Lecture 3: Upper and Lower Motor Neuron Pathology Flashcards
Golgi Tendon Organs (GTO) structure
-Encapsulated receptor located at the musculotendinous junction
-In series (follows in line with tendonitis fibers) with extrafusal fibers/sensory organ
-2-50 GTO per muscle
-Innervated by afferent fiber branches, 1b by which the distal and the proximal parts of the tendon-spindle are innervated
GTO function
1) Detect small change in muscle contraction (<1g force)
2) Sensitive to twitch contractions
3) Compensate for fatigue in motor units
4) May facilitate for inhibit muscle contractions
5) Reflex regulation of alpha motor neuron activity
6) Context and task dependent
7) Determines FORCE and speed and organizes it so that we do not get fatigued as easily
8) Stimulates the alpha motor neuron to regulate like a police
9) Able to shut the muscle down if needed
GTO Mechanoreceptors
-Monitoring and regulating the tension of muscle force
-Prevents muscle damage
what does the GTO inhibit
its own muscle Autogenic inhibition
How does autogenic Inhibition work
- 1B innervation at the tendinous junction
-Stimulated by tension of the muscle to the tendon
-Too much force = Inhibitory interneuron inhibits muscle contraction (also called inverse stretch reflex)
Muscle Spindle axon
1a sensory
muscle spindle functioning
monitoring length and velocity of the muscle
Muscle spindle activation
tendon reflex
gamma motor neurons axon
2 (motor)
gamma motor neurons function
resetting the muscle spindle after activation
gamma motor neurons activation
brain modulats muscle spindle to stretch
GTO axon
1B (sensory)
GTO function
monitoring and regulating the tension of the muscle force. workload distributor
GTO activation
inverse stretch reflex
alpha motor neuron axon
alpha motor
alpha motor neuron function
activates the muscle
alpha motor neuron activation
force production
Upper motor neuron Definition of a Syndrome Involves
-Motor cortex and pathways
-brainstem
-cerebellum
-Spinal cord reflex and coordination
Upper motor neuron neurologic signs and symptoms
postures, postural responses, movements (passive and active) and involuntary responses that correspond with an upper motor neuron lesion
Lower motor neuron Syndrome
-injury resides in the anterior horn cell or peripheral nerve
- involves the peripheral nerve or cranial nerves
what is an upper motor neuron syndrome the result from
the disruption of central motor pathways that arise from the cerebral cortex and pathways in the spinal cord
Pathways (connection to motor system)
1) Corticospinal tracts
2) corticobulbar tracts
3) lateral and medual reticulospinal tracts
4) lateral and medial vestibulospinal tracts
5) rubrospinal tracts
6) tectospinal tracts
Classic Upper Motor Neuron Syndrome weakness
loss of CNS drive
Classic Upper Motor Neuron Syndrome Spasticity
increase in muscle tone with a velocity - based muscle stretch (changes in tone)
Classic Upper Motor Neuron Syndrome decreased muscle control
changes in selective function
Classic Upper Motor Neuron Syndrome Hyperreflexia or exaggerated deep tendon reflexes
increase muscle response to tendon tap
Classic Upper Motor Neuron Syndrome clonus
repeated rhythmic contractions of individual muscle groups
muscle tone definition
Resistance to passive stretch as a patient is attempting to maintain a relaxed state of muscle activity
muscle tone reflexes
-Muscle state (at relaxation): test at every joint flextion/extention, Ab.Ad
-Independent of strength, coordination or involuntary movement
Range of muscle tone hypo to hyper
- Flaccidity (LMN)
- Hypotonia
-normal
-hypertonia (UMN)
-rigidity (UMN)
Hypertonia definition
Increase in passive muscle tightness
Hypertonia spasticity
-velocity dependent
-muscle spindle not reseting
-need to be tested very fast
-UMN
Hypertonia: rigidity
-tight throughout
-Significant increase in resistance to multi directional external force about a joint
Hypertonia Dystonia
-State of abnormal muscle tone resulting in muscular spasm and abnormal posture, typically due to neurological disease or a side effect of drug therapy
-Tone fluctuate throughout
-Goes with the basil ganglia
-In huntingtons or with children growing really fast
Common postures in UMN syndrome: CVA, TB, Cerebral palsy
-Flexed elbow
-Bent wrist
-Pronated forearm
-Clenched fist
-Thumb in palm
Ataxia definition
-loss of coordination, trimmers, overshooting, loss of velocity
-Associated with cerebellum
Bradykinesia
slow movement
Associated with basal ganglia (parkinsons)
Dystonia
-a state of abnormal muscle tone resulting in muscular spasm and abnormal posture
-Associated with basal ganglia
Chorea Distonia definition
continuous stream of slow flowing, writing involuntary movements
Ballistic Dystonia
explosive movement of the extremities
Contractures with UMN
1) Neuromuscular changes
- Loss of selective movement
- Muscle hyper-reflexia
- Muscle hypertonia
- Loss of ROM over time leads to contracture
2) Associated with sensory loss
- Loss of proprioception
- Loss of light touch
- Loss of pin prick
Hyperactive reflexes
-Is an increase in the reflex response
-Clonus
-Associated movements: moving one part of the body and another limb moves involuntary
Brainstem involvement: advanced brain lesion
-Causes severe motor disruption (sensory and motor): posturing all limbs are fixed in a postures with limited limb movements
-Associated with rigidity (severe increase in tone)
-Extension or flexion posturing
Extension posturing
extension of both limbs
abnormal flexion posturing
flexion of UE and extension of LE with slight internal rotation
CVA UMN signs
1) Initially flaccid
2) Later develops spasticity
3) Reflexed hyperactive
4) Synergistic movements
5) Clonus (variable)
6) Loss of joint position sense
7) CN changes or loss of vision or facial
8) weakness
9) Bladder changes
CVS signs
Headache
Mental changes
Aphasia
RESP problems (decreased neuromuscular control)
Decrease in cough and swallow reflex
agnosia
Incontinence
seizures
Hemiparesis or hemiplegia
Emotional lability
Visual changes
Vomiting
Perceptual defects
hypertension
Spinal cord injury UMN vertebra body fracture leads to
1) compression injury
2) flexion injury
3) extension injury
Clinical syndromes of incomplete spinal cord injury
1) central cord
2) brown sequard
3) anterior horn
Central cord
-Large lesion
-cervical
-Hyperextension
-Slight pain and temperature loss localized
-Due to spinothalamic crossing over at the specific level of the injury
Brown Sequard injury
-Hemisection of spinal cord
-Ipsilateral UMN signs below the level of lesion
-Ipsilateral loss of tactile vibration, proprioception sense 1-2 levels below the level of the lesion
-Contralateral pain and temperature loss below the level of the lesion
-Ipsilateral loss of all sensation at the level of the lesion
-Ipsilateral LMN signs
anteiror cord
1) incomplete (hemicord)
-Ispilateral vibration, position, and motor loss
-Contralateral pain and temperature loss
2) Complete
-Everything below the injury not working
Lower Motor Neuron Lesions
1) Loss of muscle function (weakness or flaccid)
- Peripheral nerve injury/spinal nerve root injury
- Range from weakness to paralysis
2) Loss of sensory function from nerve damage (proprioception , touch and pain)
3 ) Tone: hyporeflexia
- No response to weak response on tendon tap
Additional LMN signs
1) Fibrillations
2) Fasciculations
3) Hypotonia or atonia
4) Hyporeflexia
4) Strength - limited to segmental or peripheral nerve pattern
5) Sensation (loss of discriminative touch, light touch, ain, temperature, vibration, pressure, and joint position)
Fibrillations Definition
muscular twitching involving individual muscle fibers acting without coordination
Fasciculations definitions
causes by increase receptor concentration on muscles to compensate for lack of innervation
Peripheral nerve injury
1) Neuropraxia
2) Axonotmesis
3) Neurotmesus
Neuropraxia
loss of myelin
weakness
axonotmesis
loss of axon and myelin
Weakness
Atrophy
Sensory loss
Neurotmesis
Complete transection of nerve
Recovery more difficult due to neuroma formation
Clinal presentation to peripheral nerve injury
1) muscle atrophy
2) weakness or paralysis
3) pain along nerve distribution
4) numbness along nerve
5) sensory loss over nerve
6) loss of ROM
Examination of a peripheral nerve injury muscle testing
-test muscles in the uninvolved side first
- test muscles in the involved side
- test muscles of adjacent peripheral nerves
Examination of a peripheral nerve injury sensory testing
- ask about pain behavior
-Test sensation uninvolved then involved
-test sensation of adjacent peripheral nerves
Injury to the common fibular (peroneal) muscles involved
fib long and brev,TA, EHL and EDL
Injury to the common fibular (peroneal)
signs and symptoms
- numbness and tingling
- shooting pain along the nerve
- pain with nerve tapping
-pain at rest
Injury to the common fibular (peroneal)
clinical presentation
1) hyporeflexia
2) muscular weakness along the fib n. distribution
3) sensory loss
Injury to the C5-6 nerve root signs and symptoms
1) hyporeflexia
2) decreases DTR
3) weakness
4) sensory loss
5) pain
6) numbness and tingling
follows dermatome pattern
Injury to C6 spinal nerve muscles
myotomal pattern of C6
Bircps, brachioradialis, and wrist extensors
Diabetic neuropathy
glove and stocking presentation
polyneuropathy
distal symmetric sensation loss
L4 motor weakness
extension of quads
L4 functional test
squat and rise
L4 reflexes
Knee jerk diminished
L5 motor weakness
dorsiflexion of great toes and foot
L5 screening and exam
heel walking
S1 motor weakness
planter flexion of great toe and foot
S1 screening and exam
walking on toes
S1 reflex
ankle jerk
Peripheral nerve LMN injury testing
1) locate specific location
2) tinels sign
3) nerve injury follows the peripheral nerve
4) muscle and sensory loss below the level of injury
5) weakness and hyporeflexia
Spinal nerve root injury LMN testing
1) injury at the spinal nerve root
2) injury follows a myotome and dermatome pattern
LMN lesion muscle strength
weakness are paralysis
LMN lesion muscle tone
decreased or absent
LMN lesion reflex
decreased or absent
LMN lesion wasting
rapid muscle wasting
UMN lesion muscle strength
weakness or paralysis
UMN lesion muscle tone
increased
UMN lesion reflex
increased + babinski sign
UMN lesion wasting
muscle mass maintained
