Motor System
• Starts at the motor cortex
• Motor cortex is located at the frontal lobe
– precentral cortex
Motor homunculus
First discovered
by
Penfield
Brodmann areas Primary motor cortex
Area 4
Motor cortex
• different areas of the body are
represented in different cortical areas in
the motor cortex
• Motor homunculus
– somatotopic representation
– not proportionate to structures but
proportionate to function
– distorted map
– upside down map
Motor cortical areas
• primary motor cortex (MI)
– precentral gyrus
• Movements are executed
• secondary motor cortex (MII)
– premotor cortex
– supplementary motor area (SMA)
• Movements are planned together with cerebellum, basal
ganglia and other cortical areas
Primary motor cortex
• Corticospinal tract (pyramidal tract) originates
from the primary motor cortex
• Corticobulbar tract also originates from the
motor cortex and supplies brainstem and the
cranial nerves
• Cell bodies of the corticospinal tracts are
called Betz cells (large pyramidal shaped
cells)
• Corticospinal tract descends down the
internal capsule
Course of the corticospinal tract
• Descends through
– internal capsule
– at the medulla
• cross over to the other side
• uncrossed tracts
– descends down as the corticospinal tract
– ends in each anterior horn cell
– synapse at the anterior horn cell (directly or through
interneurons)
Medulla
internal capsule
Upper
motor
neuron
Lower
motor
neuron
anterior horn cell
Primary and secondary cortical
areas
• Primary areas are primarily connected with the
peripheral organs/structures
– Primary motor cortex (area 4)
• Secondary areas are inter-connected to each
other by cortico-cortical pathways and perform
complex processing
– Premotor cortex (area 6)
– Supplementary motor area (superomedial part of
area 6)
Functional role of primary and
secondary motor areas
• SMA (Supplementary motor area)
assembles global instructions for
movements
• It issues these instructions to the
Premotor cortex (PMC)
• Premotor cortex works out the
details of smaller components
• And then activates specific Primary
motor cortex (MI)
• Primary motor cortex through
Corticospinal tracts (CST) activate
specific motor units
SMA
PMC
MI
CST
Motor units
Complex nature of Cortical
Control of Movement
8.15
idea
•premotor area
•supplementary
motor area
(SMA)
•Prefrontal
cortex (PFC)
Primary
motor cortex
movement
basal ganglia
cerebellum cerebellum
plan execute
memory, emotions
Motor system
• Consists of
– Upper motor neuron
– Lower motor neuron
Lower motor neuron
• consists of mainly
• alpha motor neuron
– and also gamma motor neuron
alpha motor neuron
gamma motor neuron
alpha motor neuron
gamma motor neuron
corticospinal tract
Arrangement at the
anterior horn cell
alpha motor neuron
• this is also called the final common pathway
• Contraction of the muscle occurs through this
whether
– voluntary contraction through corticospinal tract
or
– involuntary contraction through gamma motor
neuron - stretch reflex - Ia afferent
motor unit
• muscle contraction occurs in terms of motor units
rather than by single muscle fibres
• a motor unit is defined as
– anterior horn cell
– motor neuron
– muscle fibres supplied by the neuron
• Muscle power/strength is obtained by the principle of
“Recruitment of motor units”
motor unit
• Innervation ratio
– motor neuron:number of muscle
fibres
• in eye muscles
– 1:23 offers a fine degree of
control
• in calf muscles
– 1:1000 more strength
Upper motor neuron
• Consists of
– Corticospinal tract (pyramidal tract)
– Extrapyramidal tracts
• Start from the brainstem
• Ipsilateral/contralateral
• Cortical pathways can excite/inhibit these tracts
• Modify the movement that is initiated by the CST
• Influence (+/-) gamma motor neuron, stretch reflex, muscle tone
• Important for postural control
• Cerebellar and basal ganglia influence on the lower motor neuron will
be through extrapyramidal tracts
Extrapyramidal tracts
• starts at the brain stem
• descends down either ipsilaterally or
contralaterally
• ends at the anterior horn cell
• modifies the motor functions
Extrapyramidal tracts
• there are 4 tracts
– reticulospinal tracts
– vestibulospinal tracts
– rubrospinal tracts
– tectospinal tracts
reticulospinal tract
• relay station for descending motor impulses
except pyramidal tracts
• receives & modifies motor commands to the
proximal & axial muscles
• maintain normal postural tone
• excitatory to alpha & gamma motorneurons
• end on interneurons too
• this effect is inhibited by cerebral influence
• mainly ipsilateral
midbrain
pons
medulla
spinal cord
reticulospinal tract
• pontine reticular formation
– medial reticulospinal tracts
• controls proximal muscles (axial), excitatory to flexor
• medullary reticular formation
– lateral reticulospinal tracts (also medial)
• excitatory or inhibitory to axial muscles
Reticular formation
• A set of network of interconnected
neurons located in the central
core of the brainstem
• It is made up of ascending and
descending fibers
• It plays a big role in filtering
incoming stimuli to discriminate
irrelevant background stimuli
• There are a large number of
neurons with great degree of
convergence and divergence
Functions
• Maintain consciousness, sleep and arousal
• Motor functions (postural and muscle tone
control)
– Reticulospinal pathways are part of the
extrapyramidal tracts
• Pain modulation (inhibition)
– Several nuclei (PAG, NRM) are part of the
descending pain modulatory (inhibitory) pathway
vestibular nuclei & tracts
• responsible for maintaining tone in antigravity
muscles & for coordinating the postural
adjustments in limbs & eyes
• connections with vestibular receptors (otolith
organs) & cerebellum
• mainly ipsilateral
• supplies extensors
midbrain
pons
medulla
spinal cord
vestibulospinal tract
mainly extensors
• vestibulospinal tracts
– lateral vestibulospinal tract
– medial vestibulospinal tract
– excitatory to antigravity alpha motor neurons &
supplies interneurons too
– lateral tract
• excitation of extensor muscles & relaxation of flexor
muscles
– medial tract
• inhibition of neck & axial muscles
red nucleus
• present in the midbrain
• rubrospinal tract originates from the red nucleus
• ends on interneurons
• control the distal muscles of limbs
• excite limb flexors & inhibit extensors
• higher centre influence (cerebral cortex)
• mainly contralateral
• supplies flexors
• Functionally this tract is not important in human motor
system
midbrain
pons
medulla
spinal cord
rubrospinal tract
mainly flexors
tectospinal tract
• tectospinal tract originates from the tectum of
the midbrain
• ends on interneurons
• mainly contralateral
• supplies cervical segments only
• Functionally this tract is not important in human
motor system
midbrain
pons
medulla
spinal cord
tectospinal tract
cervical segments
inferior olivary nucleus
• present in the medulla
• function:
– motor coordination
• via projections to the cerebellum
• sole source of climbing fibres to the cerebellum
– motor learning
– Functionally this nucleus is not important in human
motor system
Upper
motor
neuron
Lower
motor
neuron
extrapyramidal tracts
pyramidal tracts
alpha motor neurone
gamma motor neurone
Clinical Importance of the motor system
examination
• Tests of motor function:
– Muscle power
• Ability to contract a group of muscles in order to make an
active movement
– Muscle tone
• Resistance against passive movement
Basis of tests
• Muscle power
– Test the integrity of motor cortex, corticospinal tract
and lower motor neuron
• Muscle tone
– Test the integrity of stretch reflex, gamma motor
neuron and the descending control of the stretch
reflex
Muscle tone
• Resistance against passive movement
– Gamma motor neuron activate the spindles
– Stretching the muscle will activate the stretch reflex
– Muscle will contract involuntarily
– Gamma activity is under higher centre inhibition
• There is a complex effect of corticospinal and extrapyramidal tracts on the alpha and
gamma motor neurons (in addition to the effect by muscle spindle)
• There are both excitatory and inhibitory effects
• Sum effect
– excitatory on alpha motor neuron
– Inhibitory on gamma motor neuron
Corticospinal
tract
Extrapyramidal
tracts
Alpha motor
neuron
Gamma
motor
neuron•Voluntary movement
•Muscle tone
Muscle spindle
Clinical situations
• Muscle power
– Normal
– Reduced (muscle weakness)
• Paralysis, paresis, plegia
• MRC grades
0 - no movement
1 - flicker is perceptible in the muscle
2 - movement only if gravity eliminated
3 - can move limb against gravity
4 - can move against gravity & some resistance exerted by examiner
5 - normal power
• Muscle tone
– Normal
– Reduced
• Hypotonia (Flaccidity)
– Increased
• Hypertonia (Spasticity)
Main abnormalities
• Muscle Weakness / paralysis
– Reduced muscle power
• Flaccidity
– Reduced muscle tone
• Spasticity
– Increased muscle tone
• Lower motor neuron lesion causes
– flaccid paralysis (flaccid weakness)
• Upper motor neuron lesion causes
– spastic paralysis (spastic weakness)
Lower motor neuron lesion
• muscle weakness
• flaccid paralysis
• muscle wasting (disuse atrophy)
• reduced muscle tone (hypotonia)
• reflexes: reduced or absent (hyporeflexia or areflexia)
• spontaneous muscle contractions (fasciculations)
• plantar reflex: flexor
• superficial abdominal reflexes: present
• eg. Brachial plexus damage
Upper motor neuron lesion
• muscle weakness
• spastic paralysis
• increased muscle tone (hypertonia)
• reflexes: exaggerated (hyperreflexia)
• Babinski sign: positive
• superficial abdominal reflexes: absent
• muscle wasting is very rare
• clonus can be seen:
– rhythmical series of contractions in response to sudden stretch
• clasp knife effect can be seen
– passive stretch causing initial increased resistance which is released
later
• eg. Stroke
Babinski sign
• when outer border of the sole of the foot is
scratched
• upward movement of big toe
• fanning out of other toes
• feature of upper motor neuron lesion
• extensor plantar reflex
• seen in infants during 1st year of life (because
of immature corticospinal tract)
positive Babinski sign
• Observation
• When the spinal cord is suddenly transected, essentially all
cord functions, including spinal cord reflexes, immediately
become depressed
• This is called “spinal shock”
• Period of spinal shock is about 2 weeks in humans
• It may vary depending on the level spinal cord injury
• Higher the animal in evolution greater is the spinal shock
period
Spinal cord transection and spinal shock
During spinal shock period
• complete loss of all reflexes
• no tone
• paralysis
• complete anaesthesia
• no peristalsis
• bladder and rectal reflexes absent
• no sweating
• arterial blood pressure decreases
Possible mechanism of spinal shock
• Normal activity of the spinal cord reflexes depends to a great
extent on continual tonic excitation from higher centers
(pyramidal and extrapyramidal tracts)
• Spinal shock may be due to the sudden cessation of tonic
bombardment of spinal cord interneuron pool by descending
influences
• During recovery from spinal shock, the excitability of spinal cord
reflexes increase due to the lack of descending inhibition and
possible denervation hypersensitivity
• After the spinal shock period typical upper motor neuron
features appear
after the spinal shock
• reflexes will reappear, mostly exaggerated
• bladder become reflex
• mass reflex will appear
– afferent stimuli irradiate to several reflex centres
– noxious stimulus causes: withdrawal response,
evacuation of bladder, rectum, sweating, pallor
Site of lesions
Cortex
Internal capsule
Brain stem
Spinal cord
Anterior horn cell
Motor nerve
Neuromuscular junction
Muscle
Neurological diseases
Disease Involvement
• Stroke UMN
• Peripheral neuropathy LMN
– Mononeuropathy
– Polyneuropathy
• Plexopathy LMN
• Radiculopathy LMN
• Myelopathy LMN, UMN
• Motor neuron disease LMN, UMN
• Monoplegia (monoparesis)
• Hemiplegia (hemiparesis)
• Paraplegia (paraparesis)
• Quadriplegia (quadriparesis)
Site of lesions
monoplegia
only 1 limb is affected either UL or LL,
lower motor neuron lesion
hemiplegia
one half of the body including
UL and LL
lesion in the Internal capsule
paraplegia
both lower limbs
thoracic cord lesion
quadriplegia (tetraplegia)
all 4 limbs are affected
cervical cord or brain stem lesion
Some common neurological
diseases
Stroke
• Cerebrovascular accident (CVA)
• A serious neurological disease
• Large number of deaths per year
• Cerebrovascular ischaemia causing
infarction or haemorrhage
• Sudden onset hemiplegia
• Hypertension, diabetes, obesity are
risk factors
Peripheral neuropathies
• Mononeuropathies
– Carpal tunnel syndrome (CTS)
– Ulnar neuropathy - claw hand
– Saturday night palsy (radial nerve lesion) – wrist drop
– Common peroneal nerve lesion – foot drop
– Posterior tibial nerve lesion – tarsal tunnel syndrome
– Sciatic nerve lesion
– Facial nerve lesion – Bell’s palsy
• Polyneuropathies
– Diabetic, vitamin deficiency, toxic
Median nerve compression
(Carpal tunnel syndrome)
Ulnar nerve lesion
(Ulnar tunnel syndrome)
Clawing of the hand
Radial nerve lesion
(Saturday night palsy)
Wrist drop
Wrist guard
Common peroneal nerve
lesion
Foot drop
Ankle guard
Posterior tibial nerve lesion
(Tarsal tunnel syndrome)
Sciatic nerve lesion
Facial nerve lesion
(Facial palsy or Bell’s
palsy)
Brachial plexopathy
(Erb’s palsy)
Cervical spondylosis
Sciatica
Cervical or thoracic
myelopathy
Paraplegia
Quadriplegia
MND or Motor neuron
disease
• Anterior horn cell disease
• MND: motor neuron disease
• ALS: Amyotrophic lateral sclerosis
• Weakness of lower limbs, upper limbs
• Speech defect: dysarthria
• Difficulty in swallowing: dysphagia
MND or Motor neuron
disease

Motor system pathways for students

  • 1.
    Motor System • Startsat the motor cortex • Motor cortex is located at the frontal lobe – precentral cortex
  • 5.
  • 6.
    Brodmann areas Primarymotor cortex Area 4
  • 7.
    Motor cortex • differentareas of the body are represented in different cortical areas in the motor cortex • Motor homunculus – somatotopic representation – not proportionate to structures but proportionate to function – distorted map – upside down map
  • 8.
    Motor cortical areas •primary motor cortex (MI) – precentral gyrus • Movements are executed • secondary motor cortex (MII) – premotor cortex – supplementary motor area (SMA) • Movements are planned together with cerebellum, basal ganglia and other cortical areas
  • 9.
    Primary motor cortex •Corticospinal tract (pyramidal tract) originates from the primary motor cortex • Corticobulbar tract also originates from the motor cortex and supplies brainstem and the cranial nerves • Cell bodies of the corticospinal tracts are called Betz cells (large pyramidal shaped cells) • Corticospinal tract descends down the internal capsule
  • 10.
    Course of thecorticospinal tract • Descends through – internal capsule – at the medulla • cross over to the other side • uncrossed tracts – descends down as the corticospinal tract – ends in each anterior horn cell – synapse at the anterior horn cell (directly or through interneurons)
  • 11.
  • 12.
    Primary and secondarycortical areas • Primary areas are primarily connected with the peripheral organs/structures – Primary motor cortex (area 4) • Secondary areas are inter-connected to each other by cortico-cortical pathways and perform complex processing – Premotor cortex (area 6) – Supplementary motor area (superomedial part of area 6)
  • 14.
    Functional role ofprimary and secondary motor areas • SMA (Supplementary motor area) assembles global instructions for movements • It issues these instructions to the Premotor cortex (PMC) • Premotor cortex works out the details of smaller components • And then activates specific Primary motor cortex (MI) • Primary motor cortex through Corticospinal tracts (CST) activate specific motor units SMA PMC MI CST Motor units
  • 15.
    Complex nature ofCortical Control of Movement 8.15
  • 16.
    idea •premotor area •supplementary motor area (SMA) •Prefrontal cortex(PFC) Primary motor cortex movement basal ganglia cerebellum cerebellum plan execute memory, emotions
  • 17.
    Motor system • Consistsof – Upper motor neuron – Lower motor neuron
  • 18.
    Lower motor neuron •consists of mainly • alpha motor neuron – and also gamma motor neuron alpha motor neuron gamma motor neuron
  • 19.
    alpha motor neuron gammamotor neuron corticospinal tract Arrangement at the anterior horn cell
  • 20.
    alpha motor neuron •this is also called the final common pathway • Contraction of the muscle occurs through this whether – voluntary contraction through corticospinal tract or – involuntary contraction through gamma motor neuron - stretch reflex - Ia afferent
  • 21.
    motor unit • musclecontraction occurs in terms of motor units rather than by single muscle fibres • a motor unit is defined as – anterior horn cell – motor neuron – muscle fibres supplied by the neuron • Muscle power/strength is obtained by the principle of “Recruitment of motor units”
  • 22.
    motor unit • Innervationratio – motor neuron:number of muscle fibres • in eye muscles – 1:23 offers a fine degree of control • in calf muscles – 1:1000 more strength
  • 23.
    Upper motor neuron •Consists of – Corticospinal tract (pyramidal tract) – Extrapyramidal tracts • Start from the brainstem • Ipsilateral/contralateral • Cortical pathways can excite/inhibit these tracts • Modify the movement that is initiated by the CST • Influence (+/-) gamma motor neuron, stretch reflex, muscle tone • Important for postural control • Cerebellar and basal ganglia influence on the lower motor neuron will be through extrapyramidal tracts
  • 24.
    Extrapyramidal tracts • startsat the brain stem • descends down either ipsilaterally or contralaterally • ends at the anterior horn cell • modifies the motor functions
  • 25.
    Extrapyramidal tracts • thereare 4 tracts – reticulospinal tracts – vestibulospinal tracts – rubrospinal tracts – tectospinal tracts
  • 26.
    reticulospinal tract • relaystation for descending motor impulses except pyramidal tracts • receives & modifies motor commands to the proximal & axial muscles • maintain normal postural tone • excitatory to alpha & gamma motorneurons • end on interneurons too • this effect is inhibited by cerebral influence • mainly ipsilateral
  • 27.
  • 28.
    • pontine reticularformation – medial reticulospinal tracts • controls proximal muscles (axial), excitatory to flexor • medullary reticular formation – lateral reticulospinal tracts (also medial) • excitatory or inhibitory to axial muscles
  • 29.
    Reticular formation • Aset of network of interconnected neurons located in the central core of the brainstem • It is made up of ascending and descending fibers • It plays a big role in filtering incoming stimuli to discriminate irrelevant background stimuli • There are a large number of neurons with great degree of convergence and divergence
  • 30.
    Functions • Maintain consciousness,sleep and arousal • Motor functions (postural and muscle tone control) – Reticulospinal pathways are part of the extrapyramidal tracts • Pain modulation (inhibition) – Several nuclei (PAG, NRM) are part of the descending pain modulatory (inhibitory) pathway
  • 31.
    vestibular nuclei &tracts • responsible for maintaining tone in antigravity muscles & for coordinating the postural adjustments in limbs & eyes • connections with vestibular receptors (otolith organs) & cerebellum • mainly ipsilateral • supplies extensors
  • 32.
  • 33.
    • vestibulospinal tracts –lateral vestibulospinal tract – medial vestibulospinal tract – excitatory to antigravity alpha motor neurons & supplies interneurons too – lateral tract • excitation of extensor muscles & relaxation of flexor muscles – medial tract • inhibition of neck & axial muscles
  • 34.
    red nucleus • presentin the midbrain • rubrospinal tract originates from the red nucleus • ends on interneurons • control the distal muscles of limbs • excite limb flexors & inhibit extensors • higher centre influence (cerebral cortex) • mainly contralateral • supplies flexors • Functionally this tract is not important in human motor system
  • 35.
  • 36.
    tectospinal tract • tectospinaltract originates from the tectum of the midbrain • ends on interneurons • mainly contralateral • supplies cervical segments only • Functionally this tract is not important in human motor system
  • 37.
  • 38.
    inferior olivary nucleus •present in the medulla • function: – motor coordination • via projections to the cerebellum • sole source of climbing fibres to the cerebellum – motor learning – Functionally this nucleus is not important in human motor system
  • 39.
  • 40.
    Clinical Importance ofthe motor system examination • Tests of motor function: – Muscle power • Ability to contract a group of muscles in order to make an active movement – Muscle tone • Resistance against passive movement
  • 41.
    Basis of tests •Muscle power – Test the integrity of motor cortex, corticospinal tract and lower motor neuron • Muscle tone – Test the integrity of stretch reflex, gamma motor neuron and the descending control of the stretch reflex
  • 42.
    Muscle tone • Resistanceagainst passive movement – Gamma motor neuron activate the spindles – Stretching the muscle will activate the stretch reflex – Muscle will contract involuntarily – Gamma activity is under higher centre inhibition
  • 43.
    • There isa complex effect of corticospinal and extrapyramidal tracts on the alpha and gamma motor neurons (in addition to the effect by muscle spindle) • There are both excitatory and inhibitory effects • Sum effect – excitatory on alpha motor neuron – Inhibitory on gamma motor neuron Corticospinal tract Extrapyramidal tracts Alpha motor neuron Gamma motor neuron•Voluntary movement •Muscle tone Muscle spindle
  • 44.
    Clinical situations • Musclepower – Normal – Reduced (muscle weakness) • Paralysis, paresis, plegia • MRC grades 0 - no movement 1 - flicker is perceptible in the muscle 2 - movement only if gravity eliminated 3 - can move limb against gravity 4 - can move against gravity & some resistance exerted by examiner 5 - normal power • Muscle tone – Normal – Reduced • Hypotonia (Flaccidity) – Increased • Hypertonia (Spasticity)
  • 45.
    Main abnormalities • MuscleWeakness / paralysis – Reduced muscle power • Flaccidity – Reduced muscle tone • Spasticity – Increased muscle tone
  • 46.
    • Lower motorneuron lesion causes – flaccid paralysis (flaccid weakness) • Upper motor neuron lesion causes – spastic paralysis (spastic weakness)
  • 47.
    Lower motor neuronlesion • muscle weakness • flaccid paralysis • muscle wasting (disuse atrophy) • reduced muscle tone (hypotonia) • reflexes: reduced or absent (hyporeflexia or areflexia) • spontaneous muscle contractions (fasciculations) • plantar reflex: flexor • superficial abdominal reflexes: present • eg. Brachial plexus damage
  • 48.
    Upper motor neuronlesion • muscle weakness • spastic paralysis • increased muscle tone (hypertonia) • reflexes: exaggerated (hyperreflexia) • Babinski sign: positive • superficial abdominal reflexes: absent • muscle wasting is very rare • clonus can be seen: – rhythmical series of contractions in response to sudden stretch • clasp knife effect can be seen – passive stretch causing initial increased resistance which is released later • eg. Stroke
  • 49.
    Babinski sign • whenouter border of the sole of the foot is scratched • upward movement of big toe • fanning out of other toes • feature of upper motor neuron lesion • extensor plantar reflex • seen in infants during 1st year of life (because of immature corticospinal tract)
  • 50.
  • 51.
    • Observation • Whenthe spinal cord is suddenly transected, essentially all cord functions, including spinal cord reflexes, immediately become depressed • This is called “spinal shock” • Period of spinal shock is about 2 weeks in humans • It may vary depending on the level spinal cord injury • Higher the animal in evolution greater is the spinal shock period Spinal cord transection and spinal shock
  • 52.
    During spinal shockperiod • complete loss of all reflexes • no tone • paralysis • complete anaesthesia • no peristalsis • bladder and rectal reflexes absent • no sweating • arterial blood pressure decreases
  • 53.
    Possible mechanism ofspinal shock • Normal activity of the spinal cord reflexes depends to a great extent on continual tonic excitation from higher centers (pyramidal and extrapyramidal tracts) • Spinal shock may be due to the sudden cessation of tonic bombardment of spinal cord interneuron pool by descending influences • During recovery from spinal shock, the excitability of spinal cord reflexes increase due to the lack of descending inhibition and possible denervation hypersensitivity • After the spinal shock period typical upper motor neuron features appear
  • 54.
    after the spinalshock • reflexes will reappear, mostly exaggerated • bladder become reflex • mass reflex will appear – afferent stimuli irradiate to several reflex centres – noxious stimulus causes: withdrawal response, evacuation of bladder, rectum, sweating, pallor
  • 55.
    Site of lesions Cortex Internalcapsule Brain stem Spinal cord Anterior horn cell Motor nerve Neuromuscular junction Muscle
  • 56.
    Neurological diseases Disease Involvement •Stroke UMN • Peripheral neuropathy LMN – Mononeuropathy – Polyneuropathy • Plexopathy LMN • Radiculopathy LMN • Myelopathy LMN, UMN • Motor neuron disease LMN, UMN • Monoplegia (monoparesis) • Hemiplegia (hemiparesis) • Paraplegia (paraparesis) • Quadriplegia (quadriparesis)
  • 57.
    Site of lesions monoplegia only1 limb is affected either UL or LL, lower motor neuron lesion hemiplegia one half of the body including UL and LL lesion in the Internal capsule paraplegia both lower limbs thoracic cord lesion quadriplegia (tetraplegia) all 4 limbs are affected cervical cord or brain stem lesion
  • 58.
  • 59.
    Stroke • Cerebrovascular accident(CVA) • A serious neurological disease • Large number of deaths per year • Cerebrovascular ischaemia causing infarction or haemorrhage • Sudden onset hemiplegia • Hypertension, diabetes, obesity are risk factors
  • 60.
    Peripheral neuropathies • Mononeuropathies –Carpal tunnel syndrome (CTS) – Ulnar neuropathy - claw hand – Saturday night palsy (radial nerve lesion) – wrist drop – Common peroneal nerve lesion – foot drop – Posterior tibial nerve lesion – tarsal tunnel syndrome – Sciatic nerve lesion – Facial nerve lesion – Bell’s palsy • Polyneuropathies – Diabetic, vitamin deficiency, toxic
  • 61.
  • 62.
    Ulnar nerve lesion (Ulnartunnel syndrome) Clawing of the hand
  • 63.
    Radial nerve lesion (Saturdaynight palsy) Wrist drop Wrist guard
  • 64.
  • 65.
    Posterior tibial nervelesion (Tarsal tunnel syndrome)
  • 66.
  • 67.
    Facial nerve lesion (Facialpalsy or Bell’s palsy)
  • 68.
  • 69.
  • 70.
  • 71.
  • 72.
    MND or Motorneuron disease • Anterior horn cell disease • MND: motor neuron disease • ALS: Amyotrophic lateral sclerosis • Weakness of lower limbs, upper limbs • Speech defect: dysarthria • Difficulty in swallowing: dysphagia
  • 73.
    MND or Motorneuron disease