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S6- Neuro 2 > Week 7- Peripheral Nerve Disorders > Flashcards

Week 7- Peripheral Nerve Disorders Flashcards

1
Q

PART 1: NEUROPATHY INTRODUCTION

A

PART 1: NEUROPATHY INTRODUCTION

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2
Q

What are the 2 major ways we will talk about peripheral nerve damage/involvement?

A
  • Neuropathy

- Radiculopathy

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3
Q

What is the difference between neuropathy and radiculopathy?

A

Location and Type of nerve involved

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4
Q
  • _________ = Damage to nerves associated with the spine.

- _________ = Damage to secondary nerves located at the peripheral of the body.

A
  • Neuropathy = Damage to nerves associated with the spine.

- Radiculopathy = Damage to secondary nerves located at the peripheral of the body.

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5
Q

Neuropathy is split into ______neuropathy and ____neuropathy.

A
  • mononeuropathy

- polyneuropathy

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6
Q

Describe each of the following for PNS Dysfunction:

  • Distribution of S/Sx
  • Nerve Conduction Study
  • Muscle Tone
  • Muscle Atrophy
  • Phasic Stretch Reflexes
  • Paraspinal Sensation and/or Paraspinal Muscles
A

PNS Dysfunction:

  • Distribution of S/Sx = Peripheral nerve pattern
  • Nerve Conduction Study = Slowed/blocked conduction; decreased amplitude of recorded potentials
  • Muscle Tone = If LMN involvement, hypotonia
  • Muscle Atrophy = Rapid muscle atrophy indicates denervation
  • Phasic Stretch Reflexes = reduced or absent
  • Paraspinal Sensation and/or Paraspinal Muscles = normal
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7
Q

Describe each of the following for CNS Dysfunction:

  • Distribution of S/Sx
  • Nerve Conduction Study
  • Muscle Tone
  • Muscle Atrophy
  • Phasic Stretch Reflexes
  • Paraspinal Sensation and/or Paraspinal Muscles
A

CNS Dysfunction:

  • Distribution of S/Sx = dermatomal/myotomal pattern
  • Nerve Conduction Study = normal
  • Muscle Tone = If UMN involvement, hypertonia
  • Muscle Atrophy = Muscle atrophy progresses slowly
  • Phasic Stretch Reflexes = Hyperactive or normal
  • Paraspinal Sensation and/or Paraspinal Muscles = involved
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8
Q

What are the 3 main dysfunctions seen with PNS syndromes and their symptoms?

A

Motor Dysfunction
-weakness/paresis of denervated muscle, hyporeflexia and hypotonia, atrophy, fatigue

Sensory Dysfunction
-paresthesias, proprioceptive losses may yield sensory ataxia; insensitivities may yield limb trauma

ANS Dysfunction
-Vasodilation and loss of vasomotor tone (dryness, warm skin, edema, OH)

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9
Q

What are other things commonly seen with PNS syndromes?

A
  • Neuropathic pain and/or muscle pain (myalgia) common

- Hyper-excitability of remaining nerve fibers

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10
Q

How does hyperexcitability present both with sensory and motor?

A
  • Sensory = hyperalgesia, pins and needles, numbness, tingling, burning
  • Motor = fasciculations
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11
Q

What are some trophic changes that can occur due to denervation? (5)

A
  • Muscles atrophy, skin becomes shiny, nails become brittle, and subcutaneous tissues thicken.
  • Ulceration of cutaneous and subcutaneous tissues,
  • Poor wound healing, infections
  • Neurogenic joint damage
  • Hair thinning
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12
Q

Which trophic change is more common with severe/chronic cases?

A

-Neurogenic joint damage

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13
Q
  • What is mononeuropathy?

- What are the most common causes?

A
  • When there is damage to only one nerve.

- Entrapment, trauma, prolonged limb immobility (surgery)

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14
Q

What are the (3) classifications of mononeuropathy nerve damage from least severe to most severe?

A
  • Neuropraxia
  • Axonotmesis
  • Neurotmesis
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15
Q

Neuropraxia:

-Local ______ damage, _____ remains intact.

A

-Local myelin damage, axon remains intact.

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16
Q

Axonotmesis:

  • Continuity of _____ is lost.
  • May or may not include damage to epineurium, perineurium, and/or endoneurium.
  • Loss of continuity leads to ________ degeneration.
A
  • axon

- Wallerian (retrograde degeneration of the distal end of an axon that is a result of a nerve)

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17
Q

Neurotmesis:

  • Complete ________ of nerve.
  • ________ necessary.
A
  • transection

- surgery necessary

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18
Q
  • With neuropraxia, can you see recovery/regeneration?
  • With axonotmesis, can you see recovery/regeneration?
  • With neurotmesis, can you see recovery/regeneration?
A
  • Yes
  • Yes
  • No
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19
Q
  • What is the MAIN difference with PNS vs CNS when it comes to recovery?
  • How does it do this?
A
  • The PNS CAN REGENERATE under certain circumstances!

- Axonal sprouting (regenerative vs collateral)

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20
Q

Multiple Mononeuropathy:

  • Involves 2 or more nerves in _______ parts of the body.
  • _________ = dangerous cause of multiple mononeuropathy. (If suspected, urgent referral should be made for electrodiagnostic evaluation)
  • Individual nerves are affected, producing a _______, __________ presentation of signs.
A
  • 2 or more nerves in different parts of the body
  • Vasculitis
  • random, asymmetrical
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21
Q

PART 2: DIABETIC POLYNEUROPATHY

A

PART 2: DIABETIC POLYNEUROPATHY

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22
Q 
Polyneuropathy:
-\_\_\_\_\_\_\_\_ involvement: sensory, motor, autonomic
-\_\_\_\_\_\_\_ → \_\_\_\_\_\_ → Autonomic 
-\_\_\_\_\_\_ → \_\_\_\_\_\_\_\_
Feet → \_\_\_\_\_ → fingertips → \_\_\_\_\_\_
A

-SYMMETRICAL involvement
-Sensory → Motor → Autonomic
Distal → proximal
Feet → legs → fingertips → hands

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23
Q

Polyneuropathy affects the ________ peripheral nerves.

-______ nerve fibers → _______ nerve fibers

A
  • longest

- small nerve fibers → large nerve fibers

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24
Q

Polyneuropathy Sensory Symptoms:

  • What sensory symptoms are seen earlier in the disease? (2)
  • What sensory symptoms are seen as the disease progresses? (3)
A

Early: (anterolateral)

  • loss of temperature
  • pain (hypo or hyper)

Later: (DCML)

  • loss of vibration
  • loss of light touch discrimination
  • loss of proprioception/kinesthesia
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25
Q

Polyneuropathy Motor Symptoms:

  • Weakness
  • Cramping
  • _________
  • Muscle Loss
  • _____ Degeneration
  • Loss of Ankle _______
  • _______ Changes
A
  • Fasciculations
  • Bone Degeneration
  • Loss of Ankle Reflexes
  • Trophic Changes
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26
Q

Polyneuropathy Autonomic Symptoms:

  • What are the 2 main symptoms seen?
  • What are some others?
  • What is unique about autonomic symptoms?
A
  • Loss of B&B control, Loss of BP control (orthostasis VERY common!)
  • Impaired breathing, GI dysfunction, dysarthria, temperature dysregulation (decreased sweating)
  • Diverse manifestations, meaning they have variable S/Sx and severity.
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27
Q

What is the most common cause of polyneuropathy?

A

-Diabetes Mellitus (60-70% of individuals with DM have mild-severe forms of PN)

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28
Q

What are some other causes of polyneuropathy? (9)

A
  • Autoimmune disorders
  • Chronic kidney disease
  • HIV and liver infections
  • Low level of vitamin B12
  • Poor circulation in LEs
  • Underactive thyroid gland
  • Trauma
  • Tumor
  • Alcoholism
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29
Q

Is polyneuropathy worse with Type I or II diabetes?

A

Type II (insulin resistance)

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30
Q

Diabetic Polyneuropathy:

  • Research suggests that up to ___% of people with diabetes have peripheral motor and/or sensory neuropathy.
  • More than ___% of people with diabetes have autonomic neuropathy.
A
  • 50%

- 30%

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31
Q

What is the cause of diabetic polyneuropathy?

A

-Blood vessel and nerve damage due to high blood glucose levels and high levels of triglycerides.

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32
Q

What are the risk factors for diabetic polyneuropathy? (6)

A
  • Obesity
  • Sedentary Lifestyle
  • Hypertension
  • Decreased Glycemic Control
  • Alcoholism
  • Smoker
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33
Q

What is the “stocking and glove” distribution?

A

-Diabetic polyneuropathy description of areas of nerves that are lost.

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34
Q

Diabetic Polyneuropathy Prognosis:

  • Can diabetic polyneuropathy be prevented?
  • Is progression slow or fast?
  • Treating diabetes may halt progression and improve symptoms of the neuropathy, but recovery is exceptionally slow. (For many, improvements do not occur)
A
  • YES, with appropriate disease management and compliance.

- Progression is generally slow (years) but ultimately depends on how well the patient manages their diabetes.

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35
Q

What are the main interventions used for patients with diabetic polyneuropathy? (4)

A
  • Aerobic Conditioning
  • Balance Training
  • Resistance Training
  • Patient Education
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36
Q

Aerobic Conditioning Recommendations:

  • ____ minutes/week
  • ___-___% HRmax (mRPE 5-7 (RPE 14-16))
A
  • 150 minutes/week

- 50-70% HRmax (mRPE 5-7 (RPE 14-16))

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37
Q

Balance Training:

  • Can we improve sensory loss?
  • What does this mean we have to do?
A
  • NO

- Have to strengthen other balance systems to COMPENSATE.

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38
Q

Patient Education:

  • Skin ______/___________
  • _____ considerations
  • __________ Consult
  • ______ ______ management
  • Importance of aerobic exercise
  • Strategies to reduce sedentary lifestyle
  • ___________ to program
A
  • Skin care/inspection
  • Shoe considerations
  • Nutritional Consult
  • Fall risk management (bathroom light, get rid of items on floor, pair of shoes by bed)
  • Importance of aerobic exercise
  • Strategies to reduce sedentary lifestyle
  • Compliance to program
39
Q

PART 3: CHARCOT MARIE TOOTH DISEASE (CMT)

A

PART 3: CHARCOT MARIE TOOTH DISEASE (CMT)

40
Q
  • CMT Disease is the most common _______ neurological disease affecting 1 in every 2500.
  • Does it affect males of females more?
A
  • most common inherited neurological disorder

- Males > Females

41
Q
  • CMT presents with progressive muscle weakness that typically becomes noticeable when?
  • Does it affect motor or sensory nerves?
A
  • Typically becomes noticeable in adolescence or early adulthood, but the onset of disease can occur at any age.
  • motor and sensory nerves
42
Q

What is the cardinal S/Sx of CMT?

A

-Progressive muscle weakness

43
Q

Describe the pathology of CMT Disorder?

A

-Caused by a mutation in genes that produce proteins involved in the structure, maintenance, and formation of primarily the myelin sheath.

44
Q

With CMT Disease, we will see secondary degeneration of axons as disease progresses as well as ____-______ CMT subtypes (though less common).

A

-axon-dominant

45
Q

What is the Hallmark Pathological Sign of CMT Disease?

A

-Hypertrophic onion bulb formation.

46
Q

What is the Hypertrophic onion bulb formation?

A

-Repetitive segmental demyelination and regeneration of myelin that causes gross thickening of peripheral nerves. This creates palpable, enlarged peripheral nerves.

47
Q

What are the (4) things included in diagnosis of CMT Disease?

A
  • Clinical Exam
  • Electrodiagnostic Testing
  • Genetic Testing
  • Nerve Biopsy
48
Q

What are the only 2 things that we must perform if we have a family history of CMT Disease?

A
  • Clinical Exam

- Electrodiagnostic Testing

49
Q

CMT Motor Clinical Manifestations:

  • Clinical signs of _______ ________ muscle weakness, atrophy, and diminished DTRs.
  • _____ loss → _______ loss.
  • ____ first → ____ as disease progresses.
A
  • Clinical signs of distally symmetric muscle weakness
  • Motor loss first → sensory loss.
  • LE first → UE as disease progresses.
50
Q

CMT Motor LE:

  • ____ and ankle ________ weakness most common.
  • Loss of muscle bulk in distal LE + hypertrophy proximal LE → “_________ ________ ______”
  • ______ arches, hammer toes, inverted heel, flat feet
A
  • DF and ankle evertor weakness most common
  • “inverted champagne bottle”
  • High arches (pes cavus)
51
Q

CMT Motor UE:

  • _____ hands
  • atrophy of lumbricals/interossei
A

-claw hands

52
Q

CMT Sensory Clinical Manifestations:

  • Do we usually have sensory symptoms initially?
  • What parts of sensory are often damaged?
  • _____ remains intact (neuropathic may be present, and if so, ________)
  • Pain can be due to what?
A
  • Not usually.
  • Discriminative touch, vibratory, and proprioceptive sensation
  • Pain (severe)
  • Pain due to postural changes, skeletal deformities, muscular fatigue, and cramping is common.
53
Q
  • Is there a cure or disease modifying therapy available for CMT Disease?
  • Medications are solely _______-__________.
A
  • NO

- symptom-management

54
Q

How is CMT Disease managed if there is no cure/drugs?

A

Overall management is REHAB!

-May require surgical interventions for more significant impairment.

55
Q

CMT is a ______ progressive disorder that has a ________ life expectancy.

A
  • slowly progressive

- normal life expectancy

56
Q

What are some CMT Intervention strategies?

A
  • Strengthening and Aerobic Activity
  • Orthoses (AFO)
  • Appropriate Footwear
  • Podiatry Consult
  • ROM Management
  • Balance Training
57
Q

Strengthening and Aerobic Activity:

  • _______ intensity (__-__% 1RM)
  • ______ muscle groups
  • _______ Therapy fantastic adjunct to over-ground!
  • Be wary of ______…
A
  • moderate intensity (60-80% 1RM)
  • large muscle groups
  • Aquatic Therapy
  • Be wary of fatigue.
58
Q

ROM Management:

  • _________ are very common.
  • HEP for ___________.
  • Are splints ever needed?
A
  • Contractures
  • HEP for stretching
  • Yes, serial casting/night splinting
59
Q

Balance Training:

  • Combo of _______ balance tasks and _____ ________ strategies.
  • Introduction of _____.
A
  • Functional balance tasks and fall reduction strategies.

- Introduction of AD

60
Q

PART 4: CRANIAL NERVE DISORDERS

A

PART 4: CRANIAL NERVE DISORDERS

61
Q

What are the 12 Cranial Nerves and their function?

A
  1. ) Olfactory - Smell
  2. ) Optic - Visual acuity
  3. ) Oculomotor - Opening of eyelids, eye movement (upward/medial, upward/lateral, medial, downward/lateral)
  4. ) Trochlear - Eye movement (downward/medial)
  5. ) Trigeminal - Facial sensation, chewing movements
  6. ) Abducens - Eye movement (lateral)
  7. ) Facial - Facial muscle movement (except chewing muscles) and eyelid closing
  8. ) Vestibulocochlear - Hearing and balance
  9. ) Glossopharyngeal - Taste on the posterior third of the tongue (not usually tested)
  10. ) Vagus - Uvula and swallowing
  11. ) Accessory - Shoulder shrug
  12. ) Hypoglossal - Tongue movement
62
Q

What is a good way to remember the 12 Cranial Nerves?

A

-Oh Oh Oh To Touch And Feel Very Good Vagina, Ah Heaven

63
Q

Are cranial nerves part of the CNS or PNS?

A

-PNS

64
Q

List of Cranial Nerve Disorders. (9)

A
  • Trigeminal Neuralgia
  • Bell’s Palsy
  • Conjugate Gaze Palsies
  • Glossopharyngeal Neuralgia
  • Hemifacial Spasm
  • Hypoglossal Nerve Disorder
  • Internuclear Opthalmoplegia
  • Acoustic Neuroma
  • Meniere’s Disease
65
Q

List of Cranial Nerve Disorder we will go over.

A
  • Trigeminal Neuralgia (tic douloureux)
  • Bell’s Palsy (facial paralysis)
  • Bulbar Palsy (bulbar paralysis)
66
Q

-What is the function of the trigeminal nerve?

A

-Responsible for sensation in the face, and control of motor functions such as biting and chewing.

67
Q

-What are the 3 branches of the trigeminal nerve?

A
  1. ) Ophthalmic Nerve (V1) - sensory
  2. ) Maxillary Nerve (V2) - sensory
  3. ) Mandibular Nerve (V3) - sensory and motor
68
Q

Which branch of the trigeminal nerve is responsible for controlling the muscles of mastication?

A

-Mandibular Nerve (V3)

69
Q

Trigeminal Neuralgia Etiology:

  • Results from _________ (etiology unknown) or ____________ (tortuous basilar artery or cerebellopontine tumor).
  • Occurs in ______ population (mean age 50).
  • ______ onset.
A
  • degeneration or compression
  • older population
  • abrupt onset
70
Q
  • What are the characteristics of Trigeminal Neuralgia?
  • What 2 branches of the Trigeminal Nerve does this affect more?
  • Is it unilateral or bilateral?
  • Can be associated with _________ instability.
A
  • Brief paroxysms of severe neurogenic pain (stabbing/shooting), reoccurring frequently.
  • Mandibular (V2) and Maxillary (V3); (Ophthalmic (V1) rare)
  • unilateral
  • autonomic instability
71
Q

Trigeminal Neuralgia Clinical Presentation:

  • Characterized by brief severe attacks of neuropathic pain described as unbearable. How long do they usually last? What is it usually followed by?
  • ________ often has triggers (eating, washing, talking, shaving, temp changes) but can be spontaneous.
  • Sometimes relieved by _____/______.
  • Also associated with cluster headaches and depression.
A
  • Usually last from several seconds to several minutes and followed by a few minutes to hours of dull, achy pain. (can see remissions of weeks to months)
  • Allodynia
  • rest/meds
72
Q

What are the major focuses of examination? (4)

A
  • Pain: location, intensity
  • Trigger points: light touch to face, lips, or gums will cause pain
  • Triggering stimuli: extremes of heat or cold, chewing, talking, brushing teeth, movement of air across face
  • Motor function: control is normal
73
Q

What are a few ways we can medically manage these patients?

A
  • Medications (anticonvulsants, anti-spasticity drugs, botox injections, tricyclic antidepressants)
  • Surgery (microvascular decompression, gamma knife, thermal lesioning)
74
Q

What is the ultimate purpose of surgery for significant Trigeminal Neuralgia cases?

A

-Slicing the nerve so that there is no signaling being sent. Will lose function of CN5.

75
Q

What is something that can be done with rehabilitative management of Trigeminal Neuralgia?

A

-TENs (evidence for pain management)

76
Q

What is the prognosis of Trigeminal Neuralgia?

A

-Over time, attacks become more frequent, more easily triggered, and more disabling.

77
Q

What CN does Bell’s Palsy involve?

A

-CN7

78
Q
  • What is the motor function of CN7?
  • What is the special sensory function of CN7?
  • What is the parasympathetic function of CN7?
A
  • Motor: Facial expression muscles, posterior belly of digastric muscle, stylohyoid muscle, stapedius muscle.
  • Special Sensory: Taste from anterior two-thirds of the tongue.
  • Parasympathetic: Submandibular gland, sublingual gland, lacrimal glands.
79
Q

What is the etiology of Bell’s Palsy?

A

-Acute inflammatory process of unknown etiology (immune or viral disease) resulting in compression of the nerve within the temporal bone.

80
Q

Bell’s Palsy Characteristics:

  • What are the characteristics of Bell’s Palsy?
  • What is the onset?
  • What is it commonly preceded by?
  • How long does it take to recover?
A
  • Muscles of facial expression on one side are weakened/paralyzed. Loss of control of salivation/lacrimation.
  • Acute onset, maximum severity in a few hours to days
  • Commonly preceded by a day or 2 of pain behind the ear.
  • several weeks/months
81
Q

What do we see on examination of Bell’s Palsy?

A
  • Drooping of corner of mouth, eyelids that don’t close.
  • Function of muscles of facial expression (test CN VII)
  • Taste of anterior 2/3 of tongue.
82
Q

What are some medications for treatment of Bell’s Palsy?

A
  • Corticosteroids

- Analgesics

83
Q

How do we know that Bell’s Palsy facial droop isn’t the first sign of a stroke?

A

-FOREHEAD has bilateral innervation, therefore with a stroke we will see preservation of those muscles.

  • Bell’s Palsy = top and bottom
  • Stroke = bottom only
84
Q

What are some rehabilitative management strategies for Bell’s Palsy? (6)

A
  • Protect cornea artificial tears/patching) until recovery allows for eyelid closure
  • E-stim to maintain tone, support function of facial mm
  • Active facial muscle exercises
  • Face sling to prevent overstretching
  • Functional retraining: easily eaten foods, chew w/ opposite side
  • Provide emotional support and reassurance
85
Q

What is the prognosis for patients with Bell’s Palsy?

A
  • Generally good. Most begin to show improvements within 2 weeks after onset.
  • With proper management, most recover some/all facial function in 6 months.
86
Q
  • What is Bulbar Palsy?

- What nerves does this include?

A

Refers to weakness or paralysis of the muscles innervated by the motor nuclei of the lower brainstem, affecting the muscles of the face, tongue, larynx and pharynx.
-CN IX, X, and XII

87
Q

What is the etiology of Bulbar Palsy?

A

-Result of tumors, vascular or degenerative diseases of lower CN motor nuclei. (can be progressive)

88
Q

Bulbar Palsy Characteristics:

  • What 2 functions do we generally lose?
  • ________/_____ Paralysis (phonation, articulation, palatal action, gag reflex, and swallowing)
  • Changes in voice quality = _________
  • ______ atrophy/fasciculations
  • What do we see with bilateral involvement?
  • What is most common complication of Bulbar Palsy?
A
  • Speaking and swallowing
  • Glossopharyngeal/Vagal Paralysis
  • Dysphonia (hoarseness or nasal quality)
  • Tongue atrophy/fasciculations
  • Severe airway restrictions with dyspnea, difficulty with coughing.
  • Aspiration pneumonia.
89
Q

Pseudobulbar Palsy:

  • ________ dysfunction of corticobulbar innervation or brainstem nuclei.
  • A central ____ lesion analogous to corticospinal lesions disrupting function of anterior horn cells.
  • Produces similar symptoms of __________.
A
  • Bilateral dysfunction
  • UMN lesion
  • Bulbar Palsy
90
Q

Pseudobulbar Palsy vs Bulbar Palsy:

-What are the MAJOR DIFFERENCES between psuedobulbar palsy and bulbar palsy? (5)

A
  • Pseudobulbar Palsy = CN5 and CN7 involvement
  • Emotional incontinence (pseudobulbar affect)
  • Tongue spasticity
  • Spastic dysarthria (“Donald Duck speech”)
  • Hyperactive reflexes (jaw jerk reflex and snout reflex)
91
Q
  • What is Jaw Jerk Reflex?

- What is Snout Reflex?

A
  • Jaw Jerk = Tap on jaw: contraction of masseter and temporalis muscles
  • Snout = Tap on lips produces pouting of lips
92
Q
  • _____ Palsy = UMN lesion

- _____ Palsy = LMN lesion

A
  • Pseudobulbar Palsy = UMN Lesion

- Bulbar Palsy = LMN lesion

93
Q

Is there a treatment for Bulbar Palsy?

A

-No

94
Q

What does management of Bulbar Palsy include?

A
  • Supportive Therapy (anticholinergics to control drooling, PEG tube for severe dysphagia or recurrent aspiration PNA)
  • Speech and Language Pathology
  • Physical Therapy (inconclusive evidence on tole of exercise, patients with progressive bulbar palsy may maintain mobility but present with severe respiratory compromise and should be managed accordingly)

S6- Neuro 2 (18 decks)

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