Lecture 13 Abnormal Muscle Tone Flashcards
Lower motor neuron lesions AND acute CNS lesions can cause ___________
Hypotonia/flaccidity
resistance to stretch in resting muscle
muscle tone
complete lack of resistance to passive stretch
flaccidity
abnormally low/less than normal resistance to passive stretch
hypotonia
in an awake person, with a normal neuromuscular system, slight muscle resistance to passive stretch is normal
normal
hypertonia has two subcategories
spasticity and rigidity
velocity dependent resistance to passive stretch
spasticity
non velocity dependent increase in resistance to passive stretch
rigidity
abnormally strong resistance to passive stretch
hypertonia
Chronic (after spinal shock has resolved) upper motor neuron lesions and basal ganglia lesions will cause…
Hypertonia/spasticity
what two mechanisms cause UMN overactivity?
- absence of corticospinal/ reticulospinal inhibition onto LMNs
- BS UMN overactivity
The lack of inhibition of which tracts causes hypertonicity (spacticity), when impacted by an upper motor neuron lesion?
Reticulospinal and corticospinal
Normal muscle rigidity : Resistance to passive mvmt is ____________ no matter how fast/slow you try to move the body part
Resistance to passive mvmt is constant no matter how fast/slow you try to move the body part
cog wheel rigidity is a combo of
-lead pipe rigidity and tremor
is cog wheel seen in BG disorders like Parkinsons?
yes
Some basal ganglia disorders can cause cogwheel rigidity, which is….
When passive movements of a muscle trigger start-stop ratchet-like rigidity
Gegenhalten
Resistance to passive stretch that remains constant no matter how fast/slow you move it
where is gegenhalten seen
severe dyspraxia, apraxia, dementia
Identify
Decerebrate
Remember more “E”s in the word for extension
Damage between brainstem and the midbrain/pons
Identify
Decorticate
flexed elbows
Damage to superior midbrain or severe B lesions of cortex
Spasticity definition
intermittent or sustained involuntary hyperactivity of a skeletal muscle associated with an upper motor neuron lesion
Normal progression of UMN lesion:
Spinal Shock (flaccidity) -> spasticity
flaccid –> decreased mvmt –> adaptations –> myoplasticity or neural overactivity –> spasticity
What are the 2 hallmarks of spasticity?
Increased velocity dependent muscle tone
Tendon jerk (deep tendon reflex - DTR) hyperreflexia
Clonus definition
involuntary, Repetitive reflex contraction of single muscle
Can be sustained or unsustained
What is the clasp-knife phenomenon
an initial resistance when attempting passive movement of the extremities, followed by a rapid decrease in resistance. Indicates UMN lesion
Biomechanical factors of spasticity
Changing viscoelasticity of muscle
Muscles and tendons become stiff
Reduced # of sarcomeres in proportion to reduced length in chronic stages
HIGH risk of contractures
PROM and/or AROM may still remain normal if no fixed shortening or contracture
Weak ________ binding can contribute to spasticity
Actin-Myosin
Benefits of spasticity
Maintain postural
Maintain muscle mass
Maintain bone mineralization
Reduce dependent edema
Prevent deep vein thromboses
Spasticity arises when pyramidal tract is interrupted at: _____ , ______ , _______
Cortex
Corona radiata
Internal capsule
What tract is inhibitory for spasticity?
Dorsal Reticulospinal
What tracts are excitatory for spasticity?
medial reticulospinal and vestibulospinal
Note: Dorsal reticulospinal is inhibitory
True or false: Lesions of primary motor cortex alone will produce spasticity
false
Lesions must include the ____________ cortex to produce spasticity
pre-motor cortex
Why do lesions of the anterior limb of the internal capsule produce spasticity?
Because fibers of supplementary motor cortex pass through here
Where in the internal capsule is the corticobulbar tract found?
Genu
Describe the contents of the posterior limb of the internal capsule
Has the Corticospinal tract inside
With the UE in the anterior portion
Trunk in the middle portion
and LE in the most posterior portion
Where does the cortico-reticular tract arise?
premotor and supplementary motor areas
Reticulospinal tract projects to __________ in SC
Motor neurons and interneurons
ventromedial reticular formation
is this formation excitatory or inhibitory?
Inhibitory
What inhibits the spinal stretch reflex (DTR)
ventromedial reticular formation
Excitatory system – diffuse/extensive areas in midbrain, pons, and bulbar medullary reticular formation
These systems facilitate ______ and ___________ but they inhibit __________
Facilitate: Extensors (anti-gravity muscles) + DTR
Inhibit: Flexors
The lateral coritcospinal tract inhibits the __________
reticulospinal tract
Excessive reticulospinal drive (lack of lateral corticospinal) can cause
Contracture, spasticity
Cell bodies of gamma motor neurons are located where?
Ventral horn
Increased fusiform drive from reticular formation -> hyperactivity of _______ -> Increased muscle spindle sensitivity
Gamma Motor Neurons
True or false: During spinal shock you will have exxagerated Deep tendon reflexes
False, they will be absent
What are examples of enhanced cutaneous reflexes due to lack of supraspinal inhibition?
Babinski sign
Flexor Withdrawal reflex
True or false: Spasticity can be triggered by both non-nociceptive and nociceptive input
True
What will a nerve conduction velocity test show when you have spasticity?
Nothing because spasticity is a CNS problem but NCV tests the PNS
-Bryan Yu, SPT 2024
