Functional Organization of Nervous Tissue

The Nervous System

Components
Brain, spinal receptors cord, nerves, sensory

Responsible for
Sensory perceptions, mental activities, stimulating muscle movements, secretions of many glands

Subdivisions
Central nervous system (CNS) Peripheral nervous system (PNS)

Central Nervous System

Consists of
Brain
Located in vault of skull cranial

Spinal cord
Located in vertebral canal

Brain cord

and

spinal

Continuous with each other at foramen magnum

Peripheral Nervous System

Two subcategories
Sensory or afferent Motor or efferent
Divisions Somatic nervous system Autonomic nervous system (ANS) Sympathetic Parasympatheti c Enteric

Spinal Nerves
Connected to the spinal cord via roots (bundles of axons) Posterior root = sensory axons Anterior root = motor axons posterior roots expand as the dorsal root ganglion - cell bodies of sensory neurons Emerge from intervertebral foramina as mixed nerves

Cells of Nervous System

Neurons cells or nerve

Receive stimuli and transmit action potentials Organization

Cell body or soma Dendrites: Input Axons: Output

Neuroglia cells

or

glial

Support and protect neurons

Types of Neurons

Functional classification
Sensory or afferent: Action potentials toward CNS Motor or efferent: Action potentials away from CNS Interneurons or association neurons: Within CNS from one neuron to another

Structural classification
Multipolar, bipolar, unipolar

Neuroglia of CNS

Astrocytes
Regulate extracellular brain fluid composition Promote tight junctions to form blood-brain barrier

Ependymal Cells
Line brain ventricles and spinal cord central canal Help form choroid plexuses that secrete CSF

Neuroglia of CNS

Microglia
Specialized macrophages

Oligodendrocytes
Form myelin sheaths if surround axon

Neuroglia of PNS

Schwann cells or neurolemmocytes

Wrap around portion of only one axon to form myelin sheath

Satellite cells
Surround neuron cell bodies in ganglia, provide support and nutrients

Myelinated and Unmyelinated Axons

Myelinated axons
Myelin protects and insulates axons from one another Not continuous
Nodes of Ranvier

Unmyelinated axons

Reflex arc Neural wiring of reflex Requires 5 functional components: 1. sensory receptor, 2. sensory neuron, 3. integrating center (SC or BS), 4. motor neuron, & 5. effector

Electrical Signals
Cells produce electrical signals called action potentials Transfer of information from one part of body to another Electrical properties result from ionic concentration differences across plasma membrane and permeability of membrane

C. N. S Metabolism 1. High blood flow (15 % OF COP ) and the O2 consump on (20 % of total O2 cons. ) of the C. N. S & grey matter > white matter. 2. Glucose is the only fuel that can pass through blood brain barrier (BBB). 3. Glutamic acid is the only amino acids that can be metabolized by the brain.

The major functional levels in C.N.S. 1. The spinal cord level:

Best studied in "Spinal animal" which is an animal with complete transection in the spinal cord immediately below the level of origin of the phrenic nerve C5 (to avoid death). Functions that are still present below the transection, as stepping reflexes, withdrawal reflex, body support reflexes and visceral reflexes.

2. The lower brain level: a) Decerebrate animal : lesion is done between the superior and the inferior colliculi of the mid brain. The animal is characterized by decerebrate rigidity (stiffness of antigravity muscles) and inability to keep his equilibrium.

b)

Mid

brain

animal

lesion is done above superior colliculi. The animal shows Normal muscle tone. can stand on his four limbs. can correct it's standing posture if disturbed. No sham rage (anger) reaction. Not feed itself. No regulation of body temperature.

The higher brain level:

Studied in "decorticate" or "thalamic" animal in which the cerebral cortex is removed. The animal shows: Normal muscle tone. Sham rage (anger) reaction. Feed itself. Regulation of body temperature. Motor disturbance and decorticate rigidity. lose of fine sensations and educated motor functions.

Sham rage reaction

very angry due to Minor stimuli (exhibits sympathetic manifestation e.g. mydriasis and acceleration of heart rate + somatic manifestation e.g. biting, clawing) . Due to release of the hypothalamus (the centers of emotions) from the inhibitory impulses from the cerebral cortex as a result of: A) Removal of neocortex. B) Stimulation of amygdaloid nucleus . C) Lesion of venteromedial n. of hypothalamus (placidity center)

In man decortications can occur in bilateral lesion of the internal capsule.

Introduction
Human life would be very different without the ability to sense and perceive external stimuli Imagine your world without the ability to see, hear, smell, touch, and feel

The next 5 weeks

Step 1: sample information 2: get it to the brain Process Sensory transduction Lecture 1 (today)

Sensory pathways and 2, 3 networks

3: Some disturbances

sensory Famous CNS lesions

4: Transmission in CNS

Synapses

Key Points
Receptor potential

Phasic and tonic receptors

Coding of sensory receptors

Sensory Information
Detection of changes in environment
external or internal

4 main functions
perception control of movement regulation of body function

Sensory Receptors: are specialized structures present in the peripheral terminations of afferent neurons , for receiving all types of sensations and inform the C.N.S. about any change in the external or internal environment . They convert various forms of energy in the environment into action potentials in the sensory nerves

Sensory Pathway
Stimulus
Sensory receptor (= transducer) Afferent sensory neurons CNS Integration, perception

Classification of Receptors
Modality
Mechanoreceptrs,Chmoreceptors,Thermoreceptors, photoreceptors, nociceptors

Site
Exteroceptors Interoceptors

Adaptation: Phasic receptors

Moderately adapting receptors Tonic or very slowly adapting receptors

Sensory Receptors
1. Mechanoreceptors i.e. stimulated by mechanical stimulation e.g. touch, equilibrium, auditory and all proprioceptors, which are found in muscles, ligaments and joints. 2.Chemoreceptors i.e stimulated by chemical stimulation e.g. taste, olfactory, O2 lack, CO2 excess receptors and osmoreceptors. 3.Electromagnetic i.e. stimulated by light they are found only in the retina. 4. Thermoreceptors i.e stimulated by temperature they are found in the skin and in the hypothalamus. 5.Nociceptors i.e stimulated by tissue damage, e.g free nerve endings, they are the receptors for pain sensation.

EXTEROCEPTORS CUTANEOUS RECEPTORS SPECIAL SENSES RECEPTORS

PAIN
Nociceptors Touch Mechanoceptors Temperature Thermoreceptors Pressure Mechanoreceptors

Taste receptors Teleceptors

Vision
Hearing

Smell

Pain receptors Touch receptors

Free nerve ending

Basket ending Hair Meissners corpuscles light touch

Merkels disc light touch

Temperature receptors

Krauses end bulb Cold Ruffinis corpuscles Hot Free nerve ending

Pressure receptors

Pacinian corpuscles deep touch& pressure

Interoceptors
Proprioceptors
Kinesthetic sensation Viscerorecptors

Hypothalamic

Golgi tendon organ

Joint receptors Pacinian C

Muscle spindle

Interoceptors
Proprioceptors
Viscerorecptors

Hypothalamic

Osmoreceptors

Baroreceptors
Chemoreceptors

Chemoreceptors Glucoreceptors

Stretch receptors

Organic sensation receptors

Hunger , thirst, vomiting, defecation, ect.

PROPERTIES OF RECEPTORS

EXCITABILITY

MODALITY OF SENSATION (MULLER'S LAW OF SPECIFIC NERVE ENERGIES)

CODING OF SENSORY INFORMATION Compression function of the receptors

Adaptation

1- Excitability: Response of a receptor to an adequate stimulus by producing a non-propagated potential = receptor potential. If magnitude is sufficient AP will propagate along the sensory nerve.

How a receptor be stimulated? 1. Mechanical deformation open ion channels 2. Application of a chemical to the receptor membrane open ion channels 3. Change of temperature change permeability 4. Effect of electromagnetic radiation (+) G protein

Receptor/Generator Potential

Receptor potentials: Changes in the transmembrane

potential of a receptor caused by the stimulus.

Generator Potential: A receptor potential that is strong

enough (reaches threshold) to generate an action potential.

Remember that APs are all-or-none. The stronger the

sitmulus (above threshold) the more APs are fired over a given time period; this is translated by the CNS as a strong sensation.

RECEPTOR POTENTIAL & ACTION POTENTIAL

Properties of the receptor potential

1- It does not obey the all or none law, so it can be graded. 2- It is not followed by an absolute refractory period and its duration is long (about 5 ms), so it can be summated 3- It is not blocked by local anesthetic drugs 4- It results in a propagated action potential on reaching the threshold level

Source of generator potential:

The generator potential is produced in the unmyelinated nerve terminal of the receptor When pressure stimulus is applied the terminal fibers of the corpuscle will be deformed opening of Na+ channels Na+ influx (to the interior of the fiber) creates high positivity inside the fiber receptor potential then the generator potential depolarizes the sensory nerve at the 1st node of Ranvier. Once the firing level is reached, action potential is produced.

Once the firing level is reached, action potential is produced:

The node converts the graded response of the receptor into action potentials The frequency of AP is proportionate to the intensity (magnitude) of the applied stimuli In other way: the more the receptor potential rises above threshold level, the greater becomes the action potential frequency

Receptor Potential

&

action Potential

2. Adequate Stimulus of Sensory Receptors

(Modality)
Each type of receptor is highly sensitive to one type of stimulus for which it is designed and yet is almost nonresponsive to normal intensities of other type of stimuli. The stimulus to which a given receptor has the lowest threshold is termed the adequate stimulus of the sensory receptor. For instance, the roes and cones are highly responsive to light but almost completely nonresponsive to heat and cold.

3.Adaptation (desensitization)
When a maintained stimulus of constant strength is applied to a receptor, the frequency of the action potentials in its sensory nerve declines over time. 1. Phasic receptors : which adapt rapidly e.g touch & pressure receptors. 2. Moderately adapting receptors i.e temperature (between 20c- 40 C) smell and taste receptors, no adaptation for temperature below 10c or above 45c. 3.Tonic or very slowly adapting receptors ; vision, hearing ,pain receptors, baro- and chemoreceptors in the carotid sinus and in the aortic bodies.

Adaptation = persistent stimulus gives

no response

Adaptation
Adaptation in a sensory receptor is related to a decline in the generator potential with time. A, The generator potential is maintained without decline, and the action potential frequency remains constant. B, A slow decline in the generator potential is associated with slow adaptation. C, In a rapidly adapting receptor, the generator potential declines rapidly.

Mechanisms of Adaptation of a Receptor :

A- Readjustments

in The Receptor Structure

- Adaptation of The Pacinian Corpuscle

- Accommodation of the Central Core Nerve Fibre (Membrane Adaptation ):

A process of accommodation occurs in the nerve fibre on contineous stimulation as a result of redistribution of ions across the nerve fibre membrane . This component of adaptation appears to be an electrical property of the membrane itself. It might be due to slow changes in PK (potassium permeability) , similar to the voltagedependent increase in PK that produces accommodation but is some hundred times longer.

Differences between adaptation and fatigue

Cause Onset O2 Lack Mechanism Site
In sensory receptors. continuous constant stimulation rapid no effect Explained before

in the skeletal muscles previous prolonged exercise. slow occurs more rapidly. lactic acid

4.Coding of sensory information

MODALITY

LOCALITY INTENSITY

QUALITY OF SENSATION

Sensations of the same modality may differ in quality e.g. heat sensation (modality) differs in quality from warm to cold

INTENSITY DISCRIMINATION (WEBER-FECHNER LAW)

The magnitude of sensation felt is proportional to the logarithm of intensity of the stimulus. "

Coding of sensory information (cont.)

The doctrine of specific nerve energies

The sensation evoked by impulses generated in a receptor depends in part upon the specific part of the brain they ultimately activate. The specific sensory pathways are discrete from sense organ to cortex. Therefore, when the nerve pathways from a particular sense organ are stimulated, the sensation evoked is that for which the receptor is specialized no matter how or where along the pathway the activity is initiated. (Mullers Law)

Coding of sensory information (cont.)

The law of projection

No matter where a particular sensory pathway is stimulated along its course to the cortex, the conscious sensation produced is referred to the location of the receptor.

Coding of sensory information (cont.)

Intensity Discrimination
The magnitude of the sensation felt (represented by number of nerve impulses) is proportionate to the log of the intensity of the stimulus (Weber-Fechner law).

Stretch Receptors:
Weak stretch
causes low impulse frequency on neuron leaving receptor.

Frequency Code

Strong stretch causes high impulse frequency on neuron leaving Membrane receptor.
potential
Time

Compression in sensory process

By a variety of means, a wide range of input intensities is coded into a much narrower range of responses that can be represented by variations in action potential frequency.

 Sensory unit: single sensory axon and its peripheral branches. Receptive field of a sensory unit: is the area from which a stimulus produces a response in that unite. Recruitment of sensory units: increases the strength of a stimulus leading to spread over a large area and recruit the surrounding receptors .

Summary
The external & internal environments are monitored by sensory receptors. Each type of receptor is excited most effectively by only one modality of stimulus known as the adequate stimulus. The stimulus is converted into an electrical potential. The intensity & duration of the stimulus is frequency coded as bursts of action potentials in the primary afferent nerve.

Sensation

Somatic
Cutaneous

Visceral

Organic

Proprioceptive

Carried by Autonomic afferent nerves

Carried by Somatic afferent nerves

Thirst, Hunger

Somatic Sensations

Cutaneous Exteroceptive

Deep Proprioceptive

Combined

Pain

Pressure

Vibration sense Stereognosis

Touch

Sense of position & movement

Temperature

Sense of muscle stretch

Pain Sensation
Pain receptors are the free nerve endings. They are slowly adaptable, needs higher threshold , widely distributed. Pain is a specific sensation

Receptors :

Types of Pain
Cutaneous - skin . Deep muscle and joint

.
referred pain.

Visceral viscera .

Fast&slow pain
pricking Immediately(fast) & last for short time. Well localized & starts protective reflexes Afferent is fast myelinated A delta fibers. Carried by neospinothalamic tract. Relay in thalamus then to sensory cortex. Slow burning Delayed (slow) & last for long time. Not well localized (diffuse). Afferent is unmyelinated C fibers. Carried by paleospinothalamic tract. Relay in thalamus and reticular formation (90%), all areas of the cortex(10%).

deep pain.
It originates from any tissue deep to the skin as
muscles , ligaments , synovial membrane and periosteum sensory motor nerve

Pathway : as cutaneous pain but it is carried by the

( C fibres ) .

It is a dull aching pain , not localised , and shows the phenomenon of referred pain
Reactions to deep pain :

Characteristics :

cutaneous hyperalgesia - Autonomic changes e.g. bradycardia , hypotension , vomiting i.e. parasympathetic effects pain - Somatic reflexes : reflex contraction of the muscle in response to deep pain.

Visceral pain.
Characteristics of Visceral Pain
It is not localised because pain receptors are few in the viscera and widely distributed. The sensory cortex is not conscious about the existence of the viscera , so any painful stimuli will be referred to the skin area supplied with the same dorsal root. There is muscle rigidity over the painful viscera accompanied with parasympathetic changes as bradycardia , hypotension , nausea and vomiting

Causes of Intestinal Pain

- Spastic contraction . Over distension
- Thrombosis of mesenteric blood vessels ischaemia

Pathway of Visceral Pain : as cutaneous pain but the afferent peripheral nerves are : .- Parasympathetic afferent from respiratory , digestive systems and pelvic organs Sympathetic from thoracic viscera (heart) and abdominal viscera (stomach and small intestine) . Somatic nerves e.g. phrenic nerve , carry pain sensation from the pericardium, pleura, biliary tract and peritoneum

Referred pain.
It is pain which is felt in some place other than that in which it originates
Cardiac Pain
referred to the inner side of the left arm and little finger , and root of neck or epigastrum referred to the loin radiating to the scrotum and inner side of the thigh

Ureteric Pain

Acute Appendicitis
Inflamed Gall Bladder

referred to skin of umbilicus referred to the tip of the right. shoulder

Mechanism of Referred Pain (A) Branching of Dorsal Root . (B) Convergence Projection Theory

Reactions to Pain

1- Autonomic Changes 2- Emotional changes 3- Somatic ReFlexes 4- CUTANEOUS HYPERALGESIA

1- Primary

B- Secondary Hyperalgesia

Hyperalgesia

primary hyperalgesia

the convergence facilitation theory of secondary

hyperalgesia

Pathway of Pain

Fast pain fibres (A d type) terminate on Lamina Marginalis neurons (2nd Order Neuron) of the posterior horn . The long axons of the 2nd O.N.(lamina marginalis neurons) then cross to the opposite side to ascend as the Lateral Spino.Thalamic Tract to the thalamus. The A d fibres secrete glutamate , it has a very short period of action lasting only few milliseconds

Slow pain fibres (C type) terminate on the Substantia Gelatinosa cells (the posterior horn cells present in Lamina II and III ) . The long axons of the neurons cross to the opposite side to ascend as the L.S.Th.T.

The C fibres secrete substance P more slowly and lasts for long period

Transmission of fast and slow pain into and through the spinal cord

Pain pathway
Primary somesthetic cortex Somesthetic association area

Thalamus

Third-order nerve fibers

Hypothalamus and limbic system

Reticular formation Second-order nerve fibers Spinothalamic tract

First-order nerve fiber Spinal cord Anterolateral system

Nociceptor

16-83

Pain control System

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Hypothalamus 1 Cerebral cortex 4 Midbrain 3 Third-order neuron relays signal to somesthetic cortex. 3 Thalamus 5 Midbrain relays signal to reticular formation of medulla oblongata. Reticulospinal tract Spinothalamic tract 6 Some descending analgesic fibers from medulla secrete serotonin onto inhibitory spinal interneurons. 7 Spinal interneurons secrete enkephalins, blocking pain transmission by means of postsynaptic inhibition of second-order pain neuron. 8 Other descending analgesic fibers synapse on first-order pain fiber, blocking pain transmission by means of presynaptic inhibition. 4 Input from hypothalamus and cerebral cortex converges on central gray matter of midbrain. Nociceptor releases substance P onto spinal interneuron.

2 Second-order neuron transmits signal up spinothalamic tract to thalamus.

5
Medulla oblongata

6
Dorsal horn of spinal cord 2 7 Neurotransmitters + 1 Nociceptor Substance P Serotonin Enkephalins

8 -

Figure 16-84 16.5

ENKEPHALINS.AND ENDORPHINS Types

Two types of enkephalins are known; metenkephalin and leu-enkephalin . Also, several types of endorphins have been isolated, however , the most potent is B-endorphin

Function
They act as excitatory transmitter substances that activate the analgesic system (the pain inhibiting system in the brain and spinal cord).

Temperature Sensation
Cold receptors (Krause's end bulb) ; stimulated by temperature between 10 and 30 C Warm receptors (Ruffini's corpuscles) ; stimulated by temperature between 25 and 45 C The temperature receptors are stimulated by the temperature of the tissues in contact with it . It is not stimulated by the atmospheric temperature

Phenomenon of Paradoxical Cold Sensation

Hot bath of 45-50C produces a temporary sensation of cold at first because the cold receptors are more in number , superficial and they are stimulated either at temperature between 10 to 35 or at 45-50 C

Pathway of Temperature
sensation

Touch (Tactile) sensation

Receptors
Free nerve endings Basket endings of hair Meissner's corpuscles Merkel's discs

as in cornea .
for hair movements

in papillae of skin , more in tips of fingers in tip of fingers in subcutaneous tissue for deep touch ( pressure touch)

Pacinian corpuscles

Mechanoreceptors: Sensory transduction

Four Types of Mechanoreceptors

Types of Touch Sensation

Crude (rough) touch
Receptors
Light touch Deep touch ( pressure touch)

Light touch Hair basket endings - Meissner's and Merkel's discs , stimulated by light contact of skin , adapt very quickly

Deep touch pacinian corpuscles in subcutaneous tissue , they are stimulated by moderate stimulus

Fine touch

Tactile localization (Topognosis). Tactile discrimination (two point discrimination).

PATHWAY OF CRUDE TOUCH (LIGHT & DEEP)

TACTILE LOCALIZATION
It is the ability of the subject to recognize the touched point on the skin with his eyes closed . It is an acquired property needs experience and training.

TACTILE DISCRIMINATION (TWO POINTS DISC.)

It is the ability to identify two points in the skin stimulated at the same time as two separate points of touch, with the eyes closed , provided that the two points must exceed a certain minimal distance (3 mm in finger tip, 70 mm in back of neck). Tactile localization and discrimination exist for other cutaneous sensation as temperature , pain , and even vision.

Explanation & pathway of TACTILE DISCRIMINATION

PROPRIOCEPTIVE ( DEEP) SENSATIONS

Sense of position & movement Sense of muscle stretch

Deep Pressure

Receptors
in joint capsules and ligaments . They are stimulated when the joint is suddenly moved . They adapt slightly at first but then transmit a steady signal. - Golgi tendon organ receptor : It is found particularly in the ligaments about the joints Pacinian corpuscles : found in the tissues around the joints . They help to detect the rate of rotation at the joints

- Slowly adapting receptors Spray-type endings : Found

- Rapidly adapting receptors -

-Muscle spindle.

Stimulated by muscle stretch

Detect changes in muscle tension

Pathway of conscious proprioceptive sensation'

Pathway of Unconscious proprioceptive sensation'

COMBINED CUTANEOUS AND DEEP SENSATIONS

VIBRATION SENSE
pacinian corpuscles (up to 500)in skin and deep tissues

Receptors : Meissner,s corpuscles (up to 80)&

Pathway : Carried by Gracile and Cuneate tracts because

it needs a thick rapid conducting fibres to carry the rapid successive separated waves of vibration

STEREOGNOSIS
(Meissner,s, Merkel,s, pacinian, spray type)

Receptors :Cutaneous and deep receptors

area 5 and 7 in cerebral cortex . In pernicious anaemia degeneration of the Gracile and Cuneate tracts occurs leading to Astereognosis ( loss of stereognosis).

Pathway : Carried by Gracile and Cuneate tracts , projected to

TYPES OF SENSORY NERVE FIBRES

- Ad fibres
that transmit (mediating) immediate pain - Diameter = 2 microns . - Conduction velocity = 15 meter/sec that transmit delayed pain - Diameter = 0.4-1.2 microns Conduction velocity = 0.5- 2 meter/sec. that transmit crude touch -Diameter =5-12 microns -- Conduction velocity =30-70 meter/sec. that transmit proprioceptive sensation - Diameter =12-20 microns . - Conduction velocity = 70 - 120 meter/sec

- C fibres - Ab fibres

- Aa fibres

Four types of primary afferents axons carry info to CNS

Propioception

Touch

SOMATIC SENSATION FROM THE HEAD AND NECK

The peripheral divisions of the trigeminal nerve . Ophthalmic, Maxillary ,and Mandibular division cutaneous fields of the head

From Nolte Fig 12-12

The central connections of the trigeminal nerve . The fibres of the spinal tract and nucleus retain the primitive segmental relationship. Showing the extent of analgesia caused by lesions at a , b and c

ASCENDING TRACTS will finally reach the cerebral cortex

Gracile Lateral Spino-Thalamic Cuneate Ventral Spino-Thalamic

not finally reach the cerebral cortex

Dorsal Spinocerebellar tract Spinoolivary Ventral Spinocerebellar tract Spinotectal tract

SENSORY PATHS IN THE BRAIN STEM (LEMNISCl)

MEDIAL LEMNISCUS
Sensation It is the 2nd order neuron for fine touch and
proprioception from the body only

Origin: From the Gracile and Cuneate nuclei in the medulla. Course The fibres cross forming the internal arcuate fibres,
decussating with the opposite fibres forming the sensory decussation , ascend upward near the midline forming the medial lemniscus

Termination End in the V.P.L.N.T. (Thalamus )

Spinal LEMNISCUS
Sensation It is the 2nd order neuron for pain. , temperature, and
crude touch ( from the body)

Origin: From the S.G. of Rolando , and main sensory nucleus (in
the spinal cord) .

Course The fibres from the S.G.R. and main sensory nucleus
(combination of the lateral and ventral spinothalamic tracts) in the lower medulla

Termination It joins the medial lemniscus to terminate in

the V.P.L.N.T

TRIGEMINAL LEMNISCUS
Sensation Pain , temperature , touch and taste (from head and neck) Origin: Spinal sensory nucleus and upper sensory nucleus in pons Termination V.P.M.N.T. (thalamus)

Lateral LEMNISCUS
Sensation Hearing

Origin: Ventral and Dorsal Cochlear nucleus

Termination Inferior colliculua in midbrain and Medial
geniculate body of thalamus

SEGMENTAL FIELDS OF SENSATION (THE DERMATOMES)

Pattern of dermatomes in man

Dermatomes
Definition: Areas of the skin which are supplied by the same dorsal root. There is a known map of the body which identifies the dermatomal distribution. The importance of dermatomes: 1. Diagnosis of the affected segments in the spinal cord lesion and in other neurological diseases. 2. Overlap between adjacent dermatomes cutting of one dorsal root dose not lead to complete loss of sensations from area supplied with it. 3. Determination of the diseased viscera ( referred pain phenomenon).

Somatotopic map in the cortex

Sensory homunculus: This model shows what a man's body would look like if each part grew in proportion to the area of the cortex of the brain concerned with its sensory perception.

SENSORY DISTURBANCES
1. Hyperalgesia 2. Tabes dorsalis:
Cause : Syphilitic lesion degeneration of the dorsal root fibers

central to the ganglia (especially in the lumbo-sacral segments or pantaloon area). Manifestation: Early: a) Severe pain due to irritation of the nerve fibers (by inflammatory process). b) Sensory ataxia:- Incoordination of voluntary movements due to loss of the proprioceptive sensations. - Because of degeneration of Gracile & Cuneate tracts (thick A fibers are more affected by compression & no regeneration due to absent neurolemma). - Positive Romberg's sign the patients unaware of his muscles and joints and he can only keep his equilibrium by his eyes and if he closes them (during washing his face) he falls immediately.

C-Stamping gait: because patient is unaware of his legs he tries during walking to feel the ground by hitting strongly on the earth. D- Late: a) Loss of pain & all other sensations due to constrictive fibrosis which destroys completely the nerve fibers. b) Loss of all reflexes : -Loss of superficial reflexes e.g. withdrawal Rulcers. - Loss of deep reflexes e.g. Stretch R loss of muscle tone & jerks. - Loss of visceral reflexes e.g. micturation, defecation retention with c) Argyll Robertson pupil due to damage of pretectal nucleus in midbrain

3. Syringomyelia:

Cause: cystic dilatation with cavitation around central canal of spinal cord due to overgrowth of glial tissue degeneration of crossing fibers of lateral & ventral spinothalamic tracts

Manifestation:
it usually affects lower cervical and upper thoracic segment of spinal cord. Loss of pain & temperature on both sides while rough touch is little affected Fine touch & proprioceptive sensations remains intact (dissociated jacket like sensory loss). In severe cases, damage of anterior horn cells, lateral horn cells & pyramidal tract LMNL, Horner's syndrome & UMNL respectively. In severe cases, extension to the brain stem paralysis of cranial nerves (syringobulbia).

4. Hemisection of the spinal cord (Browen-sequard syndrome):

Cause: Destruction of dorsal & ventral horns in one side only sensory & motor manifestation (lesion may involve one or more segments). Manifestations (sensory part): Above level of lesion 2ry hyperalgesia at the same side At the level of the lesion Loss of all sensations in the same side. Below level of the lesion: 1. Loss of pain & temperature at opposite side. 2. Loss of fine touch and proprioceptive sensations on same side. 3. rough touch in both sides.

5. Thalamic syndrome:
Cause: Occlusion of the thalmo-geniculate artery damage postero-ventral nucleus of the thalamus (PVLNT), while PVMNT is little affected. Manifestation: 1) Loss of all sensations (especially fine (epicritic) from opposite half of the body, while face is less affected. 2) Sensory ataxia due to loss of proprioceptive sensation. 3) Thalamic hyperpathia: few weeks later the crude or protopathic sensations (e.g. pain, extremes of temperature & excessive joints movements) return but need strong stimuli, become poorly localized and always very painful.

 4) Emotional & autonomic disturbances: patient sometimes perceive extreme unpleasant sensations or extreme pleasant ones (due to intact medial nuclei which become facilitated with enhanced sensitivity to pain & emotions). 5) Motor manifestation due to damage of ventrolatral nucleus: a. Loss of cerebellar function motor ataxia , hypotonia & pendular knee jerk. b. Loss of basal ganglia function chorea & athetosis.

6- Peripheral neuritis: Causes: Vitamin deficiency, Dibetes mellitus, toxins. Manifestatios: Sensory disturbances: Hypothesia or anathesia. (glove&stock) Motor disturbances: paresis or paralysis of the distal parts.

7-Internal capsule haemorrhage Rupture of lenticulostriate artery and degenerartion of sensory radiation leading to contralateral hemianathesia.

Headache
Pain Sensitive Areas in the Cranial Cavity Not all of the intracranial structures are pain sensitive. The meninges of the anterior and posterior fossa , the venous sinuses f the major arteries , the falx and tentoriurn cerebelli are supplied with fibres carrying pain sensation to the fifth , ninth , and tenth cranial nerves . The parenchyma of the brain is insensitive to pain

Common Causes of Headache

1-Vascular Headache
2- Meningeal Irritation 3- Tumour Headache 4- Decreased cerebrospinal fluid pressure 5- Referred Headache 6-Tension Headache (Emotional Headache):

Extra-cranial causes : - Sinusitis. - Toothache. - Middle ear disease. - Spasm of the neck muscles. - Errors of refraction. - Fevers. - Stimulation of lower esophagus by cold or hot food. - Psychogenic headache

NEURONAL SYNAPSE
Definition: the junction between two neurons (with no protoplasmic connections). Types: 1. Chemical synapse - All synapses in human C.N.S. - Impulse transmission is through release of chemical substance (chemical transmitters). - Transmitter affects the permeability or the metabolic rate of the second neuron. 2. Electrical synapse - Found in heart and smooth m. & rare in C.N.S. - There are direct protein channels (connexon) between adjacent cells that permit ion passage from one cell to another (gap junctions). 3. Conjoint synapse: very rare in CNS, both electrical & chemical transmission occur.

Physiologic anatomy of the synapse:

Types of post synaptic potential

A) Excitatory post synaptic potential (EPSP): Transient depolarization in the postsynaptic membrane (that lasts 2 5 msec). Occur in excitatory synapse (where excitatory ch. Transmitter is released e.g. Ach ). Mechanism: one of the following 1. Opening of Na+ channels Na+ influx. 2. K+ outflux. 3. Cl- influx. 4. metabolic activity inside cells.

Summation of PSPs:
EPSP cannot alone depolarize the whole postsynaptic membrane and summation must occur to bring membrane to the firing level. Summation occur by 2 way: 1. Spatial summation: as a result of simultaneous excitation of several presynaptic neurons. 2. Temporal summation: as a result of repeated stimulation of single presynaptic neuron provided that the interval between stimuli < 15 msec ( > 15 m sec the previous EPSP decay). Presynaptic facilitation: in which certain neurons release serotonin at the presynaptic membrane cyclic AMP concentration keep Ca ++ channels opened for long time more Ca ++ influx inside the synaptic knob release of excitatory chemical transmitter EPSP.
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B) Inhibitory post synaptic potential (IPSP):

a. Post - synaptic inhibition: Local state of hyperpolarization occurs in the post synaptic membrane. The inhibitory transmitter is commonly glycine. Mechanisms: 1. Opening of K+ channels K+-outflux. 2. Cl- influx. 3. metabolic activity in post synaptic membrane 4. Closure of Na+ channels.

b. Pre-synaptic inhibition
Inhibition that occurs on the presynaptic membrane by a special inhibitory neurons which anastomose with presynaptic membrane shortly before the area of the synapse. Pre-synaptic inhibition is slower but longer than post synaptic inhibition. Mechanisms: 1. Inhibitory neurons closure of Ca++ channels in presynaptic membrane less Ca++ entry inside the synaptic knob amount of excitatory transmitter release. 2. Inhibitory interneuron opening of Cl- channels (or K+ efflux) hyperpolarization of the presynaptic membrane action potential 3. Closing of Na+ channels hyperpolarization of presynaptic membrane action potential Ca++ entry inside synaptic knob.

c. Renshawa or negative feedback inhibition:

Special type of inhibition that occur in the spinal cord due to presence of Renshaw cells (occur also in the cerebral cortex & in the limbic system). + + Anterior horn cells + + surrounding Renshaw cells inhibit this activated A.H.C (ve feedback inhibition) & other surrounding A.H.Cs (lateral inhibition) localize action & prevent prolonged excitation.

Properties of the synaptic transmission:

1) Unidirectional: only from presynaptic to the postsynaptic. 2) Synaptic delay: Time elapses between arrival of the impulse to the synaptic knob & the excitation of the postsynaptic membrane ( = 0.5 msec). The synaptic delay is caused by: a) Time taken by release of the transmitter & binding with its receptors. b) Time taken by Na+ influx to produce EPSP. c) Time taken for summation of many EPSPs till reach the threshold value. Total reflex time is the time that elapses between the application of the stimulus and the appearance of response. Central delay = difference between Total reflex time & time of conduction of afferent and efferent nerves. Number of synapses in a reflex = Central delay / synaptic delay.

3) Potentiation:
Slow repetitive synaptic stimulation EPSP tetanic discharge from the postsynaptic neurons (this discharge may continue up to many hours). It explain some higher functions of the brain as memory or learning. There 2 types of Potentiation: a. Short term Potentiation (post-tetanic facilitation): lasts few minutes & it due to excess Ca++ accumulation in synaptic knobs. b. Long term Potentiation: lasts few hours or days (e.g. in hippocampus secrete glutamate) & it is due to: Presynaptic component: released glutamate due chemical substances released from postsynaptic neuron. Postsynaptic component: glutamate Ca++ influx in postsynaptic neuron PSPs.

 4) Fatigue: Repeated stimulation of presynaptic knobs progressive decline in discharge from the postsynaptic membrane (protective mechanism e.g. in epilepsy). It is due to depletion of the stored ch. transmitters in the synaptic knobs. 5) High sensitivity to Some chemical and biological variations: A- BLOOD PH: 1. Alkalosis excitability ( at PH to 7.8 convulsion). 2. Acidosis e.g. diabetic keto-acidosis synaptic transmission (at pH 7 coma). B- Hypoxia marked inhibition of synapses loss of consciousness within 3-5 sec. C- Drugs : Sedatives. D-bacterial toxins: tetanus

DESCENDING (MOTOR) TRACTS

PYRAMIDAL TRACT

EXTRAPYRAMIDAL TRACT

CORTICOSPINAL

UPPER PORTION

To AHCs of spinal cord CORTICOBULBAR

To Motor nuclei of cranial nerves

Start from the cerebral cortex to mid brain

LOWEWR PORTION Start from mid brain to Spinal cord

DIFFERENCES BETWEEN THE & EXTRA TRACTS

-One neuron carries the -Many neurons carry the impulses from the cerebral impulse from the cerebral cortex to the A.H.C. cortex to the A.H.C.
-In the medulla it occupies -In the medulla they do not the pyramid. occupy the pyramid -Arises from localized - Arises from widely regions of the cerebral cortex distributed areas of the , area 4 ,6, 8 mainly and different lobes of the brain. Somato-sensory area I (SI).

-The fibres cross to reach the -Some tracts are AHC of the opposite side. others are direct.

crossed,

-Function: Excitatory, (fine - Some are excitatory , others isolated movements. inhibitory , two carry autonomic fibres; Lateral and Ventral Reticulospinal tracts .

PYRAMIDAL TRACT

PYRAMIDAL TRACT

FUNCTIONS OF THE PYRAMIDAL TRACT

Initiation of voluntary movements on the opposite side of the body, especially the fine, well coordinated, unfamiliar movements of distal extremities like piano-playing

Area 4 is excitatory to muscle tone and reflexes

Corticobulbar tract is concerned with the head muscles ,while the corticospinal with the rest of the body