Peripheral Neuropathies Flashcards
(41 cards)
1
Q
3 types of Peripheral Neuropathies discussed
A
- Complex Regional Pain Syndrome
- Bell’s Palsy
- DM Peripheral Neuropathy
2
Q
types of Complex Regional Pain Syndrome (CRPS)
A
o CRPS I: initiating “noxious” event (crush/soft tissue injury) or immobilization (tight cast, frozen shoulder)
o CRPS II: defined nerve injury
3
Q
CRPS definition
A
- Types:
CRPS I: initiating “noxious” event (crush/soft tissue injury) or immobilization (tight cast, frozen shoulder)
CRPS II: defined nerve injury - History of edema, skin blood flow abnormality or abnormal sweating in the region of the pain since the inciting event
- No other conditions can account for the degree of pain and dysfunction
4
Q
IASP proposed diagnostic criteria for CRPS
A
At least 1 sign during presentation in at least 2 of the following categories:
- Sensory: evidence of hyperalgesia (to pinprick), allodynia
- Vasomotor: temperature asymmetry (>1C), skin colour changes /asymmetry,
- Sudomotor/edema: edema, sweating changes/asymmetry
- Motor/Trophic: decreased ROM, weakness, tremor, dystonia (muscle contractions result in twisting and repetitive movements or abnormal fixed postures) or trophic changes
No other diagnosis that better explains signs & symptoms
5
Q
Pathophysiology of CRPS
A
- Persistent noxious stimuli from injured body region whereby primary afferent nociceptive mechanisms demonstrate abnormally heightened sensation
- Extend out beyond originally injured area (hence ‘regional’)
- Impairment of CNS processing leads to motor aberrancies as well
6
Q
Temperature Pathophysiology- WARMTH
A
Early inhibition of central cutaneous vasoconstrictor activity → vasodilation →warmth
7
Q
Temperature Pathophysiology- COOL
A
Late increased sensitivity to circulating catecholamines due to upregulation of cutaneous adrenoreceptors → vasoconstriction and coolness
8
Q
Protective Disuse
Decreased use of an injured body part is a normal post injury reaction to promote healing.
HOWEVER, Excessive protection and guarding can result in what?
A
dependent edema, coolness from decreased blood flow, and trophic changes from decreased blood flow
9
Q
epidemiology-
what is % of CRPS that is work related?
A
50% work related
10
Q
epidemiology-
is It more common in males or females?
A
FEMALES
F:M from 2-4:1
11
Q
epidemiology- what is peak age of CRPS?
A
Peak age 37-50
12
Q
Symptoms of CRPS is considered chronic after how long?
A
- Acute <2 months
- Chronic > 2months
13
Q
CRPS symptoms
A
- Immediate to weeks after injury, usually only one limb but in a few cases bilateral, even rarer can extend to 3-4 extremities
- Other locations: external genitalia, nose, ulnar styloid, malleolus
- Most often burning but can be aching, throbbing, tingling. Pain aggravated by movement or use of extremity
- Neglect–> refers to when pt is ignoring that limb and have to force themselves to look at it and appreciate it in order to move it. so if they aren’t paying attention to it they can’t move it.
- Altered temperature sensation
- Rapid fatigability in later stages
14
Q
CRPS Prognosis
A
- Duration: up to 80% (CRPS I) resolved within 18 months from onset with or without treatment. If longer →worse prognosis, worse sensory symptoms
- Despite treatment, many will be left with varying degrees of chronic pain and disability (usually from pain)
15
Q
Signs of CRPS
A
- Paresis, pseudo-paralysis or clumsiness
- Limited ROM
- Tremor
- Dystonia
- Muscle spasms
- Hypoesthesia
- Anesthesia dolorosa
- Allodynia
- Hyperpathia
- Hyperhidrosis
- Edema (2/2 to autonomic dysfxn)
- Skin colour changes due to vasomotor changes
- Atrophy
16
Q
Imaging for CRPS
A
- Plain x-ray: In chronic CRPS- bone resorption, and/or osteoporosis, bony demineralization
- Bone scintigraphy: higher sensitivity than plain film in early post fx CRPS
- MRI: very sensitive to joint changes (effusion) and soft tissue changes but not specific
17
Q
Treatment for CRPS
A
- Corticosteroids: pulsed dose 60-80mg/d for 14days
- Calcium regulating drugs: Calcitonin intranasally TID can significantly reduce pain, clodronate IV, alendronate (IV or PO) improve pain, swelling, ROM
- Opioids
- NSAIDs
- Lidocaine IV pain
- Baclofen (GABA Agonist) for dystonia
- Clonidine patch for local allodynia
- Gabapentin analgesia
18
Q
name diagnosis: facial muscle weakness with no other neurologic deficits, no apparent cause
A
Bell’s Palsy
19
Q
> 60% of Bell’s palsy occurs on what side of the face?
A
> 60% occur on right
20
Q
what 2 other conditions is Bell’s Palsy more commonly associated with.
A
More common in pregnancy, DM Persons
21
Q
if forehead is not involved with Bell’s palsy what do you need to be worried about?
A
stroke
22
Q
% of recurrence of Bell’s palsy
A
Recurs in 4-14% of patients
23
Q
~80-90% recovery if Bell’s palsy without disfigurement within what time frame?
A
6 weeks to 3 months
24
Q
what is Bell Phenomenon?
A
On attempted eye closure, the eye rolls upward and outward on the affected side
(can see because of Ptosis)
25
what reflex is absent in many cases of Bell palsy?
tear reflex
26
Bell’s Palsy Presentation
- Muscle weakness peaks before 21d
- Acute onset of unilateral upper and lower facial paralysis (over a 48-h period)
- Posterior auricular pain, otalgia sometimes precedes palsy
- Decreased tearing
- Hyperacusis
- Taste disturbances
- Forehead involvement
27
Bell’s Palsy Work Up
- Clinical Diagnosis
- HgA1c--> DM get this more than general population so need to check this.
- Lyme Titres
- Imaging
- Nerve conduction tests
28
Bell’s Palsy Diagnosis
- Diagnosis: clinical
- Nerve/EMG testing if atypical or prolonged symptoms
- If need be: r/o CVA, Lyme, AIDS
- Imaging
29
Bell’s Palsy Treatment
- Gradual resolution over time in 80-90%
- Supportive care: lacrilube for eyes
- Course of prednisone started as soon as possible increases chance of complete recovery
- Anti-virals? Acyclovir, Valacyclovir
- Surgical options
Facial nerve decompression
Subocularis oculi fat (SOOF) lift
Implantable devices (eg, gold weights) placed into the eyelid
Tarsorrhaphy
Transposition of the temporalis muscle
30
Bell’s Palsy Prognosis
- Some restoration of function noted within 3 weeks → recovery most likely to be complete
- Recovery beginning between 3 weeks - 2 months → ultimate outcome usually satisfactory
- Recovery not beginning until 2-4 months from onset → likelihood of permanent sequelae, including residual paresis and synkinesis, is higher
- If no recovery occurs by 4 months, then the patient is more likely to have sequelae from the disease, which include synkinesis, crocodile tears, and (rarely) hemifacial spasm
31
what is the MC type of neuropathy in western hemisphere
Diabetic peripheral neuropathy
32
Diabetic peripheral neuropathy can present as a Mixed neuropathy (motor, sensory, autonomic) in what percent of patients?
70%
33
what percent of DM Pts have some peripheral neuropathy
47%
34
Diabetic neuropathy can occur at any age but is more common with what?
increasing age and severity and duration of diabetes
35
DM Peripheral Neuropathy Presentation
- Lower extremities (A fibres)
- Numbness, paresthesias, pain, dysthesias (burning)
- Impaired vibration sense or impaired DTRs
- Autonomic: postural hypotension, cardiac arrhythmias, impaired sweating. Disturbances of bowel movements, bladder, gastric or sexual functions
- Sensory – Negative or positive, diffuse or focal; usually insidious in onset and showing a stocking-and-glove distribution in the distal extremities
- Motor – Distal, proximal, or more focal weakness, sometimes occurring along with sensory neuropathy (sensorimotor neuropathy)
- Autonomic – Neuropathy that may involve the cardiovascular, gastrointestinal, and genitourinary systems and the sweat glands
36
DM Peripheral Neuropathy Physical Exam
- Peripheral neuropathy testing
- Gross light touch
- Pinprick sensation
- Vibratory sense
- Deep tendon reflexes
- Strength testing and
- Muscle atrophy
- Dorsal pedal and posterior tibial pulses
- Skin assessment
- Tinel testing
- Cranial nerve testing
37
DM Peripheral Neuropathy Diagnosis
- Serial nerve conduction studies for presence & severity
- Uremia, EtOH/nutritional deficiencies, CTD, vasculitis, B12 deficiency, hypothyroid, amyloid
- Autonomic neuropathy testing
38
DM Peripheral Neuropathy Treatment
- Tight control of glucose levels to slow progression or prevention
- Neuropathic pain: pregabalin, gabapentin, valproate. Can try NSAIDs, Opioids. TCAs, SNRIs- 2-3rd lines
- Specific autonomic therapies
Gastroparesis: Erythromycin and metoclopramide are used to treat diabetic gastroparesis, jejunostomy
ED: sildenafil and related phosphodiesterase type 5 (PDE5) inhibitors. Penile prosthesis, urology consult
Gustatory sweating: Glycopyrrolate
- Ulcers: debridement, IV abx, amputation
39
Patient Care Instructions on How to help prevent diabetic neuropathy?
```
o Control blood sugar level
o Maintain normal blood pressure
o Exercise regularly
o Stop smoking
o Limit the amount of alcohol
o Eat a healthy diet and avoid elevated levels of triglycerides in the blood
o Maintain a healthy weight
o Keep follow-up appointments with the healthcare provider
```
40
DM Peripheral Neuropathy Consultations
- Neurologist early in course of neuropathy
- Rehabilitation provide a functional-based comprehensive evaluation and treatment
- Ulcer management/wound clinic or vascular surgeon
- Cardiologist should monitor patients with ECG abnormalities
- A gastroenterologist can monitor gastroparesis and diarrhea
- PCP: regular monitoring every 4 weeks to 3 months to assess therapy. Objective measures of function and improvement should be taken at every visit. Feet assessment with monofilament and tuning fork on every visit.
41
Patient Care Instructions for DM Peripheral Neuropathy
- No treatment available to reverse neuropathy
- Muscle weakness is treated with support, such as braces
- Physical therapy and regular exercise may help patients maintain the muscle strength they have
- Pain medications may help make pain more tolerable, medications can be used to treat nausea, vomiting, and diarrhea
- Preventing injuries such as burns, cuts, or broken bones is especially important, because patients with neuropathy have more complications from simple injuries and may not heal as quickly as healthy individuals.
- Patient Care Instructions
- Diabetes patients can take the following self-care measures:
- Work with primary care physicians and endocrinologists to control glucose levels
- Examine the skin of feet and lower legs regularly
- See a healthcare provider promptly for calluses, sores on the skin, or other potential problems so they can be treated properly
- Wear good-fitting, comfortable shoes that protect the feet
