Week 7- Peripheral Nerve Disorders Flashcards
(94 cards)
1
Q
PART 1: NEUROPATHY INTRODUCTION
A
PART 1: NEUROPATHY INTRODUCTION
2
Q
What are the 2 major ways we will talk about peripheral nerve damage/involvement?
A
- Neuropathy
- Radiculopathy
3
Q
What is the difference between neuropathy and radiculopathy?
A
Location and Type of nerve involved
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.
5
Q
Neuropathy is split into ______neuropathy and ____neuropathy.
A
- mononeuropathy
- polyneuropathy
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
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
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)
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
10
Q
How does hyperexcitability present both with sensory and motor?
A
- Sensory = hyperalgesia, pins and needles, numbness, tingling, burning
- Motor = fasciculations
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
12
Q
Which trophic change is more common with severe/chronic cases?
A
-Neurogenic joint damage
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)
14
Q
What are the (3) classifications of mononeuropathy nerve damage from least severe to most severe?
A
- Neuropraxia
- Axonotmesis
- Neurotmesis
15
Q
Neuropraxia:
-Local ______ damage, _____ remains intact.
A
-Local myelin damage, axon remains intact.
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)
17
Q
Neurotmesis:
- Complete ________ of nerve.
- ________ necessary.
A
- transection
- surgery necessary
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
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)
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
21
Q
PART 2: DIABETIC POLYNEUROPATHY
A
PART 2: DIABETIC POLYNEUROPATHY
22
Q
Polyneuropathy: -\_\_\_\_\_\_\_\_ involvement: sensory, motor, autonomic -\_\_\_\_\_\_\_ → \_\_\_\_\_\_ → Autonomic -\_\_\_\_\_\_ → \_\_\_\_\_\_\_\_ Feet → \_\_\_\_\_ → fingertips → \_\_\_\_\_\_
A
-SYMMETRICAL involvement
-Sensory → Motor → Autonomic
Distal → proximal
Feet → legs → fingertips → hands
23
Q
Polyneuropathy affects the ________ peripheral nerves.
-______ nerve fibers → _______ nerve fibers
A
- longest
- small nerve fibers → large nerve fibers
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
25
Polyneuropathy Motor Symptoms:
- Weakness
- Cramping
- _________
- Muscle Loss
- _____ Degeneration
- Loss of Ankle _______
- _______ Changes
- Fasciculations
- Bone Degeneration
- Loss of Ankle Reflexes
- Trophic Changes
26
Polyneuropathy Autonomic Symptoms:
- What are the 2 main symptoms seen?
- What are some others?
- What is unique about autonomic symptoms?
- 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.
27
What is the most common cause of polyneuropathy?
-Diabetes Mellitus (60-70% of individuals with DM have mild-severe forms of PN)
28
What are some other causes of polyneuropathy? (9)
- Autoimmune disorders
- Chronic kidney disease
- HIV and liver infections
- Low level of vitamin B12
- Poor circulation in LEs
- Underactive thyroid gland
- Trauma
- Tumor
- Alcoholism
29
Is polyneuropathy worse with Type I or II diabetes?
Type II (insulin resistance)
30
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.
- 50%
| - 30%
31
What is the cause of diabetic polyneuropathy?
-Blood vessel and nerve damage due to high blood glucose levels and high levels of triglycerides.
32
What are the risk factors for diabetic polyneuropathy? (6)
- Obesity
- Sedentary Lifestyle
- Hypertension
- Decreased Glycemic Control
- Alcoholism
- Smoker
33
What is the "stocking and glove" distribution?
-Diabetic polyneuropathy description of areas of nerves that are lost.
34
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)
- YES, with appropriate disease management and compliance.
| - Progression is generally slow (years) but ultimately depends on how well the patient manages their diabetes.
35
What are the main interventions used for patients with diabetic polyneuropathy? (4)
- Aerobic Conditioning
- Balance Training
- Resistance Training
- Patient Education
36
Aerobic Conditioning Recommendations:
- ____ minutes/week
- ___-___% HRmax (mRPE 5-7 (RPE 14-16))
- 150 minutes/week
| - 50-70% HRmax (mRPE 5-7 (RPE 14-16))
37
Balance Training:
- Can we improve sensory loss?
- What does this mean we have to do?
- NO
| - Have to strengthen other balance systems to COMPENSATE.
38
Patient Education:
- Skin ______/___________
- _____ considerations
- __________ Consult
- ______ ______ management
- Importance of aerobic exercise
- Strategies to reduce sedentary lifestyle
- ___________ to program
- 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
PART 3: CHARCOT MARIE TOOTH DISEASE (CMT)
PART 3: CHARCOT MARIE TOOTH DISEASE (CMT)
40
- CMT Disease is the most common _______ neurological disease affecting 1 in every 2500.
- Does it affect males of females more?
- most common inherited neurological disorder
| - Males > Females
41
- CMT presents with progressive muscle weakness that typically becomes noticeable when?
- Does it affect motor or sensory nerves?
- Typically becomes noticeable in adolescence or early adulthood, but the onset of disease can occur at any age.
- motor and sensory nerves
42
What is the cardinal S/Sx of CMT?
-Progressive muscle weakness
43
Describe the pathology of CMT Disorder?
-Caused by a mutation in genes that produce proteins involved in the structure, maintenance, and formation of primarily the myelin sheath.
44
With CMT Disease, we will see secondary degeneration of axons as disease progresses as well as ____-______ CMT subtypes (though less common).
-axon-dominant
45
What is the Hallmark Pathological Sign of CMT Disease?
-Hypertrophic onion bulb formation.
46
What is the Hypertrophic onion bulb formation?
-Repetitive segmental demyelination and regeneration of myelin that causes gross thickening of peripheral nerves. This creates palpable, enlarged peripheral nerves.
47
What are the (4) things included in diagnosis of CMT Disease?
- Clinical Exam
- Electrodiagnostic Testing
- Genetic Testing
- Nerve Biopsy
48
What are the only 2 things that we must perform if we have a family history of CMT Disease?
- Clinical Exam
| - Electrodiagnostic Testing
49
CMT Motor Clinical Manifestations:
- Clinical signs of _______ ________ muscle weakness, atrophy, and diminished DTRs.
- _____ loss → _______ loss.
- ____ first → ____ as disease progresses.
- Clinical signs of distally symmetric muscle weakness
- Motor loss first → sensory loss.
- LE first → UE as disease progresses.
50
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
- DF and ankle evertor weakness most common
- “inverted champagne bottle”
- High arches (pes cavus)
51
CMT Motor UE:
- _____ hands
- atrophy of lumbricals/interossei
-claw hands
52
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?
- Not usually.
- Discriminative touch, vibratory, and proprioceptive sensation
- Pain (severe)
- Pain due to postural changes, skeletal deformities, muscular fatigue, and cramping is common.
53
- Is there a cure or disease modifying therapy available for CMT Disease?
- Medications are solely _______-__________.
- NO
| - symptom-management
54
How is CMT Disease managed if there is no cure/drugs?
Overall management is REHAB!
| -May require surgical interventions for more significant impairment.
55
CMT is a ______ progressive disorder that has a ________ life expectancy.
- slowly progressive
| - normal life expectancy
56
What are some CMT Intervention strategies?
- Strengthening and Aerobic Activity
- Orthoses (AFO)
- Appropriate Footwear
- Podiatry Consult
- ROM Management
- Balance Training
57
Strengthening and Aerobic Activity:
- _______ intensity (__-__% 1RM)
- ______ muscle groups
- _______ Therapy fantastic adjunct to over-ground!
- Be wary of ______...
- moderate intensity (60-80% 1RM)
- large muscle groups
- Aquatic Therapy
- Be wary of fatigue.
58
ROM Management:
- _________ are very common.
- HEP for ___________.
- Are splints ever needed?
- Contractures
- HEP for stretching
- Yes, serial casting/night splinting
59
Balance Training:
- Combo of _______ balance tasks and _____ ________ strategies.
- Introduction of _____.
- Functional balance tasks and fall reduction strategies.
| - Introduction of AD
60
PART 4: CRANIAL NERVE DISORDERS
PART 4: CRANIAL NERVE DISORDERS
61
What are the 12 Cranial Nerves and their function?
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
What is a good way to remember the 12 Cranial Nerves?
-Oh Oh Oh To Touch And Feel Very Good Vagina, Ah Heaven
63
Are cranial nerves part of the CNS or PNS?
-PNS
64
List of Cranial Nerve Disorders. (9)
- Trigeminal Neuralgia
- Bell's Palsy
- Conjugate Gaze Palsies
- Glossopharyngeal Neuralgia
- Hemifacial Spasm
- Hypoglossal Nerve Disorder
- Internuclear Opthalmoplegia
- Acoustic Neuroma
- Meniere's Disease
65
List of Cranial Nerve Disorder we will go over.
- Trigeminal Neuralgia (tic douloureux)
- Bell’s Palsy (facial paralysis)
- Bulbar Palsy (bulbar paralysis)
66
-What is the function of the trigeminal nerve?
-Responsible for sensation in the face, and control of motor functions such as biting and chewing.
67
-What are the 3 branches of the trigeminal nerve?
1. ) Ophthalmic Nerve (V1) - sensory
2. ) Maxillary Nerve (V2) - sensory
3. ) Mandibular Nerve (V3) - sensory and motor
68
Which branch of the trigeminal nerve is responsible for controlling the muscles of mastication?
-Mandibular Nerve (V3)
69
Trigeminal Neuralgia Etiology:
- Results from _________ (etiology unknown) or ____________ (tortuous basilar artery or cerebellopontine tumor).
- Occurs in ______ population (mean age 50).
- ______ onset.
- degeneration or compression
- older population
- abrupt onset
70
- 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.
- Brief paroxysms of severe neurogenic pain (stabbing/shooting), reoccurring frequently.
- Mandibular (V2) and Maxillary (V3); (Ophthalmic (V1) rare)
- unilateral
- autonomic instability
71
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.
- 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
What are the major focuses of examination? (4)
- 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
What are a few ways we can medically manage these patients?
- Medications (anticonvulsants, anti-spasticity drugs, botox injections, tricyclic antidepressants)
- Surgery (microvascular decompression, gamma knife, thermal lesioning)
74
What is the ultimate purpose of surgery for significant Trigeminal Neuralgia cases?
-Slicing the nerve so that there is no signaling being sent. Will lose function of CN5.
75
What is something that can be done with rehabilitative management of Trigeminal Neuralgia?
-TENs (evidence for pain management)
76
What is the prognosis of Trigeminal Neuralgia?
-Over time, attacks become more frequent, more easily triggered, and more disabling.
77
What CN does Bell's Palsy involve?
-CN7
78
- What is the motor function of CN7?
- What is the special sensory function of CN7?
- What is the parasympathetic function of CN7?
- 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
What is the etiology of Bell's Palsy?
-Acute inflammatory process of unknown etiology (immune or viral disease) resulting in compression of the nerve within the temporal bone.
80
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?
- 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
What do we see on examination of Bell's Palsy?
- 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
What are some medications for treatment of Bell's Palsy?
- Corticosteroids
| - Analgesics
83
How do we know that Bell's Palsy facial droop isn't the first sign of a stroke?
-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
What are some rehabilitative management strategies for Bell's Palsy? (6)
- 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
What is the prognosis for patients with Bell's Palsy?
- 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
- What is Bulbar Palsy?
| - What nerves does this include?
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
What is the etiology of Bulbar Palsy?
-Result of tumors, vascular or degenerative diseases of lower CN motor nuclei. (can be progressive)
88
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?
- 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
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 __________.
- Bilateral dysfunction
- UMN lesion
- Bulbar Palsy
90
Pseudobulbar Palsy vs Bulbar Palsy:
| -What are the MAJOR DIFFERENCES between psuedobulbar palsy and bulbar palsy? (5)
- 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
- What is Jaw Jerk Reflex?
| - What is Snout Reflex?
- Jaw Jerk = Tap on jaw: contraction of masseter and temporalis muscles
- Snout = Tap on lips produces pouting of lips
92
- _____ Palsy = UMN lesion
| - _____ Palsy = LMN lesion
- Pseudobulbar Palsy = UMN Lesion
| - Bulbar Palsy = LMN lesion
93
Is there a treatment for Bulbar Palsy?
-No
94
What does management of Bulbar Palsy include?
- 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)
