PRESENTER: Dr.

Mayur Surana
PROFESSOR & H.O.D: Dr. S.S.Sant ASSOCIATE PROFESSORS: Dr R.M.Bansode & Dr.Kiran Pabitwar ASSISTANT PROFESSORS: Dr.J.J Pawar & Dr.Shilpa Ingale
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S In Vertebral Column P LOCATION I N A From Foramen Magnum to L lower border of L1 Vertebra EXTENT
C O R D

LENGTH

M: 45cm F : 43 cm
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MENINGES OF SPINAL CORD

3.PIA MATER (pia=delicate) --Innermost meninx. --Subarachnoid space:CSF- a shock absorber & suspension system for SC. 2.ARACHNOID MATER (arachn=Spider) --Middle meninx --Subdural space:Interstitial fluid

1.DURA MATER (=tough mother) --Most superficial -- From Foramen Magnum to S2 Vertebra. --Epidural Space: Fat & Connective tissue.

EXTERNAL ANATOMY OF SPINAL CORD

CYLINDRICAL SHAPE C & L ENLARGEME NTS

CAUDA EQUINA

FILUM TERMINALE

CONUS MEDULLARIS
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TERMINAL PORTION OF SC

SPINAL SEGMENTS & INNERVATION

BLOOD SUPPLY OF SPINAL CORD

ARTERIAL SUPPLY: 3 longitudinal arteries viz.Anterior spinal artery & L & R posterior spinal art.
Below cervical level,major contribution by Radical arteries. Largest ant.radicular arteries is artery of Adamkiewicz or Anterior Radicularis Magna(ARM)

APPLIED ASPECT: Damage to these radicular arteries leads to Spinal cord infarction & Paraplegia.

3 anterior & 3 posterior spinal veins drained by Radicular veins into internal vertebral (epidural) venous plexus. There is free communication between internal & external vertebral venous plexus. APPLIED ASPECT OF VENOUS DRAINAGE: No valves in Spinous venous network.As the Prostatic plexus is continuous with Vertebral venous plexus, neoplasms originating in Prostate may metastatize & lodge in Vertebrae or SC.
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PWF

LWF

AWF

NEURONS IN ANTERIOR GRAY HORN (send motor nerve fibers to muscles) 1.lpha motor neurons: Large and multipolar cells. Axons end in groups of SMF(extrafusalfibers)

NEURONS IN GRAY MATTER OF SPINAL CORD

2.Gamma motor neurons: Smaller cells scattered among motor neu. Axons to intrafusal fibers of muscle spindle. 3.Renshaw cells: Inhibitory neurons Role in synaptic inhibition at Spinal Cord
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Lateral gray horn(LGH) is a small projection between the ant. & post. horns present in thoracic & upper two lumbar segments only.

Cells in LGH called intermediolateral horn cells.

These cells give rise to sym. preganglionoc fibers. These fibers leave the SC through ant.nerve root.
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These contain the sensory neurons which receive impulses from receptors of the body through post.nerve root fibers.

1.SUBSTANTIA GELATINOSA OF ROLANDO: Cap like material at the apex of post.horn. 2.MARGINAL CELLS: Cover the Substantia gelatinosa at the tip. 3.CHIEF SENSORY CELLS: Present in remaining portion of Posterior column
4.CLARKES COLUMN OF CELLS: 12 Well-defined cells present in the innermost part.

The different collection of nerve fibers passing through the spinal cord.
Long Tracts

Short tracts

Association

Commisural

Ascending

Descending

Connect adjacent Connect opp.halves of Sensory impulses Motor impulses from segment of SC same segment of SC from SC to brain Brain to SC 13

ASCENDING TRACTS
These tracts carry various sensations. The ascending tracts in PWF formed by FON. All other ascending tracts formed by fibers of SON of sensory pathway. AT IN AWF AT IN LWF 1.Ant.spinothalamic 1.Lat spinothalamic tract. tract 2.Ventral spinocerebellar AT IN PWF 1.Tract of Gall(Fasciculus gracilis) 2.Tract of Burdach (Fasciculus cuneatus) 3.Comma tract of Schultze(Fasciculus interfascicularis)
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3.Dorsal spinocerebellar . 4.Spinotectal tract.

5.Fasciculus dorsolateralis. 6.Spinoreticular tract. 7.Spinoolivary tract. 8.Spinovestibular tract.

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ANTERIOR SPINOTHALAMIC TRACT INTRODUCTION: Formed by fibers of second order neurons of the pathway of Crude touch.

SITUATION: Anteriior white funiculus near periphery.

ORIGIN: From FON situated in post.nerve root ganglion. (FON receive impulse of Crude touch sensation from the pressure receptors. Fibers:Chief sensory cells;which form SON of Crude touch pathway. COURSE: Fibers ascend and enter the AWF Medulla Pons Midbrain Thalamus

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TERMINATION: Ventral post.lat nucleus of Thalamus. The cells of Thalamic nucleus form TON of pathway and reach somesthetic area of Cerebral cortex. FUNCTION: Impulse of Crude touch(protopathic sensation) APPLIED PHYSIOLOGY: Unilateral lesion: Loss of crude touch in opp. Side,below the level of lesion. Bilateral lesion: Loss of crude touch & sensations like itching & tickling.
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TRACT OF GALL (FG) & BURDACH (FC)

INTRODUCTION: Ascending tracts in PWF;uncrossed fibers of FON. SITUATION: PWF of SC. Medially FG; Laterally FC. ORIGIN: Cell bodies of neurons in post.root ganglion. FON so no synapse in SC. TERMINATION: 1. The fibers of FG terminate in nucleus gracilis & fibers of FC terminate in nucleus cuneatus of MO. 2. Fibers from medullari nuclei form SON & ascend as medial lemniscus & end in PLN. of Thalamus. 3. From here fibers of TON relay to Cerebral cortex.

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FUNCTIONS : 1.Fine i.e.epicretic tactile sensation. 2.Tactile localization.

3.Tactile discrimination. 4.Sensation of vibration.

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5.Conscious kinesthetic sensation.

6.Stereognosis
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APPLIED PHYSIOLOGY:
Lesion of these two tracts lead to loss of following functions in same side of body: 1.Fine i.e.epicretic tactile sensation. 2.Tactile localization. 3.Tactile discrimination. 4.Sensation of vibration. 5.Conscious kinesthetic sensation. 6.Stereognosis

Loss of Proprioception leads to condition called Sensory ataxia or posterior column ataxia.
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Tract
1. Ant.spinothalamic 2. Lat spinothalamic

Origin
Chief sensory cells Subst.gelatinosa

Course
Crossing in SC. Crossing in SC

Termination
Ventral PLN of Thalamus Ventral PLN of Thalamus

Function
Crude touch. Pain & temp.

3. Gowers tract
4. Flechsigs tract 5. Spinotectal tract 6. Spinoreticular

Marginal cells
Clarkes column Chief sensory cells Intermediolateral

Crossing in SC
Uncrossed Crossing in SC Cr & Uncrossed

Ant. Lobe of Cerebellum

Ant.lobe of Cerebellum Superior colliculus RF of Brainstem

Sub.kinesthetic
Sub.kinesthetic Spinovisual ref. Consciousness Awareness

7. Spinoolivary & 8. Spinovestibular

Not specific

Both

Olivary & lat.vestibular nucleus

Proprioception

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Formed by motor nerve fibers arising from brain & descending into SC.

Two types of descending tracts;viz:

1.PYRAMIDAL 2.EXTRAPYRMIDAL

Newer control system Responsible for fine,specific,Isolated & precise movements.

Primitive Alternate route for volitional impulses The platform on which PT works. Cortical regions (area 8 & 6) control these tracts. 23

PYRAMIDAL TRACTS
INTRO: Tracts concerned with voluntary motor activities. Also called Corticospinal Tracts. Two Corticospinal tracts.viz.Anterior & lateral SPECIALITY: All fibers of PT present since birth. But myelination only about two years after birth. The fibers of PT are nothing but axons of UMN. ORIGIN: 1)Mostly from Giant cells/Betz cells of area no.4 in Precentral gyrus of frontal lobe. 2) Some fibers arise from Premotor area(no.6) & Somatosensory areas (3,1,2)

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COURSE: Corona radiata. Descent through IC,midbrain & pons. App. of Pyramid on upper surface of Medulla Lateral White funiculus crossing-Crossed PT 20% fibers uncrossed;descend down through AWFAnterior Corticospinal tract

TERMINATION: All fibers terminate in motor neurons of ant.gray horn. WHAT ARE UMN AND LMN?? Neurons giving origin to fibers of PT & their axons UMN motor neurons in the SC & their axons-LMN

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FUNCTIONS OF PT: 1)Transmission of motor impulse from motor area of Cerebral cortex to alpha motor neurons of SC. 2)Concerned with fine,skilled movements. APPLIED PHYSIOLOGY: 1)Lesion in neurons of Motor cortex & fibers of PT called UMN lesion. 2)Lesion in ant.gray horn cells in SC & motor neurons of Cranial nerve nuclei situated in Brain stem-LMN lesion
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EFFECTS 1.) Muscle tone 2.) Paralysis 3.) Wastage of muscle 4.) Sup.reflexes 5.)Plantar reflexes

UMN Lesion Hypertonia Spastic type No wastage Lost Abnormal(Babinski)

LMN lesion Hypotonia Flaccid type Wastage Lost Plantar reflex absent

6.) Deep reflexes

7.) Clonus 8.) Elec.activity

Exaggerated
Present Normal

Lost
Lost Absent

9.) Muscles affected

10.) Fascicular twitch in EMG

Groups of muscles
Absent

Individual muscles
Present
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Applied Physiology Of Spinal Cord

A].TRAUMATIC INJURIES: oTrauma such as accidents,violence,falls,diving etc. oMost common sites :Cervical,lower Thoracic & Upper Lumbar. oAny of the following paralysis may occur: 1)Monoplegia 2)Diplegia

3)Paraplegia
4)Hemiplegia 5)Quadriplegia
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B] COMPLETE TRANSECTION (tran=across; -section =a cut) of SC

--results in complete loss of sensations & voluntary movements below the level of the transection.
C] HEMISECTION:-( a partial transection)

Hemisection results in triad of symptoms below the level of the injury called Brown-sequard syndrome:
1)Loss of ipsilateral Proprioception. 2)Ipsilateral paralysis( damage to lat CT) 3.)Contralateral loss of pain & temp sensations (damage to spinothalamic tract)
D] SPINAL SHOCK(immediate response to SC injury)

Areflexia Flaccid paralysis Low blood pressure Urinary bladder dysfunction Loss of somatic sensations

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1.MULTIPLE SCLEROSIS: Introduction: Autoimmune progressive disease causing destruction of myelin sheaths surrounding neurons in the CNS. Usually appears between age of 20-40 Most common in whites & in females(F:M2:1)
Causes: Genetic susceptibility? Environmental factors (herpes virus?) Pathology In multiple regions myelin sheath deteriorates to scleroses,which are hardened scars or plaques. 32 Destruction of myelin sheaths slows & short-circuits nerve impulse propagation.

SYMPTOMS OF MS 1.Heaviness or weakness in muscles. 2.Abnormal sensations. 3.Diplopia. N.B: One attack follows another over the years resulting in progressive loss of functions. TREATMENT OF MS: -- Injection of beta interferon. This treatment lengthens the time between relapses,decreases the sensitivity of relapses & slows formation of lesions.

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2.AMYOTROPHIC LATERAL SCLEROSIS(ALS).. (a=without;myo=muscle;trophic=nourishment)

A progressive degenerating disease attacking motor areas of Cerebral cortex,axons of UMN in lateral white columns & LMN cell bodies Begins from sections of SC that serve hands & arms and spreads rapidly affecting whole body. Does not affect intellect or sensation. Death occurs in 2 to 5 years. ALS is commonly known as Lou Gehrigs disease.

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1)Acc to one theory there is build up in synaptic cleft of NT glutamate released by motor neurons. This excessive build up is due to mutation of protein that normally deactivates & recycles the NT. The excess glutamate causes malfunction of motor neurons & eventually their death.

2.)Damage to motor neurons may be due to: Free radicals viral infection Autoimmune deficiency of NGF responses environmental apoptosis toxins

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SYMPTOMS OF ALS: 1.Fatigue 2.Muscle pain 3.Spasticity of muscles 4.Excess salivation 5.Insomnia

TREATMENT: 1)Riluzole-a drug which decreases release of glutamate. 2) Symptomatic. 3.)Supportive care & hospice nurses.
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INTRODUCTION:

A slow,progressive disease affecting both motor & sensory functions of SC.

PATHOPHYSIOLOGY:

Selective degeneration,affecting dorsal root Fibers of Post. white column of SC also affected.
FEATURES OF TABES DORSALIS:

1.Exaggeration of pain sensation. 2.Loss of sensations leading to Charcots joint. 3.Loss of tactile & kinesthetic sensations. 4.Loss of all reflexes due to loss of sensations. 5.Ataxia,awkward & stamping gait. 6.Hypotonicity of bladder muscles & loss of micturition reflexes

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4.SYRINGOMYELIA Presence of fluid filled cavities in SC is known so. PATHOPHYSIOLOGY: 1)Overgrowth of neuroglial cells accompanied by cavity formation. 2)Cavity appears in gray matter near central canal & later extends to white matter. 3)Lower Cervical & upper Thoracic seg.affected the most. FEATURES 1)Loss of pain & temperature sensations. 2)Muscular weakness. 3)Loss of sensations makes the person prone to injury. 4)Involvement of Pyramidal & extrapyramidal system results in complete paralysis of limbs.

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5. SHINGLES
FEATURES: An acute infection of PNS caused by herpes zoster virus. After recovery from Chicken pox,the virus retreats to post.root ganglion. The reactd virus overcomes weakened immune system & leaves the ganglion. It travels down sensory neurons of the skin by fast axonal transport. Clinical features include pain,skin discoln & characteristic line of skin blisters. The blister line marks the dermatome of sensory nerve.

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Definition:
A fast automatic unplanned sequence of actions in response to a peripheral nervous stimulation that occurs without our consciousness.

Reflex arc:
The pathway followed by nerve impulses that produce a reflex is called Reflex arc.

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COMPONENTS OF REFLEX ARC 1.RECEPTOR: End organ receiving the stimulus & generating impulse.

2.AFFERENT NERVE: Transmits sensory impulse from receptor to the centre

3.CENTER: Receive sensory impulse & transmits motor impulse.It may be in the Brain or SC 4.EFFERENT NERVE: Transmits motor impulse from center to effector organ. 5.EFFECTOR: Muscle or gland which responds to stimulus.

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A.]Depending on whether inborn or acquired:

1.Unconditioned reflex:
E.g.Secretion of saliva on placing any object in mouth.

2.Conditioned reflex:
E.g.Secretion of saliva by sight,smell etc. of known edible substance.

B] Depending upon situation of center:

1.Cerebellar reflex. 2.Cortical reflex. 3.Midbrain reflex. 4.Bulbar reflexes. 5.Spinal cord reflexes.
a.Segmental : e.g.Tendon reflex. b.Intersegmental : e.g.crossed extensor. c.Suprasegmental : e.g.Postural reflex
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C] Depending upon purpose:

1.Protective/Flexor/Withdrawl reflexes: Protect the body from nociceptive stimuli. 2.Antigravity/Extensor reflexes: Protect the body against gravitational force.

D]Depending upon no. of synapse:

1.Monosynaptic reflex: e.g.Stretch reflex due to stimuln of muscle spindle. 2.Polysynaptic reflex: e.g.Withdrawl reflex

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E]Depending upon clinical basis:

1.Superficial reflexes. a).Mucus membrane reflexes. b.)Cutaneous reflexes. 2.Deep reflexes. 3.Visceral reflexes. 4.Pathological reflexes.
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ONE WAY CONDUCTION: Bell Magendie law: Unidirectional transmission of impulseR C E SUMMATION a.)Spatial Summation: Separate stimulation of nerve fibersNo response. If both nerve fibers stimulated together with stimulus of same strength then muscle contracts. AB AB A B NO RESPONSE RESPONSE b.)Temporal summation: Stim n of one nerve fiber repeatedly with subliminal stimulussumm n -- RESPONSE A+A+A+A+A+A = RESPONSE 45

OCCLUSION: Occurs due to overlapping of nerve fibers. A = 9 ; B = 9;..A + B = 12 AFTER DISCHARGE Even after cessation of stimulus,the reflex activity i.e. contraction may be prolonged for some time.

REBOUND PHENOMENON: The reflex activity if inhibited for some time & inhibition suddenly removed,the reflex activity becomes more forcerful than the force before inhibition.
FATIGUE: Failure to respond to the continuously elicited response

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Four important somatic spinal reflexes are: 1.The stretch reflex 2.The tendon reflex. 3.The flexor (withdrawl) reflex 4.The crossed extensor reflex

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THE STRETCH REFLEX

Characteristics:
The reflex causes contraction of skeletal muscle in response to stretch. A feedback mechanism to control muscle length causing muscle contraction Muscle spindle monitor changes in length. Integrating center axon terminal form NMJs with skeletal muscle fibers. Ipsilateral reflex. Muscle tone a small degree of contraction present when muscle at rest. Reciprocal innervation: prevents conflict between agonist & antagonistic muscles Relay of nerve impulses to the brain: coordination of muscle movement & awareness that reflex has occurred.
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THE TENDON REFLEX

CHARARCTERISTICS: A feedback mechanism to control muscle tension. Causes muscle relaxation before muscle force becomes so great that tendons might be torn. Sensory receptors are tendon organs (Golgi tendon) Tendon organs detect & respond to changes in muscle tension caused by passive stretch or muscular contn . Inhibitory NT hyperpolarizes motor neuron causing muscle relaxn relieving tension Reciprocal innervation: Tendon reflex brings relaxn of muscle attached to tendon organ;it also triggers contraction of antagonists. 49 Relay of nerve impulses to brain as in stretch reflex.

THE FLEXOR REFLEX (WITHDRAWL REFLEX)

CHARACTERISTIC A Polysynaptic,ipsilateral ,intersegmental reflex.

THE CROSSED EXTENSOR REFLEX

CHARACTERISTIC: A Polysynaptic,contralateral, intersegmental reflex. Synchronizes extension of contralateral limb with the withdrawl (flexion) of the stimulated limb.
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REFLEX

STIMULUS

RESPONSE

AFFERENT NERVE

CENTRE

EFFERENT NERVE

1.Corneal

Irritation of cornea

Blinking of eye

V Cranial nerve

Pons

VII Cranial

2.Conjunctival

Irritation of conj.

Blinking of eye

V Cranial nerve

Pons

VII Cranial

3.Nasal reflex

Irritation of nasal mucus membrane

Sneezing

V Cranial nerve

Motor nucleus of X Cranial nerve

X Cranial & UCN

4.Pharyngeal

Irritation of pharynx

Retching of mouth

IX Cranial nerve

Nuclei of X Cr.nerve

X Cranial

5.Uvular reflex

Irritation of uvula

Raising of uvula

IX Cranial nerve

Nuclei of X Cr.nerve

X Cranial

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REFLEX 1.Scapular

STIMULUS Irritation of skin at interscapular space

Stroking abdominal wall below costal margin Stroking abdominal wall at umbilical & illiac level

RESPONSE Contraction & indrawing of scapula

CENTER C5 T1

2.UAR

Ipsilaterral abd . muscle contraction & movement of umbilicus towards stroke Ipsilaterral abd . muscle contraction & movement of umbilicus towards stroke

T6 T9

3.LAR

T10 T12

4.Cremastric

Stroking at upper & inner aspect of thigh

Stroking the gluteal skin

Elevation of testicles

L1 ,L2

5.Gluteal

Contraction of glutei

L4,L5; S1,S2

6.Plantar
7.Bulbocavernous

Stroking the sole

Stroking dorsum of glans

Plantar flexion of toes

Contraction of Bulbocavernous

L5 S2
S3 S4

8.Anal

Stroking the perianal region

Contraction of anal sphincter

S4,S5

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DEEP REFLEXES
REFLEX 1. Jaw jerk STIMULUS Tapping miiddle of chin RESPONSE Closure of mouth CENTER Pons V Cranial nerve C5,C6 C6 C8

1. Biceps jerk 2. Triceps jerk

Percussion of biceps tendon Percussion of triceps tendon

Flexion of forearm Extension of forearm

3. Supinator jerk
4. Wrist endon / Fiexion reflex 6. Knee jerk/ Patellar tendon

Percussion of tendon over styloid

Percussion of wrist tendons

Supination & flexion of forearm

Flexion of corresponding finger

C7,C8
C8,T1

Percussion of patellar ligament

Extension of leg

L2 L4

7. Ankle jerk/ Achilles tendon

Percussion of Achilles tendon

Plantar flexion of foot

L5 S2
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VISCERAL REFLEXES
a)Direct Light reflex b)Consensual/Indirect light reflex c) Accomodation reflex:constriction of pupils,convergence of eyeball & increase in ant. curvature of lens d ) Ciliospinal reflex: stimulation of skin over neck causes pupil dilatation.

Pressure over eyeball causes decrease in heart rate.

Pressure over carotid sinus causes decrease in heart rate& blood pressure.
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1.BABINSKIS SIGN Abnormal plantar reflex named after the discoverer N .plantar reflex:Plantar flexion of all toes & dorsiflexion &inversion of foot. But in Babinskis sign: Dorsiflexion of great toe & fanning of other toes.

BABINSKI SIGN IS SEEN IN: Physiologically in infants below age of 1 year. In normal subjects during deep sleep. UMN lesions such as CVD (capsular hemiplegia,disseminated sclerosis etc.) Spinal cord tumors (the PT being very sensitive to pressure) Deep narcosis,Coma. 55

 Older extrapyramidal system concerned with protective nociceptive flexor withdrawl reflex. The newer control system (PT) keeps the primitive activities under check. When damaged,older activities are released from its inhibitory effect This is expressed as nociceptive flexor withdrawl reflex,a part of which is Babinski response. Thus,Babinski sign is a release phenomenon
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Clonus is a series of rapid & repeated jerky movements,occuring during eliciting deep reflex. It occurs when deep reflexes are exaggerated due to hypertonicity of muscles in PT lesion. Well seen in calf muscles-Ankle clonus & quadriceps patella clonus

a)Patellar clonus: Patients leg is extended & patella is suddenly pushed down towards foot. Results in clonic contractions of quadriceps muscle resulting in rhythmic movements of leg.
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b)Ankle clonus: Supporting knee of patient in slightly flexed position,perform dorsiflexion of foot.The sudden stretch of calf muscles causes their rhythmic,alternate contractions. Ankle clonus is a characteristic of UMN lesions.

While eliciting a tendon jerk,some slow oscillatory movements are developed instead of brisk movements.These movements are called pendular movements. Unlike clonus,PM occur because of hypotonicity of muscles. Very common in Cerebellar lesions.
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S E E

Y O U
S O O N

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