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PHTH 527: Neuro > Lec 3: UMN and LMN Pathology > Flashcards

Lec 3: UMN and LMN Pathology Flashcards

1
Q

UMN Syndrome may involve what?

A

-Motor cortex and pathways
-Brainstem
-Cerebellum
-SC reflexes and coordination

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1
Q

What corresponds with an UMN lesion?

A

-collection of neurologic signs and symptoms (postures, postural responses, passive mvmts, active mvmts, and involuntary responses)

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2
Q

UMN syndrome injuries reside where?

A

-several areas of brain and SC
-major areas: motor cortex or brainstem
-motor pathways from major brain areas
-SC involving motor output

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3
Q

LMN syndrome injuries reside where?

A

-AHC or peripheral nerve
-cranial nerve (PN)

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4
Q

UMN Syndrome is the result of….

A

-a disruption of central motor pathways (arise from cerebral cortex and pathways in SC)

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5
Q

Define central motor pathways?

A

connections to the motor systems from cerebral cortex and in spinal cord

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6
Q

What are the six central motor pathways?

A

-Corticospinal Tracts (voluntary motor control)
-Corticobulbar Tracts (cranial nerves)
-Lateral and Medial Reticulospinal Tracts (muscle tone/cerebellum)
-Lateral and Medial Vestibulospinal Tracts (AMN/reflexes)
-Rubrospinal Tracts (cerebellum and BG)
-Tectospinal Tracts (vision and auditory stimulation to turn head)

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7
Q

Classic UMN Syndrome

A

Weakness, Spasticity, Decreased Muscle Control, Hyperreflexia (exaggerated DTR), Clonus

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8
Q

Define weakness and decreased muscle control?

A

Weakness: loss of CNS drive (groups of muscles vs PN innervated muscles)

Decreased muscle control: changes in selective function

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9
Q

Define hyperreflexia, and clonus in UMN syndrome

A

Hyperreflexia: Increase muscle response to tendon tap

Clonus: repeated rhythmic contractions of individual muscle groups

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10
Q

Tone definition and what tone reflects

A

Tone is resistance to passive stretch as a patient is attempting to maintain a relaxed state of muscle activity (excludes joint, skeletal, ligamentous abnormalities). Tone is a normal balance between excitatory and inhibitory control.

Tone reflects the muscle’s state of relaxation (must test at every joint in flexion, ext, ABD, & ADD). It is independent of strength, coordination or involuntary movement.

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11
Q

What is the range of muscle tone and where is UMN and LMN in the range?

A

Range= flaccidity–hypotonia–normal–hypertonia–rigidity

LMN characterized by flaccidity, while UMN is characterized by flaccidity only initially. UMN is later classified by hypertonia.

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12
Q

Define hypertonia and it’s 3 classifications

A

Increase in passive muscle tightness (abnormally increased resistance to an external force about a joint)

  1. Spasticity
  2. Rigidity
  3. Dystonia
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13
Q

Definition of Spasticity

A

A motor disorder characterized by velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex, as one component of the UMN syndrome.

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14
Q

Definition of rigidity and dystonia

A

Rigidity: significant increase in resistance to multidirectional external forces about a joint

Dystonia: a state of abnormal muscle tone resulting in muscular spasm and abnormal posture, typically d/t neurological disease or side effect of drug therapy

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15
Q

Movement based sign of UMN lesion

A

Synergistic movements or abnormal movements
e.g. flexor synergy/extensor synergy

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16
Q

Common upper limb postures or joint positions in UMN syndrome

A

Flexed elbow, Bent wrist, Pronated forearm, Clenched fist, Thumb in palm

17
Q

Movement based problems associated with additional brain structures

A

Ataxia (loss of coordination, tremors, overshooting mvmt, loss of velocity) associated with cerebellum

Bradykinesia (slow mvmt) associated with BG (common in PD)

Dystonia (state of abnormal muscle tone resulting in muscular spasm and abnormal posture) associated with BG (esp in Huntington’s chorea)

18
Q

Loss of ROM over time in UMN lesions leads to…

A

contracture development

19
Q

Neuromuscular changes and associated sensory loss with UMN lesions

A

-loss of selective mvmt, muscle hyperreflexia, muscle hypertonia
-loss of proprioception, light touch, pin prick

20
Q

Range of hyperactive reflexes

A

Absent -4
Just Elicitable -3
Low Response -2
Mod Low -1
Normal 0
Brisk +1
V Brisk +2
Exhaustible Clonus +3
Continuous Clonus +4

21
Q

What are “associated movements” in hyperractive reflexes

A

Moving one body part causes involuntary movement of another body part

22
Q

Advanced brain lesions are involved with what structure and cause what?

A

-involved with the brainstem
-cause severe motor and sensory disruption “posturing”

23
Q

What is “posturing” in advanced brain lesions

A

All limbs are “fixed” in a posture with limited limb movements, associated with rigidity.
-extension posturing, elbows extended (decerebrate rigidity)
-abnormal flexion, bent elbows (decorticate rigidity).

24
Q

UMN Signs

A

-initially flaccid, later develops spasticity
-reflexes hyperactive
-synergistic movement
-clonus variable
-sensory loss variable (loss of joint position sense)
-CN changes or loss (vision/facial weakness)
-bladder changes

25
Q

CVA or stroke signs

A

-hemiparesis or hemiplegia
-visual changes (Horner’s syndrome, Homonymous, Hemianopsia)
-headache, mental changes, aphasia
-hyperthermia, vomitting
-apraxia

26
Q

SCI Vertebral Body Fracture Types

A

Compression injury, flexion or extension injury

27
Q

Clinical Syndromes of incomplete SCI

A

-Central cord (large lesion, cervical, hyper extension)
-Brown Sequard (hemisection of spinal cord)
-Anterior Cord

28
Q

Brown Sequard SCI presentation

A

Ipsilateral vibration and position sense loss and motor loss
Contralateral pain and temperature sense loss

29
Q

Central Cord SCI

A

bilateral pain and temperature loss
spinothalamic crossing over at specific level of injury

30
Q

LMN Lesion Signs

A
  1. Loss of muscle function (weakness or flaccid)
    -peripheral nerve injury/spinal nerve root injury
    -range is from weakness to paralysis
  2. Loss of sensory function from n. damage
    -proprioception, touch, and pain (peripheral) n.
  3. Tone: Hyporeflexia
    -no response to weak tendon tap
31
Q

Additional LMN Lesion Signs

A

-Fibrillations= muscular twitching involving indv muscle fibers acting w/o coordination
-Fasciculations= caused by increased receptor concentration on muscles to compensate for lack of innervation
-Hypotonia or atonia
-Hyporeflexia= along with DTR and cutaneous reflexes also decreased/absent
-Strength= weakness limited to segmental or PNerve pattern (myotome nerve roots OR PNerve presentation)
-Sensation= loss of discriminative touch, light touch, pain, temperature, vibration, pressure, and joint position

32
Q

Peripheral Nerve Injury Types

A
  1. Neuropraxia: loss of myelin = weakness
  2. Axonotmesis: loss of axon and myelin= weakness, atrophy, sensory loss. Wallerian Degeneration (anything distal to injury degenerates)
  3. Neurotmesis: complete transection of nerve, recovery more difficult due to neuroma formation. Wallerian Degeneration.
33
Q

Peripheral Nerve Injuries of Nerve Root

A
  1. Herniated disc compressing spinal nerve
  2. Foraminal Stenosis
34
Q

Injury to PNerve in Carpal Tunnel Syndrome: Clinical Presentation and Muscles Involved

A

Median Nerve Injury
-Atrophy muscle, Weakness/Paralysis, Pain along nerve distribution, numbness along nerve, sensory loss (light touch and position sense) over nerve, ROM loss over time
-Flexor pollicis brevis, opponens pollicis, abductor pollicis, distal to injury site

35
Q

Examination of Peripheral Nerve Injury

A
  1. Muscle Testing
    -test muscles in uninvolved side first, test muscles in involved side, test muscles of adjacent peripheral nerves (ulnar and radial)
  2. Sensory Testing
    -ask about pain (type, location, aggravation, reduction)
    -test sensation (light touch, pin prick to uninvolved side first)
    -be sure to test sensation of adjacent peripheral n.
36
Q

Injury to Deep Peroneal Nerve: Clinical Presentation, Signs & Symptoms, and Muscles Involved

A

-Hyporeflexia, muscular weakness along PN distribution, sensory loss in common fibular distribution
-Numbness and tingling, shooting pain along nerve, pain w/ nerve tapping, pain at rest
-Peroneus longus and brevis, TA, EHL, EDL

37
Q

Injury to Cervical 5-6 Nerve Root: Signs & Symptoms and Muscles Involved

A

Radiculopathy
-follows C6 dermatomal pattern, hyporeflexia, decreased DTR, weakness, sensory loss, pain, numbness, and tingling following nervous system distribution
-Biceps, brachioradialis, wrist extensors (ECR)

38
Q

Other neuropathy: LMN

A
  1. Diabetic Neuropathy
    -diseased blood vessels —> nerves shrivel when BV disappear
    -length dependent
    -first symptoms in feet
    -glove and stocking presentation
  2. Polyneuropathy
    -distal symmetric
39
Q

Testing for LMN Injury: Peripheral vs Spinal N Root

A
  1. Peripheral nerve:
    -locate injury at a specific location
    -Tinel’s sign
    -nerve injury follows pathway of the peripheral n
    -muscle and sensory loss below level of injury
    -weakness and hyporeflexia
  2. Spinal Nerve Root:
    -injury at a spinal nerve
    -injury follows a myotome and dermatome pattern
40
Q

Upper Motor Neuron and Lower Motor Neuron Chart: Strength, Tone, Reflex Strength, Wasting, Causes

A
  1. LMN
    Strength: weakness/paralysis
    Tone: decreased or absent tone
    Reflex: decreased or absent reflex strength
    Wasting: rapid muscle wasting
    Causes: poliomyelitis, motor neuron disease, SCI at segmental level, PN dysfunction, muscle myotonias, myasthenia gravis, muscular dystrophies
  2. UMN
    Strength: weakness/paralysis
    Tone: increased tone
    Reflex: increased reflex strength + Babinski sign
    Wasting: muscle mass maintained
    Causes: Stroke (contralateral symptoms), cord section

PHTH 527: Neuro (7 decks)

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