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Neuromuscular PT 1 > Disorders of impaired neutral conduction and transmission > Flashcards

Disorders of impaired neutral conduction and transmission Flashcards

1
Q

Myelination

A
  • a sheath of proteins and fats surrounding an axon
  • provides insulation, prevents current flow across the axonal membrane
  • increases speed of action potentials and distance a current can spread
  • thicker myelin leads to faster condution and greater chances for action potential propagation
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2
Q

Demyelination

what does it do to the function of a neuron

A
  • lower membrane resistance
  • allows leakage of electrical current across membrane
  • decreases speed or blocks propagation of action potentials
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3
Q

Disorders of impaired conduction in the NS

A
  • CNS: multiple sclerosis
  • PNS: peripheral neuropathy; Guillain-barre
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4
Q

Describe what happens with MS

A
  • CNS demyelination
  • immune system produces antibodies that attack oligodendrocytes
  • patches of demyelination called Plaques in CNS white matter
  • damage to myelin sheaths in brain and SC which slows/blocks transmission of signals
  • also lose grey matter volume
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5
Q

Where can the plaques in MS occur

A
  • subcortical
  • brainstem
  • spinal cord
  • CNS white matter
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6
Q

Incidence of MS

A
  • Onset 20-40 years
  • women are 3x more affected than men
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7
Q

List some risk factors for MS

A
  • whites of European ancestry,
  • living further from equator (prior to puberty),
  • smoking,
  • low levels of Vitamin D,
  • obesity during adolescence.
  • OS&S: 2% risk for child, 5% for sibling or fraternal twin, 25% identical twin.
  • Viruses: Epstein-Barr, measles, canine distemper, herpes virus-6, chlamydia pneumonia.
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8
Q

MS

Symptoms

A
  • fatigue
  • weakness
  • impaired cognition
  • visual probelms
  • decreased sensation
  • slurred speech
  • pain
  • bowel/bladder changes
  • cognitive/affective disorders
  • exacerbations/remssions
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9
Q

MS

Diagnosis

A
  • difficult as signs may resolve when edema decreases
  • Lumbar puncture and evoked potentials (EP) also used.
    improved with use of imaging (plaques).
    looking for oligodendorcytes that are broken up
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10
Q

MS

PT role

A
  • exercise at lower intentsity
  • Avoid overexertion and high temperatures.
  • Small ↑’s (½ºF) in body temp may alter activity of membrane proteins in axons, further disabling AP conduction.
  • Sweating, dizziness, muscle weakness, slowed reaction times, reduced energy, difficulties with attention/ concentration.
  • Uthoff’s sign: better in 30 minutes.
  • “Pseudo exacerbation”: last < 24 hours.
  • exacerbations last >24 hours \, separated y ≥30 days
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11
Q

MS

Types

A
  • Relapsing remitting
  • secondary progressive
  • primary progressive
  • progressive relapsing
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12
Q

Relapsing/remitting MS

A
  • During relapses, new signs/sxs + old signs/symptoms recur or worsen.
  • Relapses f/b remission (full or partial recovery from deficits acquired during relapse.
  • without treamtent most transition to secondary progressive MS
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13
Q

Secondary progressive MS

A
  • continuous neurological decline
  • fewer or no relapses
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14
Q

Primary progressive MS

A
  • steady functional decline from time of onset
  • predominantly SC s&s
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15
Q

progressive relapsing MS

A
  • steady functional decline with superimposed relapses + partial remission s
  • Fxn never fully recover during remission
  • PRMS is now considered to be a form of PPMS
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16
Q

Peripheral Polyneuropathy

A
  • any pathologic change in peripheral nerves
  • destruction of myelin surrounding largest most myelinated sensory and motor fibers
  • results in disrupted proprioception and weakness due to desctruction of myelin in sensory and motor neurons
17
Q

Causes of periperhal polyneuropathy

A
  • autoimmune disease
  • metabolic abnormalities
  • toxic chemcials
  • hereditary disorders
18
Q

What damage is done with a diabetic polyneuropathy, what symptoms might be felt and how can one limit the pogression

A
  • both axons and myelin are damaged
  • decreased sensation along with pain, paresthesias and dysesthesias
  • glycemic control (A1C<7) can limit progression in type 1 but not type 2
19
Q

PT role with diabetic polyneuropathy

A
  • balance and strength training to reduce fall risk
  • gait and balance improve with exercise
  • orthoses may be used to stabilize weight-bearing joint
  • prevent sprains and strains
  • prevent dropping of forefoot during gait
  • prevent deformities from paresis, paralysis and lack of sensation
20
Q

Guillain-Barre Sydrome

A
  • acute inflammation demyelinated polyneuropathy
  • AIDP is most common form
21
Q

What happens with

Guillian Barre Syndrome

A
  • immune system attacks schwann cells
  • affects sensory and motor function
  • if severe, peripheral autonomic function
  • often occurs 1-2 weeks after a mild infection (resp. or GI)
22
Q

DX of Guillian Barre

A
  • EMG
  • lumbar puncutre
  • MRI
23
Q

Guillain-Barre

Signs and symptoms

A
  • Primary sign is ascending skeletal Muscle paralysis
  • difficulty with chewing, swallowing, speaking, facial expressions if motor CN’s affected
  • weakness>sensory loss; may have deep aching pain or hypersensitivity to touch
  • 3-10% die of cardiac or respiratory failure
  • in some cases demyelination is extreme and axons within myelin sheath degenerate resulting in residual complications
24
Q

Guillain-barre Syndrome

Treatment: medical

A
  • plasmapheresis: removes antibodies
  • intravenous immunogoblin therapy: neutralizes antibodies
  • 25% of patients require ventilatory
25
Q

Guillian-Barre

Treatment: PT/OT

A
  • Acute phase: stretching and ROM
  • Recovery phase: gentle exercise and functional mobility
  • monitor for DVT, PE, autonomic symptoms
  • use BORG scale and monitor during submax aerobic training for dysautonmia
26
Q

Guillain-barre

Treatment: SP/RT

A
  • SP: chewing, swallowing, speaking, breath support for speech
  • RT: breathing, secretions
27
Q

Guillain-barre

poor prognostic signs

just be aware of

A
  • over 60
  • reach peak of symptoms withing 7 days
  • being on a vent
28
Q

Synpatic Transmission

A
  1. action potential reaches axon terminal
  2. the change in electrical potential causes opening of voltage-dependent Ca2+ channels and influx of Ca2+
  3. increase leves of Ca2+ then promote movement of synpatic vesicles to the membrane
  4. Synaptic vesicles bind with membrane, then release NT into synaptic cleft
  5. NT diffuses across the synpatic cleft and activates a membrane receptor
29
Q

Neuromuscular junction transmission

A
  1. AP reaches presynaptic terminal of neuron, membrane of presynaptic terminal depolarizes.
  2. Voltage-gated calcium ion (Ca+2) channels open; Ca+2 influxes into the nerve terminal.
  3. Synaptic vesicles move toward a release site in membrane, fuse with membrane, then…
  4. Rupture to release a NT (Ach) into synaptic cleft.
  5. When ACh binds to receptors associated with membrane channels on mm cell; Na+ channels open briefly.
  6. Influx of Na+ initiates a series of events that produce contraction of mm cell.
30
Q

disorders of Impaired tranmission in the NMJ

A
  • disease of NMJ interfere with the lock (receptor) or the key (AcH)
  • Myasthenia Gravis
  • Lambert-Eaton Syndrome
31
Q

Myasthenia Gravis

what is it and incidence

A
  • Autoimmune disease
  • antibodies attack and destroy nicotinic receptors on muscle cells
  • onset in women: 20-30 years of age
  • onset in men 60-70
  • women more often than men
32
Q

How does myasthenia gravis affect the NMJ

A
  • normal amounts of AcH are released into the cleft
  • BUT
  • few receptors are availble for bindign, resulting in increaseing weakness with repetitive muscle contractions
33
Q

Which muscles tend to be most affected in myasthenia gravis

A
  • affects muscles that contract a lot
  • eye, fascial, respirtory muscles, proximal stabilizing muscles
34
Q

Myasthenia Gravis

Signs and symptoms

A
  • Muscles that contract frequently = dropping of eyelids, misalignment of eyes
  • facial expression
  • swallowing
  • proximal limb movements
  • respiration
35
Q

Myasthenia gravis

Diagnostic testing

A
  • Tensilon is used.
  • Tensilon inhibits the enzyme that breaks down ACh, thus leaving more ACh in the synaptic cleft to bind repeatedly with muscle cell receptors.
  • This rapidly improves muscle strength by increasing muscle response to nerve impulses.
  • The muscle strength increase occurs within a minute of administration of the drug and lasts only a few minutes
36
Q

Disorders of impaired transmission

Lambert-Eaton Syndrome

A
  • antibodies destroy voltage-gated Ca2+ channels in the presynpatic terminal
  • less ACh released
  • decreased excitation of muscle cells cause muscle weakness
  • Botox works same way– inhibits release of Ach @ NMJ so mm’s can’t contract

Neuromuscular PT 1 (32 decks)

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