Differential Diagnosis Test 2 - Emg And Neuromuscular Disorders

Front 1

What neuromuscular disorder is ongoing, usually symmetric, and involves muscle wasting w/ deformity and disability

Back 1

Muscular Dystrophy

Front 2

What are the 6 types of muscular dystrophy?

Back 2

Duchenne's,
Becker's
Fascioscapulohumeral (Landouzy-Dejerine)
Limb-girdle
Myotonic
Muscular dystrophy congenita, aka congenital muscular dystrophy

Front 3

Duchenne's Muscular Dystrophy - onset and progression

Back 3

Duchenne's – apparent at 2-4 years, x-linked, recessive mutation in dystrophin, rapidly progressive, loss of walking by 9-10, death in 20s

All dystrophies genetically based – some recessive (DMD and BMD) and some dominant (FSHD)

Front 4

Becker's MD - progression

Back 4

Becker's – diagnosed 5-10 yr, x-linked, recessive, mutation in dystrophin, slowly progressive, walking maintained past early teens, lifespan until adulthood

All dystrophies genetically based – some recessive (DMD and BMD) and some dominant (FSHD)

Front 5

Fascioscapulohumeral MD - progression

Back 5

Fascioscapulohumeral (Landouzy-Dejerine) – autosomal dominant, onset in early adolescence, 50% risk of children inheriting, slowly progressive, loss of walking in later life, variable life expectancy

All dystrophies genetically based – some recessive (DMD and BMD) and some dominant (FSHD)

Front 6

Limb-girdle MD - progression

Back 6

Limb-girdle – recessive or dominant, onset in late adolescence or early childhood, slowly progressive, mild impairment

Front 7

Myotonic MD - progression

Back 7

Myotonic – more common in some groups, phenotypic severity increases with each generation, variable onset, classically adolescence, autosomal dominant, rate of progression depends on age of onset; mild involvement, greater functional independence, greater longevity

All dystrophies genetically based – some recessive (DMD and BMD) and some dominant (FSHD)

Front 8

Congenital MD - progression

Back 8

Muscular dystrophy congenita, aka congenital muscular dystrophy – onset at birth or shortly after, autosomal recessive or de nova autosomal dominant, progressive; death for some in first years, others more slowly progressive and ambulation achieved

Front 9

what causes some types of muscular dystrophy?

Back 9

Protein dystrophin discovered to be causative for DMD and BMD in 1980s. Other causes for other types.
dystrophin links sacolemma with actin, abnormal causes damage to sarcolemma during contraction/relaxation → necrosis, especially with eccentric contraction.
Muscle cells replaced by fatty and connective tissues and contractures develop

Front 10

Clinical manifestations of Duchenne's Muscular Dystrophy

Back 10

Duchenne's – Grower's sign, falls, waddling gait and lumbar lordosis, walk on toes because of contracture, Trendelenburg's sign, shoulder girdle involved – winging and hypertrophy, shoulder girdle weakness and need to have weight line behind hips and anterior to knees often prevents using crutches, scoliosis, spinal fusion considered, comorbidities – cognitive, respiratory, cardiac, gastrointestinal dysfunction

Front 11

Clinical manifestations of Becker's Muscular Dystrophy

Back 11

Becker's - similar to DMD but slower progression. Proximal muscles most affected, scoliosis and contractures, but less frequent and severe than Duchenne's

Front 12

Clinical manifestations of limb-girdle Muscular Dystrophy

Back 12

Limb-girdle – both proximal and distal muscles, slow course, early – weakness in upper arm and pelvic muscles (usually in late adolescence or early adulthood, but could be late as 40s), winging, lordosis, wadling, poor balance, inability to raise arms, less consistent and more difficult to diagnose

Front 13

Clinical manifestations of congenital Muscular Dystrophy

Back 13

Congenital – spectrum, commonly severe in infancy and rapidly progressive muscle strength loss and respiratory symptoms, involves brain/muscle/visual

Front 14

Clinical manifestations of Fascioscapulohumeral Muscular Dystrophy

Back 14

Fascioscapulohumeral – mild form, weakness and atrophy of facial and shoulder girdle muscles, usually presents in 2nd decade, more females carriers, more males express, progresses to leg or hip muscles, contractures/deformities/hypertrophy uncommon

Front 15

Clinical manifestations of Myotonic Muscular Dystrophy

Back 15

Myotonic – spectrum depending on size of genetic triple repeat, most severe – weakness and myotonia at birth, classic – weakness and some disability w/ mild myotonia and cataracts, weakness and wasting with delayed relaxation and increased excitability, ocular cataracts

Front 16

Diagnosis of muscular dystrophy

Back 16

Diagnosis – clinical presentation, family history, testing such as muscle US, genetic testing, EMG, muscle biopsy, serum enzymes

Front 17

Treatment of muscular dystrophy

Back 17

Treatment – No known treatment halts the progression, aim to maintain function in unaffected muscle, remain active to avoid contractures, ulcers, infections and deconditioning, strengthening (esp eccentric) is not helpful, splinting, stretching, and serial casting for contracture management. Glucocorticoid therapy slows progression of DMD and BMD.

Front 18

Prognosis of muscular dystrophy

Back 18

Prognosis – varies, generally earlier signs → more rapid, progressive, disabling dystrophy, generally rapid progression and death in third decade, respiratory dysfunction often causes death

Front 19

Muscular dystrophy: Implications for PT

Back 19

Implications for PT: encourage mobility and ambulation, avoid strenuous exercise which facilitates breakdown, best in pool, only minimal fatigue, monitor breathing techniques, respiratory movements, and o2 sat, train inspiratory muscles for force and endurance. For more disabling forms – PT provides guidance and information, help with adaptive equipment, computer adaptation, overhead slings and mobile arm supports, splinting and night positioning and AROM and PROM to delay contractures and reduce morbidity, home environmental assessment, ambulation and pool therapy programs for endurance

Front 20

categories of myopathy and examples

Back 20

Myopathies – problem in muscle
Endocrine
-Addison's Disease, Cushing's syndrome, Hyper and hypothyroid myopathies
Metabolic
-Hyperkalemic, McArdles, and Pompe's disease
Hereditary
-Dystonia (myotonia)
-Muscular Dystrophy
Inflammatory condition
-Polymyositis, dermatomyositis

Front 21

Examples of myelopathies

Back 21

Myelopathies – anterior horn cell destroyed – no signal sent to muscle
Spinal Muscular Atrophy
Amyotropic Lateral Sclerosis
Poliomyelitis

Front 22

Examples of peripheral neuropathies

Back 22

Peripheral neuropathies – axon unable to send signal
Demyelinating – diabetic, alcoholic, Guillian-Barre, Hansen's disease (Leprosy)
Axonal -
Trauma
Entrapment
Hereditary
Chemical toxicity

Front 23

Examples of neuromuscular junction disorders

Back 23

Neuromuscular junction disorders – connection between nerve and muscle
Myasthenia Gravis
Botulism

Front 24

addison's disease

Back 24

Addison's disease: destruction of adrenal cortex → not enough cortisol, so muscle has no energy.
Fatigue, loss of appetite, GI trouble, skin pigment changes

Front 25

Cushing's disease

Back 25

Cushing's: also adrenal gland, but this time excess cortisol, weakens proteins, esp. muscle
Often obese, with “buffalo hump” and/or “moon face,” often affects women over 40

Front 26

Hyperthyroid/thyrotoxic myopathy:

Back 26

Hyperthyroid/thyrotoxic myopathy: too much thyroid hormone from thyroid gland, often affects women 20-40 years old
weakness, primarily in proximal muscles, arthralgias (joint pain), often develop diabetes and cardiac problems, wide eyes from retraction of surrounding tissues

Front 27

Hypothyroid myopathy:

Back 27

insufficient thyroid hormone, women 30-60
Generalized muscle weakness and joint pain, weight gain, goiter, behavioral and emotional problems such as apathy/lethargy/depression, cold intolerance, dry skin

Front 28

Hyperkalemic myopathy:

Back 28

inherited condition with low levels of potassium, men>women
sudden transient weakness or paralysis, “periodic paralysis” - triggered by physiologic or psychological stressors, can last minutes-days,

Front 29

McArdles myopathy

Back 29

McArdles: deficiency of phosphorylase, inability to produce glucose because it helps fuel glycolysis
Not a problem of adrenal gland, but lack of enzyme
Generalized proximal muscle weakness
Presents in childhood

Front 30

Pompe's myopathy

Back 30

Pompe's: deficiency of acid maltase, inability to produce glucose because it helps fuel glycolysis
Not a problem of adrenal gland, but lack of enzyme
Generalized proximal muscle weakness
Presents in childhood

Front 31

Inflammatory myopathies:
Polymyositis and dermatomyositis:

Back 31

Inflammatory myopathies:
Polymyositis and dermatomyositis: autoimmune, though can be caused by direct infection
Difference is whether skin is involved in addition to muscle
Muscle weakness, fatigue, pain, joint pain, fever, weight loss

Front 32

Hereditary myopathies:
Dystonia (myotonia):

Back 32

Hereditary myopathies:
Dystonia (myotonia): neurologic condition, but singular finding is involuntary sustained muscle contraction
Contraction can be focal or generalized
often lead to abnormal postures, distortions, limb deformity, and difficulty swallowing or talking
Usually hereditary, can also be caused by trauma, infection, or drug reaction
seen more in adults than children (do they die young?)
Contractions create hypertrophy - “tiny Hercules”

Front 33

Hereditary myopathies:
Muscular Dystrophy:

Back 33

largest group of myopathies, several inherited, progressive neuromuscular disorders
Destruction of muscle tissue with resulting weakness
Duchenne's (childhood) and Becker's (adulthood) most common
Muscle weakness – primarily proximal
Pseudohypertrophy – muscle replaced with fat (and connective tissue)

Front 34

Spinal Muscular Atrophy:

Back 34

Spinal Muscular Atrophy: (myelopathy) congenital, deterioration of anterior horn cell pool
Progressive muscle weakness – proximal > distal
low muscle tone - “floppy infant” syndrome
Delayed motor development
Absent DTR

Front 35

Myelopathies:
Amyotropic Lateral Sclerosis:

Back 35

Amyotropic Lateral Sclerosis: “Lou Gerhig's Disease”, progressive motor neuron degeneration, congenital, but symptoms typically don't manifest until 40s or 50s
Progressive muscle weakness begins in distal muscles and later affects proximal
Degree/pattern of progression is highly variable
Muscle cramps or fasiculations are common

Front 36

Lower motor neuron symptoms of ALS

Back 36

Lower motor neuron death – asymmetric weakness, extensor weaker than flexors, drooping head and lumbar lordosis to compensate, Bulbar signs – medulla, chewing, swallowing, eye muscles, difficulty speaking, drooling. Claw hand, muscle wasting, cramping and stiffness in the morning, twitching

Front 37

Upper motor neuron symptoms of ALS

Back 37

Upper motor neuron symptoms – loss of inhibition – spasticity, extensors of UE and flexors of LE weakened. Spastic bulbar palsy – speech, mastication, and swallowing, pseudobulbar palsy, may manifest as inappropriate laughter, irritability, anger, and tearfullness. reflexes hyperactive, clonus, Babinski

Front 38

What are some non-physical effects of ALS?

Back 38

Cognitive impairment in up to 50% - visual attention, working memory, cognitive flexibility, problem solving, visual-perceptual skills

Front 39

What palsies are associated with ALS?

Back 39

Pseudobulbar palsy – damage in corticobular tract
Progressive bulbar palsy – cranial nerve nuclei

Front 40

Primary lateral sclerosis in ALS

Back 40

Primary lateral sclerosis – neuronal loss in cortex, hyperactive tendon reflexes with spasticity

Front 41

Progressive spinal muscular atrophy in ALS

Back 41

Progressive spinal muscular atrophy – progressive loss of motor neurons in anterior horns, often in cervical area, progressive weakness, wasting, fasiculations in small muscles of hands

Front 42

Diagnosis of ALS

Back 42

Diagnosis – clinical presentation and EMG, criteria for suspected, possible, probably, and definite ALS, other disorders mimic ALS

Front 43

Treatment of ALS

Back 43

Treatment – medication(s) that target pathogenic pathways may slow disease progression, Riluzole – inhibit glutamate, neuroprotective, antiinflammatories...
see implications for PT

Front 44

ALS - Special implications for PT

Back 44

Special Implications for PT – ALS-specific QOL instrument for assessing, ALS functional rating scale for following progression, cognitive deficit screen, staging helps determine intervention, rate of loss fluctuates in first year (stable after) – maintain activity and muscle tone, exercise in moderation. Consistent slow stretching may help decrease tone/spasticity. Gait analysis to assess need for Assistive Devices. Stretch contractures, change positions and educate caregivers. May use braces and assistive devices, evaluate home environment. Have friends come over to hang out! Talk openly about sexual frustration and end of life plans. Respiratory training.
Table of programs for clients depending on stage of ALS

Front 45

Myelopathies: Poliomyelitis

Back 45

Poliomyelitis: Viral infection of anterior horn cells
Flaccid paralysis or weakness (permanent!)
LE more involved than UE
Virtually eradicated in US, but some cases, usually immigrants without immunization
absent DTRs

Front 46

Demyelinating peripheral neuropathies

Back 46

Demyelinating
Diabetic, alcoholic, Guillian-Barre, Hansen's disease (Leprosy)
All involve destruction of myelin around axon
Diminished conduction → progressive paresthesia and weakness
Symmetrical, distal sensory → proximal sensory and motor (“stocking/glove”)
Axons eventually die – further paresthesia and weakness
Significant secondary problems

Front 47

Axonal Neuropathies:

Back 47

Axonal Neuropathies: largest category of neuromuscular disorders – many different causes
Trauma
Entrapment
Hereditary – Charcot-Marie-Tooth (peroneal neuropathy): onset of symptoms before 20, both myelin and axonal degeneration are common, like others – sensory and motor changes, distal > proximal, but commonly affects peroneal nerve which leads to very high arches
Chemical toxicity
All axonal neuropathies feature destruction of axon, sensory and motor changes (consistent with nerve or nerve root), diminished deep tendon reflex, sympathetic changes

Front 48

Classification of Peripheral Neuropathies
Neuropraxia

Back 48

mildest, always transient, (foot falling asleep!), transient physiological block from ischemia with no Wallerian degeneration, symptoms of pain, mild paresthesia and weakness that pass in minutes to days

Front 49

Classification of Peripheral Neuropathies
Axonotomesis

Back 49

Axonotomesis – from prolonged or severe pressure (seen with entrapment), internal architecture of nerve preserved, but axons damaged resulting in Wallerian degeneration, symptoms of pain, complete motor and sensory loss with atrophy, recovery in weeks to months

Front 50

Classification of Peripheral Neuropathies
Neurotomesis

Back 50

Neurotomesis – result of direct trauma such as lacerations, structure of nerve destroyed and Wallerian degeneration occurs, no pain, complete motor and sensory loss with atrophy, recovery in months with surgery

Front 51

Neuromuscular Junction Disorders
Myasthenia Gravis:

Back 51

not one disease, but collection. Common feature is defect in transmission of motor impulses to muscle, deficit can be pre or post-synaptic, can be insufficient release, receptors, or uptake/recycling of acetylcholine
Women > men (onset in 20s or 30s)
Rapid fatigue of muscles, especially facial (eye droop, difficulty swallowing, chewing, coughing)
Normal DTR
Mistaken for other disorders, e.g. MS or fibromyalgia

Front 52

Myasthenia Gravis: characteristics, prevalence, process

Back 52

Fluctuating weaknesss and fatiguability
Peak in 20s and 30s, women:men = 3:2
Decreased Ach receptors on motor endplate – decreased efficiency of neuromuscular transmission
Repetition causes fatigue, rest restores

Front 53

Four categories of Myasthenia gravis

Back 53

Four categories: ocular, mild generalized, acute fulminating, or late severe

Front 54

How is myasthenia gravis diagnosed, what helps, what's affected first

Back 54

Cranial muscles often first to show weakness (eyelids and eye muscles)
Diagnosed with immunologic, pharmacologic, and electrophysiologic testing
ACh inhibitor meds improve weakness temporarily
Surgical removal of thymus successful 85% of people

Front 55

Course of myasthenia gravis

Back 55

Course is variable – daily fluctuation, spontaneous relapses, overall slowly progressive

Front 56

Myasthenia crisis –

Back 56

medical emergency requiring ventilatory assistance b/c of weakness of respiratory muscles

Front 57

Myasthenia gravis - special implications for PT

Back 57

PT
Deep breathing and coughing encouraged. Monitor tidal volume, vital capacity, and inspiratory force.
Never speak with food in the mouth. (or foot)
Be alert to signs of crisis and signs of toxicity from medications
Plan therapy and activities for max energy, frequent rest periods, avoid stress, excess sun or cold
Strength training with max isometric contractions could help clients with mild-to mod MG
Watch out for osteoporosis from corticosteroid medication

Front 58

Diabetic neuropathy - presentation and cause

Back 58

May be focal or diffuse, involve autonomic or somatic PNS
Typically, distal symmetric pattern – diabetic polyneuropathy
Cause: hyperglycemia? Endoneurial microvascular thickening? Reduced nerve growth factor?

Front 59

Classification of diabetic neuropathies

Back 59

Classification:
Rapidly reversible – hyperglycemic neuropathy
Generalized symmetric polyneuropathies –
-acute sensory neuropathy (rapid onset, painful, allodynia)
-Chronic sensorimotor neuropathy (diabetic polyneuropaty, up to 50% of patients affected, usually insidious onset, sensory loss – pain and paresthesias at night in stocking pattern or painless paresthesia and loss of ankle DTRs), motor involvement is not pronounced, may have autonomic involvement
- Autonomic Neuropathy – SNS and PSNS, in type 2 PSNS is more affected, cardiovascular, gastrointestinal, genitourinary, and cutaneous/ocular involvement
Focal neuropathies – mononeuropatheis – less common, median, ulnar and peroneal nerves most commonly affected

Front 60

Treatment of diabetic neuropathies

Back 60

Treatment: control of hyperglycemia and management of symptoms
Drugs
Physical modalities
Early detection of DN and prophylactic foot care has decreased ulcerations and amputations
Consider orthotic devices
(more info in other chapter)

Front 61

Guillain-Barre - what happens?

Back 61

flaccid paralysis, areflexia, and albuminocytologic dissociation
max weakness in 2-3 weeks
all ages, but peaks in young adults and 5th-8th decade
Believed to be immune mediated disorder. Bacterial and viral infection, surgery, and vaccinations associated with development
Can involve motor fibers only, or sensory as well.
Antibody-mediated demyelination
Sometimes axonal degeneration
Diff Dx: hysteria is most common misdiagnosis, also stroke of brainstem, tick paralysis, porphyria

Front 62

Treatment of Guillain-Barre

Back 62

Treatment: control autoimmune response with plasmapheresis, high-dose IV administration of immunoglobulin

Front 63

Prognosis for Guillain-Barre

Back 63

Prognosis: most people recover, up to 20% can have remaining deficits, after 1 year 67% completely recovered

Front 64

Special implications for PT for Guillain-Barre

Back 64

PT: maintain joint ROM and monitor muscle strength, prevent complications associated with immobilization, skin care, massage to pressure points for circulation, monitor ventilation and O2, ventilation if loss of resp muscle control, when conditions stabilizes initiate movement in pool, gentle stretching and active or active-assistive exercise, watch out for overstretching and overuse, appropriate positioning and splinting, modalities

Front 65

What are entrapment neuropathies from? Examples?

Back 65

Entrapment Neuropathies
From proximity to bony, muscular, and vascular structures – changes in sensation and motor function from compression. Or, traction on a nerve.
Carpal tunnel, sciatica, bell's palsy, tardy ulnar palsy, TOS, Saturday Night Palsy, Morton's neuroma

Front 66

Carpal Tunnel - description and treatment

Back 66

Pain, tingling, numbness, paresthesia, muscular weakness in median nerve distribution
70% in women
associated with occupational activities, any disorder that increases volume of contents of tunnel or decreases volume of tune will create rise in pressure and impingement
Normal pressure 7-8 mm Hg, CTS above 30 mm Hg or up to 90 mm Hg with wrist fully flexed
Treatment: many approaches
mild – conservative management, steroid injection, ergonomic training, wrist splints, not good long-term results/cure
surgical intervention for those without resolution within 2-3 months. Typically release of transverse carpal ligament. 76% experience return of normal 2 point discrimination, up to 70% normal muscle strength. Nerve and tendon gliding after surgery to reduce scarring, adhesions, and fibrotic tissue

Front 67

Sciatica

Back 67

Sciatica:
Most common 40-60 years
herniation of intervertebral disk?
Low back pain, radiating pain into one or both legs
Treatment: medications not so effective, epidural injection of steroids – short-term pain relief, along with NSAIDs
Prog – recovery in unmyelinated and small myelinated fibers in 1 year, but not larger myelinated fibers
PT – visual analog scale – minimal clinically relevant change reported varies

Front 68

Idiopathic Facial Paralysis/Bell's Palsy: incidence, cause, and diagnosis

Back 68

Idiopathic Facial Paralysis/Bell's Palsy:
20; 100,000 each year. Common 15-45 years
Cause: latent herpes virus reactivated? Inflammatory response
Unilateral facial paralysis develops rapidly. Taste, lacrimation and salivation may be affected.
Diagnosis: observe facial asymmetry (make faces!), EMG with degeneration. UMN involvement of facial nerve – can close eye and wrinkle forehead but can't smile voluntarily, with LMN – can't do any.

Front 69

Idiopathic Facial Paralysis/Bell's Palsy: prognosis

Back 69

Prognosis: 94% with incomplete involvement recovery fully, w/i 3 weeks, with complete involvement 75% recover motor function but takes longer. Poorer outcome with age over 60, comorbidities, and symptoms indicating lesion and autonomic involvement.

Front 70

Idiopathic Facial Paralysis/Bell's Palsy: complication

Back 70

Complication - “crocodile tears” - motor synkinesis – motor fibers of facial nerve cross-innervate autonomic branch of greater superficial petrosal nerve, when face contracts tears appear, noted up to 1 year after start of treatment
Some evidence that E-stim should not be used, twice daily facial exercise program

Front 71

Tardy Ulnar Palsy/Retroepicondylar Palsy

Back 71

Common complication of elbow fractures, may occur years after fracture – associated with callus formation or valgus deformity
Or repeated trauma for long periods of time in people with shallow ulnar groove
compression – neuropraxia with demyelination, if unrelieved, progresses to axonotmesis with denervation below elbow
Clawhand deformity with MCP extension and IP flexion of ring and little fingers because of unopposed action of extensor muscle group and paralysis of 3rd and 4th lumbricals.
Atrophy and impaired abduction and adduction, radial deviation with wrist flexion
Mild entrapments managed conservatively, mod-severe require surgery (medial epicondylectomy or transportation of ulnar nerve to anterior aspect of elbow)

Front 72

Thoracic Outlet Syndrome

Back 72

Complex and poorly defined
entrapment on brachial plexus from interscalene triangle, rib, pec minor... vascular symptoms can also occur
Neurogenic (brachial plexus), vascular (subclavian artery and/or vein) or disputed (nonspecific TOS with chronic pain and symptoms of brachial plexus involvement
Initial neurapraxia that can progress to axonotmesis and wallerian degeneration
parasthesias and pain, often nocturnal
provocative tests must include sensory symptoms as well as pulse obliteration
PT – rule out cervical radiculopathy or shoulder dysfunction, evaluate ROM and posture, evaluate strengthen

Front 73

Saturday Night Palsy/Sleep Palsy

Back 73

Saturday Night Palsy/Sleep Palsy
radial nerve compression typically after deep sleep on arm, or in axilla from crutch
Causes segmental demyelination
axilla involvement – elbow extension, flexion and supination weakness
Upper arm – triceps is spared
Both will have paralysis of wrist extensors and extensors of the fingers and thumb
May have sensory involvement
Treatment – cock-up splint to maintain extended position until return of function
Prognosis – if neurapraxia, normal conduction within a few months

Front 74

Morton's Neuroma:

Back 74

Entrapment neuropathy in forefoot, aka interdigital perineural fibroma, most often involving third toe interspace
Average age 45-60, women 5:1 over men, bilateral involvement uncommon
two nerves from medial plantar nerve, and one from lateral plantar nerve pass between plantar aponeurosis
burning, tingling, or sharp lancinating pain in one of the interspaces of the forefoot, may radiate, stop and massage foot, may be apprehensive about stepping
rule out metatarsal stress fractures, metatarsalgia, and metatarsal phalangeal derangement
non-op management is pressure relief, injection of local anesthetic or corticosteroid from dorsal direction, surgical treatment = neural decompression by releasing intermetatarsal ligament or neurectomy
Prognosis – orthoses 45-50% relief, surgical 65-100%

Front 75

What are CNAP and CMAP?

Back 75

Set of changes is called compound nerve action potential, CNAP, from group of muscle fibers is CMAP (muscle)
Characterized by shape, amplitude, and duration
Use parameters to establish normal values, so conditions such as denervation, demyelination, conduction block, and axonal loss can be measured
Bipolar or monopolar (larger area) recording electrode placement

Front 76

Electromyography –
Electromyogram (EMG) –

Back 76

Electromyography – recording action potentials
Electromyogram (EMG) – muscle, record of CMAPs

Front 77

Electroneurography –
Electroneurogram –

Back 77

Electroneurography – nerve action potentials
Electroneurogram – record of nerve action potentials

Front 78

What electrodes are preferred for recording from small areas

Back 78

Needle electrodes – preferred for recording from small areas

Front 79

3 types of electrode –

Back 79

3 types of electrode – monopolar, concentric needle electrode, bipolar

Front 80

Amplifiers –

Back 80

increase signal, “gain” is magnitude of increase, should have High Input Impedance relative to electrodes so it won't draw too much current from tissue (more accurate)
Simple – enhances all voltage, might not show stuff up well biologically
Differential – rejects common signals and enhances different (common mode rejection), usually with bipolar or concentric needles,

Front 81

Filters

Back 81

Filters – remove background noise, “pass” (keep) high or low or everything but 60, and remove others

Front 82

Signal averagers –

Back 82

diminish random signals and amplify ones consistent after the stimulus

Front 83

Integrators –

Back 83

area under waveform or curve, volt-seconds, only for rectified signal

Front 84

What's the difference between analog and digital and what tool might you use?

Back 84

Analog (continuous) to digital (discrete or digitized) convertors
Display and storage – on FM tape recorder, or computer

Front 85

What nerves are most commonly tested in nerve conduction studies?

Back 85

Answer questions about where/what type or lesion
Ulnar, median, sural, peroneal, posterior tibial are most commonly tested

Front 86

Where are electrodes placed in nerve conduction studies?

Back 86

Active electrode on motor point, reference electrode on tendinous insertion, ground electrode between them on bony area

Front 87

Latency

Back 87

Latency – time from stimulus to detection of CMAP

Front 88

How do you calculate conduction velocity? How about in most distal segments?

Back 88

Calculate conduction velocity in meters per second (forearm segment length/L2-L1)
Can't accurately determine distal conduction velocity, compare to normal distal latencies

Front 89

Amplitude of CMAP proportional to

Back 89

Amplitude of CMAP proportional to number of muscle fibers stimulated by nerve

Front 90

What's measured in sensory nerve conduction studies?

Back 90

Short-duration shocks stimulate all sensory fibers
Summated effect monitored with needles or electrodes as compound sensory nerve action potential (CSNAP)
Biphasic or triphasic
CSNAP is smaller amplitude than CMAP

Abnormalities in sensory nerves may be first indication of pathology

Front 91

In example with ulnar nerve, Sensor Latency =

Back 91

In example with ulnar nerve, Sensor Latency = time between stimulus and peak of negative phase of CSNAP (can't tell exactly when potential begins)

Front 92

Principles of Nerve Conduction Testing

Back 92

Test sensory and motor
Test several segments of suspected nerve
Test contralateral side as well
Probably check out upper and lower extremity
Do tests at appropriate time in context of suspected disorder

Front 93

Neuropraxia – again (from big electrophysiology reading)

Back 93

Neuropraxia – most mild level, localized conduction block, axon not interrupted or degenerating, too much compression/stretching/inflammation, temporary

Front 94

Axonotmesis – again (from big electrophysiology reading)

Back 94

Axonotmesis – type II lesion, disruption in axon continuity without significant damage to connective tissue layers, degeneration of distal axonal segments, early NCV on distal segments may not show changes because they haven't degenerated yet

Front 95

Neurotmesis – again (from big electrophysiology reading)

Back 95

Neurotmesis – type III, IV, or V lesion, axonal disruption and damage to 1 or more CT layers,

Front 96

Interpretation of NCV data depends on:

Back 96

Interpretation of NCV data depends on: type of lesion, partial or complete, time after lesion

Front 97

UE nerves tend to be ___m/s faster than LE
How about proximal vs. distal?

Back 97

UE nerves tend to be 7-10 m/s faster than LE
Proximal generally faster than distal

Front 98

How does age affect NCV?

Back 98

Age – infants and youngins may be 50% slower than adult, 60s-70s ~ 10 m/s slower than normal adult

Front 99

F-wave testing

Back 99

2nd wave from 2nd set of action potentials
Smaller amplitude – smaller population of motor units
Purpose – examine conduction in proximal nerve segments, when normal not possible, e.g. with nerve compression from TOS

Front 100

Axon reflex –

Back 100

U-turn at axon branch, but not real reflex, between M and F-wave

Front 101

H-reflex –

Back 101

H-wave, Hoffman's, stimulation of Ia muscle spindle afferents, activates smallest motor neurons and motor units first, same pathways as stretch reflex (electrically excited monosynaptic reflex)

Front 102

Blink reflex test –

Back 102

Blink reflex test – integrity of trigeminal and facial nerves, R1 and R2 times, facial neuropathy (e.g. Bell's palsy) – diminished ipsilateral reflex and normal contralateral

Front 103

What test is conducted to measure function of NMJ?

Back 103

Repetitive nerve stimulation test (RNS), or Jolly test, for function of NMJ, decreased voltage of AP with myasthenia gravis

Front 104

Why is EMG done, and what is measured?

Back 104

To answer questions about innervation and lesions
Active, reference, and ground
Insertional activity, activity at rest, activity upon minimal recruitment and activation, and activity during max activation

Front 105

Unnatural activity at rest during EMG

Back 105

Unnatural activity at rest – fibrilation potentials, positive sharp waves, wave goes down first
Myotonic discharges – spontaneous repetitive activation
complex repetitive discharges/bizarre high-frequency discharges, machine-gun fire
myokymic discharges, even in sleep, can be blocked, found in MS

Front 106

Normal EMG during volitional activity

Back 106

Amplitude: 200 mV -3 mV
Duration: 5-15 msec
Rise time: 100-200 msec
Frequency: 5-15 per sec
volitional: 1st motor units have lowest threshold, Type I, small alpha neurons

Front 107

EMG findings with myopathic disease

Back 107

Myopathic disease – small-amplitude motor unit potentials of short duration
Vigorous normal contraction – interference pattern, generated with lower effort in people with myopathic disease
Polyphasic potentials are abnormal

Front 108

Principles of EMG

Back 108

examine above and below suspected pathology
m innervated by other nerves in same limb
Sample EMG of full cross-section of muscle tested
contralateral limb or upper and lower may be indicated
Time in context of suspected pathology

Front 109

What type of EMG and NCV data would you get for myopathic condition?

Back 109

Myopathic if abnormal EMG w/ normal NCV, (Or, could be neuropathic condition with partial damage)
May have mild/mod neuro problems w/o abnormal EMG

Front 110

Contraction depends on stimulus ___ and ___

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Contraction depends on stimulus amplitude and duration (high-amp short to low-amp long... product of amp and duration is equal at any point, stimulus below curve not sufficient, above activates more)

Front 111

Lvl of stimulus for denervated muscle

types of tests

Back 111

Denervated muscle – requires more stimulation, no response at short duration

Strength-duration testing: to determine lvl of innervation, rare today
Reaction of degeneration (R.D.) test – assess innervation, smooth response or not, rare today
Galvanic twitch-tetanus ratio test – DC, amplitude normal:tetanus response, rare today

Front 112

Contraindications/precautions for electrophysiologic testing

Back 112

abnormal blood clotting factors
Extreme Swelling
Dermatitis
Uncooperative patient
Recent MI
blood-transmittable disease
immune-suppressed condition
Central-going lines
pacemakers
hypersensitivity to stimulation (wounds, etc)

Front 113

Case studies from reading: Carpal tunnel –

Back 113

Carpal tunnel – prolonged distal sensory latencies, Conduction velocities WNL, as were motor/sensory response amplitudes, no spontaneous activity, consistent with demyelinating process

Front 114

Case studies from reading: Case 2 – absent H-reflexes, changed amp and conduction values,

Back 114

Case 2 – absent H-reflexes, changed amp and conduction values, indicate mixed axonal and demyelinating process, more distal, LE>UE, peripheral neuropathy involving sensory/motor

Front 115

Case studies from reading: Case 3 – weakness/numbness in right foot, MMT – 5/5, 1/5 peroneal, 0/5 Anterior Tib and EDL, NCV – deep portion of peroneus is absent, EMG – motor recruitment in deep peroneal is absent, diminished superficial peroneal.

Back 115

Case 3 – weakness/numbness in right foot, MMT – 5/5, 1/5 peroneal, 0/5 Anterior Tib and EDL, NCV – deep portion of peroneus is absent, EMG – motor recruitment in deep peroneal is absent, diminished superficial peroneal. Complete lesion of deep, severe involvement of superficial

Front 116

Case studies from reading: Case 4 – hx of low back and right leg pain, leg pain worse with flexion, extends into foot, strong but painful, Sensory superficial peroneal and sural missing H-reflex on right, spontaneous activity in right S1 myotome, and increased polyphasic motor units,

Back 116

Case 4 – hx of low back and right leg pain, leg pain worse with flexion, extends into foot, strong but painful, Sensory superficial peroneal and sural missing H-reflex on right, spontaneous activity in right S1 myotome, and increased polyphasic motor units, lesion around S1 nerve root. NCV normal, sensory normal, sharp waves and fibrillation indicate degeneration,

Front 117

Motor Nerve Conduction Velocity (MNCV)

Back 117

The measurement of the speed of conduction of an impulse along either a motor or sensory peripheral nerve
Dr. C's slides
Artificial depolarization of a motor axon
Single pulse square wave
Record the resulting muscle twitch
Compound Motor Action Potential (CMAP)

Front 118

Aspects of Compound Motor Action Potential (CMAP)
- what do you see on graph

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Compound Motor Action Potential (CMAP)
Onset = onset of excitation in the innervation zone
Amplitude = number of motor units stimulated
Duration = territorial size of the stimulated motor units

Front 119

Each latency is composed of:

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Each latency is composed of:
Axonal conduction time
Neuromuscular junction
Muscle fiber conduction time
Two stimulation points are used
NCV = distance between stimulation sites / (proximal latency – distal latency)
Example: 180mm / 3.5msec = 51.4 m/sec

Front 120

Common Sites for Upper Extremity MNCV

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Median Nerve (AbPB)
Wrist
Elbow
Axilla
Erb’s Point
Ulnar Nerve (AbDM)
Wrist
Elbow
Axilla
Erb’s Point
Radial Nerve (EI)
Forearm
Mid-Arm
Axilla
Erb’s Point

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Common Sites for Lower Extremity MNCV

Back 121

Deep Peroneal Nerve (EDB)
Ankle
Fibular Head
Popliteal Fossa
Sciatic and Tibial Nerve (AbH)
Ankle
Popliteal Fossa
Buttocks
Femoral Nerve (VMO)
Mid-Thigh
Femoral Triangle

Front 122

Factors Influencing Motor Nerve Conduction Velocity

Back 122

Age
Decreased < 5 & > 60
Temperature
Increased 2 m/s @ 1o C
Gender
Females > Males
Stimulus Intensity
Use supramaximal stimulus
Limb Dominance
Dominant > Non-Dominant
Physical Activity
Increased in LE of distance runners
Increased in UE of weight lifters
Disease

Front 123

Sensory Nerve Conduction Velocity (SNCV)

Back 123

The measurement of the speed of a sensor nerve action potential
Recording of the nerve action potential (NAP)
Single-point stimulation
SNCV = d / t

Front 124

Common SNCV Stimulation Sites

Back 124

Median Nerve
1st or 2nd finger to wrist
Ulnar Nerve
5th finger to wrist
Radial Nerve
Thumb to mid-forearm
Sural Nerve
Lat Mal. to posterior calf
Superficial Peroneal Nerve
Dorsum of foot to fibular head
Saphenous Nerve
Ant-Med leg to Ant-Med knee

Front 125

F-wave

Back 125

Measurement of the result of an antidromic activation of the anterior horn cell
(signal travels both directions, when antidromic activity gets to cell body it stimulates another action potential, which travels orthodromically)
Normal Values
UE 25 – 31 msec
LE 48 – 55 msec
Abnormal Values
> 1.5 msec difference between extremities
> 2.5 msec from the predicted value
Diagnostic Use
Indicate conduction in the proximal nerve segments (eg. Nerve roots)

Front 126

H-reflex

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Measurement of the conduction time over the monosynaptic reflex arc
(sensory nerve stimulated, follows reflex loop)
Normal Values
UE 20 – 25 msec
LE 30 – 35 msec
Abnormal Values
> 1 msec difference between extremities
Diagnostic Uses
Indicate conduction in the proximal nerve segments (eg. Nerve roots)
Integrity of reflex loop

Front 127

Repetitive stimulation test

Back 127

Repetitive stimulation of a motor nerve to determine the rate of amplitude change
Normal is < 10% decrease over 5 twitches
Diagnostic Uses
Detection of neuromuscular junction problems
Myasthenia Gravis

Front 128

NCV findings with myopathy

Back 128

Myopathy
Normal MNCV & SNCV
Decreased CMAP amplitude

Front 129

NCV findings with Anterior horn cell disease

Back 129

Anterior Horn Cell Disease
Normal MNCV & SNCV
Increased CMAP amplitude

Front 130

NCV findings with neuromuscular junction disorders

Back 130

Neuromuscular Junction Disorders
Normal MNCV & SNCV
Positive Repetitive Stimulation test

Front 131

NCV Findings in Neuromuscular Pathology: Neuropathy

Back 131

Neuropathy
Demyelinating
Systemic evidence of slow NCV
Sensory > Motor
Axonal
Segmental slowing of MNCV in the area of the injury
Radiculopathies have abnormal F-Wave and H-Reflex values
SNCV is generally normal

Front 132

NCV Results in Common Peripheral Neuropathies

Back 132

Carpal Tunnel
Increased Median motor distal latency at wrist
Decreased Median SNCV
“Saturday Night Palsy”
Decreased Radial MNCV between axilla & forearm
L5, S1 Spondylolethesis
Abnormal Tibial F-Wave and H-Reflex

Front 133

Diagnostic Electromyography

Back 133

Observation of voluntary individual motor unit potentials as an indication of Neuromuscular Disease
Monopolar needle
Coaxial (Concentric) needle
Double Coaxial (Bipolar) needle
Single Fiber needle

Front 134

Equipment Components of Diagnostic EMG

Back 134

Electrodes
Amplifier
Speakers
Computer
-Analysis
-Storage

The amplifier is the most important part because it must faithfully reproduce the electrical potentials being measured
Differential Input
High Common Mode Rejection Ratio
Uniform amplification over a large frequency range
> 10,000 times
2 – 10,000 Hz
Low noise, high impedance

Front 135

Composition of the Motor Unit Potential

Back 135

Amplitude
Number of muscle fibers in the motor unit
Duration
Temporal dispersion of the muscle fibers in the motor unit
Phases
Organization of the muscle fibers within the motor unit

Front 136

Components of a Diagnostic Electromyographic Examination

Back 136

Insertion Activity
At Rest
Minimal Contraction
Maximal Contraction

Front 137

Normal Electromyogram: insertion activity

Back 137

Insertion Activity
Loud “burst” of activity
Stops immediately (< 300msec)
Caused by the needle entering the muscle membrane
Mechanical stimulation
Muscle fibers injured and release ions

Front 138

Normal Electromyogram: at rest

Back 138

At Rest
Electrical silence
Flat baseline

Front 139

Normal Electromyogram:Minimal Contraction (individual Motor Units)

Back 139

Minimal Contraction (individual Motor Units)
Waveform Shape
Monophasic, Diphasic (most common), or Triphasic
Motor Unit Amplitude
100 – 1000 uV
Dependent upon the type of electrode used
Motor Unit Duration
3 – 10 msec
Dependent upon the type of electrode used

Front 140

Normal Electromyogram: Maximal Contraction (multiple motor units)

Back 140

Maximal Contraction (multiple motor units)
Orderly recruitment (Henneman’s size principle)
Small diameter axons first
Increase firing frequency before recruitment of larger axons
Interference Pattern
Ability to recruit large number of motor units
Amplitude
3000 – 7000 uV

Front 141

The Abnormal Electromyogram: Insertion Activity

Back 141

Insertion Activity
Increased
Muscle irritability
Decreased
Global loss of motor units or muscle fibers

Front 142

The Abnormal Electromyogram: At rest

Back 142

At Rest
Spontaneous Activity
Fibrillation potentials
Low amplitude
Short duration
Positive Sharp Waves
Low amplitude
Fasciculations
Normal amplitude and duration
Indication of possible denervation or Anterior Horn Cell Disease

Mytonic Discharges
“Dive Bomber”
Variable amplitude and frequency
Indication of Myotonia
Bizzare High Frequency Discharges (“Myotonic-Like”)
Variable frequency only
Indication of a disease similar to Myotonia

Front 143

The Abnormal Electromyogram: Minimal Contraction (individual Motor Units)

Back 143

Minimal Contraction (individual Motor Units)
Waveform Shape
> 15% Polyphasic (> 3 phases)motor units
Motor Unit Amplitude
Decreased = Loss of muscle fibers in motor unit
Increased = Gain of muscle fibers in motor unit (“sprouting”)
“Giant” potentials
Motor Unit Duration
Decreased = Loss of muscle fibers
Increased = Gain of muscle fibers

Front 144

The Abnormal Electromyogram: Maximal Contraction (multiple motor units)

Back 144

Maximal Contraction (multiple motor units)
Incomplete Interference Pattern
Loss of motor units
Pain
Non-compliance
Early or reversed order of recruitment
Alteration in amplitude of Interference Pattern
Decreased = Loss of muscle fibers in motor units
Increased = Gain of muscle fibers in motor units (taking over for loss of innervation)

Front 145

Abnormal EMG Signals

Back 145

Fibrillation Potentials

Positive Sharp Waves

Endplate Potentials

Fasciculations

Front 146

EMG Findings in Neuromuscular Disease: Myopathy

Back 146

Myopathy
Increased or decreased insertion
Increased incidence of polyphasic potentials
Decreased motor unit duration and amplitude
Decreased Interference Pattern if severe
Early recruitment
Myotonic or Bizarre High Frequency discharges*
Occasionally Spontaneous activity (fibrillations, positive sharp waves)

Front 147

EMG Findings in Neuromuscular Disease: Anterior Horn Cell Disease

Back 147

Anterior Horn Cell Disease
Increased insertion activity
Occasionally Spontaneous activity
Fasciculations
Fibrillations, positive sharp waves
Increased incidence of polyphasic potentials
Increase motor unit amplitude and duration
Also Interference Pattern
Decreased Interference Pattern

Front 148

EMG Findings in Neuromuscular Disease: Neuromuscular Junction Disorders

Back 148

Neuromuscular Junction Disorders
Normal EMG exam
No spontaneous activity
Occasionally decreased motor unit amplitude and duration

Front 149

EMG Findings in Neuromuscular Disease: Demyelinating Neuropathy

Back 149

Demyelinating Neuropathy
Essentially normal if no axonal neuropathy

Front 150

EMG Findings in Neuromuscular Disease: Axonal Neuropathy

Back 150

Axonal Neuropathy
Increased insertion activity
Spontaneous
Fibrillations, positive sharp waves
Increased incidence of polyphasic potentials
Increased motor unit duration
Decreased motor unit amplitude
Decreased Interference pattern

Front 151

Case Study 1
42 y/o female
Referred for evaluation of back & leg pain
Complains that legs feels weak
Past Medical History
Relatively sedentary
Considers herself to be in otherwise good health
Medications
Prescription pain killers
History of Symptoms:
5 year history of episodic LBP and R leg pain
Usually resolves with:
Rest, medication, and home exercises
Re-injured 3 months ago while lifting at work
Immediate minor LBP, but did not limit her mobility
Severe back and leg pain with loss of motion the next morning
Observation:
Ambulates slowly with trunk held rigidly and slightly shifted to Left
Physical Findings:
Radiating pain down leg to foot and ankle
Pain worse with spinal flexion
Pain increases with coughing or sneezing
Decreased sensation over lateral foot
Denies loss of bowel or bladder control
ROM:
Trunk motion limited in all planes
Pain with flexion & R rotation
Muscle Strength:
Both UE 5/5
Left LE 5/5
Right LE 4/5
DTRs:
Intact & symmetrical in Quads, L Gastroc/Soleus
Absent R Gastroc/Soleus
Positive SLR at 30o
Pain with piriformis test
Tenderness over lumbar paraspinals and R buttocks

Back 151

Axonal neuropathy affecting tibial nerve
Problem in nerve root - H-reflex longer

Front 152

Case Study 2
22 y/o female
Complaint of inability to “let go” of objects in her hand, but no difficulty walking or running
Physical Findings:
AROM and PROM WNL for all extremities
No muscle stiffness
MMT is normal for all extremities
No loss of sensation
DTRs brisk and symmetrical
NCV: median and ulnar slower on right
EMG Findings:
-R deltoid- Normal motor units
Decreased duration & amplitude motor units
Decreased interference pattern
- R biceps - Normal motor units
Decreased duration & amplitude motor units
Decreased interference pattern
Myotonic discharges
- R Abd Pol Brev
Normal motor units
Decreased interference pattern
- R abd dig min
Normal motor units
Decreased duration & amplitude motor units
Decreased interference pattern
Myotonic discharges

Back 152

Myopathy - myotonic issues, different nerves and roots affected, no set pattern

Front 153

Case Study 3
28 y/o female
3 month history of episodic:
Facial weakness and paralysis
Dysphagia
Generalized fatigue
Physical Findings:
Ptosis of R eye
AROM and PROM WNL
Muscle strength is generally 4+/5 to 5/5
Appears to fatigue rapidly
Abd pol brev - Postitive Rep Stim
EMG findings - WNL

Back 153

Neuromuscular Transmission Disease - Myasthenia Gravis

Front 154

Case Study 4
17 y/o female
Complains of LBP
Gymnast
Physical Findings:
Radiating pain down R LE to heel and lateral foot
Normal DTR at knee
Decreased DTR at R ankle
MMT of R EH is 4-/5
EMG Findings:
Normal except for
R Abd Hallucis - Increased insertion activity
Fibrillation, positive sharp wave potentials
Normal motor units
R Gastroc -
Increased insertion activity
Fibrillation, positive sharp wave potentials
Normal motor units
Increased incidence of polyphasic potentials
R Glut max -
Increased insertion activity
Fibrillation, positive sharp wave potentials
Normal motor units
Increased incidence of polyphasic potentials
Decreased interference pattern
R paraspinals -
Increased insertion activity
Fibrillation, positive sharp wave potentials
Normal motor units
Increased incidence of polyphasic potentials
Decreased interference pattern
Decreased interference pattern
Increased incidence of polyphasic potentials
Decreased interference pattern

Back 154

Root issue - L5, S1 Axonal neuropathy. Ventral and dorsal rami involved - lesion in root, can't test that proximally with NCV
Not anterior horn cell issue because it's only in 1 leg, would have more flaccid paralysis and not radiating pain

Front 155

Case Study 5
18 y/o
Complains of numbness and weakness in R UE
Sustained hyper-extension of R shoulder while playing football
Physical Findings:
PROM is WNL
MMT of R UE is between 3+/5 and 4-/5
MMT of L UE is 5/5
DTRs decreased on R UE
Slower Median NCV on left, including at shoulder
slightly slower on ulnar
EMG Findings:
R AbDM and Ab Pol Brev
Increase insertion activity
Fibrillation and positive sharp wave potentials
Normal motor units
Increased incidence of polyphasic potentials
Decreased interference pattern
R 1st DI
Fibrillation and positive sharp wave potentials
Normal motor units
Decreased interference pattern
R FCR
Increased insertion activity
Fibrillation potentials
Normal motor units
Increased incidence of polyphasic potentials
Decreased interference pattern
R Triceps -
Increase insertion activity
Fibrillation potentials
Normal motor units
Decreased interference pattern
R biceps, R Serratus Ant, R paraspinals, L muscles:
-WNL

Back 155

Neuropathy - axonal
Plexopathy - ulnar, median, and radial nerves involved

Front 156

Compare and contrast ALS and Poliomyelitis

Back 156

Both Myelopathy - affect Anterior horn motor cells (sensory not involved)
LMN, flaccid paralysis, hyporeflexive
ALS - distal to proximal progression, sometimes cognitive, 40s-50s, cause?, affects speech, fasiculations (more than polio), could be spastic, slowly progressive, respiratory
Polio - viral, no DTR, LE>UE, flaccid paralysis, often in childhood, mostly eradicated, not cognitive, acute onset

Front 157

What causes post-polio syndrome?

Back 157

1. virus never goes away, wakes up
2. not a syndrome, ppl w/ weakness less functional as they age
3. Overused remaining motor units, killed them
A MMT of 3/5 means about 50% motor units lost, others have to contract more often

Front 158

Compare and contrast Thoracic Outlet compressing the radial nerve and a C7 radiculopathy

Back 158

Radial nerve: Thumb side of palm sensation, elbow and wrist extensors, rounded shoulders
C7 Radiculopathy: Myotome - Triceps, Dermatomes - mid hand sensation, radial, median and ulnar, forward head, rounded shoulders

Both: motor and sensory, triceps weakness, pain, tingling, burning, sensory before motor, postural changes (forward head)

Front 159

Compare and contrast Tarsal Tunnel syndrome and Lumbar Spinal Stenosis

Back 159

TTS - posterior tibial nerve, from entrapment, also artery, nerve, FDL, FHL, foot numbness, pain, weakness

Stenosis - symptoms could be in single nerve or multiple, radicular pain involving lumbar/sacral roots, LE, could radiate to foot (but doesn't start there), could be bilateral, +SLR, back pain?, more debilitating

Both: compression, nerve symptoms!

Front 160

Describe the findings from a clinical examination (history and physical) for each of the following disorders: Myasthenia Gravis

Back 160

Myasthenia Gravis
History - woman in 20-30s? Men have later onset
Weakness w/ repetition of activity, fluctuates through day and across time, (not much of a pattern, ok sometimes), no other neuro signs, facial muscles often affected first (eyelid movement, chewing, talking). Respiratory trouble, fatigue quickly, not easy to diagnose (by elimination), puffy face from steroids
Bilateral, generalized weakness

Front 161

Describe the findings from a clinical examination (history and physical) for each of the following disorders: Muscular Dystrophy

Back 161

MD
Family history, slow or rapid onset, weakness, wasting, increased lumbar lordosis, reflexes decreased because of muscle pseudohypertrophy (esp. calves and forearms), contractures, may be myotonic

Front 162

Describe the findings from a clinical examination (history and physical) for each of the following disorders: Diabetic Neuropathy

Back 162

Diabetic Neuropathy
History of Diabetes
Distal to proximal ("stocking-glove"), decreased sensation, or hypersensitive (more in early diagnosis), motor involved later, insensate neuropathy/parasthesia, 5.07 g - loss of protective sensation
May involve ANS - orthostatic hypotension