Neurogenic Dysphagia Flashcards

1
Q

Causes of Neurogenic Dysphagia:

...
-P
-H
-H
-M
-A
-G
-A
B
-B
-M
-N
A

cerebrovascular accident/stroke

parkinson’s disease

huntington’s

head injury/TBI

Multiple Sclerosis

amyotrophic lateral sclerosis/ALS/ Lou Gherig

guillan barre syndrome

alzheimers

brain tumors

bulbar /pseudobulbar palsy

myasthenia gravis

neurotoxins

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2
Q

Sources:

-

-

A
Brain/CNS
-cerebral cortex/cortical motor areas
-midbrain/basal ganglia
-corticobulbar tract 
-brainstem 
cerebellum 
-medulla 

meninges

  • PNS/cranial nerves
  • disease vs acute insult ?
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3
Q

CVA/stroke

A

hemorrhagic

ischemic

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4
Q
Site of lesion: 
-
-
-
-
A

cerebral cortex

subcortical (basal ganglia, thalamus, cerebllum)

higher brainstem/pons

lower brainstem/medulla

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5
Q

Sequelae:

dependent on ?

A

site and extent of lesion

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6
Q

sequelae:
-h
-oral
-….. coordination
-…impairments
-…. timing
-reduced
-reduced
…..disturbances

A

hemiparesis

oral acceptance

lingual/labial/velum strength

sensory impairments (including reactive/non-reactive aspiration)

pharyngeal swallow timing

reduced contraction

reduced laryngeal excursion

cognitive disturbances

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7
Q
Brain Injury: 
often very complex with considerations including: 
-severity of 
-... injury 
-... trauma 
-type of ? 

limited ?

often dysphagia is

can be

A
  • damage
  • open or closed injury (meninges/intraparenchymal)
  • multi-system trauma
  • type of force causing damage

evidence to assist in predictive outcomes

secondary

  • respiratory status
  • behavioral issues
  • impulsivity

difficult to plan treatment

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8
Q
Treatment/Considerations: 
most often ? 
-
-
-

-
-

-
-ability to actively ?

A

adaptive in nature during most acute phases

  • positioning
  • assistance, orthopedic injuries
  • diet modifications
  • strengthening
  • sensory
  • presence of partial/total nerve damage

supervision
impulsivity
ability to actively participate in compensations/exercises (family particiaption)

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9
Q
Multiple Sclerosis: 
-
-immune? 
-...disease
-not ? but ? 
-near ? will exhibit dysphagia
A

demyelination

  • immune-mediated disorder
  • inflammatory disease
  • not hereditary but genetics can impact
  • 30%
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10
Q
Sequelae of MS: 
dependent on ? 
-
-
-
-

oral?
pharyngeal ?

A

site of lesions

  • brainstem
  • cerebellum
  • corticospinal tracts
  • cranial nerves

oral dysphagia (motor)

pharyngeal dysphagia (sensory/constriction/delay)

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11
Q
Classifications of MS: 
-
-
-
-
A

progressive-relapsing

secondary progressive

primary progressive

relapsing -remitting

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12
Q

Treatment/considerations MS;
medical

  • E
  • P
  • T
  • M
  • Supplemental
A

medical management

education (insight)

positioning

thermal/tactile stimulation

maneuvers (supraglottic,cough, etc)

supplemental/non-oral nutrition

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13
Q
Parkinsons's disease: 
degenerative disorder of the ?
cell death in the ? 
reduction in> 
-
-
-
-
-
63-81% of patients will experience
A
CNS 
substantia nigra (part of the midbrain and basal ganglia) 

dopamine

  • neurotransmitter
  • movement disorder
  • difficulty initiating /slowed movements
  • tremors
  • cognition, mood, behavior

dysphagia

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14
Q
Sequelae of PD: 
oral movement ? 
-
-
-

-
-

-

A

deficits

  • tremors
  • bolus formation/containment
  • tongue rocking/pumping

pharyngeal deficits:

  • some delay
  • reduced pharyngeal wall contraction
  • reduced laryngeal excursion
  • dementia
  • rigidity
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15
Q
Huntington's disease: 
... disease
-... dominant mutation 
-mutation causes? 
-excessive ? 
-life expectancy: 
pneumonia is the primary cause of ?
A

neurogenic genetic disorder

autosomal dominant mutation

gradual damage

involuntary movements

20 years post Dx

death in patients with HD

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16
Q

Sequelae Huntingtons:
involuntary

-
-
difficulty ? 
deceased? 
decreased? 
delayed ? 
uncoordinated ?
A

movements

  • rigidity
  • chorea (writhing/rhythmic motions)
  • difficulty self feeding
  • decreased bolus control
  • decreased effective mastication
  • delayed pharyngeal swallow onset
  • uncoordinated oropharyngeal swallow
17
Q
ALS 
form of? 
-no 
-both ? 
-....
-...
-intact 
-... effect 
-ever-decreasing: 
-all patients will exhibit
A

motor neuron disease (MND)

no known cause

upper and lower motor neurons that control voluntary movement (may attack any at first)

progressive

fatal

intact cognition

pseudobulbar affect (40-45%)

respiratory function

dysphagia at some point

18
Q
Sequelae ALS: 
... involvement 
-reduced
-decreased ? 
-decreasing ability to ? 
-reduced? 
.... involvement 
-later developments: 
1. reduced
2. reduced
3. reduced
4. delayed
A

corticobulbar/corticospinal tract involvement

tongue mobility

bolus formation/intraoral pressures

orally handle more viscous liquids/foods

labial seal/drooling

velopharyngeal port involvement

BOT
pharyngeal contraction
airway protection
pharyngeal swallow initiation

19
Q
Myasthenia Gravis: 
autoimmune: 
antibodies ? 
decrease function of 
easily 
.../....
normal  ?
A
neuromuscular disease
block post-synpatic receptors from accepting acetylcholine 
nAChR
fatigued musculature 
remissions/exacerbations 
life expectancy (in length)
20
Q
Sequelae MA: 
dysphagia is often ? 
-often 
-flaccid 
-hyper
-... symptoms (...,...,...) 
-... muscles ? 
oral dysphagia is usually ? 
reduced? 
delayed ?
decreased?
A

sentinel presentation

  • silent
  • dysarthria
  • hypernasality
  • bulbar symptoms (pons,cerebellum, medulla)
  • striated muscles: lips, mandible, tongue, velum, hypopharynx
  • pharyngeal contraction
  • pharyngeal swallow
  • BOT retraction
21
Q
Important considerations: 
these pts may appear less ? 
-.. is primary concern 
-.... status 
-collab with ? 
-generally higher risk for ?
A

effected under a 2-3 min MBS/VFSS/FEES -sensitive eval

  • fatigue
  • respiratory status
  • physicians
  • aspiration pneumonia than persons after a stroke