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Neuro SKS > Motor disfunction/reflexes > Flashcards

Motor disfunction/reflexes Flashcards

1
Q

Deep tendon reflexes

A

aka stretch, myotatic
Spindle -> gray matter -> alpha (inhibits antag)
Wide normal range -> assym, symptoms
Hypo: peripheral sensory, gray or motor (lower)
- trace = flicker
- “0” = no movement even with distraction
Hyper: upper motor neuron damage
- clonus - stretch -> rhythmic beats
- pathologic spread (nearby muscles)

Jaw jerk: CNV
Biceps: C5,6
Triceps: C6,7
Brachiorad: C5-7
Finger flex: C6-8 (musc-cut)
Patella: L2-4
Achilles: S1,2
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2
Q

Superficial reflexes

A

Scrape skin -> nearby muscles
Sensory -> spinal -> brain -> spinal -> motor
- assesses spinal cord damage

Abdominal: umbilicus towards quadrant (T7-12)
- abnormal if obese, mult preg, old, etc
Cremaster: medial thigh -> elevate testes (S1)
Plantar: scrape -> down-going toe (S1-2)
 - often + withdrawal
Anal wink: S2-4
Corneal, nose tickle: V5 -> V7
Gag: V9 -> V10
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3
Q

Pathological reflexes

A

Babinski = superficial scrape -> up-going toe + fanning

- normally abolished by 6 mo

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4
Q

Reflex pathology

A

Muscle or NMJ: dec stretch, proportional
Peripheral nerve: dec stretch, more than proportional (afferent limb)
Nerve root: dec stretch, proportional, rare change to superficial (overlap)
Spine/brain stem:
- stretch hypo at, hyper below
- acute initial hypo/shock/diaschisis (degree and time proportional to damage) -> extreme hyper
- superficial hypo below/at, normal below
Cerebellar: normal or hypo, pendular (poorly checked)
Basal ganglia: no effect, may have primitive
Cortex: hyper stretch, dep or absent superficial, may have Babinski
- bilateral -> primitive, emotional released from inhibition (pseudobulbar)

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5
Q

Primitive reflexes

A

Suppressed unless b/l cortical disfunction

Feeding (rooting, suck, bite)
Grasp
Glabellar - tap on forehead -> blink
Oculoceph, nuccoceph

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6
Q

Visceral reflexes

A 
Pupillary - CN 2 -> 3
Oculo-cardiac - CN 5 -> 10
 - eyeball pressure or traction -> brady
Baroreceptor, carotid sinus - CN 9 -> 10/SNS
Bulbocavernosus - S2-4
Rectal (internal sphincter) - S2-4
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7
Q

Overview of upper motor neuron disease

A

Distal weakness
Inc tone (“clasp knife”), reflexes (-> clonus)
No atrophy
+ Babinski (LE), Hoffmans (UE)

+ LMN disease = “motor neuron disease” - ex ALS

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8
Q

Overview of lower motor neuron disease

A

Paralysis, variable
Dec tone, DTR
Significant atrophy
Fasciculations (discharge of motor unit, visible)

+ UMN disease = “motor neuron disease” - ex ALS

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9
Q

Overview of NMJ disease

A

Normal function - AP -> quantum vesicle release of Ach -> end-plate potential -> spread (4 m/s) -> Ca entry -> term by end-plate Ach-esterase

Variable strength
 - MS - decreases with repetitive
 - Lambert-Eaton - increases with repetitive
Normal tone and reflexes, no atrophy
Often improves with cold (ice pack test)
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10
Q

Overview of muscular disease

A 
Dec strength (proximal, symmetrical)
 variable atrophy (pseudohypertrophy with storage dis)
Normal tone and reflexes
Aching, high CK
EMG -> small, brief polyphasic
Biopsy -> special stain, genetic

Destructive -> progressive weakness, wasting
- inflammatory - polymyositis, dermatomyositis (+ rash)
- metabolic - ex thyroid, statins
- dystrophy = genetic, r/o metabolic and inflamm, progressive, not curable
- Duchenne’s, Becker’s, myotonic, LGMD
- inclusion body - begins distal!
Functional - channelopathy
- myotonic, paralysis

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11
Q

Overview of peripheral nerve disease

A

Often includes sensory (paresthesias)

  • Root/radiculopathy - rarely sensory dt overlap
  • peripheral - specific sensory and motor distribution
  • C5 -> shoulder abduct and ext rotators
  • C6 -> elbow flexors
  • C7 -> wrist and finger extension
  • C8-T1 -> intrinsic hand
  • L3-4 -> knee extension
  • L5 -> great toe, ankle extension
  • S1 -> plantar flexion

Positive - pain, dysesthesia
Negative - loss of sensation, weakness, areflexia
Irritant - fasciculations, paresthesias

Mononeuropathy - Tinel’s sign - trauma, compression
- multiplex - multiple, assymetrical - vasculitis
Polyneuropathy - stocking -> glove - metabolic
- axon - DM, EtOH
- myelin - GBS, B12
Radiculopathy - regional, worsened by provocative

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12
Q

Nerve conduction studies

A

Standard NCS - stimulate peripheral nerve -> outside of muscle
- measure latency (prolonged demyelinating)
-> compound muscle potential
(amplitude dt loss of axonal or NMJ conduction)

Electromyography - similar but needle inside muscle
- spontaneous activity (damage to nerve)
- size of motor unit potential
(inc if axonal injury due to collateral sprouting)

Compound nerve action potential - measure downstream on nerve
- only measures large, myelinated (dominate early)

MS - repeat stimulation -> decreasing muscle potentials

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13
Q

Struture of peripheral nerves

A

Connective tissue - endoneur, perineurium, epineurium
- nerve roots less protected from traction, trauma
Vessels - high metabolic demand, little reserve - collaterals usu sufficient but ischemia poorly tolerated
Myelination - Schwann -> inc velocity
- large myelinated - 40-70 m/s - most sensory (somatic, spindle, Golgi)
- intermediate - touch, proprioception
- lightly myelinated - sharp pain, autonomic pregang
- small, unmyelinated - 1 m/s - aching, burning pain, temp, SNS postg
Microtubules - necessary for transport of mitochondria, enzymes
- orthodromic (to periphery), antidromic (to nerve)
- trophic factors both directions (ex atrophy with LMN damage)
Innervation - nervi nervorum - most SNS -> pain with injury

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14
Q

Motor unit physiology

A

Nerve fiber -> multiple motor fibers (motor unit)

  • impulse -> motor unit potential (amplitude = #, duration = range of latency)
  • effort -> inc # of units, inc firing rate
  • uneven LMN (neuron or axon) damage -> high firing rates of remaining
  • UMN damage -> low firing rates (sim to low effort)

Fasciculations - entire motor unit (visible) dt irritation or damage of nerve -> spontaneous impulses
Fibrillations - hyperirritable motor fibers dt denervation (days-weeks)
- detect only through needle EMG

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15
Q

ALS

A

amyotrophic lateral sclerosis, aka “motor neuron disease”

LMN degeneration (anterior horn) -> fascic, atrophy
CN nuclei degeneration -> tonge, face, pharynx, palate
- eye movements spared
UMN degeneration (corticobulb, corticospinal) -> spastic, hyperreflex

40-60 yo
Assymetric -months> b/l -> 3-5 y (resp failure)
Toxins, low chronic inflammation
Genetic -> lack of antioxidants
Riluzole slightly delays progression
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16
Q

“Motor neuron disease”

A

Both upper and lower

Most common ALS
Variations: (all progress to ALS)
- primary lateral sclerosis (UMN -> both -> 10 yrs)
- progressive muscular atropy (LMN only -> both)
- progressive bulbar palsy (cranial only -> general)
Rare inherited ALS forms

LMN only but degenerative

  • Werdnig-Hoffman - infant
  • Kugelberg-Welander - children, young adults
17
Q

Mononeuropathy

A

Trauma (acute) or compression, entrapment (chronic)
Higher risk if underlying polyneuropathy
Negative (loss of sensation, weakness, atrophy), positive (pain, paresth)
- Tinel’s sign - tap on site -> electrical paresthesia

Carpal tunnel - median nerve
- congenitally small tunnel, thick ligaments, inflammation
- numb, paresthesias in radial digits, thenar weakness/atrophy
- pain radiates past median nerve, unpredictable
Ulnar - elbow joint problems, flexion pressure
-> intrinsic atrophy, sensory loss
- bicycle riding -> wrist (minimal sensory)
Radial - humerus, lateral elbow -> extensor weakness, dorsal sensory
- wrist pressure (handcuffs) -> superficial -> paresth, numb dorsal
- supinator -> deep branch -> weak extensors, spares brachiorad
Lateral femoral cutaneous - inguinal (weight, preg, belt) -> lat thigh
Fibular - fibular head -> numb dorsal, weak dorsiflex, eversion
Tibial - medial ankle trauma, RA
Interdigital neuromas - between metatarsal heads

18
Q

Thoracic outlet syndrome

A

Mechanical compression in upper thorax
- ex cervical rib, scalene, connective tissue

Vascular - subclavian or axillary in certain arm positions
- shoulder dep, arm abd and ext rotated, neck rotation and extension
- ischemic sx, no pulse
Neurogenic - lower brachial plexus -> ulnar nerve, ulnar side of elbow

19
Q

Radiculopathy

A

Damage to nerve root
Herniation (young)
Degenerative (old) -> thickening -> narrowed foramina
- most common lower lumbar, mid-lower cervical

Sx follow nerve distribution - weak, dec reflex, less sensory (overlap)
Distal sx + spinal pain - burning, aching
- worsened by stretch (straight leg raise, lat neck bend) or compression (arch back, compress neck) or cough/strain

20
Q

Polyneuropathy clinical

A

Affects longest nerves first -> stocking -> glove
- usu symmetrical
- numb, paresthesia
- sometimes proprioception/vibration (-> gait, Romberg)
- can have weakness, loss of reflexes
- small fibers - may lose pain, temp
Axon (dec transmission) or myelin (dec velocity) or both

May be idiopathic (25-40%, older, slowly progressing)
NCS/EMG routine
CBC, ESR, glu, A1c, TSH, serum protein electrophoresis
Acute - ? GBS, acute metabolic or toxic
Consider RPR, Lyme, HIV, ANA, rheumatoid, anti-neutrophil, heavy metals, porphyrins, sural or skin biopsy (young)
f/u months, sooner if rapid

Tx underlying cause, foot care, stability (cane)

21
Q

Charcot-Marie-Tooth

A

aka hereditary motor sensory neuropathy (HMSN)

Genetic - multiple genes/defects -> genetic testing
- Type 1 - autosomal dom -> demyelin (inc latency on NCS)
- Type 2 - axonal degen
Begins in childhood -> high arches and hammer toes dt weakness
Slowly progressing

Other familial neuropathies - may not have clear pattern
- NCS/EMG -> genetic

22
Q

Metabolic polyneuropathy

A

Most common = DM -> axons and myelin

EtOH, B12 deficiency -> myelin
Pyridoxine, porphyria, sprue
Heavy metals, solvents, industrial (carbon disulfide)
Meds - chemo, seizure, ARV’s
Syphilis, Lyme, HIV
Leprosy -> patchy
Abnormal proteins - amyloid, monoclonal gammopathy

23
Q

Immune polyneuropathy

A

Acute immune demyelinating polyradiculoneuropathy
= Guillain-Barre syndrome (aka AIDP)

Antibodies vs myelin
- post viral/diarrheal - Campylobacter
Rapid weakness -> respiratory paralysis, autonomic
Early loss of reflexes (muscle stretch), ascending or descending, +/- sensory
CSF - high protein, no change cells (WBC)
Most recover, shorten with IVIg, plasmapheresis

Chronic (CIDP) - relapsing or progressing AIDP

  • > assymetric weak, sensory, areflexia
  • long-term immunosuppression
24
Q

Mononeuritis multiplex

A

Multiple patchy mononeuropathies

Diabetes - poorly controlled, systemic sx (weight loss, fatigue)
-> lumbar plexus, rarely brachial
-> weak quad, adductors, iliopsoas absent patellar reflex (amyotrophy)
- control DM, IVIg, pulse steroids
Vasculitis
- SLE, polyarteritis nodosa, Sjorgren’s, Wegner’s
- infectious - Lyme (syphilis, HIV)
Idiopathic - rare -> middle age men, brachial plexus
- painful onset -> atrophy, weakness -> slow improvement
- “neuralgic amyotrophy” aka Parsonage-Turner, “idiopathic brachial neuralgia”
- IVIg, pulse steroids

25
Q

Myasthenia gravis

A

Autoimmune vs nicotinic Ach receptors (end plate)
-> more Ach needed = dec safety factor (excess Ach above necessary)
- not all impulses followed by contraction -> fewer fibers involved per unit
Young adult women, middle aged men (thymic tumors cross-react)

Ocular (ptosis, diplopia) -> bulbar (pharynx, palate) -> generalized -> diaphragm, autonomic instability
- will generalize in first 2 years or not at all
-> weakness -> neurogenic atrophy (specific type II fibers)
Sustained, repetitive -> depletes presynaptic Ach -> worsens
- nerve stimulation -> decreasing compound muscle potential

Tx: immune suppression (IVIg, plasma exchange, meds/steroids)
Ach-esterase inhibitors (pyridostigmine)
thymectomy

26
Q

Myasthenic syndrome

A

aka Lambert-Eaton

Ca channel defect in pre-synaptic -> dec quanta of Ach released
Improves with repetitive (facilitation)

Paraneoplastic - esp bronchogenic small-cell
Tx: Ach releasing - 4-aminopyridine

27
Q

Meds/toxin vs NMJ

A

Botulism - injection, wound, infant gut
- cleaves synaptobrevin -> no vesicle release
- neck -> descending paralysis -> autonomic
Curare - blocks nicotinic receptor
Depolarization block - excess stim -> no repolarization
- organophos, insecticide, chemical warfare

28
Q

Functional myopathies

A

aka channelopathies
Little wasting, atrophy vs destructive
EMG myotonic potentials, clinical dx, rare!

Myotonia -
- congenital myotonia - Cl- channel - improves with exercise
- paramyotonia congenita - Na channel - worse exercise, cold
Periodic paralysis - generalized periodic paralysis
- worse after meal, exercise
- thyrotoxic or familial (hypo, hyper or normoK, Anderson syndrome)
-

29
Q

Metabolic myopathies

A

Acquired
- thyroid - both hypo and hyper
- Rx - statin, colchicine, hydroxychloroquine, EtOH
Genetic
- impaired metabolism of carbs or fats -> intracellular inclusions, myoglobinuria, cramping with exercise
- poorly defined inclusions - nemaline, myotubular
- mitochondria - excess replication of abnormal mitochondria -> accum
- eyes (tonic activity), heart, also brain
- exercise intolerance, elevated lactate

30
Q

Inflammatory myopathies

A

aka myositis

Acquired - sarcoidosis, HIV, trichinosis
Autoimmune
- often paraneoplastic (lymph, lung, bladder, breast, ovary)
  -> immunosuppression, treat CA
- often high ESR, CRP, CK
  • polymyositis - 30-60yo, insidious, symmetrical, proximal (stairs, lifting of arms), sore
  • dermatomyositis - 5-15yo, 50-60’s yo - usually underlying CA or auto
    • insidious, proximal, more sore
    • rash - red/purple - eyelid (heliotrope), extensor joints (fingers/toes, elbow, knee), face, chest, affected muscles
  • inclusion body - > late middle-age, insidious
    • > proximal, finger/wrist flexion
    • inclusion bodies on biopsy, no tx
31
Q

Duchenne muscular dystrophy

A

X linked -> dystrophin - attaches actin to membrane
Infancy - second protein with same fx
-> sx in childhood (walk don’t run)
- pseudohypertrophy of calves, hip and shoulder girdle weakness
- very high CPK, aldolase
-> progressive (wheelchair) -> death (20’s) dt cardiomyopathy

No tx, steroids may prolong

Becker - same gene, less severe mutation -> later onset

32
Q

Myotonic dystrophy

A

Myotonia (delayed relaxation) + dystrophy

Type I - autosomal dominant - myotonic protein kinase

  • trinucleotide repeat (longer -> earlier, usu childhood, young adult)
  • distal - hands, face, neck
  • non-neuro - frontal balding, testicular atrophy, DM, cardiac arrhythmias, cataracts
  • progresses slowly -> respiratory, PNA in 40’s

Type II - complex repeat (CCTG) - transcription factor

  • 20-30’s, less common
  • proximal - elbow extension, hip flexor
33
Q

Limb girdle muscular dystrophy

A

Heterogenous, 15 different mutations - some recessive or dominant
Adolescence, adult

Proximal -> slow progression or spontaneously stop

34
Q

Facioscapulohumeral dystrophy

A

Chromosome 4 hypomethylation
- 2 defects (recessive, dominant) -> gene or methylation

Adolescence, early adult
Face -> scapula and upper arm
Slow progression, normal life expectancy
Mental retardation, cardiac arrhythmias

35
Q

Oculopharyngeal dystrophy

A

Trinucleotide repeat, autosomal dominant
-> accumulation of intranuclear mRNA trafficking protein

40’s -> ptosis -> extraocular paralysis -> swallowing
Manage sx (feeding tube)
Must r/o MG, mitochondrial (Kearn-Sayer)

Neuro SKS (19 decks)

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