Lecture 10 Flashcards

1
Q

Lower motor neuron lesions AND acute CNS lesions can cause ___________

A

Hypotonia/flaccidity

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2
Q

Chronic upper motor neuron lesions will cause…

A

Hypertonia/spasticity

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3
Q

The lack of inhibition of which tracts causes hypertonicity (spacticity), when impacted by an upper motor neuron lesion?

A

Reticulospinal and corticospinal

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4
Q

Normal muscle rigidity : Resistance to passive mvmt is ____________ no matter how fast/slow you try to move the body part

A

Resistance to passive mvmt is constant no matter how fast/slow you try to move the body part

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5
Q

Some basal ganglia disorders can cause cogwheel rigidity, which is….

A

When passive movements of a muscle trigger start-stop ratchet-like rigidity

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6
Q

Gegenhalten

A

Resistance to passive stretch that remains constant no matter how fast/slow you move it

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7
Q

Identify

A

Decerebrate

Remember more “E”s in the word for extension

Damage between brainstem and the midbrain/pons

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8
Q

Identify

A

Decorticate

Damage to superior midbrain or severe B lesions of cortex

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9
Q

Spasticity definition

A

intermittent or sustained involuntary hyperactivity of a skeletal muscle associated with an upper motor neuron lesion

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10
Q

Normal progression of UMN lesion:

A

Spinal Shock (flaccidity) -> spasticity

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11
Q

What are the 2 hallmarks of spasticity?

A

Increased velocity dependent muscle tone

Tendon jerk (deep tendon reflex - DTR) hyperreflexia

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12
Q

Clonus definition

A

Repetitive reflex contraction of single muscle
Can be sustained or unsustained

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13
Q

What is the clasp-knife phenomenon

A

an initial resistance when attempting passive movement of the extremities, followed by a rapid decrease in resistance. Indicates UMN lesion

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14
Q

Biomechanical factors of spasticity

A

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

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15
Q

Weak ________ binding can contribute to spasticity

A

Actin-Myosin

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16
Q

Benefits of spasticity

A

Maintain postural
Maintain muscle mass
Maintain bone mineralization
Reduce dependent edema
Prevent deep vein thromboses

17
Q

Spasticity arises when pyramidal tract is interrupted at: _____ , ______ , _______

A

Cortex
Corona radiata
Internal capsule

18
Q

What tract is inhibitory for spasticity?

A

Dorsal Reticulospinal

19
Q

What tracts are excitatory for spasticity?

A

medial reticulospinal and vestibulospinal

Note: Dorsal reticulospinal is inhibitory

20
Q

True or false: Lesions of primary motor cortex alone will produce spasticity

A

false

21
Q

Lesions must include the ____________ cortex to produce spasticity

A

pre-motor cortex

22
Q

Why do lesions of the anterior limb of the internal capsule produce spasticity?

A

Because fibers of supplementary motor cortex pass through here

23
Q

Where in the internal capsule is the corticobulbar tract found?

A

Genu

24
Q

Describe the contents of the posterior limb of the internal capsule

A

Has the Corticospinal tract inside

With the UE in the anterior portion

Trunk in the middle portion

and LE in the most posterior portion

25
Q

Where does the cortico-reticular tract arise?

A

premotor and supplementary motor areas

26
Q

Reticulospinal tract projects to __________ in SC

A

Motor neurons and interneurons

27
Q

ventromedial reticular formation

is this formation excitatory or inhibitory?

A

Inhibitory

28
Q

What inhibits the spinal stretch reflex (DTR)

A

ventromedial reticular formation

29
Q

Excitatory system – diffuse/extensive areas in midbrain, pons, and bulbar medullary reticular formation

These systems facilitate ______ and ___________ but they inhibit __________

A

Facilitate: Extensors (anti-gravity muscles) + DTR

Inhibit: Flexors

30
Q

The lateral coritcospinal tract inhibits the __________

A

reticulospinal tract

31
Q

Excessive reticulospinal drive (lack of lateral corticospinal) can cause

A

Contracture, spasticity

32
Q

Cell bodies of gamma motor neurons are located where?

A

Ventral horn

33
Q

Increased fusiform drive from reticular formation -> hyperactivity of _______ -> Increased muscle spindle sensitivity

A

Gamma Motor Neurons

34
Q

True or false: During spinal shock you will have exxagerated Deep tendon reflexes

A

False, they will be absent

35
Q

What are examples of enhanced cutaneous reflexes due to lack of supraspinal inhibition?

A

Babinski sign

Flexor Withdrawal reflex

36
Q

True or false: Spasticity can be triggered by both non-nociceptive and nociceptive input

A

True

37
Q

What will a nerve conduction velocity test show when you have spasticity?

A

Nothing because spasticity is a CNS problem but NCV tests the PNS
-Bryan Yu, SPT 2024