Acute and Chronic Polyneuropathies Flashcards

1
Q

Pain Pathways

A

Stimulus (painful stimuli) –> Relay (synapses in the spinal cord that connect neural pathways) –> Pain (pain signals are processed in different parts of the brain) –> Regulation (the brain generates signals that descend along the spine and either inhibit or amplify the pain signals in the spine)

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2
Q

Types of Pain

A

Acute, Chronic, Referred, Central neuropathic, Autonomic, Peripheral

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3
Q

Acute Pain

A
  • Normal predicted physiological response
  • Serves as a warning
  • Localized
  • Occurs in proportion to the intensity of the stimuli or tissue damage
  • Associated with anxiety, increased autonomic activity
  • Usually relieved by interventions correcting the injury
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4
Q

Chronic Pain

A
  • Referred to as “intractable pain” if persists for 6 months or greater
  • Pain that continues after the stimulus has been removed and tissue is healed
  • Believed to result from hyper-sensitization of pain receptors and enlargement of the receptor field in response to localized inflammation that follows tissue damage
  • Poorly localized, has ill-defined time of onset and is strongly associated with subjective components
  • Associated with: depression, difficulty sleeping, poor mental and physical function and fatigue
  • *Pt’s with high anxiety and other personality traits may be able to be flagged as people that may turn into pt’s with chronic pain. **
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5
Q

Referred Pain

A
  • Pain felt at a point other than it’s origin
  • Can be referred from an internal organ, a joint, a trigger point or a peripheral nerve to a remote musculoskeletal structure
  • Usually follows a specific pattern (ex/ cardiac pain to left UE/jaw)
  • Result of a convergence of the primary afferent neurons from deep structures and muscles to secondary neurons that also have a cutaneous receptive field
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6
Q

Central Neuropathic Pain

A
  • Pain initiated or caused by a primary lesion or dysfunction of the CNS, can be at many levels: nerves, nerve roots and central pathways in the spinal cord and brain
  • Medically diagnosed by it’s defining neurological signs and symptoms
  • Verified with neuroimaging tests
  • Can be caused by vascular insult; traumatic, neoplastic and demyelintating diseases; surgery (including vascular compromise during surgery)
  • Patients have difficulty describing their pain and report burning, aching, pricking, squeezing or cutting pain after cutaneous stimulation
  • Difficult to treat
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7
Q

Autonomic Pain

A
  • Under normal conditions there is a fine balance between parasympathetic and sympathetic branches of the ANS
  • Parasympathetic activity maintains homeostasis, whereas sympathetic activity function to make “flight or fight” changes in response to stress
  • Stimulation of the autonomic efferent fibers is not normally painful, but the balance between afferent input and descending sympathetic nervous system is disrupted when there is injury resulting in exaggerated and prolonged sympathetic activity, allodynia and hyperalgesia and therefore autonomic pain (CRPS)
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8
Q

Peripheral Pain

A
  • Results from noxious irritation of the nociceptors
  • character of peripheral pain depends on location and intensity of the noxious stimulation as well as which fibers carry the information into the dorsal gray matter
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9
Q

Phantom Limb

A
  • Any non painful sensation in the amputated limb
  • Cortically perceived
  • Sensations such as:
    - ->Kinesthetic (posture, length, volume)
    - ->Kinetic (willed movements, spontaneous movements
    - ->Exteroceptive sensations (touch, temperature, coldness, bugs crawling = formication)
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10
Q

Phantom Limb Pain

A
  • Painful sensations that seem to occur in the lost limb
  • Cortically perceived
  • Cannot usually be ended by nerve blocks
  • Often described as excruciating, sticking, cramping, burning, squeezing
  • Cortical map still retains the anatomic image of the amputated part.
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11
Q

Another name for residual limb pain

A

“stump pain”

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12
Q

Residual Limb Pain

A
  • Painful sensations localized to the stump of an amputated body part.
  • Pain in the residual limb with an organic reason: blister, in grown hair, etc.
  • Mediated by peripheral nerves
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13
Q

What kind of therapy works well for pt’s with amputation experiencing phantom limb pain?

A

Mirror therapy

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14
Q

Is phantom limb pain a CNS or PNS phenomenon?

A

CNS

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15
Q

When a pt is experiencing phantom limb pain and they undergo Transcranial Magnetic Stimulation (TMS) does their cortical map change to show amputation?

A

No, the cortical map is the same as it would be before the amputation, the brain does not recognize that a limb was amputated.

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16
Q

Over time will other areas of the cortical map eventually appropriate the cortical region that once mediated the sensation/movement of the amputated limb? Will TMS show these changes?

A

Yes and yes.

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17
Q

What is one thing that is good about phantom limb pain?

A

Pt can use these sensations (as long as they are not painful) to propel prosthesis.

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18
Q

Treatments for phantom limb pain

A
  • Often ineffective, TENS
  • Vibration
  • Analgesics or painkillers may work temporarily
  • Compression such as residual limb wrapping, shrinkers, or wearing the prosthesis may decrease the pain.
  • *Mirror therapy works well for these patients**
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19
Q

Can phantom limb sensations occur in patients with SCI?

A

Yes, these tend to resolve quickly.

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20
Q

Guillain-Barre Syndrome describes a broad group of ___

A

demyelinating inflammation poly radiculoneuropathies

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21
Q

What are the two forms of GBS (guillain-barre syndrome)?

A

Dymyelinating polyradiculoneuropathy (AIDP)

Acute Axonal Neuropathy (AMAN)

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22
Q

Why does GBS result in flaccid paralysis?

A

Because nerve roots (radiculopathy) and peripheral nerves (polyneuropathy) are affected

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23
Q

What kind of motor neuron lesion is GBS considered?

A

Lower motor neuron lesion

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24
Q

Cranial nerves may be affected in GBS. What kind of lesion is this? upper/lower

A

Cranial nerves are LMN

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25
Q

What age group are affected by GBS?

A

Trick question: Occurs in all age groups

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26
Q

What symptoms of GBS do pts experience before the onset of weakness and sensory?

A

Most experience respiratory or GI illness before weakness and sensory.

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27
Q

Causes of GBS?

A

campylobacter jejuni, viruses, bacterium, surgery, vaccinations

28
Q

GBS has an overall good prognosis because:

A

it is a reactive and self limiting auto-immune disease.

29
Q

What happens to nerve conduction in GBS?

A

slowed or blocked

30
Q

What type of cells are affected in GBS?

A

Schwann cells in the PNS that produce myelin.

31
Q

How fast do schwann cells begin to proliferate after initial demyelination?

A

2-3 weeks after. Inflammation subsides and remyelination begins.

32
Q

What is Nadir?

A

Point of greatest severity

33
Q

Which type of GBS progresses faster to NADIR?

A

AMAN has more rapid progression to NADIR.

34
Q

What is used to determine if GBs is axonal or nonaxonal?

A

Through an electrodiagnostic test.

35
Q

What are some potential sensory impairments in GBS?

A

paresthesias of toes (burning/tingling)

hypesthesias (abnormal sensitivity to touch)

36
Q

In which direction does GBS progress?

A

From distal to proximal

37
Q

What is affected if a GBS patient needs a mechanical ventilator?

A

Diaphragm and CNs

38
Q

What are the ANS changes 50% of GBS patients suffer with?

A

BP fluctuations, pooling of blood/poor venous return, tachycardia, Arrhythmias

39
Q

What are some Oral-Motor problems in pts with GBS and what do they mean functionally?

A

Dysarthria (difficulty speaking)- need alternative communication

Dysphagia (difficulty swallowing)- measure to prevent aspirations

40
Q

A GBS pt that has a lesion of the facial nerve (CN VII) would present with what impairment?

A

Bilateral facial weakness

41
Q

What cranial nerves are affected in a GBS pt with diplopia?

A

CN III, IV, VI

42
Q

GBS pts present with DTRs that are:

A

absent due to demyelination of peripheral nerves

43
Q

Signs of overwork weakness

A

DOMS (worse 1-5 days after exercise), Reduction in amount of force muscle able to generate

44
Q

Use gravity-eliminated plane for muscles at what MMT grade?

A

2/5 strength

45
Q

May progress to anti-gravity plane exercises only when the patient is able to move limb _______.

A

against resistance equal to the weight of the limb

46
Q

Gravity eliminated exercise examples

A

pool, overhead sling apparatus, or powder board

47
Q

Techniques used to engage muscles

A

Stroking, Brushing, Vibration, or Tapping

48
Q

What changes need to be made with W/C use as patients recover?

A

acclimated to upright, mobility

49
Q

General Progression of HEP

A

Low reps, short bouts—> Endurance

50
Q

Progression of adaptive equipment as patient recovers

A

parallel bars–> walker–> forearm crutches–> cane

51
Q

In GBS: As PNS recovers, muscle weakness is______.

A

reversed

52
Q

Prognosis for GBS

A

Very good but patients usually immobilized for long period of time

53
Q

How can patients with GBS make the most of their function as recovery occurs?

A

By safeguarding the MSK and cardiorespiratory systems

54
Q

Biggest challenge in treating GBS

A

Improve function without causing damage

55
Q

Family education in acute phase of GBS

A
  • Progression of disease
  • Positioning
  • ROM exercises
  • Interactions and keeping pt engaged
56
Q

Family education in plateau phase of GBS

A
  • Upright positioning for all meals
  • Diaphragmatic breathing, coughing, inspiration spirometer 1x hour
  • ROM, light bicep curls in bed, quad sets, glute sets
57
Q

Family Education in recovery phase of GBS

A

transfers, progression of ADs, what coming home to

58
Q

Plasmapheresis

A

red and white blood cells are separated from the plasma

blood cells are then returned to pt

59
Q

reason for plasmapheresis

A

thought to eliminate some immune factors that are responsible for the disease process
reduces length of illness, shortens time on ventilator, earlier ambulation

60
Q

IV Immunoglobulins (IVIG)

A

helps in recovery
just as effective as plasmapheresis
fewer side effects

61
Q

Phases of GBS

A

Acute (about 4 weeks)
Plateau (about 4 weeks)
Recovery (few months to several years)

62
Q

poorer prognosis of GBS is due to?

A

ventilatory support
rapid progression of demyelination
low distal motor amplitudes on EMG

63
Q

Management for ACUTE phase of GBS

A

prevent contractures and skin break down
postural drainage with percussion
gentle stretching of chest wall
manage pain (PROM, massage, TENS, pressure wrap)

64
Q

Management for PLATEAU phase of GBS

A
tolerance to being upright
maintain ROM
improve pulmonary function
avoid fatigue & overexertion
pressure relief
65
Q

Management for RECOVERY phase of GBS

A

muscle strength recovered 2-4 weeks
muscles recover in descending order
tilt table
positioning splints

66
Q

guidelines for strength recovery

A

short periods of non-fatiguing exercises
increase difficulty ONLY if pt improves or there is no deterioration
improve function not just strength