touch, pain, temperature

DESCENDING (MOTOR) TRACTS

• Lateral corticospinal tract
• From the motor cortex of the brain
• Ventral corticospinal tract
• Also from the motor cortex of the brain
• Rubrospinal tract
• From the red nucleus of the mesencephalon
• Reticulospinal tracts
• From the reticular substance of the mesencephalon, pons, and medulla.
• Olivospinal tract
• From the inferior olive of the medulla
• Vestibulospinal tract
• From the vestibular nuclei of the medulla and pons
• Tectospinal tract
• From the tectum of the mesencephalon.
Excitatory tracts –stimulation of most motor tracts causes either increased muscle tone or actual muscle contraction.
Inhibitory tracts – stimulation of some tracts can decrease muscle tone

In the cervical region of the cord, the grey commissure is invaded by white fibres leading to the appearance of the
reticular formation

Five different classes of fibres:

• afferent fibres extending short or long distances in the cord

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• long ascending fibres (from supra-spinal levels)
• long descending fibres (from supra-spinal levels)
• intra-segmental and inter-segmental fibres
• efferent fibres
In addition there are
• decussating fibres (crossing the median plane to unlike structures
• commissural fibres – crossing the median to like structures
These different fibres allow the sensory information to be integrated to allow both simple and complex processing of
stimuli:
• Simple processing of sensation - such as flutter, contact, vibration, and pressure (such sensations can be
explained by activity of primary peripheral afferent fibres)
• Complex processing of sensation – such as tactile recognition of unseen objects and the determination of
direction of movement of cutaneous stimuli.

Peripheral nerves allow the determination of the position of the stimuli and its modality.
Central integrative functions are required to create perceptions and the remainder of our somaesthetic experience.

PERIPHERAL NERVE ORGANISATION

Somatosensory signals travel in fibres in peripheral nerves whose diameters range from the smallest unmyelinated
fibres to the largest and fastest fibres.
These neurons are pseudo-unipolar cells with their cell bodies in the dorsal root ganglion.
The neurons are randomly organised within the nerves.
Each nerve collects signals from a region of skin called a dermatome:
• Dermatomes overlap so that adjacent dermatomes are innervated by more than one spinal nerve.
• Overlap is more extensive for pain and temperature than for discrimination and touch

Damage to a peripheral nerve may produce a limited anaesthetised area.

• Such anaesthetised regions may still have preserved pain sensibilities while very reduced or absent other
modalities (termed intermediate zones).

Pathological conditions:
• Axotomy (transection) of a peripheral nerve
• Causes axonal degeneration to the cell body or degeneration of myelin sheath by Schwann cells
• regeneration may occur at up to 4 mm per day.
• Demyelination (common form of neuropathy; chronic alcoholism, diabetes, toxins)
• Can cause slowing or failure of conduction
• Ischaemias lasting longer than 7 hours
• May lead to permanent impairment.
• Acute distortion may not affect smaller fibres, only the large myelinated ones.

DORSAL ROOT ORGANISATION

Afferent fibres enter the CNS by the dorsal (posterior) root ganglion of the spinal cord.
There is a loose correlation between spinal nerve locations and the dermatomes innervated by them.

Pathological conditions:
• Dorsal root lesions
• Similar effects to damage of peripheral nerves (eg herniation of intravertebral disc)
• Irritation can cause paraesthesia (tingling) or hyperaesthetic regions (heightened sensitivity).

SPINAL CORD ORGANISATION

Afferent neurons enter the dorsal root ganglion and:

• Synapse with secondary neurons within the same segment of the cord
OR
• Ascend or descend a few segments of the cord before synapsing with a secondary neuron
OR
• Enter a major ascending spinal tract

Divergence: a single neuron may influence many other neurons through contact made via a highly branched axon
• The output from a single neuron then spreads onto many neurons.

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Convergence: the opposite, with a single neuron receiving the outputs from a large number of other neurons
• The inputs from many cells converge on one.

Smaller diameter, unmyelinated neurons aggregate into a lateral mass (mainly nociceptive and thermoceptive).
Larger diameter, myelinated neurons aggregate in a medial mass (proprioceptive and discriminative touch).
Small diameter neurons which branch and ascend or descend only 1 or 2 segments in the dorsal funiculus synapse
on secondary neurons in lamina 1 and the outer zone of lamina 2.
Larger neurons also branch with many ascending in the dorsal funiculi to terminate in the nucleus gracilis and
nucleus cuneatus of the medulla.
They may also ascend or descend only a few segments to synapse on secondary neurons in the outer portions of
lamina 2 and in laminae 3 to 5.
Usually afferent fibres entering a single dorsal root synapse over a number of spinal cord segments.
Neurons with receptors with receptive fields on the proximal limbs or the dorsal body surface tend to synapse in
laterally placed grey matter neurons.
This imposes a topographical mapping of the skin surface in a medio-lateral way in the cord axial columns.

ORGANISATION OF SECONDARY SPINAL CORD NEURONS

A spinal cord neuron can be identified by its location, morphology and response to natural stimuli.
While its cell body is restricted to an individual lamina, the dendritic trees can extend over several laminae.
This means neurons can be influenced by many other inputs.

The dendritic trees of Rexed’s laminae are arranged as follows:

Lamina 1 (marginal zone) disk-shaped dendritic trees confined to lamina 1;
Mostly nociceptive Aα and C fibres.
Lamina 2 (substantia gelatinosa) outer stalked cells and inner islet cells; both are mainly restricted to
lamina 2 with some extension to lamina 3; islet cells terminate mainly in L2 while stalk cells terminate in
L1 or project intersegmentally in the dorsal funiculus too the substantia gelatinous of nearby laminae;
Mostly C fibres and so nociceptive and strong mechanical outputs; L2 cells habituate to repeated stimuli.
Lamina 3-6 contain most of the axons of cells which ascend into main ascending somatic sensory pathways;
contain large, complex dendritic arbor which can extend along many laminae and so mixing with other
inputs.
As a generality, moving ventrally from lamina 3 to lamina 6, the neurons change from being biased towards
light mechanical stimuli to responding to several modalities – ie they become multi-modal.
Cells found in the more ventral parts of the dorsal column have more complex receptive fields as a consequence of
their more extensive dendritic trees.
EG. Cells in lamina 4 have simple excitatory receptive fields while those in lamina 5 have both excitatory
and inhibitory sub-regions.

In some cases, for axons which ascend in the dorsal columns and excitatory field may be surrounded by an
inhibitory field. This surround inhibition may sharpen the spatial acuity of the somatic sensations.

Cells in any given region may be excited by one modality and then inhibited by a less noxious light stimulus to the
same site; or intense excitatory stimulus may be inhibited by activating other sites in the body. Such a
response may explain the subjective relief obtained by rubbing an injury.

EXAMPLE: Inhibition of reference response to stimuli applied to DIFFERENT locations.

EXAMPLE: Inhibition of reference response (background response at approx 25 impulses/s) to different stimuli
applied to SAME location.
• Brush depresses the response (lower than original background signal).
• Pressure has initial increase in activation and then returns to a slightly depressed response (lower than
original background signal).
• Pinch and Squeeze both have stronger initial responses and then return to enhanced levels – result of
damage to the area caused by the pinching and squeezing.

INHIBITION AND EXCITATION

Influences from higher centres, mainly the cerebral cortex via the corticospinal tract, can cause inhibition or
excitation of many of the dorsal column neurons.
These are DESCENDING influences.

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 ASCENDING PATHWAYS

The thalamus is an integral part of the relaying of ascending signals from the spinal cord to the somatosensory
regions of the cerebral cortex.
Such communications can occur over a variety of pathways, including the dorsal (posterior) column, spinothalamic,
spinocervicothalamic and spinoreticulothalamic.
The dorsal (posterior) column pathway is the most extensive (by 10 to 100 fold).

DORSAL (POSTERIOR) COLUMN PATHWAY

Carries sensations of highly localised (fine) touch, pressure, vibration and proprioception (position sense).
Pathway begins at a peripheral receptor.
Processes ascending in the dorsal column of the spinal cord terminate in the dorsal column nuclei of the medulla:
the nucleus gracilis and the nucleus cuneatus.
There is one relay neuron between the primary afferent fibre travelling in the dorsal columns and the thalamic
nuclei.
These dorsal columns have reached the peak of their development in primates in which they occupy about 40% of
the total cross section of the sub-mudullary cord.

The axons ascending within the dorsal column are organised according to the region innervated.
• Axons carrying sensations from the inferior half of the body ascend within the fasciculus gracilis and synapse
in the nucleus gracilis of the medulla oblongata.
• Axons carrying sensations from the superior half of the trunk, upper limbs and neck ascend in the fasciculus
cuneatus and synapse in the nucleus cuneatus.

Axons of the second-order neurons of the nucleus gracilis and nucleus cuneatus CROSS OVER to the opposite side
of the brain stem and ascend to the ventral nuclei of the thalamus.
Decussation: the crossing of an axon from the left side to the right (or vice versa).

At the level of the cortex, the sensory modalities are arranged in a simple gross topographical map (much less well
defined than the visual map).
Some of this topographical mapping is evident in the dorsal columns with the more caudal spinal nerves represented
by more lateral positions in the dorsal columns of the lumbar region of the spinal cord.
This dorsal column topography is re-sorted in higher levels of the cord so as to allow a proper somatotopic
organisation.

Two major pathways are involved in somatic sensory perception:

• Dorsal (posterior)-medial lemniscus pathway
• Spinothalamic pathway
They have the following features in common:
• Both comprise 1st-order, 2nd-order and 3rd-order sets of sensory neurons.
• The somas of the 1st-order neurons (primary afferents) occupy posterior root ganglia.
• The somas of 2nd-order neurons occupy CNS grey matter on the SAME side as the 1st-order neurons.
• The 2nd-order neurons cross the midline and then ascend to terminate in the thalamus.
• The 3rd-order neurons project from the thalamus to the somatic sensory cortex.
• Both pathways are somatotopic: an orderly map of body parts can be identified experimentally in the grey
matter at each of the three loci of fibre termination.
• Synaptic transmission from primary to secondary neurons and from secondary to tertiary, can be modulated
(inhibited or enhanced) by other neurons.

DORSAL-MEDIAL LEMNISCUS PATHWAY

In the dorsal column nuclei of the medulla – nucleus gracilis and nucleus cuneatus – the column of influence of
receptive fields can be shown to be less for more caudal parts of the body.
Nucleus gracilis – receives from the hind limb and trunk (cat)
Nucleus cuneatus – receives from forelimb (cat)
The most dorsal cell in these nuclei receives from the most distal sensory receptors.
Ventrally situated neurons receive from more proximally located receptors.
Cluster neurons: there are regions in these nuclei which receive direct dorsal column inputs providing a direct
pathway to the thalamic nuclei via the lemniscus.
• Receive signals from such receptors as the hair receptors in the cat which respond to light touch or the
displacement of only a few hairs

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 • Specially involved in rapidly changing, spatial, tactile stimuli.
• May be a highly suitable way of ensuring that information about spatial pattern so rapidly changing
tactile stimuli are not retarded in any detrimental way.
Extra-cluster neurons are of mixed modality.

The characteristics of the dorsal column transmissions are that it involves the fastest propogating fibres and that it
can handle rapidly changing signals – up to at least 400 Hz in follow mode, up to 700 Hz in detection mode.
Such high frequency signals can only travel in the dorsal column. Use of a tuning fork to test dorsal column function
by neurologists is a reflection of this feature.

SPINOTHALAMIC TRACTS

There is only one relay neuron between the primary afferent fibre and thalamic cells.
Provide conscious sensations of poorly localised (crude) touch, pressure, pain and temperature.
Begins at the peripheral receptors and ends at the primary sensory cortex of the cerebral hemispheres.
Axons of first-order sensory neurons enter the spinal cord and synapse on second-order neurons within the posterior
grey horns.
Axons of these interneurons cross to the opposite side of the spinal cord and ascend within the anterior
or lateral spinothalamic tracts.

Spinocervicothalamic tract :
Originates from the dorsal column nuclei in lamina 4 (cat) and lamina 4 to 5 (monkey).
Axons from these neurons form the spinocervical tract which ascends in the ipsilateral dorsolateral column to the
lateral cervical nucleus in C1 and C2 regions of the spinal cord.
Lateral cervical neurons project axons to the thalamus by first crossing in the anterior commissure, then travelling
to the inferior olivary nucleus then to the pons and then via the medial lemniscus to the thalamus.
Spinothalamic tracts :
Anterior spinothalamic tracts: Carry crude touch and pressure sensations.
Lateral spinothalamic tracts: Carry pain and temperature sensations.
These tracts end in the third-order neurons in the ventral nucleus group of the thalamus.
Ventral posterolateral nucleus (VPL)
Posterior group of nuclei (PO)
Intralaminar nuclei (IM).
After sensations are sorted and processed, they are relayed to the primary sensory cortex.
Spinocerebellar pathway :
Sends proprioceptive information about the position of skeletal muscles, tendons and joints to the cerebellum.
This information does NOT reach our conscious awareness.
First-order neurons synapse on interneurons in the dorsal grey horn.
The axons of the second-order neurons ascend in one of the spinocerebellar tracts.
Axons that enter the R or L posterior spinocerebellar tract DO NOT CROSS OVER – they reach the cerebellar
cortex via the inferior cerebellar peduncle of that side.
Axons that DO CROSS OVER enter the L or R anterior spinocerebellar tract. And reach the cerebellar cortex via
the superior cerebellar peduncle.

LOCALISATION OF SENSATION

Information arriving at the thalamus is sorted by thalamic nuclei according to

• The nature of the stimulus
• The region of the body involved.
Processing by the thalamus determines whether we perceive a given sensation as fine touch, or pressure or
vibration.
Localisation of sensation depends on the projection of information from the thalamus to the primary sensory cortex.
• Sensory information from the toes – arrives at one end of the primary sensory cortex
• Information from the head arrives at the other end.
Electrical stimulation of primary sensory cortex has resulted in functional mapping of the primary sensory cortex.

SENSORY HOMUNCULUS: “little man”.

Proportions are different to that of an individual.
Represents the area of sensory cortex devoted to a particular body region, relative to the number of
sensory receptors the region contains.

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 DETERMINATION OF PAIN

In the dorsal column and the spinothalamic tracts, determination that a stimulus is painful (rather than hot, cold, or
vibrating) is determine by the projection of the sensation to different populations of second-order and
third-order neurons.
Any abnormality along the pathway can lead to inappropriate sensations:
• Phantom limb pain: following amputation, pain may be experienced in the missing limb, caused by activity in
the sensory neurons or interneurons along the spinothalamic pathway. The neurons involved once monitored the
intact limb.
• Referred pain: when pain is felt in an uninjured part of the body, when the pain actually originates at
another locations. Eg heart attack (pain typically in the left arm); appendicitis (generally felt in lower right
quadrant); liver and gallbladder pain felt in right shoulder.

THALAMIC NUCLEI

The thalamus is the largest nuclear mass in the entire nervous system.
The afferent and efferent connections of the 12 main nuclear groups are so diverse that the thalamus cannot be said
to have a unitary function.
Thalamic nuclei can be categorised into 3 functional groups: specific or relay nuclei; association nuclei; non-
specific nuclei.

Specific relay nuclei:

Thalamic nuclei responsible for handling most of the afferent signals.
Reciprocally connected to specific motor or sensory areas of the cerebral cortex.
• Ventral anterior nucleus (VA): projects to prefrontal cortex.
• Ventral lateral nucleus (VL):
 Anterior part projects to supplementary motor area.
 Posterior part projects to motor cortex.
• Ventral posterior nucleus (VP): projects to somatic sensory cortex (SI) and smaller projection to second
somatic sensory area (SII). Somatotopically arranged:
 Ventroposteromedial nucleus (VPM) devoted to face and head.
 Ventroposterolateral nucleus (VPL) devoted to trunk and limbs.
 Modality segregation is a feature of both these nuclei
• Proprioceptive neurons most anterior
• Tactile neurons in mid-region
• Nociceptive neurons at back (posterior nucleus)
• Medial geniculate nucleus: (hearing): projects to primary auditory cortex.
• Lateral geniculate nucleus (vision): projects to primary visual cortex.

Association or non-specific nuclei: other thalamic nuclei containing thalamic interneurons or diffuse projections to
the cortical and sub-cortical structures.

Association nuclei:
Reciprocally connected to the association areas of the cerebral cortex.
• Anterior nucleus: projects to cingulate cortex. Involved in limbic circuit; function related to memory.
• Mediodorsal nucleus: inputs form olfactory and limbic systems; reciprocally connected with prefrontal cortex.
Some functions in relation to cognition, judgement, mood.
• Lateral posterior nucleus and pulvinar: belong to a single nuclear complex. Project to entire visual association
cortex and entire parietal association cortex.

Non-specific nuclei: (not specific to any one sensory modality)

• Intralaminar nuclei: project widely to cerebral cortex.
• Reticular nucleus: all thalamo-cortical projections pass through the reticular nucleus and give collateral
branches to it.

Somatosensory information reaches all of these thalamic nuclei.

Contralateral somatosensory signals provide the sources for the four thalamic terminations.
• Dorsal (posterior)-medial lemniscus pathway: cells terminate in VPL with a few in PO.
• Spinothalamic pathway: cells go to VPL, PO and IM nucleus

Ventral posterolateral nucleus (VPL):

• Core of cutaneous receptors

2008 HET227 18
 • Shell of deep receptors
• Relays discriminative touch, pressure and joi9nt position.
• Small percentage of VPL neurons show surround inhibition where they are inhibited by stimulation of
areas just outside their excitatory receptive fields.

Posterior group of nuclei (PO):

• Large receptive fields
• Multi-modal
• Not somatotopic
• Convergent inputs.

Intralaminar nuclei (IM):

• Mainly convergent inputs (including pain)

DAMAGE TO SOMATOSENSORY CORTEX:

Thalamic centres provide a slight degree of crude tactile sensibility even when the somatosensory cortex is
destroyed.
This suggests that there are perceptions in thalamic or lower centres.
Pain and temperature are not affected.

SOMATOSENSORY CORTEX

Varies in thickness from 2 to 4 mm,

• thinnest in primary sensory areas;
• thickest in motor and association areas.
More than half is hidden from view in the walls of the sulci.
Cortex has both a laminar and a columnar structure.
• Varies in detail from one region to another
• Permits the cortex to be mapped into different histologically different areas.

LAMINAR ORGANISATION - Six layers of cortex:

1. PLEXIFORM LAMINA (molecular) layer:
• contains the most dendritic branches of pyramidal cells, and the most distal branches of axons
projecting from the intralaminar nuclei of the thalamus.
• Signals from lower brain centres, excitability adjustment.
2. EXTERNAL GRANULAR (outer granular) layer:
• Contains small pyramidal and stellate cells
• Signals from lower brain centres, excitability adjustment.
• Signals to other related cortical layers
3. PYRAMIDAL (outer pyramidal) layer
• Contains medium-sized pyramidal cells projecting to other parts of the cortex.
• Signals to other related cortical layers
4. INTERNAL GRANULAR (inner granular) layer
• Contains stellate cells receiving afferents from the thalamic nuclei
• Entry level for most sensory signals
5. GANGLIONIC LAMINA (large, inner pyramidal) layer
• Contains large pyramidal cells projecting to corpus striatum, brainstem, and spinal cord.
• Signals to more distant parts of CNS.
6. MULTIFORM LAMINA (FUSIFORM or polymorphic cell) layer.
• Contains modified pyramidal cells projecting to the thalamus.
• Signals to more distant parts of CNS.

MAIN CELL TYPES within the laminae:

1. PYRAMIDAL CELLS:
• Bodies ranging from 20-30 µm in laminae II and III, more than twice that height in lamina V.
• Apical and basal dendrites branch freely and are studded with spines.
• The axon gives off recurrent branches before leaving the grey matter.
• ALL are excitatory.
2. SPINY STELLATE CELLS:
• Have spiny dendrites
• Are generally excitatory
• Receive most of the afferent input from the thalamus and other areas of the cortex

2008 HET227 19
 • Synapse upon pyramidal cells.
3. SMOOTH STELLATE CELLS:
• Have non-spiny dendrites
• Are generally inhibitory
• Receive recurrent collateral branches from pyramidal cells
• Synapse upon other pyramidal cells.
• Inhibitory GABA-secreting neurons make up 25% of all neurons in the cerebral cortex.
• Some synapse on bases of dendritic spines, some synapse upon somas, some synapse on initial
axonal segments.

COLUMNAR ORGANISATION
Neurons arranged functionally in terms of columns 50-100 µm in diameter, extending radially through the laminae.
Within each column, all of the cells are modality-specific.
• Eg, a given column may respond to movement of a particular joint but not to stimulation of the overlying
skin.
• Somatosensory modalities are conveyed by anatomically different pathways.
• Cells making up these pathways have distinctive response properties.
• Sensory receptors and primary sensory neurons responsive to one sub-modality (such as pressure or
vibration) are connected to clusters of cells in the dorsal column nuclei and thalamus that receive inputs
only for that sub-modality.
• These relay neurons in turn project to modality-specific cells in the cortex.
Columns are also organised by receptive field.
• Receive inputs from the same local area of skin and respond to a single class of receptors.
• Receptive fields of a column share a common centre (although are not precisely congruent).
Columns therefore provide an anatomical structure that preserves the properties of location and modality.

Somatic sensory cortex has 3 major divisions:

1. Primary (S I)
2. Secondary (S II)
3. Posterior parietal cortex.

PRIMARY SOMATOSENSORY AREA (S-I)

In post-cental gyrus
• Lesions in the area cause impairment of contralateral senses.
• Stimulation provides somatosensory experiences.
• Receives projections from ventrobasal thalamus.
• Responds to touch, pressure, pain, proprioceptive modalities, BUT NOT TO ANY OTHERS.
• S-1 neurons make point-to-point connections with caudal portion of VPL.
• Topographical mapping of S1 which is replicated in at least areas 1 and 3b.
Vertical columns respond to some modality-columnar organization.
The S-I in primates has 60% of the cells which respond to somatic stimulation.
Caudal to central sulcus – receptive fields become larger and more neurons are driven by non-cutaneous stimuli.
Contains four cytoarchitectural areas (defined by Brodmann) which differ functionally:
Brodmann’s areas 3a, 3b, 1, and 2.
• Thalamic fibres mostly terminate in 3a and 3b, which project axons to areas 1 and 2.
• Thalamic neurons also send small projections directly to areas 1 and 2.
Topographical organisation:
• All four areas receive input from all areas of the body surface, but one modality dominates in each area.
 Area 1 receives information from receptors it in the skin – rapidly adapting cutaneous receptors (with
receptive fields often covering several adjacent fingers).
 Area 2 receives convergent input from slowly and rapidly adapting cutaneous receptors or from
cutaneous receptors and proprioceptors in the underlying muscles and joints.
 Area 3a also receives proprioceptive information from receptors in muscles and joints, with the
dominant input from proprioceptors signalling muscle stretch.
 Area 3b receives information from receptors it in the skin – primarily from cutaneous
mechanoreceptors.
The four areas are extensively interconnected, with serial and parallel processing involved in higher-order
elaboration of sensory information.
Lesions of S-1: Critical to discrimination of size and form
• Impaired kinaesthesis
• Pain and temperature not affected.

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SECONDARY SOMATOSENSORY AREA (S-II)
At level of Sylvian Fissure under temporal lobe.
Innervated by neurons from each of the four areas of S-I.
• The projections of S-I are required for the function of S-II.
• EG. If neural connections from the hand area of S-I are removed, stimuli applied to the skin do not activate
neurons in S-II.
• Removal of parts of S-II has no effect on the response of neurons in S-I.
Projects to the insular cortex, which in turn innervates regions in the temporal lobe important for tactile memory.
Modality properties of S2 differ to those of S-1.
• Most activated by light mechanical stimulation of the hairs or of the skin surface.
Adapt rapidly to maintained stimuli.
Shows similar columnar organization and spatial distribution of receptive fields.

POSTERIOR PARIETAL CORTEX (BRODMANN’S AREAS 5 AND 7)

Immediately posterior to S-I.
This area receives input from S-I as well as input from the pulvinar and therefore has an associational function.
Projects to motor areas of the frontal lobe, and plays an important part in sensory initiation and guidance of
movement.
Also connected bilaterally through the corpus callosum.
Area 5: Integrates tactile information from mechanoreceptors in the skin with proprioceptive inputs from the
underlying muscles and joints.
• Also integrates information from the two hands.
Area 7: Receives visual information as well as tactile and proprioceptive inputs
• Allows integration if stereognostic and visual information.

PLASTICITY OF SOMATIC SENSORY CORTEX

• [Monkeys] cortical sensory representations of the individual digits of the hand can be defined very exactly
by recording the electrical response of cortical cell columns to tactile stimulation of each digit in turn.
• These digital maps can be altered by peripheral sensory experience:
 The median nerve supplies to ventral surface of the outer 3 digits of the hand, and the
radial nerve supplies the dorsal surface. If the median nerve is crushed, representation of dorsal
surface on digital map increases at the expense of the ventral representation.
 If the middle (3rd) digit is denervated, the corresponding cortical area is unresponsive for
a few hours and then becomes progressively (over weeks) taken over by expansion of the
representations of the 2nd and 4th digits.
• These experiments show that the somatic sensory maps are plastic – being modified by peripheral events.
• Lesion studies (in monkeys) have shown the reorganisation of topographical allocations following
peripheral lesions
• Experimental conditions (cats) have shown the number of cortical columns responding to a particular
thalamocortical input can be increased by local infusion of a GABA antagonist drug which suppresses
lateral inhibition. The effect of removal of a peripheral sensory field is comparable:
 If one set of thalamocortical neurons falls silent due to loss of sensory input, it no longer
exerts lateral inhibition and cortical columns within its territory are taken over by neighbouring
active sets.
 EG: in the human somatosensory body map, the digits are represented next tot eh face. In
several well-documented cases of upper limb amputation, patients had later experiences of
“phantom finger” sensations on touching their face on that side with an implement such as a comb
held in the other hand. This illusion can occur within 2 weeks of amputation [explained on the basis
of unmasking of pre-existing over-lap of thalamocortical neurons.

Cortical signals are transmitted to thalamic, medullary and cord relay centres which can control the sensitivity of the
sensory input.
• These inhibitory signals are termed corticofugal.
• If stimulus intensity becomes too high, the corticofugal signals will decrease the transmission through the
relay centres.
• Such control capacity ensures that the operating range of the somatosensory system is always appropriate
and never too low or too high.

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 POSITION SENSES

Also called proprioceptive senses

• The sense of position and movement of one’s own limbs and body without using vision.
Divided into 2 categories:
• STATIC POSITION – limb position sense
• DYNAMIC or KINAESTHETIC PROPRIOCEPTION – limb movement sense.
Important for controlling limb movements, manipulating objects that differ in shape and mass, maintaining an
upright posture.

Receptors involved in propriuoceptioon:

• Loose connective tissue and fascial receptors
 Fasciae: connective tissue layers supporting and surrounding organs
• Skin receptors.
 Pacinian corpuscles (sensitive to deep pressure) also occur in the superficial and deep
fasciae, in joint capsules – particularly suitable for dynamic proprioception.
• Direct proprioceptors: Types of mechanoreceptors in muscle and joints which signal the stationary
position of the limb and the speed and directions of limb movement:
• Muscle spindle receptors
• Golgi tendon organs
• Receptors located in joint capsules.

DIRECT PROPRIOCEPTORS
Muscle spindle receptors - specialised stretch receptors in muscle; monitor skeletal muscle length and trigger stretch
reflexes.
Golgi tendon organs - receptors in the tendon that sense contractile force or effort exerted by a group of muscle
fibres.
• Similar in function to Ruffini corpuscles (sensitive to pressure and distortion of the skin)
• Located at junction between skeletal muscle and its tendon.
• Dendritic branches repeatedly branch and wind around densely packed collagen fibres of the tendon.
• Stimulated by tension in the tendon; they monitor the external tension developed during muscle
contraction.
Receptors located in joint capsules - sense flexion or extension of the joint.
• Joint capsules are richly innervated by free nerve endings that detect pressure, tension, and movement at
the joint.
• Sense of body position results from the integration of information from these receptors with the
information provided by muscle spindles, Golgi tendon organs and the receptors of the inner ear.
Proprioceptors do not adapt to constant stimulation
• Each receptor continuously sends information to the CNS.
Most proprioception is processed at sub-conscious level:
• A relatively small proportion of the arriving information reaches your conscious awareness over the
posterior column pathway.

SPINOCEREBELLAR PATHWAY to the cerebellum outside our conscious awareness.

Delivers proprioceptive information about the position of skeletal muscles, tendons and joints to the cerebellum.
This information does NOT reach our conscious awareness.

• First-order neurons synapse on interneurons in the dorsal grey horn.

• Second-order neuron axons ascend in one of the spinocerebellar tracts.
 Axons that enter the R or L posterior spinocerebellar tract DO NOT CROSS OVER – they reach the
cerebellar cortex via the inferior cerebellar peduncle of that side.
 Axons that DO CROSS OVER enter the L or R anterior spinocerebellar tract. And reach the
cerebellar cortex via the superior cerebellar peduncle.
Proprioceptive information from each part of the body is relayed to a specific position of the cerebellar cortex.

PROPRIOCEPTIVE PATHWAYS
Dorsal column-lemniscus system
The dorsal column-lemniscus system is the principal pathway for perception of touch and proprioception.
• Large-diameter axons with fast conduction velocities to the dorsal horn of the spinal cord then to the brain
stem and thalamus.
The proprioception and tactile axons in this column are segregated anatomically.

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 • Proprioception axons – more ventrally in the dorsal column than those of tactile receptors, which are
located dorsally.
• Proprioceptors terminate more rostrally in the gracile and cuneate nucleus.
• Proprioceptive afferents terminate in the Lamina VII, on interneurons in laminae V and VI and on motor
neurons in lamina IX.

Thalamic processing of proprioception

Thalamic neurons responses occur selectively at either one or two extents of joint rotation:
• Maximum –when joint is at full rotation
• Maximum when joint at minimum rotation.
• This contrasts with the actual joint receptors which are maximally stimulated at specific degrees of rotation
of the joint.
• Ventral posterior nucleus (VP): projects to somatic sensory cortex (SI) and smaller projection to second
somatic sensory area (SII). Somatotopically arranged:
 Ventroposteromedial nucleus (VPM) devoted to face and head.
 Ventroposterolateral nucleus (VPL) devoted to trunk and limbs.
 Modality segregation is a feature of both these nuclei
• Proprioceptive neurons most anterior
• Tactile neurons in mid-region
• Nociceptive neurons at back (posterior nucleus)

CLINICAL CONSIDERATIONS

Loss of sensory function is one of our most sever of disabilities.

Removal of sensory input (sensory deprivation) can have severe effects on normal behaviour.
Loss of sensory function is generically termed “agnosia”
Specific loss or number of sensory modalities is given a combining form so that we have terms such as
astereognosia – loss of sense of one’s body.

Loss of any sensory modality is not always easy to definitively prove:

• A subject may not be aware of the loss, they may never experience the sensation and so are not then
aware of its absence.
• A subject may have subconscious reception but have not conscious awareness – ie, they may not know
they can sense something.

This situation arises through the site of a lesion or dysfunction, if it is at the primary receptor or affects the pathways
to the CNS it is usually clear that a problem is present.
If the damage is in one of the target areas of the CNS for the information, then only one level of the sense may be
destroyed, including perceptual aspects.
Any loss of somatosensory function is suggestive of damage to the post central gyral regions of the cortex
(Brodmann’s areas 3a, 3b, 1 and 2) and also the adjacent cortex (areas 5, 7 and S2).
Lesions of the somatosensory system results in a variety of deficiencies:
• Reduced capacity or loss of tactile localisation
• Reduced capacity or loss of tactile discrimination
• Reduced capacity or loss of tactile recognition of objects
• Reduced capacity or loss of limb position sense

SOMATOSENSORY LESIONS
In 1920, Henry Head proposed that lesions of the somatosensory cortex cause three mainly independent effects:

1. Increased somatosensory thresholds for tactile, thermal, painful stimuli

• poor detection
• poor two-point discrimination
• poor sense of limb position
• clumsy hand/finger movements
2. Impaired tactile appreciation of object qualities – impaired touch recognition
e.g. impaired object identification or recognition by touch
Astereognosis – inability to match or identify shapes by touch.
3. Impaired perception of limb position in space – ie, impaired spatial recognition
e.g. impaired limb placement (reaching)
• loss of knowledge of own body (illness, pain, body parts)

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These categories are still in use today.
Many studies on the changes to somatosensory processing have been undertaken on subjects with cortical head
wounds or who had surgery to reduce epilepsy.

Damage to the post-gyrus region

Any damage to the post-central gyrus region has been seen to result in abnormally high sensory thresholds and
impaired stereognosis.

Examples of patient somatosensory changes:

• difficulty in detecting light touch to the skin
• poor two-point discrimination
• difficulty locating point touch on skin contralateral to side where lesion was present.
• If blindfolded – difficulty in knowing if the contralateral hand was passively moved.
Another symptom of lesions has been called
• A symptom of lesions in post-gyrus region efferent paresis
 Patients have clumsy movements of the fingers as a result of loss of positional feedback.
This consequence occurs whether the lesion is in the right or left hemisphere.
• If the lesion is in the region of the face representation area in the somatosensory cortex
 a symptom termed motor aphasia occurs in which the patient has difficulty in
controlling the lips and tongue to pronounce desired sounds.
 These symptoms do not occur if the lesion is in the right hemisphere.
• Even though the thresholds for somatosensory perceptions may be normal, this does not preclude disorders
of the somatosensory system.

Normally we process several stimuli simultaneously.

We distinguish between them and process accordingly.

Damage to the secondary somatosensory region

Simultaneous extinction: Another somatoperceptual disorder
• Failure to distinguish between simultaneous stimuli
• One or more of the simultaneous stimuli are not appreciated and therefore are extinguished.
• Commonly produced by damage to the secondary somatosensory cortex, particularly in the right parietal lobe
Damage to the posterior parietal region (including secondary somatosensory areas 5 and 7)
• Often results in patients unable to accurately position their limbs.
• Specially pronounced if the use of visual feedback clues is prevented.
• Impaired kinaesthesia or disruption of the coordination between tactile sensory and visual information
processing in the cortex.

SOMATOSENSORY AGNOSIAS
• Astereognosis: Loss of tactile appreciation of objects.
• Asomatognosia: Loss of knowledge about one’s own body
Astereognosis:
• Rarely demonstrated by itself in the absence of other somatosensory disorders.
• Other spatial deficiencies are not uncommon.
• Associated with damage to more posterior portions of the somatosensory cortex.
• Primary Agnosias:
 Result in loss of the ability to recognise the tactile qualities of an object
 Because the tactile image is incomplete or absent.
• Secondary Agnosias or asymbolia
 Occur when the tactile image is preserved but is disconnected from other sensory
representations
 The subject is confused about the full significance of the object.
Asomatognosis:
• Most distressing condition.
• Unaware of illness or problems caused by neglect of their body.
• Several variations of the condition:
 Anosognosia: lack of awareness of illness
 Anososiaphoria: indifference to illness
 Autopagnosia: inability to locate or name body parts
 Asymbolia for pain: absence of normal response to pain.
• May affect both sides or only one side.

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SENSORY ILLUSIONS AND HALLUCINATIONS
Sensory illusions
 More likely to involve the visual sense than tactile sense
 Phantom touches and tickles are experienced in normal and abnormal patients.

Sensory hallucinations
 Can be considered to occur when the cortex is stimulated BUT the receptors are not
 In normal conditions the frontal cortical lobes control this discrepancy.
 Absence of frontal lobe control can produce a pathological state
 Visual hallucinations more common than tactile.
 Normal processing of sensory hallucinations is thought to be the result of the cortex resolving the
ambiguity between cortical responses and absence of any receptor signal.
 Schizophrenics or people under the influence of psychogenic drugs may fail to resolve the ambiguity and
so experience the sensations as if they were actually occurring.

STIMULUS INTENSITY

Sensory quality depends on which nerve is actuated and where in the brain it leads.
But can the brain distinguish between sensory quantity or magnitude of the sensation (stimulus intensity) as well as
quality?
• Laws have been devised in an attempt to define the perception of stimulus intensity.

THE WEBER-FESCHNER PRINCIPLE:

An approximate psychological law relating the degree of response or sensation of a sense organ and the intensity of
the stimulus.
The law asserts that equal increments of sensation are associated with equal increments of the logarithm of the
stimulus, or that the just noticeable difference in any sensation results from a change in the stimulus which bears a
constant ratio to the value of the stimulus.
The just-noticeable difference is the smallest difference perceivable between two similar stimuli

FOR EXAMPLE:
• In the bright midday sun you light a candle. Does anyone notice it getting brighter?
• Will you identify my voice if I call you on your mobile phone at a concert?
• You're carrying the downside of a refrigerator up a flight of stairs and someone puts a hammer on the
fridge, do you sense the difference?
Mostly, the Fechner Weber Principle or Law holds that you won't notice a difference.

WEBER’s LAW
Background: Ernst Heinrich Weber (1795-1878) was the German anatomist and physiologist who first
introduced the concept of the just-noticeable difference. Weber was a professor at the University of Leipzig from
1818 until 1871. He is known chiefly for his work on sensory response to weight, temperature, and pressure.
Weber determined that there was a threshold of sensation that must be passed before an increase in the intensity of
any stimulus could be detected; the amount of increase necessary to create sensation was the just-noticeable
difference.
He further observed that the difference was a ratio of the total intensity of sensation, rather than an absolute figure;
thus, a greater weight must be added to a 100-pound load than to a 10-pound load for a man carrying the load to
notice the change. Similar observations were made on other senses, including sight and hearing. Weber also
described a terminal threshold for all senses, the maximum stimulus beyond which no further sensation could be
registered.

• Weber’s Law found that the just noticeable difference or difference threshold is a constant ratio of the
standard stimulus:
k = ΔI / I
ΔI (delta I) represents the difference threshold, I represents the initial stimulus intensity, and k signifies the
proportion on the right side of the equation remains constant despite variations in the intensity (I).

That is: the ratio of the increment threshold to the background intensity is a constant.
Weber's Law predicts a linear relationship between the increment threshold and the background intensity.
Here is a plot of some hypothetical data showing Weber's Law. The slope of the line is the Weber fraction.
A TVI plot
Threshold Versus Intensity

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 sometimes called a TVR plot for thresholds
for detecting light (threshold versus radiance).

FECHNER’S LAW or the WEBER-FECHNER LAW

Gustav Theodor Fechner (1801-1887) was a German physicist and philosopher and a key figure in the founding of
psychophysics. At the age of 16 he enrolled in medicine at the University of Leipzig where he studied anatomy
under Weber.

Fechner developed Weber’s theory into the Weber-Fechner law that to increase the intensity of a sensation in
arithmetical progression, it is necessary to increase the intensity of the stimulus in geometric progression

The Weber-Fechner Principle states that the gradations of stimulus strength are discriminated approximately in
proportions to the logarithm of stimulus strength.
• This means that the ratio of the change in stimulus strength for a detectable change is always about 1:30.
ϕ = k*log(φ)
Perceive signal strength = Constant * Log (STIMULUS)
• This is only true for higher level visual, auditory and cutaneous stimuli.
• Also does not hold for weak and very strong stimulus intensities.

Assumptions made:
• JND provides the basic unit of perceived magnitude
• One JND is perceptually equal to another JND

Fechner's Law holds across a wide range of situations, but there are some exceptions:
• Within limits perceived length changes precisely with actual length; and experienced pain grows more
rapidly than the pain stimulus.
• The decibel scale (logarithmic unit) marked off in equal ratios of intensity do not mark off equal steps in
perceived loudness.
• The growth of apparent loudness departed widely from the predicted logarithmic function:
• A tone of 100 decibels sounds about 40 times louder than 50 decibels.
This highlighted some of the problems associated with Fechner’s law:
• The intervals between JNDs are unequal
• Weber's law breaks down at the extremes

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Steven’s Power law was first proposed in 1957 to relate sensation magnitude to stimulus intensity, addressing
problems associated with the Fechner and Weber laws:

The Weber-Fechner concept was complemented and modified by Stevens. While maintaining a relationship between
JNDs and sensory metrics, Stevens replaced the logarithmic Weber-Fechner law by a power-law.

Steven’s Power Law states that the perceived stimulus intensity varies with the logarithm of the stimulus strength.
This law has demonstrated a better fit to the experimental data for a number of sensory channels
P = k Sn
where P is the perceived magnitude, S is the physical stimulus intensity and n is a modality-dependent exponent.

Testing of these laws has demonstrated that the brain CAN distinguish between sensory quantity or magnitude of the
sensation (stimulus intensity) as well as quality
BUT they have also served to demonstrate that in addition to different topography for sensory qualities, there are
also differences in the somatosensory system for the sensory quantitative assessment.

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