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Rehab Med > Nerve and Muscle > Flashcards

Nerve and Muscle Flashcards

1
Q

Any Disorder of the peripheral nervous system involving either the axon or the myelin sheath

 May be localized or generalized

A

nerve and muscle

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2
Q

toxic substance

A

lead neuropathy

steroid neuropathy

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3
Q

demyelinating disease

A

Guillain Barre Syndrome

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4
Q

Axonopathies

A

Crohn’s Disease

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5
Q

Demyelinating/ axonal loss

A

Diabetes Mellitus neuropathies

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6
Q

tells the 3 types of destruction of the nerve

A

SEDDON’S CLESSIFICATION

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7
Q

often times can recover, normally it would present as conduction block

A

Neuropraxia

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8
Q

axon are severed

A

Axonotmesis

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9
Q

totally no connection anymore

A

Neurotmesis

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10
Q

this classification is very important in surgery because the nerve transection repair should be approximated properly depending on the level of severity

A

SUNDERLAND’S CLASSIFICATION

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11
Q

neuropraxia)

 Focal conduction block

A

FirstDegree

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12
Q

Axonotmesis)

 Concentric needle

 Axonal damage and wallerian degeneration with intact supporting structures

A

Second degree injury

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13
Q

Neurotmesis)

 Interruption of axon and endoneurium

A

Third Degree Injury

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14
Q

Interruption of perineurium and endoneurium

A

Fourth Degree Injury

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15
Q

Complete cut

A

Fifth degree injury

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16
Q

often times the mainstay in dx, b/c some conditions are demyelinating.

It evaluates the integrity of the nerve and muscle

A

Electrodiagnosis

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17
Q

Nerve Conduction study, Somatosensory evoke potentials,

A

Nerve conduction study (NCS)

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18
Q

Divided into 2: electromyography and single fiber testing

A

Electromyography

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19
Q

nerve usually have faster response b/c of saltatory conduction

A

myelinated

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20
Q

slower b/c they don’t have the myelin sheath and nodes of ranvier.

A

unmyelinated

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21
Q

Will require you to have electrodes and stimulators.

 Electrodes are placed in a certain area and you will find where it will pass through.

A

Nerve conduction study (NCS)

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22
Q

needle that has 2 needles inside.

 Has one major outer needle, which is usually positive

 Third Degree Injury (Neurotmesis)

 Interruption of axon and endoneurium

and the reference, and the much inner needle which is the active and is negative.

 It can pick up a very huge number of signals

A

Concentric needle

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23
Q

one polar needle, which is usually positive.

 Fifth degree injury

 Complete cut

 The active electrode which is usually negative is the one incorporated with the monopolar needle.

A

Monopolar needle

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24
Q

Antidromic (studies are performed by recording potentials directed toward the sensory receptors)

A

Non-Physiologic response

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25
Q

will stimulate a portion and placed the recording electrode near the proximal portion, which is called as orthodromic testing. (Studies are obtained by recording potentials directed away from these receptors.

A

physiologic response

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26
Q

Sensory Nerve Action potential

 Smaller signal, 10 microvolts

 More sensitive

A

SNAP

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27
Q

Compound Motor Action Potential

 Signal is bigger because it has 2 mv

A

CMAP

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28
Q

It will tell amplitude, latency and duration.

A

CMAP

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29
Q

tells us how far or how fast that signal came to u from point A to point B.

A

Conduction velocity

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30
Q

Primary sensory peripheral neuropathy (acroneuropathy)

 Antidromic (studies are performed by recording potentials directed toward the sensory receptors)

o Autonomic Peripheral Neuropathy

o Acute painful Neuropathy

o Subclinical Neuropathy

 SNAP

 Sensory Nerve Action potential

 Smaller signal, 10 microvolts

 More sensitive

o Proximal lower extremity motor neuropathy (diabetic amyotrophy)

A

Symmetrical

Diabetic neuropathy

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31
Q

Neuropathy of individual nerves (mononeuropathy)

o Some Painful Neuropathy

o Truncal Neuropathy or radiculopathy

o Entrapment Neuropathy

A

Asymmetrical DN

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32
Q

Rare

 Severe pain in the distal lower extremities

 Associated with weight loss, depressionand insomnia

 Mild sensory loss

 Inappropriately labeled “neuritis”

A

Acute Painful Neuropathy

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33
Q

Sensory loss and:

o Orthostatic hypotension

o Gastrointestinal dysautonomia

o Esophageal dysmotility

o Gastroparesis

Diarrhea or Constipation
neurogenic bladder
erectile dysfunction
impaired distal sweating

A

Autonomic Peripheral Neuropathy

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34
Q

Initially thought of as a “spinal cord lesion”

 Earlier called “diabetic amyotrophy”

 Electrodiagnostically noted as a dysfunction in the proximal peripheral nerve

 May be acute or subacute

 Weakness of quads, iliopsoas, or thigh adductors or in combination

 May also include gluteal muscles, hamstrings and gastrocnemius

 Pain (Severe, Deep and aching)

 Sensory is usually intact

Recovery occurs over a 12 to 24 month period

 Prognosis for recovery is good

A

Lower Extremity Proximal Motor Neuropathy

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35
Q

Seen in older patients (50 and above)

 May be acute or gradual

 Unilateral distribution

 Usually T3 through T12

A

Truncal Neuropathy or Radiculopathy

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36
Q

Studies suggest by Frasier et al that there is no clear cut relationship between this neuropathies and diabetes

A

Entrapment Neuropathy

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37
Q

Also known as Acute Demyelinating Polyradiculopathy (AIDP)

 An acquired symmetrical polyneuropathy

 Affects the lower extremity first

 Etiology: unknown

 May be due to a viral insult on the myelin and schwann cell

IDIOPATHICBRACHIAL NEURITIS

 Onset: 1 to 4 wks post illness, vaccination or surgery

 Males affected more than females

A

GUILLAIN-BARRÉ SYNDROME

38
Q

Ascending sensory abnormalities

 Ascending symmetrical weakness

 Possibly bedridden in two days

 CN VII most affected

 CN I and II not affected

 Respiratory or autonomic failure

A

GUILLAIN-BARRÉ SYNDROME

39
Q

GUILLAIN-BARRÉ SYNDROME

ancillary

A

CSF

 increased protein, few mononuclear cells

 EMG

40
Q

GUILLAIN-BARRÉ SYNDROME

tx

A

Plasmapharesis

 IV immunoglobulins

 Respiratory support

 Steroids usually not effective

41
Q

GUILLAIN-BARRÉ SYNDROME

rehab aims

A

Maintain Muscle bulk and range of motion

 Splinting to prevent Contractures

 Orthotics and assistive devices

 Improve endurance

42
Q

HEREDITARY MOTOR SENSORY NEUROPATHY I)

A

CHARCOT MARIE TOOTH DISEASE

43
Q

Most frequently inherited neurologic disease

Prevalence rate: 125,000 in US

Chromosome 17

Autosomal Dominant

Age onset: Early childhood (1st to 2nd decade of life)

A

CHARCOT MARIE TOOTH DISEASE

44
Q

Progressive

 Abnormal Vibration and proprioception

 Abnormal muscle stretch response

 Foot intrinsic atrophy

 Pes Cavus -Hammer Toes

 Bilateral foot drop

 Stork leg appearance

 Hypertrophy of peripheral nerves

 Greater auricular nerve

A

CHARCOT MARIE TOOTH DISEASE

45
Q

CHARCOT MARIE TOOTH DISEASE ancillary

A

CSF tap-increased protein

 Onion bulb formation on schwann cell

 EMG/NCV

46
Q

rehab aims

CHARCOT MARIE TOOTH DISEASE

A

Correct deformity

 Improve strength

 Orthotic devices

47
Q

IDIOPATHICBRACHIAL NEURITIS

A

PARSONAGE-TURNER SYNDROME

48
Q

PARSONAGE-TURNER SYNDROME commonly affects

A

Radial nerve

 Long thoracic nerve

 Suprascapular nerve

Spinal Accessory Nerve

Males>Females

1/3 has both shoulders affected

49
Q

Sharp pain on shoulder followed by aching sensation

 Weakness

 Atrophy

 Prognosis: Good

A

PARSONAGE-TURNER SYNDROME

50
Q

A disease that causes degeneration and loss of the motor neuron in the spinal cord, brainstem motor nuclei and the motor cortex

 Men> women

 Familial in 5%- Autosomal dominant

A

ALS

51
Q

Appears middle to late life

 10% may have symptoms by age 40 yrs

 No geographical or racial predilection

 Invariably leads to death within a few yrs of diagnosis

 Slower progression noted in patients who suffered at a younger age

 Pathogenesis and etiology is unknown

 Diagnosis is based on History and Proper PE

 Diagnostics: EMG-NCV

A

ALS

52
Q

Weakness, asymmetric with no sensory loss

 Tongue fasciculations

 Extraocular muscles are rarely involved

A

early onset ALS

53
Q

Dysphagia

 Immobility

 Dyspnea

 Atrophy

 Occasional cramps

 Dementia may occur

 Emotional lability-bulbar involvement

A

ALs late

54
Q

ALS rehab

A

Keep the patient at the highest level of function

 Range of motion exercises

 Communication devices

 Assistive devices to improve ADL

 Psychological support

 Medications

 Death may bedue to respiratory complications

55
Q

A disabling disease of the anterior horn cell in the spinal cord

 Caused by a picornavirus

 Has 3 strains which are distinguished by antigenic strains

A

POLIOMYELITIS

56
Q

picornavirus virus replicates at oropharynx

A

alimentary phase

57
Q

Infective phase, seeding occurs from the lymphatic tissue

picorna

A

lymphatic phase

58
Q

virus gains access into the blood stream and migrates to the central nervous system: cervical and lumbar segments greatly affected

picornavirus

A

viremic phase

59
Q

Polioencephalitis

 Decreased Tendon reflexes

 Paralysis (distal and asymmetric)

 Atrophy

 Bulbar signs (CN IX, X most affected)

 Constipation, gastric atony

 Clumsiness, frequent fall, poor walking skills

 Symmetrical

 Affects pelvic muscles first

 Pseudohypertrophy of calves

 Gower’s sign

 Other associated abnormalities

o Scoliosis

 Minor illness

o Pain

 Sore throat

 Vomiting

 Abdominal pain

 Fever

 Minor headache

 Easy fatigability

o Cardiac abnormalities-cardiac failure

o Restrictive pulmonary disease

o Decreased IQ

ANCILLARY PROCEDURES

 Muscle biopsy

CPK (elevated)

 Recovery may usually last up to 4 to 8 yrs

EMG/NCV

 Due to anterior horn cell recovery

A

poliomyelitis

60
Q

poliomyelitis recovery due to

A

collateral sprouting

61
Q

 Is the subsequent addition of paresis or paralysis roughly 30 yrs after the initial attack of Poliomyelitis

 May occur in 25% to 60% of Polio victims

 2 Broad categories:

 Late Stages

 Primary musculoskeletal symptoms

 Dysphagia

 Immobility

 Dyspnea

 Atrophy

 Occasional cramps

 Dementia may occur

 Emotional lability-bulbar involvement

 Post-poliomyelitis progressive muscular atrophy (PPMA)

A

POST POLIO SYNDROME

62
Q

New onset of fatigue (80 to 90%)

 Multiple joint pains

 Decreased mobility due to altered body biomechanics or scoliosis

 Physical decompensation following a recent weight gain or brief period of immobility owing to some form of physical trauma

A

PRIMARY MUSCULOSKELETAL SYMPTOMS

63
Q

GOALS IN REHABILITATION OF POST POLIO

A

Focused on maintaining strength of the weakened muscles (those with muscle strength of 3)

 Regaining function

 Use of assistive device

 Use of braces

64
Q

Group of muscle diseases whose common primary symptom is proximal limb muscle weakness

Majority has no cure

Treatment is focused on:

Prevention

Maximizing function

A

MYOPATHIES

65
Q

causes MYOPATHIES

A

Congenital-Collagen-vascular

 Metabolic-Toxic

 Endocrine-secondary to other etiologies

 Infectious

66
Q

X linked recessive myopathy

 Incidence: 1/3,500 live male births

 Prevalence: 3/ 100,000 live males

 1/3 of cases are due to spontaneous mutation

 Severe or absent Dystrophin

 Abnormality in short arm of Chrom X (Xp21 locus)

 Evident at age 3-5 y/o

 Polioencephalitis

 Decreased Tendon reflexes

 Paralysis (distal and asymmetric)

 Atrophy

 Bulbar signs (CN IX, X most affected)

 Constipation, gastric atony

 Clumsiness, frequent fall, poor walking skills

 Symmetrical

 Affects pelvic muscles first

 Pseudohypertrophy of calves

 Gower’s sign

 Other associated abnormalities

o Scoliosis

 Minor illness

o Pain

 Sore throat

 Vomiting

 Abdominal pain

 Fever

 Minor headache

 Easy fatigability

o Cardiac abnormalities-cardiac failure

o Restrictive pulmonary disease

o Decreased IQ

A

Duchenne

67
Q

ancillaru duchenne

A

Muscle biopsy

CPK (elevated)

EMG/NCV

68
Q

duchenne loses ability to walk age

A

12

69
Q

duchenne die at

A

20

70
Q

duchenne cause of death

A

respiratory insufficiency

71
Q

duchenne rehab aims

A

Maintain strength

 Prevent deformities

 Maintain Mobility

 Maintain hand function and ADL

 Fatigue should not happen!

72
Q

Milder variant of DMD

 X linked recessive disorder

 Incidence: 1/50,000 live male births

 Weakness starts at 10-15 yrs of age

 Has lower amounts of Dystrophin

 Prognosis: better than DMD

A

MUSCULAR DYSTROPHY

73
Q

Weakness

 Pseudohypertrophy

 Cardiac abnormalities-cardiomyopathy

 Gower’s sign

A

MUSCULAR DYSTROPHY

74
Q

life expectancy muscular dystrophy

A

milder, may live up to 6th decade

75
Q

Weakness of hips and then shoulders

REHABILITATION AIMS

LIMB GIRDLE DYSTROPHY

 Autosomal Dominant or recessive

 May also be seen as:

 Sarcoglycan gene mutation has been identified in four forms

 Facial muscles are spared

A

limb girdle

76
Q

limb girdle ancillary

A

cpk
muscle biopsy moth eaten whorled fibers
emg/ncv

77
Q

death limb girdle

A

cardiopulmo, pneumonia

78
Q

an inflammatory disease of the central nervous system characterized by areas of demyelination

 3rd most common cause of disabling illness between 15 and 50

 1.1 million affected worldwide

 More common in females

 Average age of onset: 32.4 for female and 34.3 for males

 Linked with Human Lymphocyte Antigen but may vary in population

 Often linked with chromosome 6 however mendelian inheritance is not well established

 May be confused with other diseases

 Occurs as “plaques” on the white matter

A

MS

79
Q

Frequently seen in white matter

 Prognosis is Poor if:

o Male

o Progressive course at onset

o Age of onset >40 yrs

o Cerebellar involvement at onset

o Multiple system involvement at onset

 Cause of Death: complication of the disease such as:

o Infection

o Pulmonary Embolism

o Malnutrition

o Dehydration

o May also be due to suicide

ANCILLARY PROCEDURES

 CSF

MRI

EMG/NCV/SSEP

o Near the lateral ventricle

o Floor of the fourth ventricle

o Corpus collosum

o Periaqueductal region

o Optic nerves, chiasm, tract in the corticomedullary junction

o White matter tracts of the spinal cord

A

MS

80
Q

Inflammatory reaction with perivascular lymphocytic cuffing, local

disruption of the blood brain barrier with edema, and migration of T lymphocytes and some plasma cells into the parenchyma, followed by macrophages, which appear foamy as they ingest fragmented myelin debris.

 Axons spared

 Chronic plaques show absent oligodendrocytes, inflammatory cells

 Presumed autoimmune reaction to myelin sheath

 Symptoms present at onset of illness in Definite MS:

o Weakness that may be accompanied by increased muscle stretch reflexes and in the lower limbs

o Paresthesia which is often painful

o Optic Neuritis

o Diplopia

o Ataxia

o Disturbed nutrition

o Gait difficulty

A

MS

81
Q

discrete attacks produced increased neurologic

impairment, which subsequently improves or resolves over ensuing weeks to months

A

Secondary progressive pattern

82
Q

in which gradual accumulation of neurologic deficit is present from the onset of the disease without superimposed relapses

A

Primary progressive

83
Q

in which the disease appears clinically quiescent without progression

A

Plateaued pattern

84
Q

individuals with initial relapses and remissions have little or no neurologic deficit 1 yrs following onset. Some patients, however may later go on to develop progressive disease

A

Benign MS

85
Q

a particularly aggressive course of primary progressive MS leading to death from fulminant disease within 5 yrs of onset

A

Malignant MS

86
Q

MS ancillary

A

CSF

MRI

EMG/NCV/SSEP

 Individualized

 PREDNISONE

 May decrease the length and severity of exacerbation

 INTERFERON

 May decrease the number of exacerbation

87
Q

May decrease the length and severity of exacerbation

MS

A

predinisone

88
Q

May decrease the number of exacerbation

MS

A

interferon

89
Q

May slow progression inchronic MS

A

azathioprine

90
Q

dec ataxia MS

A

isoniazid

91
Q

Ameliorating Fatigue:

MS

A

amantadine

permoline (liver toxicity)

Rehab Med (3 decks)

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