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
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
3
Q
What are some examples of motor dysfunction found in PNS syndromes?
A
- weakness/paresis of denervated muscle
- hyporeflexia and hypotonia
- atrophy
- fatigue
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
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
6
Q
What is sensory dysesthesias? Examples?
A
abnormal sensation
- hyperalgesia
- pins and needles
- numbness
- tingling
- burning
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
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
9
Q
What are common causes of mononeuropathy?
A
- entrapment
- trauma
- prolonged limb immobility (surgery)
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
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)
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
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
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
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
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
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
18
Q
What sensory symptoms are seen early in the disease progression with polyneuropathy?
A
- loss of temp
- pain (hypo or hyper)
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
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
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)
22
Q
Why does polyneuropathies occur with DM?
A
- blood vessel and nerve damage from high blood glucose and high triglyceride levels
23
Q
What are the risk factors associated with developing diabetic polyneuropathy?
A
- Obesity
- Sedentary lifestyle
- HTN
- Decreased glycemic control
- Alcoholism
- Smoker
24
Q
What is the prognosis for diabetic polyneuropathy?
A
- Slow progression over years that can be prevented with disease management and compliance
25
General treatment interventions for polyneuropathy?
- aerobic conditioning
- balance training
- resistance training
- patient education
26
amount of aerobic conditioning for polyneuropathy intervention
- 150 min/week
- 50-70% HRmax
mRPE 5-7 (RPE 14-16)
27
T/F: Balance training can improve sensory loss in polyneuropathy
false - balance training CANNOT improve sensory loss
- strengthen other balance systems to compensate
28
What are some patient education things for polyneuropathy?
- 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
What is Charcot Marie Tooth Disease? Who is more likely to be diagnosed and when?
- progressive muscle weakness that eventually effects motor and sensory nerves
- males > females
- diagnosed in adolescence but onset can occur at any age
30
What is the hallmark pathological sign of CMT?
- Hypertrophic onion bulb formation
o Schwann cells keep reproducing and creating more layers leading to decreased nerve function
31
How is CMT diagnosed?
- Clinical exam
- Electrodiagnostic testing
- Genetic testing
- Nerve biopsy – if diagnostic workup is negative
32
clinical signs of CMT
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
LE clinical signs of CMT
- DF and ankle evertor weakness most common
- inverted champagne bottle
- High arches (pes cavus), hammer toes, inverted heel, flat feet
34
UE clinical signs of CMT
- claw hands (wasting of dorsal and palmer interossei)
- atrophy of lumbricals/interossei
35
When does sensory impairment begin in CMT? What sensory tract is affected?
- seen later in the progression
- medial lemniscus affected - discriminative touch, vibratory and proprioceptive sensation
36
What sensory tract remains intact with CMT? What does that cause?
anterolateral remains intact
- neuropathic pain present, often severe
- pain due to postural changes, skeletal deformities, muscular fatigue and cramping is common
37
What are the major considerations for medical management of CMT?
- No cure
- Medications for symptoms
- Rehab and surgical interventions for significant impairments
38
What are some intervention strategies for CMT?
- strengthen and aerobic activity
- orthoses
- appropriate footwear
- podiatry consult
- ROM management
- balance training
39
At what intensity should strengthen and aerobic activity be done at? What type of therapy is better for achieving this?
- moderate intensity - muscles are quick to fatigue
- large muscle groups
- aquatic therapy > ground therapy
40
What are the 12 cranial nerves?
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
responsibility of trigeminal nerve (CN V). Which sections are sensory and which are motor?
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
What causes trigeminal neuralgia?
Caused by abnormal physical contact from nerve and other structure (like blood vessel)
- abrupt onset
43
What population does trigeminal neuralgia typically occur in?
- older population (mean age 50)
44
characteristics of trigeminal neuralgia
- brief neurogenic pain, reoccurring frequently along mandibular and maxillary divisions
- unilateral
- has triggers like stress and cold
- relieved by relaxation
45
How long do trigeminal neuralgia attacks last? What follows the attack?
- several seconds to minutes that is usually followed by a few minutes to hours of dull, achy pain
46
What is a hallmark sign of trigeminal neuralgia?
really bad neuropathic pain
- pain has triggers
47
What should the major focuses of the exam be for trigeminal neuralgia?
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
How is trigeminal neuralgia managed? What is prognosis?
- medications
- surgery
- rehab
over time, attacks become more frequent, more easily triggered, and more disabling
49
medications used for trigeminal neuralgia
- anticonvulsants
- Anti-spasticity drugs
- BOTOX injections
- tricyclic antidepressants
50
What are the 3 surgery techniques discussed for trigeminal neuralgia?
- 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
What is the focus of rehab for trigeminal neuralgia?
TENS for pain reduction
52
What are the primary functions of the facial nerve (CN VII)?
- motor - facial expressions
- sensory - hearing
- special sensory - taste
- parasympathetic - saliva and tear production
53
etiology of Bell's palsy
Acute inflammatory process of unknown etiology (immune or viral disease) resulting in compression of the facial nerve within the temporal bone
54
What age range is Bell's palsy most seen in?
20s-40s
55
risk factors for Bell's palsy
o Pregnancy
o Preeclampsia - high blood pressure disorder that can occur during pregnancy
o Obesity
o HTN
o DM
o Respiratory illness
56
What are the major characteristics of Bell’s Palsy?
- 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
What will be seen in a Bell's palsy exam?
- 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
What are the medicinal options for Bell’s Palsy?
- Corticosteroids
- Analgesics
59
How do we know the facial droop isn’t the first sign of a stroke?
- 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
What does rehabilitative management of Bell’s Palsy involve?
- 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
How is the prognosis for Bell’s Palsy?
- Very good
- Show improvements within 2 weeks w/ or w/o treatment
- w/ proper management – most recover all facial function within 6 months
62
What is the involved anatomy behind Bulbar Palsy?
- Muscles innervated by glossopharyngeal (CN IX), vagus (CN X), and hypoglossal nerve (CN XII)
o Muscles of face, tongue, larynx, and pharynx
63
etiology of Bulbar palsy
- 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
What are the major characteristics of Bulbar Palsy?
- 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
How can Bulbar Palsy be differentiated from Pseudobulbar Palsy?
- 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
How is Bulbar Palsy managed?
- 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
