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distal, spinal nerves, cranial nerves, outside skull
PNS includes structures _____ to _____ and axons of _____ that are _____
nerve roots, dorsal root ganglia, spinal nerves, sensory, motor, autonomic
PNS includes _____, _____, and _____, contains _____/_____/_____ neurons
spinal, myotomal, dermatomal, peripheral
PNS lesion distributions are _____ (_____/_____) and _____
31, 10, optic, olfactory, telencephalon
PNS includes _____ pairs of spinal nerves and _____ pairs of cranial nerves (_____ and _____ attach to _____ and are part of CNS)
enclosed by bone
if nervous tissue is _____ = CNS
brainstem, spinal cord
PNS cell bodies are located in _____ and _____
motor, cell body, axon, motor endplate, muscle fiber, sensory, ganglion, axon, sensory receptor
potential sites of involvement are _____ (_____/_____/_____/_____) or _____ (_____/_____/_____)
synapse, motor axon, muscle fiber
neuromuscular junction is location of _____ between _____ and _____
ACh, depolarization, muscle membrane, contraction, excitatory
neuromuscular junction releases _____ to facilitate _____ of the _____ to facilitate _____, action is ALWAYS _____
spontaneously, muscle health, endplate potential, atrophy, generate contraction, connection
even with inactive motor neurons small amounts of ACh are released _____ to maintain _____, cause miniature _____ (avoid muscle _____) but not enough to _____, keep _____ between LMN and muscle
impaired, pattern, weakness, fibrillation
sensory changes include _____ sensation, autonomic dysfunction depends on _____, motor changes include _____ and _____
trophic, nutrition
denervation causes _____ changes due to lack of _____
demyelination, axon, bare, myelin, segmental, conduction, speed, blunt, compression, ischemia
neurapraxia is _____ (leaves _____ intact but _____ where _____ is lost = _____), affects _____ through decreased _____, results from _____ injury/_____/_____
degeneration, directly, axon, connective tissue covering, physical, crush, stretch, laceration, disease, wallerian degeneration
axonotmesis is _____ that _____ affects the _____, _____ that support/protect the nerve remain intact, results from _____ injury (_____/_____/_____) or _____, causes _____
severe, complete severance, axon, disruption, connective tissue coverings
neurotmesis is most _____ loss, _____ of the _____ and _____ of _____
endoneurium, perineurium, epineurium
connective tissue covering layers (3)
immediately, separation, distal, cell body, few weeks, death, distal, communication
wallerian degeneration begins _____ after _____ of the _____ axonal segment from the _____ and is completed over period of _____, results in _____ of entire _____ segment, NO _____ between segments
single, focal
mononeuropathy is _____ nerve, _____ dysfunction
several, multifocal, asymmetrical, individual
multiple mononeuropathy is _____ nerves, _____ dysfunction, _____ involvement of _____ nerves
many, generalized, distally, symmetrically
polyneuropathy is _____ nerves, _____ disorder that presents _____ and _____
axon, myelin, both
neuropathy dysfunction results from damage to _____, _____, or _____
trauma, demyelination, complete, rapid, remyelination
traumatic myelinopathy cause _____, pathology _____, recovery is _____ and _____ by _____
trauma, axonal, slow, axonal regrowth, good, connective tissue, intact
traumatic axonopathy cause _____, pathology _____ damage, recovery is _____ by _____ but _____ because _____/Schwann cells are _____
trauma, axon, myelin degeneration, slow, poor, inappropriate reinnervation, neuroma
traumatic severance cause _____, pathology _____ and _____, recovery is _____ with _____ results due to _____ and traumatic _____
complication, diabetes, blood vessel inflammation, ischemia, slow, axonal regrowth, good
multiple mononeuropathy cause is _____ of _____ or _____, pathology is neuron _____, recovery is _____ by _____ usually _____
complication, diabetes, autoimmune disorder, genetic, metabolic, inflammatory
polyneuropathy cause is _____ of _____/_____ or _____, pathology is _____ or _____, recovery is variable based on type
mechanical stimuli, blood flow, transport, edema, thickening, myelin, axonal damage
traumatic myelinopathy is caused by repeated _____ = decreased epineurial _____ and axonal _____ = _____ of endo/epineurium = _____ of epi/perineurium = _____ and _____
sensitization, ectopic foci, sensation, movement
traumatic myelinopathy can also cause _____ of nociceptors, development of _____, and impaired _____/_____
symmetrical, distal to proximal, feet, hands, longest axons, stocking glove, gradient
polyneuropathy has _____ involvement progressing from _____ (symptoms begin in _____, then appear in _____ = areas of body supplied by _____), _____ distribution (_____)
toxic, metabolic, autoimmune, genetic, diabetes, nutritional, alcoholism, autoimmune, drugs, toxins, nutritional
polyneuropathy cause can be _____/_____/_____/_____, most common include _____, _____ deficiencies secondary to _____, and _____ diseases, other causes are therapeutic _____, industrial/agricultural _____, and _____ disorders
diabetes mellitus, distal, symmetrical, polyneuropathy, single
diabetic neuropathy occurs in setting of _____, occurs in _____/_____ pattern, termed _____ but _____ nerve involvement is possible
I, hyperglycemia, regeneration, duration
diabetic neuropathy is greater in type _____, risk factors include chronic _____ (control is known to enhance _____) and diabetes _____
myelinated, unmyelinated, vascular, ischemia, hypoxia, axonal degeneration
diabetic neuropathy causes loss of _____ and _____ axons, _____ changes affect peripheral nerves (multifocal regions of _____ and _____ result in _____)
rapidly reversible, hyperglycemic, generalized symmetric, acute sensory, chronic sensorimotor, autonomic, focal, cranial, focal limb
classification of diabetic neuropathy includes _____ (_____), _____ polyneuropathies (_____/_____/_____) and _____ neuropathies (_____/_____)
history, examination, electrodiagnostic, sensory, autonomic, single
diabetic neuropathy diagnosis is made based on _____, clinical _____, _____ studies, quantitative _____ evaluation, and _____ function testing, NOT based on _____ item
cardiovascular, gastrointestinal, genitourinary
autonomic diabetic neuropathy can manifest in _____/_____/_____ symptoms
control hyperglycemia, address symptoms, impairments, health condition, slowly progressive, body systems
diabetic neuropathy treatment includes _____ and _____, target _____ and _____, prognosis is _____ metabolic disorder that affects many _____
chronic alcoholism, distal, symmetric, direct toxic, alcohol, nutritional deficiencies, dietary habits, segmental demyelination, axonal degeneration
alcoholic neuropathy is seen with _____, _____/_____ involvement, attributed to _____ effects of _____ on nerve and _____ from poor _____, causes _____ and _____
muscle bulk, ankle reflexes, sensation, feet, aching, calves, pain, paresthesia, numbness, symmetrical stocking glove, weakness, atrophy
alcoholic neuropathy mildly presents with minor loss of _____/diminished _____/impaired _____ in _____/_____ in _____, distal sensory changes include _____/_____/_____ in _____ pattern, advanced presents with _____ and _____ of distal musculature
history, examination, electrodiagnostic, action potential amplitude, sensory, motor
alcoholic neuropathy diagnosis is made by _____, clinical _____, and _____ studies showing loss of _____ (_____ and _____)
aerobic, stress, coping, symptomatic, orthotics, mild improvement, total alcohol abstinence, slow, incomplete
alcoholic neuropathy is treated by _____ exercise to decrease ____/improve _____ mechanisms and _____ treatment (_____), prognosis is _____ with _____ but _____ recovery and often _____ with axonal degeneration
hereditary, autosomal dominant, mutation, schwann cell myelination, demyelination, hypertrophic onion bulb, remyelination, fibular, forearm, hand
charcot marie tooth is _____ neuropathy (_____), _____ in proteins associated with _____ create extensive _____ along with _____ formation as _____ is attempted, initially involves _____ nerve, later progresses to muscles of _____/_____
childhood, adulthood, history, examination, hereditary, electrodiagnostic, biopsy
charcot marie tooth onset may occur in _____ or _____, diagnosis is by _____, clinical _____, _____ picture, _____ studies, and nerve _____
alter course, symptomatic, function, safety, monitor, progression, stretching, ROM, strengthening, endurance, bracing
charcot marie tooth has no treatment to _____, _____ treatment is used to maximize _____ and _____, _____ disease and modify based on _____, implement _____/_____/_____/_____/_____ to improve ambulation
slowly progressive, incurable, deformities, secondary complications, contractures, gait, hand
charcot marie tooth is _____ and _____, need to prevent _____ due to _____ (_____ further reduce _____ and _____ function)
clawing, varus, hammer
charcot marie tooth foot deformities include great toe _____, _____ alignment, and _____ toe
rapidly evolving, immune mediated, seasonal relationship, bacterial, viral infection, surgery, vaccination
guillain barre is most common cause of _____ motor/sensory deficits, _____ disorder, possible _____ associated, risk factors include _____/_____, _____, and _____
spinal nerve roots, distal termination, motor, sensory, antibody, demyelination, schwann cells
guillain barre has lesions throughout the PNS from _____ to _____ of fibers, can involve _____ only or with _____ degeneration, _____ mediated _____ primarily attacking _____
rapidly ascending, bilateral, symmetrical, distal, paresthesia, toes, weakness, distal legs, spreads, arms, trunk, face, mechanical ventilation
guillain barre has _____/_____/_____ motor and _____ sensory impairments, first neurologic symptom is _____ in _____ followed by _____ in _____ which _____ to _____/_____/_____, some require _____
4 weeks, less, 2-4 weeks, static, 2-4 weeks, recovery, months, years
guillain barre time from onset to peak is typically _____ or _____, progression lasts _____, then _____ phase begins for _____ before _____ which takes _____ to _____
proximal to distal
guillain barre recovery occurs in _____ progression
progressive weakness, more than one extremity, DTRs, rapidly, ceases, 4 weeks, symmetric, sensory, facial, oral bulbar, 2-4 weeks, ceases, tachycardia, arrhythmia, blood pressure, fever, CSF, nerve conduction velocity
guillain barre diagnosis requires _____ in _____ and loss of _____; supported by weakness developing _____ that _____ by _____, _____ weakness, mild _____ signs, _____ weakness common and _____ with involved _____ musculature, recovery begins _____ after progression _____, _____/cardiac _____/labile _____, absence of _____; _____ protein levels increase and _____ is slowed
high, IV, immunoglobulin, plasmapheresis, morality, complete, remaining neurological deficits, neuropathic pain, autonomic, distal weakness
guillain barre is treated with _____ dose _____ administration of _____ and _____, prognosis is variable from _____ to _____ recovery, some have _____, complications include _____/_____ changes/_____ in extremities
older, recovery, artificial respiration, evoked motor potential amplitude, younger, diarrhea, disability, admission, longer, ventilator support
factors that predict poor outcome with guillain barre include _____ age, increased time before _____, need for _____, significantly reduced _____
factors that predict better outcome with guillain barre include _____ age, absence of preceding _____, lower levels of _____ and _____, _____ interval between symptoms and admission, and absence of _____ need
ROM, pain tolerance, monitor, strength, prevention, complications, immobilization, skin care, positioning, splinting, movement, stretching, active, active assisted, strength, resistive, higher, functional, disability, assistive, mobility, home
guillain barre therapy acute = maintain _____ within _____ and _____ muscle _____; ascending phase focus on _____ of _____ associated with _____ (_____/_____/_____); stabilization phase initiate _____ through gentle _____ and _____/_____ at level consistent with _____; descending phase integrate _____ exercise _____ intensity produces greater _____ improvements and reduces _____; impaired function may require use of _____/_____ equipment and _____ modifications
slower, relapses, remissions
chronic inflammatory demyelinating polyneuropathy is guillain barre variant with _____ onset with _____/_____
eradicated, vaccine, resurgence, infectious, deadly, person to person contact
poliomyelitis was virtually _____ in 1950s with _____, _____ due to antivaccination movement, highly _____ and potentially _____ disease that is transmitted through _____
new neuromuscular symptoms, decades, 25 years, recovery, weakness, functional mobility, fatigue
postpolio syndrome is _____ that occur _____ (average is _____) after _____ from acute paralytic episode, characterized by _____, decline in _____, and reports of _____
muscle denervation, original, alpha motor neuron, compensated, axonal sprouting, maintained, prunes, metabolic, support, new denervation
postpolio syndrome has ongoing _____ = evolution of _____ motor neuron dysfunction that began after poliovirus affected _____, _____ reinnervation (via _____) cannot be _____ = nervous system _____ back without _____ ability to _____ = _____
strength, affected, recovered, stability, 3-10 years, pain, atrophy, bulbar, myalgia, joint, atrophy, new, fatigue, vasomotor, endurance
postpolio syndrome causes declines in _____ in muscles that had previously been _____ with polio and had fully/partially _____, with periods of _____ for _____, experience _____/_____/_____ problems, may have _____/_____ pain/increased muscle _____/_____ weakness/excessive _____/_____ abnormalities/diminishing _____
clinical, exclusion, slowly progressive, stable
postpolio syndrome diagnosis is _____ by _____, prognosis is _____ with _____ periods
symptomatic, lifestyle, energy conservation, surgery, nonexhaustive, general conditioning, functional, submaximal, endurance, functional, exercise, rest, fatigue
postpolio syndrome treatment is _____ and modification of _____ (_____), _____ for residual ankle deformities, _____ exercise and _____, _____ exercises of _____ intensity, goal of maintaining and improving _____ and _____ capacity, balance between _____ and _____ for _____ management
fifth cranial nerve, intense paroxysms, lancinating pain, distribution
trigeminal neuralgia is disorder of _____ with _____ of _____ within nerve’s _____
women, 50-70, herpes zoster, MS, vascular, tumor
trigeminal neuralgia typically occurs in _____ between ages _____, associated with _____/_____/_____ lesions/_____ that affect the nerve
demyelinated, hyperexcitable, sudden, sharp pain, maxillary
trigeminal neuralgia occurs from _____ fibers becoming _____, _____ onset described as _____, restricted to _____ division
subjective report, pain, typical pattern, sodium channel blockers, carbamazepine, neurosurgery, unresponsive, difficult, spontaneous remittance, remain, remission
trigeminal neuralgia diagnosis is _____ of _____ in _____, treatment is _____ (oral _____) and _____ for _____ patients, prognosis is _____ to determine may have _____/_____/_____
sensory, carcinomas, subacutely, chronically, precede, tumor
cancer induced paraneoplastic neuropathies are _____ neuropathies associated with other _____, development of symptoms occurs _____ or _____ over weeks/months and may _____ discovery of _____ from months/years
autoimmune, cancer antigen, membrane receptors, within neuron
cancer induced neuropathies are _____ response initially directed against _____ subsequently attacks _____ or those _____
numbness, paresthesia, asymmetric, all extremities, weakness, sustain contraction, proprioceptive feedback, cerebellum
cancer induced neuropathies present with _____ and _____ initially _____ but progress to involvement of _____, _____ is NOT common but related to inability to _____ secondary to impaired _____ (_____ indirect involvement)
extensive, medical, holistic, neuropathy symptoms, health condition, immunosuppression, integumentary, safety, falls, deterioration, stabilization, disability
cancer induced neuropathies differential diagnosis is _____, treatment has minimal _____ options, care should be _____ addressing _____, overall _____, and effects of _____, recognize and prevent _____ problems, preserve _____ with gait and mobility, and prevent _____, prognosis is _____ over weeks/months and then _____ with _____
toxic, environment, medications
_____ substances in the _____ and some _____ prescribed to treat condition can be toxic to PNS
segmental demyelination, upper extremities
lead neuropathy causes _____ in CNS and PNS, affects neurons innervating _____
inhibition, acetylcholinesterase, overstimulation, neuromuscular junction, nausea, vomiting, diarrhea, fasciculations, weakness, paralysis, death, vasomotor, respiratory paralysis, 1-4 days, chronic, delayed
pesticides and organophosphates cause _____ of _____ activity = _____ at _____, symptoms include _____/_____/_____ and muscle _____/_____/_____, _____ can result from _____ collapse that coincides with _____, symptoms appear within _____, _____ can persist for months/years, _____ can have onset weeks after exposure
neuromuscular transmission, autoimmune, fluctuation, weakness, fatigability, skeletal muscle
myasthenia gravis is most common disorder of _____, _____ disorder, characterized by _____ of _____ and _____ of _____
thymic, diabetes, immune, familial, exacerbations, menstrual period, pregnancy
myasthenia gravis risk factors include _____ disorders, _____/_____ disorders, _____ association, and _____ may occur before _____/shortly after _____
ACh receptors, neuromuscular junction, efficiency, neuromuscular transmission, impulses, pass, neuromuscular junction, stimulate contraction
myasthenia gravis has impaired _____ at _____ resulting in decreased _____ of _____, nerve _____ fail to _____ the _____ to _____
skeletal muscle weakness, fatigability, normal, ocular, mild generalized, acute fulminating, late severe, history, observation, symptoms, weakness, continued use, rest
myasthenia gravis presents with _____ and _____, other neurologic findings are _____, classified as _____/_____/_____/_____, diagnosis is made by _____ and clinical _____ of _____ of _____ with _____ and improvement with _____
acetylcholinesterase inhibitor, weakness, underlying disease, surgical, thymus, immunosuppression, plasmapheresis, slowly progressive, complete, permanent, fluctuate, day
myasthenia gravis treatment includes _____ medication for improvement of _____ but does NOT treat _____, _____ removal of _____, _____, and _____, prognosis is _____, remissions are rarely _____ or _____, symptoms _____ in intensity during the _____
supportive, respiratory, crisis, weakness, respiratory, talking, chewing, swallowing, strength, maximal isometric, secondary, corticosteroid, monitor, participation, quality of life
myasthenia gravis therapy should be _____ care, _____ management, being alert to signs of impending myasthenic _____ (increasing _____, _____ distress, difficulty _____/_____/_____), establish _____ training eliciting _____ contractions, reduce _____ complications from long term _____ use, and _____ symptoms and impact of _____/_____
normal, quiet, no motor unit potential, decreased
segmental demyelination EMG has _____ insertional noise, _____ at rest, affected fibers have _____ during minimal contraction and _____ interference pattern during maximal contraction
increased, spontaneous potentials, fibrillation, positive sharp wave, no motor unit potential, decreased, no
axonal degeneration EMG has _____ insertional noise, _____ (_____/_____) at rest, affected fibers have _____ during minimal contraction and ______ (partially affected) or _____ (completely affected) interference pattern during maximal contraction
increased, quiet, fibrillation potentials, low amplitude polyphasic potential, low amplitude full, frequency, firing, effort
myopathy EMG has _____ insertional noise, _____ at rest with _____ at end stage, _____ during minimal contraction, and _____ interference pattern during maximal contraction with increased _____ of _____ and moderate _____