1. Spinal shock occurs immediately after complete transection of the spinal cord and is characterized by a complete loss of all reflexes below the level of lesion lasting 2-6 weeks.
2. Early recovery of reflexes begins after spinal shock and includes weak return of the stretch reflex and appearance of new reflexes like the plantar reflex.
3. Full recovery of reflexes may take 6 months as reflexes further strengthen and autonomic functions partially return through reorganization at the spinal level.
Chandrapur Call girls 8617370543 Provides all area service COD available
Â
motor system.pptx
1. ⢠Motor nervous system
⢠Reflex arc :
⢠Consists of :
⢠Stimulus
⢠Receptor
⢠Afferent
⢠Center
⢠Efferent
⢠Response
2.
3. ⢠White matter Grey matter
posterior horn
sensory neurons
anterior horn
motor neurons
4. ⢠Spinal reflexes:
Monosynaptic reflexes Polysynaptic reflexes
-Reflex having only one synapse
-No interneurones
-The strech reflex is the only mono
synaptic reflex
-Reflex containing more than one synapse
---may reach 100 interneurones
-Ex âFlexor withdrawal reflex
5. ⢠Stretch reflex:
⢠Def: Reflex contraction of the muscle in response
to stretch.
⢠Components of the stretch reflex:
Stimulus âstretch of the muscle extrafusal fibers
Receptor â Muscle spindle
Afferent -thick myelinated fibers (primary,secondary)
Center â spinal cord (monosynaptic)
Efferent â thick myelinated A alpha fibers
Response â muscle contraction
6. ⢠Structure of the muscle spindle:
⢠1-mehanoreceptors
⢠2-monitor change in muscle length
⢠OR rate of change of muscle length
⢠3-spindle shape
⢠4-encapsulated & ends of capsule are attached to
tendons on both sides of muscle
⢠5-distributed through out the muscle length
⢠6-each muscle has many spindles
⢠7-each spindle contain 2-10 intrafusal muscle
fibers
7.
8. ⢠Intrafusal muscle fibers:
⢠-smaller than extrafusal fibers
⢠-less striated than ordinary fibers
⢠-Parallel with muscle fibers
⢠-intrafusal muscle fibers are 2 types
⢠-end of chain fibers are attached to side of bag
fibers
Nuclear bag fibers Nuclear chain fibers
- Thicker than nuclear chain
- Longer than nuclear chain
- 1-3 nuclei in each spindle
-thinner
-shorter
-3-9 nuclei in each spindle
9. ⢠-the central portion of the intrafusal fibers is
⢠*the receptor area
⢠*stretcheable
⢠*not contractile
⢠*contain no Actin or Myosin
⢠-the peripheral part of intrafusal fibers is
contractile (contain actin & myosin)
10. ⢠Innervation of muscle spindle:
⢠Afferent (sensory) ----*primary ending
⢠*circle central part of nuclear bag and chain
⢠*secondary ending
⢠*circle nuclear chain only
⢠Efferent (motor)
⢠*dynamic gamma efferent---to peripheral
contractile part of nuclear bag
*static gamma efferent ----to peripheral contractile
part of nuclear chain
11.
12.
13. ⢠Properties of stretch reflex:
⢠-monosynaptic
⢠-fastest reflex in body
⢠-restricted to stretched muscles
⢠-show receprocal innervation
⢠-more in antigravirty muscles
⢠-does not show fatigue
14. ⢠Components (types) 0f stretch reflex:
⢠Static stretch reflex
⢠Dynamic stretch reflex
⢠Static stretch reflex Dynamic stretch reflex
*It is the base of MUSCLE TONE as the
tone in the antigravity muscles
*its stimulus is SUSTAINED STRETCH of the
muscle
*the receptor is muscle spindle(NUCLEAR
CHAIN TYPE)
*afferent ---primary & seondary endings
*response is CONTINUOUS CONTRACTION
OF THE MUSCLE
*it is the base of TENDON JERK
*its stimulus is SUDDEN STRETCH OF
MUSCLE
*the receptor is muscle spindle (NUCLEAR
BAG TYPE)
*afferent ---primary ending
*response is SUDDEN CONTRACTION
FOLLOWED BY RELAXATION
15. ⢠Supraspinal regulation of stretch reflex:
⢠*the stretch reflex is a spinal reflex which is
controlled by supra spinal centers
⢠The supra spinal centers regulating the stretch
reflex are:
Facilitatory supra spinal centers Inhibitory supra spinal centers
1-facilitatory reticular formation
2-motor area 4
3-neocerebellum
4-vestibular nuclei
NB:
*facilitatory reticular formation has
intrensic activity
*send impulses through facilitatory
reticular formation then to gamma motor
neurons
1-inhibitory reticular formation
2-area 4 S (cortical suppressor area)
3-paleocerebellum
4-red nucleus
5-basal ganglia
NB:*inhibitory reticular formation has no
intrensic activity
*send impulses through inhibitory reticular
formation
16. ⢠Function of stretch reflex:
⢠1-static stretch reflex is the base of MUSCLE TONE
⢠2-role of stretch reflex in controlling voluntary
movement.
⢠3-clinical importance of stretch reflex
17. ⢠Static stretch reflex is the base of muscle tone:
⢠Skeletal muscle tone:
⢠Def:
⢠reflex
⢠subtetenic contraction of skeletal muscle fibers
⢠alternating
â˘
⢠lead to muscle tension
⢠it occurs especially in antigravity muscles
18. ⢠Mechanism:
⢠During rest the muscle is continuously stretched as
length of the muscle is shorter than the distance
between the origin and insertion
⢠(Intrensic activity) of higher centers form
continuous impulses from them through gamma
fibers-----keep muscle spindle stretched
19. ⢠NB:
⢠The muscle tone acquire NO FATIGUE.
⢠Causes:
⢠1-alternating activity of different motor neurons ---
alternating contraction of group of muscle fibers
and the other group relax and rest
⢠2-the reflex contraction is SUBTETANIC
20. ⢠Function of muscle tone:
⢠1-keep body position against gravity
⢠2-keep viscera in position
⢠3-maintain body temperature----muscle contract --
-release energy----increase metabolic rate
⢠4-help venous return and lymph drain
21. ⢠2-role of stretch reflex in controlling voluntary
movements.
⢠1-Damping function of stretch reflex:
⢠the brain discharges the impulses irregularly
⢠to motor neurones
⢠this leads to JERKY OSCILLATORY movements
⢠The stretch reflex prevents oscillation of movements &
make them smooth
⢠due to
⢠Simultaneous discharge to gamma motor neurones &
alpha motor neurones
⢠this leads to
⢠Contraction of extra & intra fusal fibers at same time
⢠This make the contraction smooth
22. ⢠2-servoassist function during muscle contraction:
⢠lift weight
⢠cortex send signals to
⢠Alpha & Gamma motor neurons
⢠(coactivation between alpha & gamma)
+++ Extra fusal fibers +++ Intra fusal fibers
At same time
(the stimulation of the gamma fibers reflexly
stimulate the alpha fibers thus potentiate it)
23. ⢠Decerebrate rigidity:
⢠make transverse section of spinal cord
⢠between SUPERIOR COLLICULI & INFERIOR
⢠COLLICULI
⢠This will remove the INHIBITORY EFFECT OF
⢠SUPRA SPINAL INHIBITORY CENTER & RED
⢠NUCLEUS
⢠&
⢠leave the facilitatory effect of facilitatory
⢠reticular formation & vestibular nucleus
â˘
24. ⢠This will lead to
⢠marked increase in the tone of antigravity muscles
⢠Animal will have---1-extended neck
⢠2-extended back
⢠3-extended limbs
⢠4-elevated tail.
⢠NB:
⢠The same condition occur in humans if there is
lesion in the INTERNAL CAPSULE ----person will
have increased tone in antigravity muscles
25. ⢠Clinical importance of stretch reflex:
⢠Tendon jerk (Deep reflexes)
⢠(Dynamic stretch reflex)
⢠Def: sudden strike of tendon of muscle
⢠lead to
⢠sudden stretch of the muscle
⢠which lead to
⢠reflex contraction of muscle followed by relaxation
26. ⢠NB: the tendon jerk is facilitated by:
⢠1- putting muscle in stretched position
⢠2- increase gamma efferent discharge by
⢠*clinching teeth
⢠* hook fingers of hands together & pull
⢠hands apart
â˘
27. ⢠1-Biceps jerk:
⢠Stimulus ---sudden tap on tendon of biceps
⢠Receptor---muscle spindle (nuclear bag)
⢠Afferent----primary ending
⢠Center -----C5,C6
⢠Efferent ----myelinated
⢠Response---contraction of biceps (flex elbow) then
⢠relax
28. ⢠2-Triceps jerk:
⢠Stimulus ---sudden tap on tendon of triceps
⢠Receptor---muscle spindle (nuclear bag)
⢠Afferent----primary ending
⢠Center -----C6,C7
⢠Efferent ----myelinated
⢠Response---contraction of triceps (extend elbow)
⢠then relax
â˘
29. ⢠3-Knee jerk:
⢠Stimulus ---sudden tap on tendon of Quadriceps
⢠Receptor---muscle spindle (nuclear bag)
⢠Afferent----primary ending
⢠Center -----L2,L3,L4
⢠Efferent ----myelinated
⢠Response---contraction of Quadriceps (extend
⢠knee) then relax
â˘
30. ⢠4-Ankle jerk:
⢠Stimulus ---sudden tap on tendon of Achilles
⢠Receptor---muscle spindle (nuclear bag)
⢠Afferent----primary ending
⢠Center -----S1,S2
⢠Efferent ----myelinated
⢠Response---contraction of gastrocnemius muscle
⢠(planter flexion of ankle)
31. ⢠Inverse stretch reflex:
⢠Def: marked stretch of the muscle ----lead to reflex
relaxation of the muscle
⢠Stimulus----increase tension in the muscle
⢠(as in marked stretch OR strong contraction)
⢠Receptor---GOLGI TENDON ORGAN
⢠*receptor
⢠*in the tendon
⢠*parallel with muscle fibers
⢠*stimulated by high tension in muscle
32. ⢠Afferent: myelinated
⢠Center: spinal cord (BI SYNAPTIC) (2 interneurons
⢠Efferent: alpha motor neuron fiber inhibitory to
⢠muscle fiber
⢠Response: relaxation of muscle (decrease muscle
⢠tone to prevent tear of muscle fibers)
33. ⢠Clinical application of inverse stretch reflex:
⢠Clasp knife rigidity:
⢠Def: resistance then sudden release
⢠felx upper limb
⢠(extensors are stretched)
⢠stimulate muscle spindle
⢠increase muscle tone (Resistance)
⢠stimulate golgi tendon receptor
⢠inhibit Alpha motor neuron
⢠relaxation of muscle (Release)
34. ⢠Polysynaptic reflexes:
⢠1-flexor withdrawal reflex:
⢠Def: flexion & withdrawal of limb away of injurious
stimulus.
⢠Stimulus: painful stimulus on limb
⢠Receptor: F.N.E. (free nerve ending)
⢠Afferent: A delta fibers , C fibers
⢠Center : spinal cord (polysynaptic)
⢠Efferent: Alpha motor neurone
⢠Response: flexion & withdraw of limb away of pain
stimulus
35. ⢠Polysynaptic reflexes:
⢠1-flexor withdrawal reflex:
⢠Def: flexion & withdrawal of limb away of injurious
stimulus.
⢠Stimulus: painful stimulus on limb
⢠Receptor: F.N.E. (free nerve ending)
⢠Afferent: A delta fibers , C fibers
⢠Center : spinal cord (polysynaptic)
⢠Efferent: Alpha motor neurone
⢠Response: flexion & withdraw of limb away of pain
stimulus
36. ⢠4-pattern of contraction depend on site of
stimulation
⢠5-tetanus (there will be continuous ontraction)
⢠Types of tetanus are:
⢠Reflex tetanus Motor tetanus
*Repeated Stimulation of AFFERENT
nerve
*conduction of impulse along
AFFERENT
INTERNEURONES
EFFERENT
MUSCLE
*continuous contraction of muscle
*Repeated stimulation of MOTOR
EFFERENT nerve of the muscle
*impulse move to muscle directly
37. ⢠Characters of reflex tetanus , & motor tetanus
Reflex tetanus Motor tetanus
*Longer latent period
*Tension rises gradually (due to increase
number of activated motor cells)
(Recrutement)
The tension decreases gradually (due to
fatigue in the synapse)
After removal of stimulus the tension
persists for short period (due to after
discharge)
*Short latent period
*Tension rise rapidly
maintained as the stimulus is applied
drop rapidly after removal of stimulus
38. ⢠2- Crossed extensor reflex:
⢠Def: application of injurious stimulus to a limb
⢠this leads to
⢠Reflex flexion of Reflex extension of
⢠Ipsilateral limb contralateral limb to
⢠support body weight
⢠*properties of C.E.R.:
⢠1-the latent period in C.E.R. LONGER than F.W.R.
⢠2-after discharge in C.E.R. LONGER than F.W.R.
⢠3-it has receprocal innervation
39. ⢠3-Reflexes of posture & locomotion:
Positive supporting reaction Stepping movement
Deep pressure on sole of foot
lead to
Reflex contraction of flexors & extensors
(make limb rigid column)
(no receprocal innervation)
Support body weight
Rhythmic stepping of limb
&
Receprocal stepping of the other limb
(walking)
41. ⢠Complete transection of spinal cord:
⢠Due to 1-accidents
⢠2-penetrating wounds
⢠The effects of complete transverse section of spinal
cord are
⢠Motor orders
⢠sensory information
42. ⢠Effect of complete T.S. of spinal cord:
Permanent loss of all
sensations below level
of lesion
No neurolemmal sheath
Permanat loss of voluntary
movements below level of
lesion
No neurolemmal sheath
*If the lesion in
1-upper cervical region
Respiratory failure & death
2-lower cervical region
Quadriplegia , respiration is
diaphragmatic
3-mid thoracic region
paraplegia
Reflexes
The reflexes pass by 3
stages which are
1-Spinal shock immediately
after T.S. & last 2-6 weeks
2-Recovery of reflexes
*Early recovery ---
immediately follow spinal
shock
*late recovery----after 6
month
3-Failure of reflexes
If infection occur
43. ⢠A: spinal shock
⢠Def: complete loss of all reflexes below level of
lesion
⢠Reflexes lost are:
⢠1-stretch reflex:
⢠Its loss leads to-----Atonia , Areflexia
⢠3-Blood pressure:
⢠there will be loss of the vasomotor tone
⢠Due to interruption of fibers connecting vasomotor
center with sympathetic
⢠this leads to -----V.D. ----decrease B.P
⢠The higher the lesion the lower is the BP
44. ⢠4-Loss of Autonomic reflexes:
⢠Loss of -----*defecation reflex
⢠*micturition reflex
⢠(retension with over flow)
⢠Accumulate urine in bladder till pressure in
bladder overcomes tone of sphincter---drippling
⢠* no Sweating reflex ---skin is dry
⢠* no erection
45.
46. he
⢠Duration of spinal shock:
⢠*The duration of the spinal shock depends on THE
DEGREE OF DEVELOPMENT OF THE BRAIN
(ENCEPHALIZATION)
⢠*lower animals as frogs----1-2 hours
⢠dogs-----days
â˘
⢠* in humans ------------------2-6 weeks
â˘
47. ⢠Cause of spinal shock:
⢠Sudden withdraw of the supra spinal facilitatory
impulses form higher centers
⢠this leads to
⢠hyperpolarization of the neurons in spinal cord &
they do not respond so there will be no reflexes
48. ⢠Recovery of reflexes:(due to denervation
hypersenstivity)
⢠I- Early recovery of reflexes:
⢠Immediately after the end of spinal shock (after 2-
6 weeks).
⢠The reflexes which return early are:
⢠1- stretch reflex:
⢠*first reflex to return
⢠*the tone in the muscles are weak
⢠*the tone appear in the flexor muscles at first---
lead to ------ paraplegia in flexion.
49. ⢠planter reflex: (NEW REFLEX APPEAR NOT PRESENT
AT PAST)
⢠Stimulus: ----scratch skin of foot
⢠Response:----dorsiflexion of big toe
50. ⢠3- Deep reflexes:
⢠First knee jerk appear----weak
⢠Later Ankle jerk ----------- weak
⢠4- Mass reflex: (NEW ABNORMAL REFLEX APPEAR
NOT PRESENT AT PAST)
⢠Stimulus: scratching the skin of the
⢠*abdominal wall
⢠*lower limb
⢠lead to
⢠Response: *flexion and withdraw lower limbs
⢠*evacuate bladder , & retum
⢠*sweating
⢠*increase Blood pressure
51. ⢠5-Autonomic reflexes:
⢠*the patient will be shifted to the automatic
bladder & automatic rectum
⢠(reflex micturition , reflex defecation)
⢠*there will be increase in the BP
⢠*there will be erection & ejaculation on
manipulating the glans but not the complete act
52. ⢠6- the skin will be warm , ulcers heal , good color due
to increased BP
⢠Late recovery:
⢠*after 6 months
⢠*marked reflex activity appear
⢠*the tone in the extensor muscles become greater
(paraplegia in extension)
⢠*Mass reflex disappear
⢠*FWR is accompanied by CER
⢠*NEW REFLEXES APPEAR
⢠1-positive supporting reaction
⢠2-stepping reflex
53. ⢠NB: if the patient had :
⢠*severe urinary tract infection
⢠*severe bed sores
⢠The patient will go to stage of FAILURE OF
REFLEXES where reflexes disappear and patient die
⢠Care of patient with complete T.S. of spinal cord:
⢠The aim of the care is to pass the patient from
stage of SPINAL SHOCK to RECOVERY OF REFLEXES
⢠1-catheterization
⢠2-rectal enema
⢠3-frequent mobilization
⢠4-antibiotics
54. Role of brain stem in controlling voluntary function:
brain stem
Mid brain pons medulla diencephalon
1-thalamus
2-subthalamus
3-hypothalamus
NB: *brain stem is formed of dense network called
RETICULAR FORMATION
*The reticular formation include nuclei as CVC,
RC,sleep centers
55. ⢠The reticular nuclei are
Pontine reticular nuclei
(facilitatory reticular formation)
medullary reticular formation
(inhibitory reticular formation)
*Discharge spontaneously
*Send the excitatory impulses to
1-UP
-Ascending reticular activating system
(RAS)
-This stimulate cortex -----lead to
alertness
2-DOWN
-stimulate STRECH REFLEX----maintain
tone in antigravity muscles
*Have NO intrensic activity
*Activated by signals from
-BASAL GANGLIA
_RED NUCLEUS
_PALEOCEREBELLUM
*They send signals to
-inhibit stretch reflex
56. ⢠RAS :
⢠Def: it is the ascending branches of the
FACILITATORY RETICULAR FORMATION
⢠*Fibers of the RAS go up to all area of the cerebral
cortex
⢠Function of the RAS:
⢠1-it is responsible for ALERT,& CONSCIOUSNESS
⢠2-If depressed -----sleep & its damage lead to coma
57. ⢠Factors affecting activity of RAS:
Factors increase activity of RAS Factors decrease activity of RAS
1-sensory signals
*Auditory signals more effective than
visual signals
*Pain signals
2-Signals from cerebral cortex
*From temporal lobe, Frontal lobe
as in Emotions
*Performing Voluntary movements
this help to resist sleep
3-Drugs---*sympathomymetics
(adrenaline)
(caffeine)
(amphetamine)
1-Decrease sensory signals
2-Decrease signals from cerebral cortex
3-Damage of RAS as by tumors
4-General anaesthesia as by *drugs
*alcohol
5- stimulation of sleep centers
58. ⢠Electroencephalogram EEG:
⢠Def: recording electric activity of BRAIN through
INTACT SKULL
⢠The normal waves are:
⢠ALPHA, BETA ,DELTA, THETA, LAMDA
Alpha waves Beta waves
*low frequency
*high amplitude
*recored when
1-person relaxed
2-closed eyes
*high frequency
*low amplitude
*recored when
1-alert
2-eyes open
3-anxiety
59. ⢠Sleep :
⢠Def: state of unconsciousness from which person is
easily aroused.
⢠The sleep occur in 2 alternate types which are:
Slow wave sleep(non REM) non Rapid Eye
Movement
Rapid eye movement (REM)
*first to occur
*represent 80% of sleep
*last for 90 min.
*No-------- rapid eye movement
-dreams
-swallowing
-teeth grinding
-erection , ejaculation
*decrease âHR
-BP
-Respiratory rate
-Basal metabolic rate
-muscle tone
*Occur later after the 4th stage of non
REM sleep.
*represent 20% of sleep
*Last 20 min.
*it is accompanied by:
-dreams
-rapid eye movement
-increase HR
BP
Respiratory rate
-teeth grinding
-swallowing
-erection , ejaculation
60. Non REM sleep REM sleep
*EEG show 4 stages:
Stage I ----waves are ---low amplitude
(BETA) high frequency
Stage II ----waves are â spindle shape
Stage III ---waves are âhigh amplitude
(ALPHA) low frequency
Stage IV ---waves are âvery large
*easy to be aroused
-decrease muscle tone.
*EEG show
-small
-rapid
-irregular
-Beta waves
-like alert
*not easy to be aroused
61. ⢠Mechanism of sleep:
⢠The sleep is due to inhibition of the RAS by:
Passive mechanism of sleep Active mechanism of sleep
*passive inhibition of the RAS by
1-fatigue after long time wakefulness
2-eleminating the visual, auditory exciting
stimuli
*active inhibition of the RAS by:
subcortical centers
release chemical transmitters
1- serotonin
2-prostaglandin
3-acetylcholine
4-noradrenaline
inhibit RAS
63. 1-Pressure receptors in foot
(detect support)
2-Body proprioceptors
(detect position of parts of body
Related to each other)
3-neck proprioceptors
(detect position of head related EQUILIBRIUM
To body)
4-visual system (position in space)
5-vestibular system
(detect position of head in space)
64. ⢠The vestibular system & its role in maintenance of
equilibrium:
⢠Vestibular apparatus(filled Endolymph)
Membranous labyrinth bony labyrinth
*inside body of labyrinth
* formed of
Non Auditory labyrinth Auditory labyrinth
Semicircular Utricle & Saccule
canals
65. Semicircular canals
3 in each vestibular apparatus
Superior posterior vertical Horizontal
(Anterior vertical)
NB: the semicircular canals contain ENLARGEMENT AT
ONE OF ITS ENDS _____AMPULLA
NB: inside the ampulla there present the RECEPTOR
(CRISTA AMPULLARIS)
*mechanoreceptor
*found in the ampulla of the semicircular canals
*formed of hair cells in gelatinous CUPOLA
*detect ANGULAR ACCELERATION
66. ⢠Mechanism of stimulation of semicircular canals:
During rotation to right
At start of rotation During rotation At end of rotation
*By ENERTIA the
ENDOLYMPH rotate to left
this lead both CRISTAE
bend to left
Left crista Right crista
Bend bend
Away from towards
UTRICLE UTRICLE
inhibited stimulated
*the unbalanced discharge
cause SENSE OF ROTATION
TO RIGHT (you feel to rotate
to right)
*constant speed
within 30 seconds
Both crista regain normal
resting position
sense of rotation disappear
*By MOMENTUM the
ENDOLYMPH continue to
rotate to right after stop
rotation
this lead both CRISTA
bend to right
Left crista Right crista
Bend bend
towards from away from
UTRICLE UTRICLE
Stimulated inhibited
*person feel sense of
rotation to left despite stop
of rotation (VERTIGO)
67. ⢠Effect of stimulation of semicircular canals:
Nystagmus Vertigo Postural reflexes
(change in muscle
tone)
Autonomic changes
*Def: oscillatory eye
movement
*it has 2 components
- FAST
componentâin
same direction of
rotation
- SLOW
- Component âin
- Opposite direction
of rotation
*causes of
nystugmus:
1-look from widow
(optokinetic)
2-Menier disease
(enlarge SCCs)
3-Neocerebellar
lesion
Def: false sense of
rotation ----leads to
loss of balance
*causes of vertigo:
1-Alcohol toxicity
2-streptomycin drug
3-Motion sickness
4-Menier disease
Stimulation of SCCs
During angular
acceleration
Change muscle tone
To maintain balance
*stimulate SCCs
1-decrease HR
2-decrease BP
3-increase RR
4-nausea
5-vomiting
6-sweating
7-pallor
68. ⢠The UTRICLE & SACCULE:
⢠Receptors (MACULAE)(OTOLITH ORGAN)
⢠mechanoreceptors
⢠in each UTRICLE & SACCULE
⢠Macula of utricle Macula of saccule
⢠Lie horizontal lie vertical
69. ⢠Function of otolith organ:
Macula detect change in position of head Macula detect linear acceleration
*Detect tilt of head to front & back or side
to side
*Macula of UTRICLE detect orientation of
head in space when person is upright
*Macula of saccule detect orientation of
head in space when person is lying
*Macula detect orientation of head in space
during SWIMMING when
-No vision
-No proprioception
*Macula in utricle -----respond to horizontal
acceleration
*Macula in saccule ----respond to vertical
acceleration
70.
71. ⢠Cortical control of motor action:
⢠The motor cortex is divided into:
Primary motor cortex, (area 4) , (pyramidal
area)
Premotor cortex
1-in the precentral gyrus
2-contain large neurones
3-contain highly excitable neurones
4-neurones are giant cells (called BETZ cells)
5-body is represented as:
-crossed
-inverted
-depend on motor value (large area
for hands , lips , less for back
6-function:
*stimulate stretch reflex
*initiate & control fine movement
7-if lesion occur in motor area 4 lead to:
*paralysis of opposite side of body
*hypotonia , hyporeflexia
*loss of superficial reflexes
*+ve babiniski sign
1-less excitable
2-the body is represented
*crossed
*inverted
3-function:
*control voluntary movement need group
of muscles to act together to form a task
*inhibit stretch reflex
*inhibit grasp reflex
*contain specific areas:
1-word formation area----memory of words
2-Head rotation area
3-voluntary eye movement
4-hand skills
72. ⢠Brocas area: (word formation area) (speech area)
⢠Function:
⢠-coordinated patern of vocalization
⢠-proper movement of tongueâform speech
⢠Damage:
⢠-
74. ⢠Function of pyramidal system:
⢠1-complex skilled movement
⢠2-facilitate Stretch reflex
⢠Lesion in pyramidal pathway results in
⢠1-paralysis of opposite side of body
⢠2-hypotonia
⢠3-hyporeflexia
75. ⢠The extra pyramidal system:
⢠Def: all parts of brain and brain stem concerned by
motor control other than pyramidal system
⢠1-premotor area
⢠2-basal ganglia
⢠3-reticular formation
⢠4- red nucleus
⢠5- vestibular nucleus
⢠Function of extra pyramidal system:
⢠-control gross movements involving group of muscles
76. UMNL LMNL
1-Causes:
*hemorrhage OR thrombosis lead to lesion
in the posterior limb internal capsule .
2-Effects:
*paralysis:
-wide spread paralysis.
-contralateral hemiplegia
-permanent loss of voluntary movement
-increase muscle tone (spastic paralysis)
*reflexes:
A-(stretch reflex) increased tone in paralyzed
muscles
-in antigravity muscles
-clasp knife spasticity
-due to cut inhibitory pathways
B-exaggerated tendon jerk
C-superficial reflexes absent
D-+ve babiniski sign
1-causes:
-Damage of LMN ---poliomyelitis
DM
B12 deficiency
myasthenia gravis
2-Effects:
*paralysis:
-on same side
-localized paralysis
-decrease muscle tone (flaccid paralysis)
-Recovery ----nerves have NEUROLEMMA
*Reflexes:
-Atonia ---absent stretch reflex
-Absent deep reflexes
-Absent superficial reflexes
*Muscle:
-marked atrophy
-abnormal response to electric stimulus
(reaction of degeneration)
-prolonged Chronaxie
77. UMNL LMNL
*muscle
-minimal wasting of paralyzed muscles
-normal response to electric stimuli (no
reaction of degeneration).
*gait:
-circumduction gait
*contralateral hemi anaesthesia
-cut sensory radiation
-some recovery for pain , temperature , touch
*hemianopia
-lesion for optic radiation
*slight affection of hearing
-bilateral representation of hearing
78. ⢠Basal ganglia:
⢠-nuclei
⢠-deep in cortex
⢠-interconnected
⢠-lateral to thalamus
⢠-have high O2 consumption
⢠-have high copper content
⢠-5 on each side
⢠-3 of them are large--*Caudate
⢠*Putamen Corpus striatum
⢠*Globus pallidus
⢠-2 of them are related functionally
⢠*Subthalamus
⢠*Substantia nigra
80. ⢠Neurotransmitters in basal ganglia:
⢠-there are EXCITATORY & INHIBITORY transmitters
⢠-the normal function of BG depends on balance
between them
⢠-the EXCITATORY transmitters are:
⢠1-Acetyl choline
⢠2-Noradrenaline
⢠-the INHIBITORY transmitters are:
⢠1-Dopamine
⢠2-GABA
81. ⢠Function of BG:
⢠1-the BG in BIRDS,& FISH do all voluntary
movement
⢠2-BG inhibit muscle tone
⢠3-BG have a role in controlling voluntary
movement:
(1)*Caudate------Convert the thoughts into plans to
⢠form complex goal
⢠*if the caudate is damaged
⢠-no thoughts are converted to plans
⢠-person can not write, or draw
⢠-no timing , no scaling of movement
82. (2)*the Putamen ----help to form SUBCONSCIOUS
⢠LEARNED MOVEMENT
⢠-store familiar automatic
⢠movement
⢠- as in driving, walking, writing
⢠*damage of PutamenâApraxia (inability to do
⢠familiar movement with no
⢠paralysis.
(3)*BG help planning & programming of movement
(4)*BG help to take posture (position) taken by body
to do certain movement
83. ⢠Lesion of BG:
⢠Involuntary movements
⢠1-Chorea----rapid
⢠involuntary
⢠jerky
⢠dancing movement
⢠due to lesion in caudate , putamen
⢠2-Athetosis---continuous
⢠slow
⢠snake like movement
⢠due to lesion in globus pallidus
85. ⢠Parkinsonism (paralysis agitans)
⢠-disease
⢠-due to lesion in substantia nigra
⢠-there is loss of Dopamine inhibitory transmitter
⢠Causes of parkinsonism:
⢠Idiopathic phenothiazine tranquilizers
⢠-old age
86. ⢠Manifestation:
⢠1-Rigidity:
⢠(lead pipe) (Cog wheel) type of rigidity :
⢠-there is resistance all through bending of limb
⢠-occur in both antigravity , & progravity muscles
⢠-more in flexors (person has flexed position)
87. ⢠2-hyperkinesia: (static tremors)
⢠-rhythmic
⢠-involuntary
⢠-alternating contraction
⢠-of antagonist muscles
⢠-occur at distal joints
⢠-with rate of 4-8/sec
⢠-occur at rest
⢠-disappear on voluntary movement
⢠-have the form of up & down movement of
mandible , or pill rolling of hands
88. ⢠3-Akinesia:
⢠-difficult to initiate voluntary movement
⢠-decrease associative movement
⢠-mask face
⢠-monotonous speech
⢠-bent forward---flexors tone are stronger
⢠-shuffling gait----short steps
⢠no swinging arms
⢠Treatment:
⢠1-L-dopa----change in CNS to dopamine
⢠2-Anticholinergic drugs---inhibit acetylcholine
89. ⢠Cerebellum:
⢠It is divided functionally into
Vestibulocerebellum
(flocculonodular lobe)
(Archicerebellum)
Spinocerebellum
(intermediate zone)
(paleocerebellum)
Cerebrocerebellum
(lateral zone of hemisphere)
(Neocerebellum)
-concerned with equilibrium -concerned with coordination -concerned with planning and
programming of movement
90. ⢠Function of cerebellum:
⢠1-control posture and equilibrium
⢠2-effect on muscle tone
⢠3-control voluntary movement
⢠*servocomparter function
⢠*prevent over shoot (damping function)
⢠*timing of movement
91. ⢠1-control posture and equilibrium:
⢠During rapid movement
⢠Vestibular apparatus send impulses to
vestibulocerebellum (archicerebellum)
⢠To maintain equilibrium through changing muscle
tone
92. ⢠2-effect of cerebellum on muscle tone:
⢠Neocerebellum is facilitatory to SR---increase
muscle tone
⢠Paleocerebellum is inhibitory to SR---inhibit muscle
tone
93. ⢠3-control voluntary movement:
⢠A* Servocomparter function:
⢠The spinocerebellum compares between the
intended plan (intention) of motor cortex
⢠&
⢠The performance of the muscles
⢠&
⢠It sends corrective signals to motor cortex
94. ⢠B-cerebellum prevent over shoot (damping
function)
⢠*The cerebellum sends signals to stop movement
at the intended point &prevent over shoot
⢠C-cerebellum function in timing of movement
⢠*Cerebrocerebellum forms the timing for the start
& termination of each movement
⢠this helps the ability
⢠To progress smooth from one movement to the
next (this is needed in complex movements )
writing, running
95. ⢠Abnormalities of cerebellum:
⢠-neocerebellar syndrome
⢠-lesion in deep cerebellar nuclei
⢠*Manifestation:
⢠-on the same side of lesion
⢠-hypotonia---due to loss of facilitatory effect of
cerebellum on muscle tone
⢠-Asthenia---muscle weakness ----due to difficult to
maintain muscle contraction
⢠-Ataxia ---incoordination of voluntary movement
in absence of UMNL , or LMNL
96. ⢠Manifestation of ataxia:
⢠-dysmetria----movement over shoot the intended
point
⢠-decomposition of movement
⢠-disdiadokinesia----inability to do rapid alternating
opposite movements
⢠-dysarthria-----(stacato-speech)
⢠Difficult to form correct speech----as the person
can not progress from one movement to another
⢠-eye ball tremors
⢠-kinetic tremors (intention tremors )---due to
absence of damping function
97. ⢠-Rebound phenomenon:
⢠Person can not stop the motor act at the intended
point
⢠-Staggering gait:
⢠Patient walks on wide base