Peripheral Nn, Pain, & CVA Flashcards

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1
Q

External mechanisms of nerve injuries

A

Laceration, avulsion, stretch, crush, compression, contusion

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2
Q

Internal mechanisms of nerve injuriese

A

Viruses, bacteria, autoimmune

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3
Q

Nerve injuries accompanied by injuries to:

A

Bone, tendon, ligament, soft tissue, vessel

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4
Q

Nerve injuries

A

Dysfunction of peripheral Nn results from damage to neuron, Schwann cells, or myelin sheath

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5
Q

Stretch injuries

A

Damage in intrafascicular area (axonal disruption, hemorrhaging); All Nn have ability to stretch & recoil, as long as nerve is free to glide within its beds, stretch can be tolerated, but if it is anchored to its bed by scar tissues, or is overstretched, injuy may occur (intraneural damage, intrafasciular pressure)

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6
Q

Compression Injuries

A

Acute & chronic; increase pressure, slowed nerve conduction/loss of conduction, mechanical deformation of axon & Schwann cells, decreased circulation

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7
Q

Laceration

A

Loss of continuity of structure

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8
Q

What happens when a nerve fiber is cut or crushed?

A

Wallerian degeneration (process by which damaged segment of nerve is phagocytosed); Regeneration

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9
Q

Response to Peripheral N injury

A

Different than other tissues; regeneration occurs 1-3mm/day, latency of 3-4 weeks, residual deficit is common

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10
Q

Neurapraxia

A

Result of blunt trauma or compression, causing contusion to nerve. Axons remain in continuity, no Wallerian degeneration, recovers spontaneously within days or weeks, N conduction preserved proximal & distal to injury

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11
Q

Axonotmesis

A

Axon severed, sheath intact, Wallerian degeneration distal to level of compression; intact endoneurial tube allows regrowth for proximal part of N to reattach to distal portion ot N; recovery usually 6 months, if cell body alive

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12
Q

Neurotmesis

A

Partial or complete laceration of axon & sheath, without directional guidance of endoneural tube, misdirected axon growth may occur; microsurgery needed, grafting may be necessary

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13
Q

Signs & symptoms

A

Force & level of injury determines the type of injury sustained & resulting deficits; motor impairment, sensory dysfunction, pain, & parasthesia

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14
Q

Diagnosis

A

Motor function tests, sensory testing, X-ray, CT scan, MRI, nerve conduction studies

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15
Q

Order of sensory return

A

1) Pain & temperature; 2) 30 hz vibration; 3) Moving touch; 4) Constant touch; 5) 256 Hz vibration; 6) Touch localization; 7) 2-pt discrimination; 8) Stereognosis

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16
Q

Treatment

A

Reduce trigger (set fracture, dislocation); analgesics (control pain), antivirals/steroids (decrease edema); operative repair (decompression, repair, neurolysis, grafting)

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17
Q

Vasomotor sympathetic function

A

skin color & skin temperature change

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18
Q

Sudomotor

A

sweat

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19
Q

Pilomotor

A

goosebumps

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20
Q

Trophic

A

hair & nail growth/changes

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21
Q

Motor return

A

Function returns along path of N regeneration; return in direction of proximal to distal (everything above should be working)

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22
Q

Prognosis

A

Varies depending on type & extent of injury, contamination of wound, age of pt, medical status/health previous, surgery to repair N within 3 mos

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23
Q

Complications

A

Paresthesias, neuromas & entrapment syndromes, hperesthesia, hypersensitivity to cold, paralysis, denervation can develop & result in muscle atrophy, joint stiffness

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24
Q

OT post op consideration

A

splinting in protective position to decrease amount of tension on healing nerve (3 wks); prevention of contractures & scar adhesions

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25
Q

Radial N Injuries

A

Wrist drop; associated /c midhumeral shaft fractures, fracture/dislocation of elbow, compression between radial head & supinator; Functional loss=ulnar & radial wrist extension, weakened supination, loss of MCP jt extension, loss of thumb ext & radial abd

26
Q

Radial tunnel syndrome

A

Compression of N in raidal tunnel, symptoms include persistent pain, cramping, & tenderness in dorsal forearm; Tx includes decreasing wrist motion, splinting, modification of activity, decrease forearm rotation, modalities, balance activity & rest, neural glides

27
Q

Median N injuries

A

Associated /c humeral fx, elbow dislocations, distal radius fx, dislocation of lunate, knife & glass lacerations at volar wrist, compression of carpal tunnel; Functional loss=thumb opposition, sensory loss of volar thumb, index & long & radial half of ring fingers & dorsal surgace of dist phalanges of thumb, index, long, & radial half of ring fingers; monkey hand

28
Q

CTS Etiology

A

Compression of median N lying directly under flexor retinaculum, associated /c pregnancy, RA, DM, Colles’ fracture, deconditioning, thyroid disease, obesity, repetitive motion

29
Q

CTS Symptoms

A

Pain & parasthesia in Median N sensory distribution; loss of power to thenar muscles & eventual wasting of thenar muscle mass, loss of opposition & fingertip pinch, decrease grip strength; Sensory loss on palmar aspect of radial 3.5 digits

30
Q

Tx for CTS

A

Anti-inflammatory meds, rest, wrist immobilization splint, ergonomic modifications, neural glides; surgical decompression (division of flexor retinaculum)

31
Q

Ulnar N injuries

A

Associated /c fracture of medial epicondyle of humerus, olecranon of ulna; glass & knife lacerations of wrist can involve Ulnar N, compression at Guyon’s canal at wrist level & in cubital tunnel proximally; Funcitonal loss=grip & pinch affected, difficulty /c lateral pinch will substitute for loss of add pollicis /c FPL, decrease power grip; Claw deformity

32
Q

Cubital Tunnel Syndrome

A

Compression to ulnar N at elbow as it passes through tendinous arch of origin of flexor carpi ulnaris; sensory loss occurs on palmar aspect of little finger & ulnar half of ring finger & dorsal cutaneous branches of ulnar N

33
Q

Nerve injury therapy Acute phase

A

Immobilization; minimize tension at site of injury, protect N to minimize inflammation; Increase ROM, functional splinting

34
Q

Recovery phase

A

Motor retraining, desensitization, sensory reeducation

35
Q

Acute pain

A

occurs in response to tissue injury, lasts less than a month

36
Q

Chronic/persistent pain

A

persists beyond typical course of recovery, no discernible cause, persists greater than 1 month after resolution of injury, OR pain that persists over months or years without discernible cause

37
Q

Referred pain

A

perceived at location other than site of stimulus

38
Q

Describing pain

A

Severity quality, location, duration, course

39
Q

Neurobiological basis of pain

A

Noxious stimulus occurs–perceived by Pacinian corpuscles & immediately travels up spinal cord to brain, nociceptors pain threshold reached–slower fibers communicate /c nociceptor in spinal cord & travel to thalamus then cortex; Brain determines how to respond to message; Pain causes brain cells to release chemicals; Can cause inflammatory response signaling injury when there is not one in chronic pain

40
Q

Central Sensitization

A

Nociceptors carry messages regarding pain danger to spinal cord & brain, repetitive firing of nociceptors results in decr threshold before pain is perceived, it no longer takes the amount of stimulation to elicit the pain respose

41
Q

Chronic pain neurosignature

A

Cortical inhibition is decreased, cortical excitation is increased; More sensitive & less precise

42
Q

Limbic system & Pain

A

Emotions & memories of sensations & experiences have strong influence on pain; Limbic system can become sensitized, eliciting pain & inflammatory responses, can be elicited /c thoughts

43
Q

Graded motor imagery

A

Provide pain-free input to aid remapping process; Sequentially graded, progressing from easy to difficult & non-threatening to threatening

44
Q

OT interventions

A

Patient education about pain; deep diaphragmatic breathing, visualization, comforting thoughts, meditation, prayer, mindfulness, biofeedback; Graded activities, exercise, functional body mechanics retraining, coping skills, physical agent modalities; Control neuroplasticity & cortical remapping as tx & preventative intervention, Promote cortical inhibition

45
Q

2 Mechanisms of Stroke

A

Ischemic; Hemorrhagic

46
Q

Ischemic strokes

A

caused by clot/blockage; thrombosis=blood clot that forms somewhere in cerebral vessel & causes block in blood supply; Embolism=occurs when blood clot formed somewhere else in vascular system (heart) breaks free & travels to cerebral vessel where it becomes lodged & interrupts blood flow

47
Q

Hemorrhagic strokes

A

rupturing in vessel wall, which causes vessel to bleed out; intracerebral hemorrhage=bleeding in brain; subarachnoid hemorrhage=bleeding around brain; Fatality rates are higher, but recovery is better

48
Q

Transient Ischemic attacks

A

stroke symptoms lasting

49
Q

Stroke risk factors

A

Older age, heredity/family hx, sex (male>female), race (African American), h/o prior stroke, TIA, heart attack; smoking, high BP, DM, high cholesterol, obesity, poor diet, sedentary lifestyle, heart disease, atrial fibrillation

50
Q

Stroke symptoms

A

Motor impairments, language impairments (Broca’s causes expressive aphasia, Wernicke’s causes receptive aphasia), visual-perceptual impairments, psychosocial, incontinence, hemiplegia on contralateral side, sensory & cognitive disturbances

51
Q

Occipital lobe

A

Vision

52
Q

Parietal lobe

A

Sensory & motor

53
Q

Frontal

A

judgment & reasoning

54
Q

Temporal

A

hearing, language, memory

55
Q

Cerebellum

A

Organization of movement

56
Q

Brainstem

A

heart rate, respiratory, everything important

57
Q

Right hemisphere impairments

A

left hemiparesis, visual field deficits, neglect, poor insight & judgement/impulsive behavior

58
Q

Left hemisphere impairments

A

right hemiparesis, aphasia, apraxia/motor planning deficits, math, abstract reasoning, analytical & sequential thinking

59
Q

FAST

A

Facial drooping, Arm weakness, Speech difficulties, Time to call 911

60
Q

Recovery from stroke

A

Early initial improvement or spontaneous recovery occurs b/c pathologic processes in brain resolve & neurotransmission resumes near & far from infarct/hemorrhage; Later ongoing improvement occurs due to neuroplasticity in brain; most rapid recovery in first 1-3 mos & slower recovery up to 1 yr

61
Q

Stroke dx

A

CT, MRI, fMRI, PET

62
Q

Stroke tx

A

Prevent progression of lesions, reduce cerebral edema, prevent secondary complications, surgical procedures to clear blocked arteries, rehab