Intr oduction
Organization of the nervous system

ANATOMICAL organization
a) Brain:

(1 ) Central nervous system

1- Cerebrum: cerebral hemisphere,

with basal ganglia.
2- Diencephalon:



3- Brain stem: midbrain, pons &

4- Cerebellum.

b) Spinal cord:

31 segments.

8 Cervical, 12 Thoracic, 5 Lumber, 5 Sacral & 1 Coccygeal.

a) Cranial nerves: b) Spinal nerves:

(2) Peripheral nervous system

(12 pairs): Sensory, motor or mixed.

(31 pairs): All are mixed nerves.

FUNCTIONAL organization
the nervous system is divided into 2 systems:

1) Somatic nervous system
It controls the activities of skeletal muscles.

2) Autonomic nervous system
controls Visceral (involuntary) functions. According to the direction of nerve impulse:
1 - Sensory division: Receptors → afferents → tracts → centre (CNS). 2 - Motor division: Centre (CNS) → upper & lower motor neurons → organ.



Major levels of CNS function:
may be at the level of

(a) Spinal cord: micturition, flexor withdrawal reflex. (b) Lower brain level: (Thalamus, hypothalamus, basal ganglia, cerebellum, pons and medulla). (Subconscious activities) Respiratory, CVS, GIT reflexes. (C) Higher brain level: i.e. cortex e.g. sensory functions, motor activities, language. Cortex usually function in association with the lower brain centers.



Synaptic Transmission
Synapse is the site of junction between two neurons. With no protoplasmic continuity.

Transmission at the synapses may be
1. Electrical By low resistance gap-channel pathway that allow passage of ions from one cell to another. Not Sensitive to drugs. Rare in CNS. (CEREBELLUM AND VESTIBULAR SYSTEM). 2. Chemical By release of a chemical substance from presynaptic terminal to act on postsynaptic cell. Sensitive to drugs.

Types of synapses
1. Axo-dendritic: most numerous, least excitable. 2. Axo-somatic: 3. Axo-axonic: least numerous, Most excitable (low threshold).

Because of the numerous Na channels in the axon hillock.



Functional anatomy
(A) Synaptic knobs: contain 1. mitochondria. (ATP synthesis). 2. Vesicles containing; neurotransmitters. 3. Large number of Ca channeles & release sites for neurotransmitters. (b) Synaptic cleft: 30-50 nm width & contains extracellular fluid. (c) Synaptic gutter: Post synaptic membrane

Contains receptors for neurotransmiiters, protein channels and enzymes for destruction of neurotransmitters.

Mechanism Of Synaptic Transmission
(1) Release of the chemical transmitter
Action potential in the presynaptic nerve opens voltage gated Ca++ channels. leading to rupture of vesicle and release of the chemical transmitter in the synaptic cleft by exocytosis. The amount of the transmitter release α amount of Ca++ in the presynaptic terminal.

(2) The chemical transmitter crosses the synaptic cleft (3) Union of chemical transmitter with its receptors
This changes the permeability of the post synaptic membrane to one or more ions.

(4) Changes in ion Fluxes:
lead to change in resting membrane potential to become: less negative causing excitatory post synaptic potential.(EPSP) More negative causing inhibitory postsynaptic potential.(IPSP)



Postsynaptic Potentials
(a) Excitatory post synaptic potential (EPSP)
It is a state of partial depolarization (2-5 msec). Occurs due to release of excitatory neurotransmitters as acetylcholine. It is caused by opening of ligand gated Na+ channels and closure of the ligand gated K+ channels or CL channeles. To reach the threshold value,

EPSPs must be summated:
(1) Time (temporal) summation: One presynaptic Knob is stimulated repetitively. Each EPSP reach postsynaptic membrane before the ending of the previous one. N.B . In temporal summation, the time between stimuli must be less than the duration of the EPSP. (2) Space (spatial) summation: Several presynaptic knobs are stimulated simultaneously. When the excitation reaches the firing level, action potential starts. 50 EPSPs are needed to reach the firing level.



(B) Inhibitory post synaptic potential (IPSP)
- It is a state of hyperpolarization (3 msc). - Occurs due to release of inhibitory neurotransmitters as glycine. - It is a local state that can be summated (temporal or spatial). - It is caused by opening of ligand gated CL & K+ channels and closure of ligand gated Na+ and Ca++ channels.

Type s Of Sy na ptic Inhib iti on (1) Inhibitory post synaptic potential (EPSP) (2) Presynaptic Inhibition
The axon terminals of a 3rd inhibitory neuron end at the axon terminals of an excitatory neuron. ►The 3rd neuron releases an inhibitory transmitter which Opens Cl- channels of the excitatory neuron which Closes the voltage gated Ca channels. ►The end result is reduced Ca++ entry to the synaptic knob and, in turn, decrease release of the transmitter.

[3] Negative feedback inhibition: (Recurrent inhibition)
Mainly occur in the anterior horn of the spinal cord. Mechanism of inhibition • Anterior horn cells gives collaterals to excite inhibitory interneurones (Renshow cells).



The inhibitory interneurones, in turn, inhibit the anterior horn cell & its surrounding cells.

Properties of Synaptic Transmission
(1) Forward direction i.e from pre to postsynaptic neuron. (2) Synaptic delay
= 0.5 msc.

It is the time needed for release of neurotransmitters and binding of the transmitter to receptors. The more the number of synapses, the slower the conduction.

(3) Fatigue
►Def: Decrease rate of discharge in post synaptic neuron due to rapid repetitive stimulation. Mainly due to decrease chemical transmitter in presynaptic terminal. ►Importance It prevents over excitation in CNS. (It is a gift from the god to the epileptic patients).

(4) Synaptic potentiation
►Def If the pre-synaptic neuron is stimulated by brief rapid (tetanizing) stimuli, the post synaptic neuron response will continue for few seconds to minutes after stoppage of the stimulus. ►Mechanism Increased Ca++ in pre synaptic neuron → continuous release of chemical transmitter.

(5) Effect of acidosis and alkalosis
[I] Alkalosis; increased excitability → increase coma. transmission convulsion. [II] Acidosis; decreased excitability & transmission



(6) Effect of Hypoxia
Due to accumulation of acids, hypoxia leading to decrease transmission. Prolonged ischaemia causes brain damage.

(7) Affected by Drugs
[I] Drugs which increase synaptic transmission. - Theophylline and caffeine (decrease threshold for excitation). - Strychnine blocks the action of the inhibitory transmitters. [II] Drugs which decrease synaptic transmission. - Analgesics, hypnotics, anaesthetics (-- the amount of excitatory neurotransmitters or enhancing the inhibitory neurotransmitters).

(8) Synaptic plasticity:
It is the ability to change the function of synapse according to the demand i.e the synaptic transmission can be increased or decreased for short or long duration by repeated stimulus.

Forms of Synaptic plasticity
A) Post-tetanic potentiation
►Def If the pre-synaptic neuron is stimulated by brief rapid (tetanizing) stimuli, the post synaptic neuron response will continue for few seconds to minutes after stoppage of the stimulus. ►Mechanism Increased Ca++ in pre synaptic neuron → continuous release of chemical transmitter.



B) Habituation
►Def It is the gradual loss of response to a benign stimulus, when it is repeated for several times at intervals. ►Mechanism Decrease Ca++ in presynaptic neuron caused by unknown gradual inactivation of Ca ++ channels → decrease release of chemical transmitter.

C) Sensitization
►Def It is the prolonged augmented response due to application of a noxious stimulus accompanying the benign stimulus. ►Mechanism

Presynaptic Facilitation
-The 3rd neuron is excitatory neuron; which secretes serotonin. - Serotonin increase cAMP in the presynaptic terminals. - cAMP Phosphorylates a protein in the K+ channels and close them. - This prevents repolarization & prolongs depolarization. - Depolarization Keeps Ca++ achannels opened → Increase release of the chemical transmitter.



Neuronal Pool
A collection of neurons having the same function.

Neuronal Pool Organization (1) Convergence
Many neurons activate one neuron It allows for spatial summation. Interpretation of many information received by one neuron.

(2) Divergence
One neuron activates many neurons. Its functions are: a. Amplification e.g One cortical cell activates 1000 AHCs in spinal cord. b. Distribution of signals.

(3) Excitation field, discharge zone & subliminal fringe
Excitation field = neurons excited by one input afferent fibre. Discharge zone = central neurons in which the excitation is above the threshold value so they discharge. Facilitation zone (sub limi nal below the threshold value. Weak stimulus → small excitation field formed mainly of subliminal Fringe.
Fri nge ) =

peripheral neurons in which the excitation is

This arrangement leads to the development of 2 other phenomena
Occlusion Facilitation Simultaneous stimulation of two afferent fibres. - Close to each other - not close to each other - by maximal stimuli - by submaximal stimuli Results in reflex reaction which is


11 less than the sum more than the sum of the separate stimulation of the two input fibres. Cause: Overlap of the Discharge zones Facilitation zones (subliminal fringe).

@ Occlusion:
This means occurrence of a smaller response when 2 near afferent neurons are maximally stimulated simultaneously than the algebraic sum obtained each afferent. of the responses

@ Subliminal fringe summation


It is the occurrence of a greater response when 2 afferent neurons (that are not very close to each other) are sbumaximally stimulated simultaneously than the algebraic sum of the responses obtained when each afferent is stimulated separately.

(4) Reciprocal Innervation
in which a sensory signal stimulates the neurons supplying group of muscles, meanwhile it inhibits their antagonists through stimulation of inhibitory interneurones. This enables the contracting muscle to function freely e.g. flexor
withdrawal reflex.

(5) After discharge
►Definition The output continues to discharge after stoppage of stimulation of the input. ►Mechanism: [a] Prolonged action of the neurotransmitter on the postsynaptic
receptor till it becomes completely inactivated.

[b] Parallel circuits: The input is connected to the output by many parallel circuits, each contains different numbers of interneurones and so different numbers of synapses. [c] Reverbrating circuits: The output neuron sends collateral restimulate itself.



It can be stopped by: Fatigue i.e decreased chemical transmitter. Inhibition from other areas.

(6) Fatigue
Decrease rate of discharge in post synaptic neuron due to rapid repetitive stimulation. Mainly due to exhaustion of chemical transmitter in presynaptic terminal.

(7) Recruitment
Recruitment is the gradual increase to a maximum in a reflex when a stimulus of unaltered intensity is prolonged. There is progressive increase in the activity of the interneurons, leading to an increase in the excitability of more and more motor neurons, until spatial summation raises the excitability to the threshold value to discharge.

(8) Central delay
Definition: It is the time passed during impulse transmission in the synapses included in the pathway of the reflex arc. Calculation Central delay = Total reflex time - time of transmission in the afferent and efferent neurons. Total reflex time = It the time passed from stimulation till appearance of response. Imprortance Estimation of the number of synapses in the reflex arc pathway = Central delay / 0.5 msec (single synaptic delay).



Synaptic Transmitters
Class I: Class II: Acetylcholine.
The Amines:

Norepinephrine. Epinephrine. Dopamine. Serotonin. Histamine. Class III: Amino Acids: gamma aminobutyric acid (GABA). Glycine. Glutamate. Aspartate. Class IV: Nitric oxide (NO).

Acetylcholine (ACh)
Sources: - neurons in many areas of the brain, - motor neurons that innervate skeletal muscles, -preganglionic neurons of the ANS, - postganglionic neurons of the parasympathetic nervous system, - some of the postganglionic neurons of the sympathetic nervous system. Effects: ACh has an excitatory effect, though it has inhibitory effects at some peripheral parasympathetic nerve endings.

Norepinephrine (NE)
Is secreted by many neurons located in the brain reach widespread areas of the brain. In most of these areas, NE probably activates excitatory receptors, but in few areas, it activates inhibitory receptors. NE is also secreted by most of the postganglionic neurons of the sympathetic neurons system.




Is secreted by neurons that originate in the substantia nigra and which terminate mainly in the basal ganglia. The effect of dopamine is usually inhibition.

Is secreted by neurons that originate in the median raphe of the brain stem, and project to many brain and spinal cord areas. Serotonin is inhibitory.

Gamma-aminobutyric acid (GABA)
Is secreted by nerve terminals in the spinal cord, cerebellum, basal ganglia and cortex. It causes inhibition.

Is secreted mainly at synapses in the spinal cord. It is an inhibitory transmitter.

Is secreted by presynaptic terminals in many sensory pathways, and in many areas in the cortex. It causes excitation.

Nitric oxide (NO)
Occurs especially in areas of the brain that are responsible for long-term behaviour and for memory. [It is synthesized instantly as needed, and diffuses into the immediately adjacent postsynaptic neuron as well as other postsynaptic neurons nearby]. It modifies neuronal excitability for seconds, minutes or even longer (by changing intracellular metabolic functions).

Classification by Function

1.Inhibitory or Excitatory? the action of a neurotransmitter can be either excitatory (allow Na+ in) or inhibitory (allow Cl- in), depending on what type of channel it opens a. generally inhibitory - glycine & GABA b.generally excitatory - glutamate c. some can be either, dependent on location: most other neurotransmitters i. ACh - exitatory on skeletal muscle, inhibitory on cardiac muscle 2.Ionotrophic vs. Metabotrophic Actions a. ionotropic - opens Na+ or Cl- channels b.metabotropic - promote longer lasting changes using "second messenger system"



i. binding of neurotransmitter causes production of intracellular "second messenger" called cyclic AMP (cAMP) ii. cAMP can activate enzymes in the cell to alter activity of channels and enzymes.

Senso r y Sys tem

It gives information & knowledge to the individuals about any change in environment & position of the individual.



Specialized structures at the peripheral end of the afferents which receive and convert different stimuli into action potentials (nerve impulse).

Two t ype s of receptor
- a nerve cell. - a specialized epithelial cell.

cel ls

Function s
1. Detectors: i.e detect changes in the surrounding environment. 2. Transducers: i.e transform stimulus energy into potential changes. With generation of action potentials in the afferent fibres.



(1) Excitability
The receptors have the ability to convert energy into action potential in the sensory nerves. When the receptor is stimulated by an adequate stimulus, it generates adepolarizing potential called receptor or generator potential which is localized, non propagated potential change. The amplitude of the generator potential is related to the intensity of the stimulus.

Mechanism of stimulation of receptors
- It is studied in paccinian corpuscle. Pacinian corpuscle: It is a straight non-myelinated nerve endings surrounded by connective tissue concentric layers giving it an onion like appearance, first node of Ranvier starts just before leaving the capsule. - Application of weak pressure to receptor, open voltage gated Na+ channels and increase Na+ influx, produce local nonpropagated potential at the receptor site. When reaching threshold value, it activates the first node of Ranvier and generates propagated action potential along the nerve fiber.

Properties of RP



1. Local state of partial depolarization which spreads passively. 2. Does not obey all or none law. 3. It can be graded i.e. its amplitude is increased by increasing the intensity of the stimulus. 4. has no absolute refractory period. 5. It can be summated. 6. Its duration is longer 5-10 msec than action potential 2 msec. 7. So it can initiate repeated action potentials, when the depolarization of the 1st node reaches the threshold value. 8. Not blocked by local anesthesia.
Relation of the R.P magnitude to the Frequency of action potentials

The frequency of action potentials produced is proportional to the amplitude of the RP.

Weber-Feshner principle
The frequency of impulses α log intensity of the stimulus. So, the frequency of action potentials (rate of firing) is not a linear relationship with the stimulus intensity.

Generator potential
Do not obey all or non law. Graded. No absolute refractory period. Summated. Not propagated. Lasts 5 msec. In receptors.

Action potential
Obey all or non law. Cannot be graded. Absolute refractory period cannot be summated. Propagated. 2 msec. In nerve axon.

(2) Adaptation of receptors



► Definition: It is the decrease in the amplitude of R.P. and the frequency of action potential with constant continuous stimulus. ► Cause:
Ea ch rece ptor ha s it s ow n pr ope rty of ada ptat ion e.g .

1. Gradual inactivation of Na+ channeles. 2. Dissipation of some stimulus energy to the surrounding. 3. decreased excitability of the receptor membrane. 4. Remodeling (Readjustement) in the shape of receptors. 5. decreased excitability of the first node of Ranvier. N.B. Pain receptors do not adapt due to their protective function.

Difference between adaptation and fatigue Adaptation Fatigue
Definition Effect of O2 lack Rate of stimulation Previous stimulation Mechanism
Gradual decrease in receptor due to continues constant stimulation. No effect No effect. No effect Decrease in the permeability of membrane to Na. Gradual decrease in organ response due to repeated stimulation. Accelerates onset of Fatigue. Accelerates onset of Fatigue. Accelerates onset of Fatigue. Accumulation of metabolites as lactic acid.

3) Specificity

Muller’s law

Each receptor responds to a specific stimulus called adequate stimulus for this receptor. e.g.: Thermal receptors arc sensitive to thermal forms of energy but completely insensitive to touch or pressure. Rods and cones are responsive to light but insensitive to hot or cold. The sensation perceived as a result of stimulation of receptor is called modality of sensation.

Muller's law of specific nerve energy
"Each receptor is sensitive to one specific stimulus called adequate stimulus and gives one type of sensation regardless the method of stimulation".

Coding Of Sensory Information



►Def It is the ability of the CNS to recognize the modality (type), locality & intensity of sensation.

[a] Modality of sensation:

depends on specificity.

Muller’s law
Each receptors give one type of sensation, irrespective of the method of stimulation.

[b] Intensity of sensation:
It is coded by change in: 1. The number of receptors activated (recruitment of receptors). Increase stimulus intensity → Increase number of receptors activated. 2. The frequency of impulses: Stronger stimulus → Increase frequency of impulses. ► according to: Weber-Feshner principle Which states that sensation felt (interpreted stimulus intensity = log intensity of the stimulus x constant).i.e. The frequency of impulses α log intensity of the stimulus.

[c] Locality of sensation:


on law of projection

Each area in the body e.g. hand or leg is represented in a particular area in the cerebral cortex. So, when an impulse reaches the specific area in the cortex, the cortex will projects the sensation to its original site.

Phantom limb;
This is the false sensation from a limb when the limb does not really exist. It occurs in amputees who complain of pain, touch, itching or pressure sensation felt in the absent limb. This false sensation is due to irritation of the cut ends of the afferent nerves of the amputated limb which send impulses up to the brain. The brain projects the sensation on to the absent limb as if it were existing.

Classification of receptors
According to mode of stimulation


21 2. Thermoreceptors. 4. Electromagnetic: Photoreceptors (rods & cones).

1. Mechanoreceptors. 3. Chemoreceptors.

5. Nociceptors (pain receptors) i.e. free nerve endings. (1) Mechanoreceptors: Stimulated by mechanical forms of energy. e.g Touch, pressure, vibration, acceleration and stretch. They are found in skin, mucous membrane, muscles, tendons, Joints, blood vessels, lungs and inner ear.. etc. (2) Thermo receptors: Respond to changes in temperature. Present in skin and mucous membranes. (3) Chemo receptors: Stimulated by chemical forms of energy. Carotid and aortic chemoreceptors, Taste & smell.

According to Adaptation
a. Slowly adapting (tonic) receptors: Pain receptors, muscle spindle, alveolar stretch receptors. The slow adaptation keeps the brain continuously alerts due to their important postural & protective signals. b. Moderately adapting receptors: temperature, smell & taste receptors. c. Rapidly adapting (phasic) receptors) They discharge while the change is actually taking place.
e.g. paccinian corpuscle (most rapidly adapting).



According to Situation
A) Exteroceptors: - Cutaneous receptors: Pain, touch and temperature. - Teleceptors: Vision, hearing, and smell.

B) Interoceptors:
- Proprioceptors: muscle spindle and golgi tendon organs. - Visceroceptors: Baroreceptors and chemoreceptors. - Hypothalamic receptors: Glucoreceptors and osmoreceptors.

Sensory unit
-Single sensory axon with peripheral branches & its receptors. -The receptors of sensory unit are sensitive to the same type of stimulus & density of receptors is higher at the centre of the receiptive field. - the receiptive field of sensory unit is the area from which stimulus produces a response in that unit. -There is overlap between receptive sensory fields.

Somato-sensory nerves
Classification of peripheral nerves:-



- According the their diameter A, B & C A is further subdivided into alpha, beta, gamma & delta. - Numerical classification I, II, III and IV. asing the diamete r.

- Conduction velocity: increased by incre

Sensation is the feeling produced by change in the environment or by the application of stimulus to the receptors, or nervous pathways.

Sensation includes the following types
I) Somatic sensations:
arising from skin and deeper structures e.g. skeletal muscles, tendons, ligaments, joints and periosteum.

2) Visceral sensations:
include sensations from the viscera.

3) Organic sensations
e.g. thirst and hunger.

4) Special sensations:
Vision, hearing, taste and smell.

5) Emotional sensations:
as fear, sadness, pleasure etc.



Physiological Classification
[1] Pain sensation. [2] Thermal sensation. [3] Mechano-receptive sensations.
(a) Tactile sensation: Touch : crude & fine. Pressure. Vibration. (b) Position Senses: Static : sense of position. Kinetic : sense of movement.

Anatomical Classification
1. Exteroceptive sensations; pain, touch and temp. 2. Interoceptive sensations. - Proprioceptive sensations; position & movement. - Deep sensations; deep pressure. deep pain & vibration. - Visceral sensations; Visceral pain, bladder & rectal distention.

Classification according to pathways
1. Spinothalamic sensations; Pain, crude touch & temperature. 2. Dorsal column sensations; - Fine touch - Proprioceptive sensations; position & movement. - Deep sensations; Pressure & vibration.

Classification perception





(A) Protopathic (Crude) sensations;



- perceived mainly at the level of the thalamus.(Poorly localized) - High threshold of stimulation. - Include; - Slow pain, Warm sensation, Crude touch. - Extremes of temperature.

(B) Epicritic ( Fine ) sensations;
- Perceived mainly at the level of the cortex.( Well localized) - Include; - Fine touch - Proprioceptive sensations; position & movement. - Deep sensations; Pressure & vibration.

Some notes; very important
A) All spinothalamic sensations carried by A delta and C. nerve fibres. B) All dorsal column sensations carried by A beta.



1. It consists of A-delta nerve fibres (mainly) and also C nerve fibres. 2. It transmits a wide variety of sensations 3. It has a low degree of lamination. 4.Poor (a) localization of sensations (b) discrimination of their intensity


(c) transport of rapidly repetitive signals. 5.Conduction of signals from the opposite side.

T he v entr al (an ter ior ) spino thal ami c tr act
This tract transmits crude touch and pressure as well as tickle and itch sensations. Its pathway consists of 3 ne ur on s; ۩ First order neurons Thes e are A-delta and C afferent nerve fibres. They enter the spinal cord via the dorsal roots, ascend or descend a few segments in the Lissauer's tract, then terminate at the main sensory nucleus in dorsal horn. ۩ Second order neurons
These constitute the tract. They start in the dorsal horn, cross to the opposite side, ascend in the anterior column of spinal cord, and terminate at the ventral posterolateral nucleus.

۩ Third order neurons These start: in the thalamus, pass in the sensory (thalamic) radiation (in the posterior limb of internal capsule) and terminate at the c ortical sensory
areas in the postcentral gyrus.

later al spino thal ami c tr act
Th is tract tra nsmi ts pain and thermal sensations. It inclu des 2 separ ate pa thwa ys;



a) paleospinothalamic pathway
This transports slow pain sensation as well as thermoreceptive sensations specially heat, and it consists of the following 3 ne ur ons;

♣ First order neurons:
These are mainly C afferent nerve fibres. They enter the spinal cord via the dorsal roots, then terminate at the substantia gelatinosa of Rolandi (SGR) in laminae II & Ill of the dorsal horn.

☻Second order neurons:
These constitute the tract. They start: at the SGR, cross to the opposite side close to the central canal, ascend in the lateral column of the spinal cord and terminate at (a) the periaqueductal gray area (PAG) (b) the reticular formation (c) the nonspecific thalamic nuclei.

♥ Third order neurons:
These start at the thalamus and project to almost all parts of the cerebral cortex (via the internal capsule). However, they are not essential for perception of the transported sensations but are essential for arousal of the nervous system.

B) Neospinothalamic pathway
This transports fast pain as well as thermoreceptive sensations specially cold, and it consists of the following 3 neurons:

۞ First order neurons
These are mainly A-delta afferent nerve fibres. terminate at laminae 1 & V of the dorsal horn

۞ Second order neurons
These constitute the tract. They start at the dorsal horns, cross to the opposite side and ascend in the lateral column of the spinal cord. Finally terminate at the thalamic VpLN These are similar to ventral spinothalamic tract.

۞ Third order neurons

It is characterized by the following : 1. It consists mainly of A-beta fibres.


2. It transmits limited (but: fine) sensations. 3. it has a high degree of lamination.

4. Fine (a) localization of sensations (b) discrimination of their intensity (c) high ability to transport rapidly-repetitive signals. 5. Conduction of signals mainly from the same side.

Gracile and Cuneate tracts
These tracts transport: (1) Fine tactile sensations (tactile localization & discrimination). (2) Stereognosis and texture of material sensation. (3) Fine pressure and muscle tension sensations. (4) Vibration sense. (5) Proprioceptive and kinesthetic sensations. (6) Some crude touch and pressure. The pathway of the gracile and cuneate tracts consists of the following 3 neurons:

® First order neurons
These are mostly A-beta afferent nerve fibres. As They enter the spinal cord, they immediately turn upwards in the ipsilateral dorsal column and ascend without relay as the gracile and cuneate tracts till relay at: the gracile and cuneate nuclei in the medulla oblongata. The gracile tract carries sensations from the lower part of the body and lies medially in the dorsal column, while the cuneate tract carries sensations from the upper part of the body and lies laterally in the dorsal column.

® Second order neurons
These start at the gracile and cuneate nuclei in the medulla, cross in the sensory decussation to the opposite side, then ascend as the medial lemniscus, and finally terminate at the thalamus specially at the VPLN. These start at the thalamic VPLN and terminate at the cortical sensory areas in the postcentral gyrus.

® Third order neurons



Items Sensations - Afferents - Spinal cord - Crossing -Brain stem - Perception - Spatial (space) - Characters of Transmission - Activation of cortex Lesion - In the sp. cd. - Decortication

Dorsal Column
Fi ne touc h a nd press ure Vibr atio n se nse Posi tion se nse A b eta Grac ile & cu nea te trac ts. Brai n st em Me dial le minis cus Main ly in co rtex Hi gh degr ee Discr ete loc aliz atio n Spe cific are as

Antero-lateral column
Crud e t ouch an d pr ssur e Pain an d t emp erat ure Sex ual sens ati on & Tickli ng A d elta an d C Lat eral Spi no thal amic tr . Ven tral spi no thal amic tr . Sp inal cor d Sp inal le minis cus Ma inly in thal amu s. Low deg ree i.e po orly loca lize d Poor loc aliz atio n wh ole cort ex & fe w fi bers go to sp ecifi c ar ea I & II Lo st on the opp osit e si de Slig htly a ffec ted & rapid reco very

Lost on th e sa me side Sev erely a ffe cted , n o reco very

Sensa tions fr om head and nec k
►1st Trig emi nal nerv e

order neuron

Trigeminal (Gasserian) ganglion.

Axo ns ent er a t po ns and divi de into 2 part s:-


a. Ascending fibres end in Sensory nucleus which is the

2nd order neuron; of fin e s ensa tio ns touc h, pr , prop rioc epti ve. cro sses to the op posi te side & asce nds to b. Desc end ing fibr es end in Spin al nucl eus. whi ch is th e 2nd order neuron
of pain and temp.

Axo ns: ►3rd

fo rm the trig emin al lemni scu s
Postro ventral nucleus of thalamus

cros ses to the opp osit e si de & as cen ds to

order neurone
Ax ons : Ce ntre :

en d in th e c ereb ral cort ex.

Fa ce area in the low est part of pos t c entr al gyrus .

Mec hanor eceptiv e sensa tions
►Tactile sensations

(1) Touch:



a) Crude touch:
Touch sensation with poor identification of site & number of stimuli.. Tested by a piece of cotton passed on the skin. (Cotton wool test) Receptors; Hair end organs & free nerve endings. Afferent: A delta fibres. (5-30 m/sc) Tract: Ventral spinthalamic tact and some fibres pass through dorsal column. Centre: Thalamus.

b) Fine touch Touch sensation with accurate identification of site & number of stimuli. Receptors; Meissner’s & Paccinian corpouscles, Merkel’s discs & Ruffini endings. Afferent: A beta fibres (30-70 m/sc). Tract: dorsal column tract. Centre: sensory cortex.

Fine Tou ch i nc lude s
1. Tactile localization
Ability to localize exact point of touch with eyes closed.

Tested by two marker test



It is tested by touching the skin of blind-folded subject by the tip of a blunt-pointed object, then asking the subject to open his eyes and point out the site where he touched. The acuity of this sense is inversely proportionate to the distance of error in localizing the stimulus.


Tactile discrimination

= 2 p oint s di scrim ina tion .

It is the ability to identify two tactile stimuli applied simultaneously as two separate points of contact regarding that the distance between these two points is more than threshold distance. Acuity of this sensation is inversely proportionate to the two-point threshold distance which is the minimal distance at which the two stimuli are felt as two separate points.

i.e. 2 mm in lips & finger tips & 60 mm in the back. Tactile localization and discrimination are more accurate (less threshold distance)
a. the more the number of receptors. b. the more the number of afferents. c. the less the convergence of afferents. d. the greater the area of cortical representation.

It is tested by the compass test.
The two blunt ends of a test compass are applied to the skin of a blind-folded subject. The distance between the two ends of the compass is increased step by step until the subject feels the two ends of the compass as two separate points.

3. Texture of material.
Ability to know the texture of material with eyes closed e.g silk, wool, cotton.

4. Stereognosis
Ability to know familiar object put in the hand with both eyes closed.



- It depends on: 1) All cutaneous & deep sensations. 2) past cortical experience regarding the object. - Stereognosis is carried on dorsal column tract.
- Its centre mainly in somatic association area (area 5,7).

- damage of dorsal column tract tracts by:

Syphilis and vitamin B12 deficiency (pernicious anaemia). - Also due to lesion in the somatic association area.

[2] Pr ess ur e S ense
It enables the person to know the weights of objects and discriminate between different weights. It is tested by applying different weights on supported hand of a blindfolded subject, then he is asked to identify the lighter or the heavier weight. Receptors: paccinian and Ruffini. Afferent: A beta fibres. Tract: dorsal column tract.

This is the sensation produced by traction on muscle tendons. The receptors are the Golgi tendon organs. It enables the person to discriminate different weights by lifting them. It is tested by applying different weights on an

unsupported hand of a blindfolded subject, then he is
asked to identify the lighter or the heavier weight.

[3 ] V ibr ation Sen se
Is a rhythmic repetitive pressure sensation which if felt when a vibrating

tensing fork is put opposite body prominences to magnify the stimulus.

- Paccinian corpuscle responds to vibration up to 500-800 Hz. - Meissner corpuscle responds to vibration up to 80 Hz.



Afferent: A beta. Tract: dorsal column tract. Centre: sensory cortex. Vibration sense is tested by putting the base of a vibrating tuning fork on the skin. A sense of buzzing or thrill is felt. The tuning fork is usually put on a subcutaneous bony prominence just to magnify the vibrations. Bone itself is insensitive to vibrations.

Depression of vibration sense is an early diagnostic sign in degeneration of posterior column of spinal cord e.g. uncontrolled diabetes, pernicious anaemia. Also, it localizes lesions of spinal cord.

[ 4 ] Tic kli ng and it ching ; Tickling= to feel light moving things on the skin as insects, which cause
local repeated mechanical stimulation.


the sensation caused by chemical substance secreted near the Receptors; Ra pidl y a dapt ing fre e n erve en ding s. Afferent: C fiber s. Tract: V entra l sp inth ala mic tact . Centre: Th ala mus.

receptors as histamine and kinin.



Pr oprioce ptiv e Sensa ti on
Sensation of the position & movement of each part of the body in Relation to each other & in relation to the space.


present in joints, ligaments and tissues around ligaments. -Slowly adapting

muscle spindle, Golgi tendon organ & Ruffini endings. -Rapidly adapting e.g paccinian to detect rate of movement.

►Proprioceptive impulses

go to the

Cerebellum via spinocerebellar tracts help to keep equilibrium. Cerebral cortex via dorsal column tracts inform the cortex
movements (dynamic). about the position of different parts of body (static) & rate of

►Types 1) Sense of position. 2) Sense of movement. ►Loss of proprioception;

lead ing to

Sensory ataxia
A) Stamping gait; patient raises his legs too high & drops them forcefully. B) +ve Romberg’s sign: the patient cannot maintain his erect
position with closed eyes.

C) Patient cannot walk in the dark . D) Patient walk with broad base .



T her ma l Sensa tions

►The Thermoreceptors Internal (Central) thermoreceptors:
These are located in the hypothalamus for detection of the core temperature.

External (peripheral) thermoreceptors:
These include cold and w armt h rec ept ors and are located under the skin. With the highest density in the face and hands.

Cold receptors
free nerve endings and Krause’s end bulbs attached to C & A delta fibers. These receptors respond to temperature from 10 to 35 ºC warm fibers discharge maximal at 25ºC. - Cold spots are greater than hot spots (10 times).

Warm receptors
free nerve endings attached to C fibers. These receptors respond to temperature from 25 to 45 ºC, warm fibers discharge maximal at 35ºC.

►Adaptation of Thermoreceptors
- Cold receptors adapt more slowly than warm receptors. (Both moderately adapting. - There is no adaptation above 45 ºC and below 10 ºC.

►Range of stimulation

of thermal receptors:

At O ºC, there is no action potentials i.e. anaesthesia. O to 10 ºC, cold pain fibres discharge, maximal at 5ºC. 10 to 35 ºC, cold fibres discharge, maximal at 25 ºC. 25 to 50 ºC, warm fibres discharge maximal at 35ºC. At 50 ºC, heat pain fibres discharge.

►Central pathway of thermal sensation
Thermal signals are transmitted to the higher centres through the lateral

spinothalamic tract, specially via the paleospinothalamic pathway.



►Perception of thermal sensation
Thermal sensation mostly protopathic (perceived at the level of the thalamus), but mild changes are epicritic which need the integrity of cerebral cortex.

►Testing the thermoceptive sensations

(Two test tube test)
Test tubes containing hot and cold water at different temperatures can be used.

►Paradoxical cold sensation
- Rise of temperature to about 45-50 ºC leading to false sensation of cold, due to increase in cold receptor discharge. - The more rapid change in skin temperature within the range leading to increased rate of discharge from receptors.


The more number of cold receptors may contribute to this phenomenon.



Damaged tissues release proteolytic enzymes, K+ & histamine Proteolytic enzymes act on globulins in the interstitial Fluid to release kinins. + e.g bradykinin, K and histamine stimulate pain receptors Pain is a protective sensation.

►Pain receptors.

Free nerve endings Three types

1. Mechanical pain Receptors.: stimulated by mechanical injurious stimuli. 2. Thermal pain Receptors.: discussed before. 3. Chemical pain Receptors.: stimulated by chemical stimuli. Chemical stimuli include: bradykinin (most important) serotonin, histamine & K+.

► Distribution of pain receptors
More: Skin, periosteum, arteries, joint surfaces, & tentorium

cerebelli and cranial sinuses.


Less: deep tissues.

Absent: liver parenchyma, lung alveoli and brain.

►Nerve fibres: ►Adaptation:

A delta


C fibres.

Slowly (static-tonic) or nonadaptive receptors.

►Types of pain

Pain is classified according to the:



(a) Site of pain
1. Cutaneous pain. 2. Deep pain. 3. Visceral pain.

(b) Quality of pain

(1) Cut aneous Pai n
Fast (Immediate, acute sharp or pricking)
1. Felts wit hin 0.1 sec ond . 2. Sh ort dura tio n. 3. Me cha nical & Th erma l R. 4. A delt a fibre s. 5. En ds in ce rebr al cort ex. 6. Wel l lo caliz ed. 7. Not felt in dee p tissu es 8. Block ed by hypo xia & pr ess ure 9. Neo spi noth ala mic trac t Neur otra nsm itte r: Glut ama te .

1. Epicritic i.e sharp pricking pain. 2. Protopathic i.e dull aching pain. 3. Burning pain.

Slow (Chronic, burning, aching throbbing nauseous)
1. Af ter one sec ond . 2. Prolo nge d; ann oyin g, intol era ble. 3. Elicit ed by All type s of R. 4. C fi bres 5. Ends in non sp ecifi c th ala mic nucl ei & Re ticu lar form atio n. 6. Poorl y lo cali zed . 7.Oc curs in skin & dee p ti ssue s 8. Blo cke d by co cain e. 9. Pale ospi nth alam ic tract Ne urot ran smit ter: Su bsta nce P.

No te

Fast pain is transmitted by A delta fibers (5-15 m/sec.) from skin (mainly), parietal pleura, peritoneum a & Synovial membrane.

Reactions to pain


Sp inal ref lex es.

(1) Somatic (motor) reflexes:(2) Autonomic reactions:-

Flexor withdrawal reflex.

Cutaneous pain: Pressor effects (increased heart rate & ABP). DEEP & visceral pain: Depressor effects (decreased heart rate & ABP).

(3) Emotional reactions:-Acute pain: Crying and anxiety.

(4) Hyperalgesia:-

mainly due to skin lesion. (increased pain sensibility).

Appreciation of pain
- Fast pain; is appreciated in thalamus and cortex. - Slow pain; is appreciated mainly in thalamus.

Functions of the cortex in pain appreciation
1. Localization of pain 2. Discrimination of type of pain. 3. Modulation of pain by emotional and behavioral factors.

Arousal reaction to pain signals
The non specific thalamic nuclei (intra-laminar nuclei) and reticular formation have a strong arousal effect on the brain which prevents sleep during pain.

(B) D eep pa in Causes:



Diffuse, Dull aching and Depressor effects. - inflammation, ischaemia or muscle spasm.

Bone fractures; due to stimulation of periosteal pain receptors.

Characters of deep pain
1. Dull aching or rhythmic cramps. 2. Diffuse (poorly localized).



3. Depressor autonomic changes: decreased heart rate, decreased arterial blood pressure ,nausea & vomiting.

►Ischaemic pain
Type of deep pain felt in muscles when their blood supply is decreased. The Patients complains of severe pain in the muscles upon walking or running due to accumulation of pain producing substances as lactic acid.

1. Cardiac muscle: angina pectoris. 2. Skeletal muscle: intermittent claudication.

(C) V iscer al pa in

C Fibres

Most of viscera contain only pain receptors. Pain from viscera is carried a long; C fibres. Pain from peritoneum, pleura or pericardium: A delta. It differs from cutaneous pain . Sharp cut in the viscera does not cause pain (why). . Diffuse stimulation of pain nerve ending → severe pain.

Causes Of Visceral Pain
1. Ischaemia: increased acidic metabolites, bradykinin & proteolytic enzymes. 2. Inflammation of peritoneal covering of viscera. 3. Irritation (chemical irritation by HCI in peptic ulcer). 4. Overdistension of a hollow viscus e.g urinary bladder. 5. Spasm of a hollow viscus e.g gut, gall bladder or ureter. Both 4 & 5: Obliteration of blood vesssels → Ischaemic pain.

Characters of visceral pain
1. Dull aching or rhythmic cramps. 2. Diffuse (poorly localized).



3. Depressor autonomic changes: decreased heart rate, decreased arterial blood pressure ,nausea & vomiting. 4. Rigidity of the overlying muscles.

Limitation of the spread of infection. Decrease the mobility of the diseased viscus for relief of pain.
5. Referred to the surface area i.e referred pain.



Ref er r ed pain
Pain originating from viscera but felt in somatic structures which supplied by the same spinal dorsal root ( the same dermatome) of the diseased viscus.

1. Cardiac pain: is felt in left shoulder. 2. Gall bladder pain: is felt in tip of right shoulder. 3. Appendicular pain: is felt around the umbilicus. 4. Gastric pain: is felt between the umbilicus & xiphoid process. 5. Renal pain: is felt in the back, inguinal region & testicles. 6. Teeth pain: referred to other teeth.

Mechanism of referred pain a. Convergence – projection theory
Afferent pain fibres from the skin and viscous converge on the same cells of SGR or thalamus and will finally activate the same cortical neurons. Whatever the source of pain, the cortex will project it to the skin being the commenst source of pain. b. Facilitation theory Afferents of diseased viscera, give facilitation to cutaneous pain cells in Substantia Gelatinosa of Rolandi (SGR), Which leads to facilitation of their stimulation.



• Pain Contr ol Systems
(I) Analgesic system
a) The neurons of the periaqueductal gray area are stimulated by B endorphin reaching them from hypothalamus (neurons of periventricular area) or pituitary (through blood). b) Fibres of periaqueductal and interneurones of secrete (Enkephalin) c) Fibres of raphe magnus nucleus secrete (Serotonin) d) Inhibitory interneurones in spinal cord secrete (Enkephalin).



(II) Brain Opiate System
Opiate receptors in the brain cause pre and postsynaptic inhibition of the nociceptive pathway.

Sites of opiate receptors
1. Periaqueductal gray area. 2. Periventricular aea. 3. Raphe magnus nucleus in medulla. 4. Substantia nigra.

Opioid peptides
(1) Enkephalins.
Act as neurotransmitters at the analgesic system.

(2) Endorphins
-In hypothalamus act as neurotransmitters. -In pituitary act as hormone. Release during stress leading to stress analgesia.

(3) Dynorphin
Very potent analgesic.

Types of opiate receptors
Delta, Mu, Kappa, Sigma & Epislon.

(III) Gate theory
1) Spinal gate:
SGR (substantia gelatinosa of Rolandi) in layers II & III acts as gate. At this level, there is a group of inhibitory enkephalinergic interneurons which form the "Pain Inhibitory complex, PIC". When stimulated, these interneurons block the transmission of pain sensation by presynaptic inhibition of pain-conducting fibers. This gate can be closed by:

Impulses from
1. A beta fibres: (rubbing of skin inhibits pain). 2. A delta fibres; counter irritant and acupuncture inhibit pain. They stimulate cutaneous receptors which send impulses through A delta fibres stimulate the PIC. 3. Cortico-fugal fibres: (thinking decrease pain).
All these fibers causes presynaptic inhibition of pain by activating an interneurone which secrete (GABA).



2)Thalamic gate:
The same "gating" mechanism for pain is found also at the thalamus where pain signals could be blocked by corticofugal fibers or facilitated by intralaminar thalamic nuclei. In this way, the thalamus considered as a secondary gate far pain transmission.

Stress analgesia; A) At the thalamus:

Du ring str ess, Pai n is bl ocke d a t tw o le vels :

(the sec ond gat e o f pa in tran smis sion ).

Corticofugal fibers to the thalamus block by presynaptic inhibition the transmission of pain signals in the thalamus before they reach the cerebral cortex.

B) At the dorsal horn of the spinal cord:
tr ansm issi on).

(the first ga te of pain

The hypothalamus, and other parts of the central analgesia system, activate the spinal PIC which blocks the transmission of pain signals at the dorsal horn.



Melzack and Wall (1965, 1988) developed a comprehensive theory of pain (‘gate-control theory’) which has generally received wide support • Fast ‘touch’ fibres and slow ‘pain’ fibres connect with substantia gelatinosa (SG) and transmission cells (T cells) in spinal cord • T cells send pain information to the brain • SG acts as “gate” to allow or inhibit T cells Activity in fast fibers tends to close the gate (touch but no pain) and slow fibers open the gate (pain) A light touch accompanying a noxious stimulus partially closes gate (reduces pain) — rub skin to alleviate pain Psychological factors? Modify gate via descending pathway and/or release of endogenous opiates (e.g. endorphins) in the CNS producing analgesic effects. Ignore pain to escape from greater danger (e.g. death!)

Headac he


49 Brain is insensitive to pain. Pain sensitive intracranial structure; (Arteries, Veins, Nerves and Dura at the base of the brain) Head ache is referre d pain

a. Supratenterial is refe rred al ong the ophth

almic n → fr ontal Head ache. → occi pital Headach e.

b. Infratentorial is referr ed alon g Cervical 2

Causes of intracranial headache:
1. Meningeal irritation;

me nin gitis ;

gen eral ize d. loca lize d.

Br ain tum our;
2. Migraine headache; 3. Hypertension:

Abn orma l va scul ar phe nom eno n.

He ada che α pu lse Pre ssur e. Rem oval of 20 ml of CS F.

4. Low CSF pressure:

→ bra in desc ent → tra ctio n of th e d ura & h ead ache .
5. Alcoholic headache

al coh ol pr odu ces dir ect meni nge al irrita tio n.
6. Constipation.

Ab sorp tion of tox ins pro duce s di rect me nin geal irri tati on.

Causes of extra-cranial headache
2. Irri tati on of the nas al si nus es. 3. Err ors of refra ctio n . 4. Oti tis medi a. 5. Toot hach e.


1. Mu scul ar spas m of sca lp and nec k m uscl es due to emot ions .

= Incr eas ed pain se nsat ion.



1. primary hyperalgesia;
It occurs in the inflammed skin due to decreased threshold of pain receptors by bradykinin, K, Histamine and prostaglandins. So non painful stimuli become painful.

2. Secondary hyperalgesia;
It occurs in normal skin due to increased threshold of pain receptors. So pain receptors need stronger stimulus, but once pain is elicited, it is very severe It can be explained by (Convergence facilitation theory). Impulses from the injured area facilitate a central neuron. Impulses from the area of secondary hyperalgesia converge on same central neuron. The convergence on a central facilitated neuron explains the exaggerated pain sensibility. Why the threshold of pain is increased in the area of secondary hyperalgesia. The facilitator neuron which arises from the area of primary hyperalgesia exerts lateral inhibition on the stimulator neuron which arises from the area of secondary hyperalgesia.

It occupies broadmann’s area 1,2,3,5,7 and 40. All are behind the central sulcus .


These areas are divided into three main areas.

(1) Somatic sensory area I
► Site:
Post ce ntra l gy rus ( ar ea 3,1, 2)

► Organization of neurons: in to layer s a nd colu mns. ► Representation
Crossed representation i. e re ceiv es sens atio n fr om the opp osit e ½. Inverted representation i.e bod y is repr ese nte d u psid e d own Large areas for thumb & lips i.e area α nu mber of rec epto rs.

► Modality orientation
- Ant erior col umn s fo r m uscl e, tend ons and joi nt move men t & str etch (pro prio cept ive) . - More po steri orly for slo wly ada ptiv e re cep tors an d pr essu re. -Mos t p oste rior for mov ing obj ects on the ski n.

► Functions

It rec eive th e fo llowi ng sen sati ons.

1. Fin e t ouch : Tact ile loca liza tion & discr imin ati on, ster eog nosi s & te xtur e o f ma teri als. 2. Dis crimi nati on of vario us weig hts (pre ssur e sens e). 3. Vib rati on sens e. 4. Se nse of posi tion an d m ove ment s o f joi nts . 5. Discri min atio n of var iou s gr ade s of te mper atur e.

►Destruction of sensory area I A) The person loses ability for:
1. Dis cret e (fi ne) but no t cr ude loc aliz atio n. 2. per cep tion of the ab ove sen sati ons .

B) Temperature; C) Pain;

sens ati on is mo der atel y a ffe cte d. sens ati on is po orly a ffec ted .

(2) Somatic sensory area II
► Site Behind and below the lower part of sensory area I. It occupies areas 40.



► Receives impulses from - Dorsal columns & spino-reticulo-thalamic fibres of both sides. -Sensory area I, visual and auditory areas. ► Representation of the body parts Head area in anterior part, leg area in posterior part, ► Functions It potentiate function of S I It gives simple meaning for the sensory signals.

(3) Somatic association area
► Site behind the lower parts of sensory area I i.e area 5,7 ► Receives signals from a. Somatic sensory area I & II. b. Ventro-basal nuclei of the thalamus. c. Other areas of the thalamus. ► Function Collects information to understand the meaning. ► Effect of removal of association area a. Denial of the existence of the opposite half of the body (Amorphosynthesis) b. Astereognosis.



T hala mus
[I] Specific projection nuclei
to specific portions of cortex.



a. Specific sensory relay nuclei:
1. Medial geniculate body relays impulses to auditory cortex. 2. Lateral geniculate body relays impulses to visual cortex. 3. Postero-ventral nuclei relay impulses to postcentral gyrus. PVMN; from the face to the cortex. PVLN; from the body to the cortex. b. Motor nuclei ventrolateral & ventro-anterior. Relay impulses from BG & cerebellum to motor cortex.

c. Anterior nuclei project to limbic cortex.
Concerned with recent memory and emotion.

d. Dorso-lateral nuclei project to cortical association areas.
Concerned with complex integrative functions as language.

[II] Non specific projection nuclei
so responsible for consciousness and alertness

Midline & intralaminar

- Relay impulses from reticular activating system to all parts of the neocortex, - Act as higher centre for crude (protopathic) sensations.

Lesion of thalamus
(Thalamic Syndrome)


Thrombosis of the thalamo-geniculate artery.

► Lesion
Postroventral nucleus Lateral ventral nucleus 3rd order neurone for all sensation. only motor nucleus in thalamus.

► Effects 1. Sensory - Loss of all sensations on the opposite side of the body initially, then Return of some crude sensations later on. - Return of pain after few months i.e thalamic pain; which needs a stronger stimulus to produce it, and once it is produced, it is very severe. (Secondary hyperalgesia). 2. Ataxia: a) Sensory ataxia: due to loss of proprioceptive sensations. - Positive Romberg sign. - Stamping gait. b) Motor ataxia: due to cutting of connection between cerebellum and cortex. (This connection passes through the lateral ventral nucleus).

- Dysmetria. - Nys tagm us .

- Adi adokokinesi a. - Rebo und.

- Dysarthe ria.

- Drunken ga it .

3. Emotional disturbance




Most of sensations pass through the thalamus except olfaction.

Lesions of the Sensory System
(1) Peripheral nerve
[ a ] Mono-neuropathy:



Loss of all sensation in the area of supply. [ b ] Poly-neuropathy Loss of sensations from the distal parts of the limbs e.g gloves and stock anaesthesia especially for pain. [ c ] Lesion of the dorsal roots: Loss of sensations from the corresponding dermatomes and decrease of deep reflexes.

(2) Spinal cord lesion
[ a ] Subacute Combined Degeneration (SCD)



This is a slowly-progressive disease due to deficiency of vitamin B12 , it is often associated with pernicious anaemia. There is polyneuropathy and bilateral degeneration of the dorsal and lateral columns of the spinal cord specially in the lumbosaeral region.

[ b ] Syringomyelia
This is a slowly progressive disease, congenital, in middle ages and females are more affected. There is abnormal overgrowth of neuroglial tissue (gliosis) associated with cavitation leading to widening of the central canal of the spinal cord. (usually cervical).

pain & temperature fibers, as they cross in front of the central canal.

- Loss of pain and temperature on both sid es at the leve l of th e le sion
→ jacket like Dissociated sensory loss. - LMNL du e to d ama ge of a nter ior horn cel ls at t he level of the les ion. - Autonomic manifestations; du e dama ge of later al horn cell s in th e a ffe cte d

seg ment s. (Horner’ s Syndrome).

Crude touch may be preserved because it passes also in the dorsal column All Sensations carried in the dorsal column e.g fine touch are not affected i.e dissociation of cutaneous sensations occurs.



[c] Tabes dorsalis

Syphilitic disease

It attacks the dorsal roots central to the dorsal root ganglion of lumbo-sacral region of spinal cord.

►Manifestations 1. Severe pain as it irritates pain fibers at first due to irritation of pain
conducting nerve fibres.

2. Then, degeneration of gracile and cuneate tracts leading to loss of fine
touch, pressure, vibration sense and proprioceptive sensation. - Loss of Proprioceptive sensation leading to;

Inco-ordination of voluntary movement in absence of paralysis characterized by the following manifestations;
A) Stamping gait ; patient raises his legs too high &drops them forcefully. B) +ve Romberg’s sign: the patient cannot maintain his erect.

position with closed eyes.


C) Patient cannot walk in the dark. D) Patient walk with broad base.

3. In advanced stage of the disease;
a. Loss of spinothalamic sensations. b. Damage of afferent limb of the reflex (e.g. Micturition) leading to loss of micturition reflex. c. Damage of pretectal nucleus leading to loss of light reflex. (Argyll-Robertson pupil).

[d] Brown Sequard syndrome 1- At the level of the lesion

i.e Hem isec tio n of th e sp . cd . sa me side

Sensory : loss of all sens ati ons at the corr esp ondi ng derm ato me . Motor : Low er m otor ne uron e lesio n i. e fl acci d p araly sis.

2- Below the level of the lesion On the same side
1. Sensory : lo ss of p ost colu mn sens ati ons i. e fi ne touc h, Press ure , vi brati on, se nse of posi tion & sens e o f mo vem ent s. 2. Motor : Upp er m otor ne uron e lesio n (UMNL ) i. e S past ic parat ysis , (h yper efle xia & +ve Ba bins ki sign) . On the opposite side 1. Sensory; lo ss of a ntro lat eral col umn sen sati ons i.e pai n, tem p,


crud e t ouch & crud e pr ess ure 2. Motor No los s.



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