TRANSECTION OF THE SPINAL CORD 1 FINAL BY DR K AMBAREESHA

drambreesh 13 views 47 slides Apr 14, 2025
Slide 1
Slide 1 of 47
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47

About This Presentation

Spinal cord transection, a complete or partial severing of the spinal cord, results in a loss of motor and sensory function below the level of injury, often caused by significant trauma.


Slide Content

TRANSECTION OF SPINAL CORD Dr. K. Ambareesha ,. PhD Associate professor Physiology

Complete transection of spinal cord Spinal cord is completely separated from the higher centers Cause : Gunshot wounds, occlusion of blood vessel due to thrombosis

Effects of complete transection of spinal cord are described in following three stages: Stage of spinal shock Stage of reflex activity Stage of reflex failure

Transection 3 types: complete, incomplete and hemisection . A. Complete Transection of Spinal Cord immediate effects 1. Stage of spinal shock (or stage of flaccidity): Features Portion above the cut-unaffected; below the section: deprived of all activities. Duration of shock: 3 weeks Cause: Stoppage of tonic bombardment of spinal motor neurons by excitatory impulses in the descending pathway. Flaccid paralysis

Subnormal body temperature. Muscle tone: completely lost. All reflexes (superficial and deep): +++ ↓ or lost. All sensations below transection : lost. Urinary bladder and rectum: paralysed Penis: flaccid, erection impossible. BP ↓ s

Later effects (after 1 wk) 2. Stage of reflex activity Autonomic reflexes recover within days or weeks retention of urine (sphincter vesical recover very soon than detrusor muscle) paralysed blood vessel tone returns Muscle tone returns slowly, reflex in character → paraplegia in flexion (limbs adopt a position of flexion) spinal man cannot stand unsupported . No muscle wasting.

Paraplegia in flexion (A) and extension (B)

3. Reflex (Failure) movements: return in approx. 2 weeks. Cause ( i ) Denervation hypersensitivity to the mediators; (ii) growing of collateral Features Abnormal Babinski response Mass reflex - advantage Deep (or tendon) reflexes: sluggish After 6 months, marked activity ↑ extensor reflexes. Coitus (sexual) reflex: absent.

B. Incomplete or Irregular Transection of the Spinal Cord Stage of spinal shock: As above Stage of reflex activity: → paraplegia in extension . Features All features of UMNL Involuntary movement: infrequent. Reflex movements ( i ) extensor thrust reflex: positive; (ii) Crossed extensor reflex: positive.

C. Hemi section of the spinal cord: Brown Sequard Syndrome (ANS functions remain normal) On the same side On the opposite side Below the level of hemisection Extensive motor loss of UMNL type Little sensory loss Below the level of hemisection Either no paralysis or paralysis of few muscles of UMNL type. Extensive sensory loss At the level of hemisection Sensory changes LMNL type Motor changes At the level of hemisection Sensory changes: Some loss of pain Motor changes : Nil 3. Above the level of hemisection A band of hyperaesthesia 3. Above the level of hemisection Hyperaesthesia may be referred .

Hemisection of the spinal cord

Brown sequard syndrome i.e. motor & sensory changes below the level of hemisection

Sensory Disturbances A. Syringomyelia ( Syrinx = cavity; myelia = S. cord) Cause: Extensive growth of neuroglial tissue round the central canal of the spinal cord with cavity formation. Common site: Cervical region

Tabes dorsalis (A) Pale dorsal columns; (B) Characteristic features of tabes dorsalis

Features Lightning pain (a) perforating ulcers at pressure points. anaesthesia round the anus, over legs, upper chest and hands. Charcot joint . Loss of position sense and vibration sense. Deep (or tendon) reflexes: lost. Marked disturbance of voluntary movements.

C. Disseminated (multiple) sclerosis Cause: Patchy widespread destruction of myelin in the CNS. Sign and symptoms manifest according to the ascending and descending pathways involved. (It is a crippling disease ).

Disseminated (multiple) sclerosis

2. CEREBELLUM

Anatomical lobes:

Functional parts of the cerebellum

Intro Cerebellum is the largest part of the hindbrain and lies behind the pons and medulla oblongata separated by the IV ventricle. It consists of a narrow, worm like central body vermis , and two lateral lobes, the right and left cerebellar hemisphere. The cerebellum is connected with the brain stem by three peduncles: i . Inferior cerebellar peduncles—Between Cerebellum and medulla oblongata. ii. Middle cerebellar peduncles—Between Cerebellum and pons iii. Superior cerebellar peduncles—Between Cerebellum and midbrain

Phylogentic classification of cerebellum:  Archicerebellum  Paleocerebellum  Neo cerebellum Anatomical division of cerebellum:  Anterior lobe  Posterior lobe  Flocculonodular lobe Functional division of cerebellum:  Vestibulocerebellum  Spinocerebellum  Cerebrocerebellum

Functional divisions:  Vestibulocerebellum ( Flocculonodular lobe)  Spinocerebellum ( Vermis & intermediate zone)  Neocerebellum ( cerebrocerebellum )

Vestibulo cerebellum:  Connected to vestibular apparatus  Role in control of body posture, equilibrium & visual fixation Spinocerebellum :  Mainly connected to spinal cord Vermis : Controls muscle movements of axial body, neck, shoulder, hips  Maintains posture via vestibulospinal & reticulospinal pathways Intermediate zone: Control of muscular contraction of upper & lower limbs via corticospinal tract

Cerebrocerebellum :  Connected with pons and cerebral cortex  Concerned with overall planning and programming of sequential motor movements  Coordinates the timing and duration of contraction of different groups of muscles

Cerebellar cortex: It is arranged in three uniform layers. a . Outer molecular layer- consists of dendrites of purkinje cells b. Intermediate purkinje layer- consists of cell bodies of purkinje cells c . Inner granular layer- consists of granular and golgi cells

Functional unit of cerebellum. PF = Parallel fi bres , P = Purkinje cell, Gr = Granule cell, Go = Golgi cell, CF = Climbing fi bre .

Afferent input to cerebellar cortex: Climbing fibers – arises from inferior olivary nucleus and conveys proprioceptive impulses from different parts of the body to cerebellar cortex Mossy fibers- main afferent fibers to cerebellar cortex and deep cerebellar nuclei

Cerebellar nuclei: These are masses of grey matter scattered in white matter of cerebellum and has four nuclei on each side. a. Fastigial Nucleus: It is placed near the midline on the roof of IV ventricle. b. Emboliform nucleus: Lies below the above nuclei. c. Dentate nucleus: This crenated nuclei situated lateral to all other nuclei and is the largest of all

Cerebellar nuclei.

Afferents to cerebellum  Cortico - ponto cerebellar fibers  Dorsal spinocerebellar tract  Ventral spinocerebellar tract  Cuneo cerebellar fibers  Vestibule cerebellar fibers  Tecto cerebellar fibers

Afferent tracts to the cerebellum

Efferents from cerebellum:  Cerebello dentato rubro thalmocortical tract  Cerebello olivary tract  Cerebello rubr spinal tract  Fastigo bulbar tract

Connections

Functions

Pathways for cerebellar control of voluntary movements

Pathways of cerebellar error control of voluntary movements

Applied aspects: Cerebellar disorder: the characteristic symtoms are seen. No sensory loss or paralysis is seen 1. Ataxia 2. Scanning of speech 3. Intention tremor 4. Nystagmus 5. Asthenia 6. Atonia 7. Dysmetria 8. Decomposition 9. Drunken gait 10. Dysdiadochokinesia

CEREBELLAR LESION

Name the features of cerebellar lesion

Thank you