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Neuro 2 > Peripheral Nerve Disorders > Flashcards

Peripheral Nerve Disorders Flashcards

1
Q

List clinical signs of PNS syndromes

A
  1. Motor Dysfunction
  2. Sensory Dysfunction
  3. ANS Dysfunction
  4. Neuropathic pain and/or muscle pain (myalgia) common
  5. Hyper-excitability of remaining nerve fibers
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2
Q

PNS symptom: Motor Dysfunction

A
  1. Weakness/paresis of denervated muscle
  2. hyporeflexia
  3. hypotonia
  4. atrophy
  5. fatigue
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3
Q

PNS symptoms: Sensory Dysfunction

A
  1. Paresthesias
  2. Proprioception losses may yield sensory ataxia
  3. insensitivity may yield limb trauma
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4
Q

PNS symptoms: ANS dysfunction

A
  1. Vasodilation and loss of vasomotor tone
    • dryness
    • warm skin
    • edema
    • OH
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5
Q

what does hyper-excitability of remaining nerve fibers look like in PNS syndromes?

A
  1. Sensory dysesthesia → hyperalgesia, pins and needles, numbness, tingling, burning
  2. Motor → fasciculations
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6
Q

Describe tropic changes due to denervaion in PNS syndromes

A
  1. muscle atrophy
  2. skin becomes shiny
  3. nails become brittle
  4. subcutaneous tissues thicken
  5. ulceration of cutaneous and subcutaneous tissues
  6. poor wound healing
  7. infections
  8. neurogenic joint damage
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7
Q

what is a mononeuropathy

A
  1. weakness, numbness, pain, paresthesias, confined to the distribution of the involved nerve
  2. most common causes:
    • entrapment
    • trauma
    • prolonged limb immobility (e.g. surgery)
  3. Example → carpal tunnel syndrome
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8
Q

Classification of nerve damage in mononeuropathy

A
  1. Neuropraxia
    • local myelin damage, axon remains intact
  2. Axontmesis
    • continuity of axon is lost
    • may or may not include damage to epinerium, perineurium, and/or endoneurium
    • loss of continuity leads to Wallerian degeneration
  3. Neurotmesis
    • complete transection of nerve
    • surgery necessary
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9
Q

how are PNS injuries different from CNS injuries?

A
  1. PNS can regenerate under certain circumstances
    • Axonal sprouting
      • regenerative
      • collateral
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10
Q

what is a multiple mononeuropathy?

A
  1. involves two or more nerves in different parts of the body
  2. Vasculitis = dangerous cause of multiple mononeuropathy
    • if suspected, an urgent referral should be made for an electrodiagnostic eval
  3. Individual nerves are affected, producing a random, asymmetrical presentation of signs
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11
Q

what is a polyneuropathy?

A
  1. symmetrical involvement: sensory, motor, autonomic
    • Sensory → Motor → Autonomic
    • Distal → Proximal
    • Feet → legs → fingertips → hands
    • Affects longest peripheral nerves in extremeties
      • small nerve fibers → large nerve fibers
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12
Q

Motor symptoms for Polyneuropathies

A
  1. Weakness
  2. Cramping
  3. Fasciculations
  4. Muscle Loss
  5. Bone degeneration
  6. Loss of ankle reflexes
  7. trophic changes
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13
Q

Sensory Symptoms for Polyneuropathies

A
  1. Earlier in disease
    • loss of temp
    • pain (hypo or hyper)
  2. As disease progresses
    • loss of vibration
    • loss of light touch discrimination
    • loss of proprioception/kinesthesia
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14
Q

Autonomic Symptoms for Polyneuropathies

A

Diverse manifestations

  1. impaired breathing
  2. dysarthria
  3. temp dysregulation
    • in particular - decrease sweating
  4. GI dysfunction
  5. Loss of bowel/bladder control
  6. Erectile dysfunction
  7. Loss of BP control
    • orthostasis very common
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15
Q

common causes of polyneuropathies

A
  1. Diabetes Mellitus
    • 60-70% of pts with DM have mild-severe forms of PN
  2. Other
    • 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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16
Q

Risk factors for diabetic polyneuropathy

A
  1. Obesity
  2. Sedentary lifestyle
  3. HTN
  4. Decreased glycemic control
  5. Alcoholism
  6. Smoker
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17
Q

Diabetic Polyneuropathy prognosis

A
  1. CAN BE PREVENTED with appropriate disease management and compliance
  2. Progression of symptoms progresses slowly over years
    • depends largely on how well the pt’s DM is managed
  3. Treating DM may halt progression and improve symptoms of the neuropathy, but recovery is exceptionally slow
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18
Q

Interventions for Diabetic Polyneuropathy

A
  1. Aerobic Conditioning
  2. Balance training
  3. Resistance training
  4. Patient education
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19
Q

parameters for aerobic conditioning in Diabetic Polyneuropathy

A
  • 150 min/week
  • 50-70% HRmax
    • mRPE 5-7(RPE 14-16)
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20
Q

Balance training in Diabetic Polyneuropathy

A
  1. Cannot improve sensory loss
  2. strengthen other balance systems to compensate
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21
Q

Aspects of pt education for diabetic polyneuropathy

A
  1. skin care and inspection
  2. shoe consideration
  3. nutritional consult
  4. fall risk management
  5. importance of aerobic exercise
  6. strategies to reduce sedentary lifestyle
  7. compliance to program
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22
Q

what is CMT?

A

Charcot Marie Tooth Disease

  1. most common inhereted neuro disorder
    • affecting 1 in every 2,500
    • Males > Females
  2. progressive muscle weakness
    • typically becomes noticeable in adolescence or early adulthood, but the onset of disease can occur at any age
  3. eventually effects both motor and sensory nerves
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23
Q

describe the pathology of CMT

A
  1. caused by a mutation in genes that produce proteins involved in the structure, maintenace, and formation or primarily the myelin sheath
    • >50 genes causing CMT ID
    • will see secondary degeneration of axons as disease progresses as well as axon-dominant CMT subtypes (though less common)
  2. Hallmark Pathologic sign
    • hypertrophic onion bulb formation
24
Q

what causes hypertrophic onion bulb formation in CMT?

A

repetitive segmental demyelination and regeneration of myelin that causes gross thickening of peripheral nerves

creates palpable, enlarged peripheral nerves

25
Q

how is CMT diagnosed?

A
  1. clinical exam
  2. electrodiagnostic testing
  3. genetic testing
    • only if no family history present
  4. nerve biopsy
26
Q

Clinical manifestation of CMT (motor signs)

A
  1. clincal signs of distally symmetric muscle weakness, atrophy, and diminished DTRs
    • Motor loss first → sensory loss
    • LE first → UE as disease progresses
    • mild scoliosis, hip dysplasia
27
Q

describe UE and LE motor signs in CMT

A
  1. LE
    • DF and ankle evertor weakness most common
    • loss of muscle bulk in distal LE + hypertrophy proximal LE → “inverted champagne bottle”
  2. UE
    • claw hands
    • atrophy of lumbricals/interossei
28
Q

Clinical manifestations of CMT (sensory)

A
  1. usually, no sensory symptoms initially
  2. discriminative touch, vibratory and proprioceptive often damaged
  3. Pain remains intact
    • Neuropathic pain may be present, and if so severe
    • pain due to postural changes, skeletal deformities, muscular fatigue and cramping is common
29
Q

Medical management of CMT

A
  1. No cure for CMT
  2. No disease-modifying therapy available
  3. Meds are solely symptom-management
  4. Overall management = REHAB
    • may require surgical interventions for more sig impairment → tendon release, etc.
30
Q

Prognosis for CMT

A
  1. slowly progressive disorder
    • but not fatal
    • normal life expectancy
    • eventual disability is likely secondary to distal muscle weakness and deformities
31
Q

CMT Intervention strategies

A
  1. Strengthening and aerobic activity
  2. Orthoses (AFO)
  3. Appropriate footwear
  4. Podiatry consult
  5. ROM Management
  6. Balance training
32
Q

describe ROM management for CMT

A
  1. HEP for stretching
  2. serial casting and night splinting may be used as contractures can be common in this population
33
Q

describe strengthening and aerobic training parameters for CMT

A
  1. moderate intensity (60-80% 1 RM)
  2. large muscle groups
  3. aquatic therapy fantastic adjunct to over ground therapy!
  4. be wary of fatigue
34
Q

describe balance training for CMT

A
  1. combo of functional balance tasks and fall reduction strategies
  2. introduce an AD/have conversation early to prepare the pt
35
Q

List some possible cranial nerve disorders

A
  1. trigeminal neuralgia (tic douloreux)
  2. bell’s palsy (facial paralysis)
  3. bulbar palsy (bulbar paralysis)
36
Q

describe the etiology of Trigeminal Neuralgia

A
  1. results from degeneration (etiology unknown) or compression (tortuous basilar artery or cerebellopontine tumor)
  2. occurs in older population (mean age 50)
  3. abrupt onset
37
Q

describe the characteristics of trigeminal neuralgia

A
  1. brief paroxysms of severe neurogenic pain (stabbing/shooting), reoccuring frequently
    • occurs along the distribution of the trigeminal nerve’s mandibular and maxillary divisions (involvement of opthalmic division in rare)
    • unilateral
    • autonomic instability → exacerbated by stress, cold; relieved by relaxation
38
Q

describe the clinical presentation of Trigeminal Neuralgia

A
  1. brief, severe attacks on neuropathic often described as unbearable
    • attacks can last from several secs to several min
    • episodes of several attacks lasting days, weeks, months or longer
    • can see remissions between attacks of weeks to months
  2. Allodynia → often has triggers, but can be spontaneous
  3. sometimes relieved by rest, some meds
  4. also → cluster HA, depression
39
Q

major focuses of exam for trigeminal neuralgia

A
  1. Pain → location, intensity
  2. Trigger points → light touch to face, lips, or gums will cause pain
  3. Triggering stimuli → extremes of heat or cold, chewing, talking, brushing teeth, movement of air across face
  4. Motor function → control is normal
40
Q

Trigeminal Neuralgia management

A
  1. Medical
    • meds
      • anticonvulsants
      • anti-spasticity drugs
      • botox injections
      • tricyclic antidepressants
    • surgery
      • microvascular decompression
      • gamma knife
      • thermal lesioning
  2. Rehab management
    • transcutaneous electrical nerve stimulation (TENs)
41
Q

prognosis of trigeminal neuralgia

A
  1. over time, attacks become more frequent, more easily triggered, and more disabling
42
Q

what is Bell’s Palsy?

A

Idiopathic Facial Paralysis

  1. Motor → facial expression muscles, posterior belly of digastric muscles, stylohyoid muscles, stapedius muscle
  2. Special sensory → taste from anterior two-thirds of the tongue
  3. Parasympathetic → submandibular gland, sublingual gland, lacrimal glands
43
Q

describe the etiology of Bell’s Palsy

A

acute inflammation process of unknown etiology (immune or viral disease) resulting in compression of the nerve within the temporal bone

44
Q

describe characteristics of Bell’s Palsy

A
  1. muscles of facial expression on one side are weakened/paralyzed
  2. Loss of control of salivation or lacrimation
  3. Onset is acute, with max severity in a few hours or days
  4. Commonly preceded by a day or 2 of pain behind the ear
  5. Most fully recover in several weeks/months
45
Q

Belly’s Palsy exam findings

A
  1. Drooping of corner of mouth, eyelids that don’t close
  2. Function of muscles of facial expression (test CN VII)
  3. Taste of anterior 2/3 of tongue
46
Q

Bell’s Palsy meds

A
  1. Corticosteroids (prednisone)
  2. Analgesics
47
Q

key differential diagnosis between Bells Palsy and a Stroke

A
  1. Look at the forehead
    • should still have the ability to raise eyebrows if its a stroke
    • if its a LMN disorder like Bells Palsy they won’t be able to raise either eyebrow
48
Q

rehab management for Bells Palsy

A
  1. protect cornea (artifical tears or patching) until recovery allows for eyelid closure
  2. E-stim to maintain tone, support of function of facial mm
  3. Provide active facial muscles exercises
  4. May require face sling to prevent overstretching of facial mm
  5. Provide functional retraining → foods that can be easily eaten, chewing with opposite side
  6. provide emotional support and reassurance
49
Q

Prognosis for Bells Palsy

A
  1. generally, very good
  2. with or without treatment, most begin to show improvements within 2 weeks after onset
  3. with proper management, most recover some or all facial function within 6 months
50
Q

what is bulbar palsy

A
  1. 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 9, 10 and 12
51
Q

what is the etiology of Bulbar Palsy?

A
  1. result of tumor, vascular or degenerative diseases of lower cranial nerve motor nuclei (ALS, MG, GBS)
    • can be progressive
52
Q

describe the characteristics of bulbar palsy

A
  1. Glossopharyngeal and Vagal Paralysis
    • phonation
    • articulation
    • palatal action
    • gag reflex
    • swallowing
  2. Changes in voice quality
    • dysphonia (hoarseness or nasal quality)
  3. Tongue atrophy, fasciculations
  4. With bilateral involvement → severe airway restriction with dyspnea, difficulty coughing
  5. possible complication = aspiration pneumonia
53
Q

compare bulbar to pseudobulbar palsy

A
  1. Bilateral dysfunction of corticobulbar innervation of brainstem nuclei
  2. Pseudobulbar palsy
    • a central UMN lesion analogous to corticospinal lesions disrupting function of anterior horn cells
    • produces similar symptoms of bulbar palsy
54
Q

major differences between pseudobulbar and bulbar palsy

A
  1. Pseudobulbar
    • +CN 5 and 7 involvement
    • emotional incontinence (pseudobulbar affect
    • tongue spasticity
    • spastic dysarthria (donald duck speech)
    • hyperactive reflexes
      • jaw jerk reflex
      • snout reflex
55
Q

Management of Bulbar Palsy

A
  1. No known treatment
  2. Supportive therapy
    • anticholinergics to control drooling
    • percutaneous endoscopic gastrostomy tube (PEG tube) for severe dysphasia or recurrent aspiration PNA
  3. Speech and Language Pathology
  4. PT
    • inconclusive evidence on the role of exercise in the management of bulbar dysfunction in pts with ALS
    • pts with progressive bulbar palsy may maintain mobility but present with severe respiratory compromise and should be managed accordingly

Neuro 2 (29 decks)

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