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Neuroconditions 2022 > Peripheral Disorders > Flashcards

Peripheral Disorders Flashcards

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1
Q

What is amyotrophic lateral sclerosis ALS

A

Progressive neuromuscular disease characterized by degeneration and eventual death of upper motor neurons and lower motor neurons causing weakness of the limbs, respiratory, and vulgar musculture. Lower motor neurons affect it first

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2
Q

What are the known risk factors of ALS

A

Older age, lower BMI, cigarette smoking, professional athletes are more at risk, repeated head injuries

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3
Q

What is the pathology of ALS

A

Dysfunction of the astrocytic excitatory amino acid transporter two, reduced uptake of glutamate from the synaptic cleft, leading to glutamate excitotoxity
The resulting glutamate induced excitotoxins city induces neurodegeneration through activation of calcium dependent in enzymatic pathways

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4
Q

What is amyotrophy

A

Loss of brain stem cranial nerve nuclei and anterior horn cells and spinal cord

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5
Q

What is lateral sclerosis

A

Loss of cortical motor cells causing corticospinal tract dysfunction

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6
Q

What is El Escorial criteria

A

Presence of three of these findings including evidence of lower motor neuron degeneration by clinical, electrophysiology goal or neuropathology goal exam, evidence of upper motor neuron degeneration by clinical exam, or progression of the motor syndrome within a hidden region or to other regions by history or exam

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7
Q

What is the most common a ALS presentation

A

Is limb onset of symptoms with distal to proximal progression including fasciculations, atrophy, weakness, spasticity

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8
Q

What form of ALS typically progresses faster

A

Bulbar onset occurs in 25% of cases including changes in speech, difficulty swallowing, involuntary tongue twitching, vocal cord spasms

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9
Q

What type of ALS is rare

A

Respiratory answer is rare under 3% which includes shortness of breath orthopnea, and sleep disordered breathing

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10
Q

What is the prognosis of ALS

A

Three years survival equals 50% five year survival equals 20% 10 years survival is 10%

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11
Q

What are negative prognostic factors for ALS

A

Bulbar onset, weight loss, cognitive impairment, impaired respiratory function

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12
Q

What are the five stages of ALS

A

Stage zero equals pre-symptomatic
Stage one is involvement of one clinical region
Stage two is involvement of two clinical regions
Stage three is involvement of three clinical regions
Stage four is substantial respiratory or nutritional failure
Stage five equals Death

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13
Q

What are the two types of medical management for ALS

A

Riluzole add three months to overall survival is taken for 18 months
Edaravone decreases oxidative stress in ALS

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14
Q

What does your examination Of historyinclude for ALS

A

Location of symptom onset, month or year of symptom onset, date of diagnosis, previous trauma, falls secondary to weakness, cervical and lumbar laminectomy’s, carpal tunnel releases

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15
Q

What are your examination items for impairments for ALS

A

ALS functional rating scale

Range of motion, strength, sensation, muscle tone, skin integrity, respiratory status

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16
Q

What are the examination items For activity limitations

A

Balance and gait measures based on the individuals current functional status including,, bread, gait speed, six minute walk test, tug

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17
Q

What are the general interventions for ALS

A

Disease progression is different for everyone, you are in LA, fall risk and prevention, energy conservvation and prioritization of activities

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18
Q

What are the early stage presentations of ALS

A

Muscle weakness in extremities, weakness and muscles with speech and swallowening, specificity, muscle fasciculations, atrophy, painful muscle cramping, shortness of breath, mild changes

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19
Q

What are the middle stage presentations of ALS

A

Muscle weakness and atrophy at the body, paralysis occurs in some muscles, has more of the lower motor neurons damage, to speed decreases, uncontrollable or inappropriate laughing or crying, further weakness of swallowing muscles with reports of choking, weakness of muscles of speech to the degree of requiring augmentative communication, difficulty breathing requiring noninvasive ventilation, increased cognitive decline

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20
Q

What are the late stage presentations ALS

A

Majority voluntary muscles are paralyzed
Respiratory muscle weakness resulted in significant respiratory insufficiency requiring mechanical ventilation for survival
String Clawson swallowing muscle significant enough to require gastrostomy tube for nutrition

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21
Q

What are epigenetic factors that influence house Health

A

Aging, obesity, physical activity and exercise, smoking, geographic variations, socioeconomic status, social support, environmental barriers healthcare, gender, race, ethnicity, generational differences

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22
Q

What is a type of myopathy

A

Myasthenia gravis

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23
Q

What is myasthenia gravis

A

Chronic peripheral autoimmune neuromuscular disease of the neuromuscular junction
Skeletal muscle weakness that worsens after bouts of activity and improves after rest

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24
Q

What are the cardinal signs of myasthenia gravis

A

Ptosis a.k.a. eyelid drooping which is usually asymmetrical

Muscle fatigue

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25
What are the signs and symptoms of myasthenia gravis
``` Ziploc Pilea Facial weakness For ptosis Dysphasia, dysarthria Shortness of breath Weakness in neck, upper extremities and lower extremities Fatigue ```
26
What is Limb girdle muscular dystrophy (LGMD)
``` mutations in many different genes that provide instructions for making proteins involvled in muscle maintenance and repair type 1= dominant inheritance type 2= recessive inheritance affects promzimal muscles of UE/LE 6/1000 affected ```
27
What is early stage of LGMD
changes in walking (waddling, waking on balls of fee), hands on knees to transition from squat to sstand
28
What are late stages fo LGMD
may require w/c , scapular wingin (due to muscle wasting), increased lumbar lordosis, pseudohypertrophy of calf muscles ( due to fatty deposits and scar tissue)
29
What are PT considerations for LGMD
resistance trianing-- both higher and lower intensity resistance training may improve strength in arms over 6 months aerobic and endurance-- may also improve aerobic capacity and walking
30
What ia fascioscapularhumeral muscular dystrophy (FSHD)
``` facial, scapular, and humeral muscles affects autosomal dominant inheritance mask like appearnce symptoms usually before 20 life expectancy not shortened ```
31
What is the management of FSHD
plumonary funciton testing testing for retinal and hearing speech therapy maintain flexibilty and minimize atrophy manage pain compensations like orthotics might be helpful
32
What muscles are affected early in FSHD?
hamstring and trunk muscles are affected early
33
What has the fasted conduction for a nerve cell?
very thick myelin = fast conduction
34
What has the slowest conduction?
no myelin= very slow
35
What type of cells make myelin in the PNS
schwann
36
What type of cells make myelin in the CNS
oligodendrocytes
37
What is neurapraxia
temporary failure of nerve conduction without structural changes. usually caused by blunt trauma, pressure, ischemia. axon remian intace and muscle does not atrophy
38
What is axonotmesis
aaxon indamages due to crush, stretch, lacerating injury or disease process. Connective tissue support for the nerve remains intact
39
what is neurotmesis
most sever axonal loss with complete severance of the acon and its connective tissue coverings if cell body remains viable, regerneative sprouting occurs with growth approx 3mm/day near the lesion and 1mmday further from lesion
40
What are the types of neuropathy?
``` wide careity of cause can be acquired and idiopathic bell's palsy trigeminal neuralgia icu acquired weakness chemotherapy induced neuropath ```
41
What is bell's palsu
typicallu preceded by a viral infection facial paralysis of one side 71% have full recovery
42
What is trigeminal neuralgia
brief, intense shock like burss of pain within a distribution of the trigeminal nerve opthalmic, maxillary, mandibular could be related to herpes zoster, inflammatory reactions, tumors, other compression of the nerve
43
What is ICU acquired weakness linked to
multi organ failure and ventilare >2 weeks
44
What is a common side affect of cancer treatment
chemotherapy induced nueropathy
45
How do you differentiate Bell;s Palsy from a stroke?
bell's palsy has full one side facial paralysis
46
What are the 4 classifications of neuropathy
infectious hereditary metabolic immune-mediated inflammatory
47
What are the infectious neuropathy's
poliomyelitis | post polio syndrom (PPS)
48
what is a hereditary neuropathy
Charcot-Marie-Tooth disease (CMT)
49
what is the metabolic neuropathy
diabteic neuropathy
50
what type of neuropathy is Guillain-barre syndrome
immune-mediated, inflammatory
51
What are symptoms of polio of the early 1950
caused by virus, highly infectious, especially <5 symptoms are fever, fatigue, headached, vomiting, tiffness of the neck and pain in th limbs it can cause toatl paralusis by affecting the anterior horn cells of the spinal cord
52
What kinds of impairments do people with polio have
focal and asymmetric motor impairments-- anterior horn cells (possible brainstem) may be affected absent DTRs equal numbers recovered, had mild residular parayis, or left with moderate to severe paralysis
53
What mimics polio currently
acute infantile paralysis
54
What is post polio syndrome
new neuromuscular sumptoms that occur decades after recovery 1/4 to 1/2 develop PPS most recovery of muscle strength is due to reinnervation of denervated muscle fibers by collateral sprouts from nearby axons
55
What are some interventions for PPS
non-exhaustive exercise and gneral body condition monitor vitals functional exercises of submaximal intensity are stressed with the goal of maintaing and improving endurance and functional capactiy lifestyle modification compensations preventions
56
What syndrome is the most common cause of rapidly evolving motor paresis, paralusis and sensory deficits?
Guillain-Barre syndrome
57
What are causes of GBS?
bacterial and viral infections, surgeries and vaccines have all been implicated GBS is an immune mediated disorder evidence supports the view that GBS is an immune mediated disorder
58
What cells are the primary targets of attack
Schwann cells
59
What is the first symptom of GBS and acute inflammatory demyelinating polyneuropathy (AIDP)
paresthesia in toes, followed within hours or days by weakness distally in the legs
60
What are the symptoms of GBS/ AIDP
first symptom if often paresthesia in toes weakness and sensory loss that is symmetric and ascending (distal to proximal) weakness spreads to involve arms, trunk, and facial muscles flaccid paralsis is accompained by absence of DTRs may result in respiratoy failure recovery takes weeks to months (body repairs myelin)
61
How do you diagnose GBS/AIDP
lumbar puncture for CSF analysis -- albumin elevated fibrillations if axonal damage may have tachycardia, cardiac arrhythmias, and labile BP
62
What is the treatme for GBS. AIDP
aimed at controlling the immune response plasmapheresis removes and filters plasma to remove or dilute circulating antibodies high-doe intravenous immunoglobulin (IVIg)
63
What is longer length of inpatient hospitalization correlated with for GBS/AIDP
presence of muscle belly tenderness sever lower limb weakness as measured by MMT FIM scores at admssion
64
What is the acute rehab look like fo rGBS/AIDP
LOS 63 days by discharge min to no assistance for mobility, max A at admission LOS double when axonal dame, ventialtor dependence, and muscle belly tenderness is present
65
What is the PT managmenet for the descending weakness phase of GBS/AIDP?
aarom and milde resitance = avoid fatigue progress functional trainin consider compensatory devices maintain jjoint ROM, and flexibility with pain tolerance monitor vitals hep with pan control
66
WHat it the PT management for outpatient of GB/AIDO
participation level goals, return to work, independence, exercise, wean from AD, fall prevention
67
What is CMT?
Charcat-marie-tooth disease is characterized by distal limb muscle wasting and weakness, usually skeltal deformities, distal sensory loss, and abnormalieites of DtRs hereditary motor and seonsroy neuropathy -- begins with peroneal nerve disorder progressing to foot and leg, ankle DF and EV affected later progresses to weakness and wasting of intrinsic hand muscles no treatment
68
What is rocker bottom deformity
bones of the foot may fracture and collapse
69
what is pes cavus
intrinsic foot and lower lef weakness resulting in imbalance of muscle action resultin in clawing of toes and high arch
70
What kind of foot is more common in children?
pes cavus
71
What is the PT management for CMT
prevent contractures, UE function pain control balance exercise-- focus on unaffectec muscles and moderated strengthen ar 40-60% 1 RM, aerobic training at 70-90%
72
What is diabetic peripheral neuropathy ?
meaning a demonstratable disorder, either clinically evident or subclinical, that occurs in the setting of M without other cuases for peripheral neuropathy affect sensory and motor nerves in a distal to proximal symmetric pattern (stocking glove pattern)
73
Within one year of DM diagnosis have many have neuropathy
7%
74
What is the pathogenesis of DN
caused by the chronic metabolic distrubances that affect neurons and schwann cells vascular changes affect peripheral nerves
75
What are the specific findings of DN
early detection and prophylactic foot care regimens have led to fewer foot ulcerations and amputations greater forefoot pressure occur during gait (decreased 1sst toe and ankle mobility) increased risk for development of metatarsal ulcers footdrop during gait

Neuroconditions 2022 (14 decks)

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