Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro 2 > Peripheral Nerve Disorders > Flashcards

Peripheral Nerve Disorders Flashcards

1
Q

neuropathy vs radiculopathy

A
  • Neuropathy – happens w/ rest of peripheral nerve (not nerve root)
  • Radiculopathy – happens at nerve root
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some of the typical signs and symptoms associated with PNS syndromes?

A
  • motor dysfunction
  • sensory dysfunction
  • ANS dysfunction
  • neuropathic pain and/or myalgia
  • hyper-excitability of remaining nerve fibers (sensory dysesthesias and motor fasciculations)
  • trophic changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some examples of motor dysfunction found in PNS syndromes?

A
  • weakness/paresis of denervated muscle
  • hyporeflexia and hypotonia
  • atrophy
  • fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some examples of sensory dysfunction found in PNS syndromes?

A
  • Paresthesias
  • proprioceptive losses may yield sensory ataxia
  • insensitivity may yield limb trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some examples of ANS dysfunction found in PNS syndromes?

A

vasodilation and loss of vasomotor tone
- dryness
- warm skin
- edema
- OH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is sensory dysesthesias? Examples?

A

abnormal sensation
- hyperalgesia
- pins and needles
- numbness
- tingling
- burning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some examples of trophic changes?

A
  • muscles atrophy
  • skin becomes shiny
  • brittle nails
  • subcutaneous tissues thicken
  • Ulceration of cutaneous and subcutaneous tissues
  • poor wound healing/infections
  • neurogenic joint damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a mononeuropathy and what are its characteristics? Example?

A
  • Weakness, numbness, pain, paresthesias confined to the distribution of the involved nerve
  • 1 nerve impacted
  • focal and specific to the nerve

ex: carpal tunnel syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are common causes of mononeuropathy?

A
  • entrapment
  • trauma
  • prolonged limb immobility (surgery)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do we classify mononeuropathies?

A
  • Neuropraxia (lease severe) – local myelin damage, axon intact
  • Axonotmesis – continuity of axon is lost which leads to Wallerian degeneration
  • Neurotmesis (most severe) – transection of nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Wallerian degeneration? Which classification do we see this with?

A
  • axon distal to the injury starts to weather away as a result of nerve lesion

seen with axonotmesis (continuity of axon is lost)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the two major ways that axons demonstrate regeneration in the PNS?

A
  • Regenerative – proximal nerve sprouts to another intact distal nerve
  • Collateral – proximal nerve sprouts to multiple distal nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is multiple mononeuropathy and what are its characteristics? What is a common cause?

A
  • several focal points (2 or more nerves) in different parts of the body
  • produces a random, asymmetrical presentation of signs

common cause is vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is vasculitis? Signs and symptoms?

A
  • dangerous cause of multiple mononeuropathy
    S&S
  • fever
  • fatigue
  • weight loss
  • muscle and joint pain alongside focal loses

THIS IS A MEDICAL EMERGENCY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a polyneuropathy and what are its characteristics?

A

symmetrical involvement of multiple nerves
- Typically starts with sensory nerve, then motor, then autonomics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some of its most common causes?

A

o DM
o Autoimmune
o Chronic kidney disease
o HIV and liver infections
o Low level of vitamin B12
o Poor circulation in Les
o Underactive thyroid gland
o Trauma
o Tumor
o alcoholism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the typical progression of polyneuropathy?

A
  • sensory to motor to autonomic loss
  • distal to proximal
  • affects longest peripheral nerves in extremities
    small nerve fibers to larger nerve fibers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What sensory symptoms are seen early in the disease progression with polyneuropathy?

A
  • loss of temp
  • pain (hypo or hyper)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What sensory symptoms are seen later in the disease progression with polyneuropathy?

A
  • loss of vibration
  • loss of light touch discrimination
  • loss of proprioception/kinesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What motor symptoms are seen in the disease progression with polyneuropathy?

A
  • weakness
  • cramping
  • fasciculations
  • muscle loss
  • bone degeneration
  • loss of ankle reflexes
  • trophic changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What autonomic symptoms are seen in the disease progression with polyneuropathy?

A

Diverse-Manifestations
- impaired breathing
- GI dysfunction
- dysarthria
- temperature dysregulation (decrease sweating in particular)
- loss of bowel/bladder control, erectile dysfunction
- Loss of BP control (orthostasis is very common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why does polyneuropathies occur with DM?

A
  • blood vessel and nerve damage from high blood glucose and high triglyceride levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the risk factors associated with developing diabetic polyneuropathy?

A
  • Obesity
  • Sedentary lifestyle
  • HTN
  • Decreased glycemic control
  • Alcoholism
  • Smoker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the prognosis for diabetic polyneuropathy?

A
  • Slow progression over years that can be prevented with disease management and compliance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

General treatment interventions for polyneuropathy?

A
  • aerobic conditioning
  • balance training
  • resistance training
  • patient education
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

amount of aerobic conditioning for polyneuropathy intervention

A
  • 150 min/week
  • 50-70% HRmax
    mRPE 5-7 (RPE 14-16)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

T/F: Balance training can improve sensory loss in polyneuropathy

A

false - balance training CANNOT improve sensory loss
- strengthen other balance systems to compensate

28
Q

What are some patient education things for polyneuropathy?

A
  • skin care and skin inspection
  • shoe considerations
  • nutritional consult
  • fall risk management
  • importance of aerobic exercise
  • strategies to reduce sedentary lifestyle
  • compliance to program
29
Q

What is Charcot Marie Tooth Disease? Who is more likely to be diagnosed and when?

A
  • progressive muscle weakness that eventually effects motor and sensory nerves
  • males > females
  • diagnosed in adolescence but onset can occur at any age
30
Q

What is the hallmark pathological sign of CMT?

A
  • Hypertrophic onion bulb formation
    o Schwann cells keep reproducing and creating more layers leading to decreased nerve function
31
Q

How is CMT diagnosed?

A
  • Clinical exam
  • Electrodiagnostic testing
  • Genetic testing
  • Nerve biopsy – if diagnostic workup is negative
32
Q

clinical signs of CMT

A

clinical signs of distally symmetric muscle weakness, atrophy, and diminished DTRs
- motor loss first then sensory loss
- LE first then UE loss as disease progresses

33
Q

LE clinical signs of CMT

A
  • DF and ankle evertor weakness most common
  • inverted champagne bottle
  • High arches (pes cavus), hammer toes, inverted heel, flat feet
34
Q

UE clinical signs of CMT

A
  • claw hands (wasting of dorsal and palmer interossei)
  • atrophy of lumbricals/interossei
35
Q

When does sensory impairment begin in CMT? What sensory tract is affected?

A
  • seen later in the progression
  • medial lemniscus affected - discriminative touch, vibratory and proprioceptive sensation
36
Q

What sensory tract remains intact with CMT? What does that cause?

A

anterolateral remains intact
- neuropathic pain present, often severe
- pain due to postural changes, skeletal deformities, muscular fatigue and cramping is common

37
Q

What are the major considerations for medical management of CMT?

A
  • No cure
  • Medications for symptoms
  • Rehab and surgical interventions for significant impairments
38
Q

What are some intervention strategies for CMT?

A
  • strengthen and aerobic activity
  • orthoses
  • appropriate footwear
  • podiatry consult
  • ROM management
  • balance training
39
Q

At what intensity should strengthen and aerobic activity be done at? What type of therapy is better for achieving this?

A
  • moderate intensity - muscles are quick to fatigue
  • large muscle groups
  • aquatic therapy > ground therapy
40
Q

What are the 12 cranial nerves?

A

I - olfactory
II - optic
III - oculomotor
IV - trochlear
V - trigeminal
VI - abducens
VII - facial
VIII - vestibulocochlear
IX - glossopharyngeal
X - vagus
XI - accessory
XII - hypoglossal

41
Q

responsibility of trigeminal nerve (CN V). Which sections are sensory and which are motor?

A

sensation in the face and control of motor functions like biting and chewing
- Ophthalmic nerve (V1) - sensory
- Maxillary nerve (V2) - sensory
- Mandibular nerve (V3) - sensory and motor

42
Q

What causes trigeminal neuralgia?

A

Caused by abnormal physical contact from nerve and other structure (like blood vessel)
- abrupt onset

43
Q

What population does trigeminal neuralgia typically occur in?

A
  • older population (mean age 50)
44
Q

characteristics of trigeminal neuralgia

A
  • brief neurogenic pain, reoccurring frequently along mandibular and maxillary divisions
  • unilateral
  • has triggers like stress and cold
  • relieved by relaxation
45
Q

How long do trigeminal neuralgia attacks last? What follows the attack?

A
  • several seconds to minutes that is usually followed by a few minutes to hours of dull, achy pain
46
Q

What is a hallmark sign of trigeminal neuralgia?

A

really bad neuropathic pain
- pain has triggers

47
Q

What should the major focuses of the exam be for trigeminal neuralgia?

A

o Pain – location and intensity
o Trigger points – light touch to face, lips, or gums will cause pain
o Triggering stimuli – extreme heat or cold, chewing, talking, brushing teeth, movement of air across face
o Motor function – control is normal

48
Q

How is trigeminal neuralgia managed? What is prognosis?

A
  • medications
  • surgery
  • rehab

over time, attacks become more frequent, more easily triggered, and more disabling

49
Q

medications used for trigeminal neuralgia

A
  • anticonvulsants
  • Anti-spasticity drugs
  • BOTOX injections
  • tricyclic antidepressants
50
Q

What are the 3 surgery techniques discussed for trigeminal neuralgia?

A
  • Microvascular decompression - small craniotomy behind the ear and remove what is causing the problems
  • Gamma Knife - radiation surgery locally
  • Thermal Lesioning - ablates nerve with heat
51
Q

What is the focus of rehab for trigeminal neuralgia?

A

TENS for pain reduction

52
Q

What are the primary functions of the facial nerve (CN VII)?

A
  • motor - facial expressions
  • sensory - hearing
  • special sensory - taste
  • parasympathetic - saliva and tear production
53
Q

etiology of Bell’s palsy

A

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

54
Q

What age range is Bell’s palsy most seen in?

A

20s-40s

55
Q

risk factors for Bell’s palsy

A

o Pregnancy
o Preeclampsia - high blood pressure disorder that can occur during pregnancy
o Obesity
o HTN
o DM
o Respiratory illness

56
Q

What are the major characteristics of Bell’s Palsy?

A
  • Muscles of face on 1 side are weakened/paralyzed (unilateral)
  • Loss of control of salivation or lacrimation
  • Onset is acute, with maximum severity in a few hours or days
  • Commonly preceded by pain behind the ear
  • Most fully recover in a few weeks/months
57
Q

What will be seen in a Bell’s palsy exam?

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
58
Q

What are the medicinal options for Bell’s Palsy?

A
  • Corticosteroids
  • Analgesics
59
Q

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

A
  • forehead has bilateral innervation
  • will see full unilateral facial paralysis with Bell’s palsy
  • If forehead moves on both sides = CVA
  • If no forehead movement on 1 side = Bell’s palsy
60
Q

What does rehabilitative management of Bell’s Palsy involve?

A
  • Protect cornea (patching, lubricating eye drops) until recovery allows for eyelid closure
  • E-stem to maintain muscle tone, support of function of facial muscles
  • Provide active facial muscle exercises
  • Face sling to prevent overstretching of facials muscles
  • Functional retraining – foods that are easy to eat, chewing on opposite side
  • Emotional support and reassurance
61
Q

How is the prognosis for Bell’s Palsy?

A
  • Very good
  • Show improvements within 2 weeks w/ or w/o treatment
  • w/ proper management – most recover all facial function within 6 months
62
Q

What is the involved anatomy behind Bulbar Palsy?

A
  • Muscles innervated by glossopharyngeal (CN IX), vagus (CN X), and hypoglossal nerve (CN XII)
    o Muscles of face, tongue, larynx, and pharynx
63
Q

etiology of Bulbar palsy

A
  • Results of tumors, vascular or degenerative diseases, malignancy, inflammation, genetic disorders impacting lower cranial nerve motor nuclei
    o Can be progressive but not always
    o Commonly seen alongside ALS
64
Q

What are the major characteristics of Bulbar Palsy?

A
  • Glossopharyngeal and vagal paralysis
    o Phonation, articulation, palatal action, gag reflex, swallowing
  • Changes in voice quality
    o Dysphonia – hoarseness or nasal quality
  • Tongue atrophy, fasciculations
  • Airway restriction with bilateral involvement
    o Dyspnea
    o Difficulty with coughing
65
Q

How can Bulbar Palsy be differentiated from Pseudobulbar Palsy?

A
  • Pseudobulbar Palsy – UMN lesion
    o + CN 5 and 7 involvement
    o Emotional incontinence – extreme swings between emotions
    o Tongue spasticity
    o Donald duck speech – spastic dysarthria
    o Hyperactive reflexes
     Jaw Jerk reflex – tap on jaw that causes contraction of masseter and temporalis muscles
     Snout reflex – tap on lips that produces pouting of lips
66
Q

How is Bulbar Palsy managed?

A
  • No known treatment
  • Supportive therapy
    o Anticholinergics to control drooling
    o PEG tube for severe dysphasia or recurrent aspiration pneumonia
  • Speech and language pathology
  • PT – inconclusive evidence on role of exercise in management of bulbar dysfunction in ALS

Neuro 2 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions