Lecture 8 Flashcards
describe upper motor neurons lesions, where can occur
Injury or disease influencing: -upper motor nuclei in motor cortex
- axons descending through brain, brainstem or spinal cord
Describe how side of lesion identifies location
distal muscles= lateral CST
- if damage below cervical medullary junction (has crossed midline), symptoms on same side- ipsilateral lesion at spinal level
- If damage occurs in the cortex (hasnt crossed midline yet), symptoms on opposite side- contralateral lesions at cortical level
4 Symptoms of upper motor neuron lesion
-muscle weakness
- increased muscle reflexes (hyper-reflexia)
- Increased muscle tone (hypertonicity)
- Positive babinski sign
Name for symptoms associated with UMN lesion
spastic paralysis
Describe muscle weakness
inability to activate muscles and produce force against resistance
Consideration for muscle weakness symptoms
associated with both UMN and LMN lesions
Describe hyperreflexia
stretch reflexes are excessivley large
Describe numbers of deep tondon reflex scale associated with hyperreflexia
> 2
Function of UMN in relation to reflexes
UMN’s help modulate stetch reflexes
Consequnces of damage to UMN (reflexes)
lose ability to modulate reflexes at spinal cord
Define clonus
repetitive vibratory contraction of the muscle in response to stretch
Describe how to test for tone
taking segmeny ad rotating around joint feeling for abonormal resistance
Testing that indicates hypertonia
resistance when moving joint through ROM
Identify the two types of hypertonic symptoms
spacticity, rigidity
Describe charcteristics of rigidity
rate and force dependant independant, associated with other disorders such as parkinsons
Describe characteristics of spaciticity
Rate and force dependant, at the end of range of motion gives way (clasp knife phenomenon), associated with upper motor neuron lesions
Describe the hairchy of infleunce on LMN function
-Cortex (boss), largest infleunce on LMN function,
-Rubrospinal tract, effects on arm muscles (net flexor),
-Vestibulospinal (net extensor effect)
Describe how type of tone helps identify infleunce
- If lesion above the midbrain- removal of cortical infleunce, rubrospinal and vestibulospinal tract is intact= “de-corticate” posture, involves rubrospinal tract- felxion of arm, extension of leg
- If lesion is below the midbrain, remove reubrospinal infleunce= “de-cerebrate” posture, vestibulospinal influence- extension of the arm and leg
Describe positive babisnki reflex
dorsiflexion of the big tow and fanning of the toes
How to test babsinski reflex
take hard object and drag on base of foot from heal on lateral side upwards
Describe when have positive babinski sign and what indicates a negative response
<1 years have babinski reflex
>1 years cortex modulates these reflexes, in adults get opposite response toes felx downwards
Dscribe how symptoms of UMN may lead to altered gait
Hemiplegic gait typical of unilateral UMN lesions. With decorticate posture, walk with arm flexed and leg extended, pelvis high on that side and circumduction of the leg
Identify causes of Upper motor neuron lesions
Injury can occur any where along UMN:
- Injury to motor cortex
- Damage to internal capsule/cerebral peduncles: *corticospinal tract tightly packed so usually will affect axons for all regions (legs, arms, face) on contralateral side
- Spinal cord lesion or compression
- Diseases attacking upper motor neuron: Primary lateral sclerosis, amyotrophic lateral sclerosis
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Describe characteristics of primary lateral sclerosis
unknown origin
Degeneration of upper motor neurons
UMN symtoms (e.g. spacicity, weakness)
No cure ( may use muscle relaxants, pain releivers, antidepressants)
Progressive and non-fatal (occurs over years, decades)- starts with cells in legs, than trunk, arms etc.
Describe amyotrophic lateral sclerosis
-“lou gehrigs disease”
-degenration of UMN’s and LMN’s
-unknown origin (potentially genetic)- genetic mutation decrease enzymes that rid free radicals and glutimate
-LMN lesion symtoms (atrophy, fasciculations etc)- LMN deficits in later stages
-UMN lesion symptoms (hypertonia, hyperreflexia)
-Problems breathing, swallowing, speaking
-fatal in 2-4 years- leads to respiratory failure, cant intake food
Describe symptoms assocated with damage to SC
if damage to lateral column, UMN symptoms below that level of injury, if damage cord and anterior horn, see LMN and UMN symptoms
Symptoms: weakness on bottom half of right side of face
damage to upper motor neuron on contralateral side. Sites: motor cortex in face region on lateral aspect (most likely) or potentially anterior region of internal capsule (small lesion, less likely)
Symptoms: loss of strength on whole right side including lower half of face, spacticity, increased reflexes, babinski sign, no other complications (i.e. sensory loss)
- injury above the level of the pons, affecting upper motor neurons. Most likely in basis pedunculi or posterior limb of internal capsule
Symptoms: weakness on whole right side of face
damage to facial nerve or facial nuclei on ipsilateral side of symptoms
Symptoms: loss of strength on whole right side except the face, spacticity, increased reflexes, babinski sign, no other complications (e.g. sensory loss)
-Most likley UMN damage below the level of the pons, e.g. pyramids, before get into spinal cord, or less likely superior lateral part of motor cortex
Symptoms: weakness in right arm and bottom half of right face, spacticity, increased reflexes, no other complications (e.g. sensory loss)
above pons because face is involved, most likley lateral aspect of corex on contralateral side of lesion
