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Stroke Pathophysiology
blood clot forms and blocks blood flow to an area of the brain
blood vessel ruptures causing bleeding into or around the brain
Stroke Disease Course & Prognosis
in general, we expect patients in recovery from a stroke to improve
spontaneous recovery period ~3-6 mos for gross motor function; speech/language/cog can be longer
consider neuroplasticity
Specific Stroke Dysphagia Features
highly variable, no two cases are identical
affects any/all swallowing events
cognition directly influences swallow safety and compliance
Brainstem Stroke Dysphagia Features
most likely pharyngeal swallow impairment
What is spontaneous recovery after a CVA?
the brain’s ability to repair the area that surrounds the lesion quickly
reprofusion, edema management, diaschisis reversal
Reprofusion
restoration of oxygnated blood to the area
Edema management
swelling goes down so oxygenated blood can return
Diaschisis Reversal
the most important spontaneous recovery mechanism
reverses depressed neural activity from loss of input from damaged areas of the brain
Wallenberg Syndrome Pathophysiology
secondary to an ischemic stroke in the lateral medulla (brainstem)
Wallenberg Syndrome Dysphagia Incidence
51-94% of patients experience severe dysphagia
Wallenberg Syndrome Prognosis
non-progressive trajectory but the rate of recovery is extremely variable across individuals
Wallenberg Syndrome Dysphagia Features
difficulty triggering the swallow
absent pharyngeal constriction (unilateral or bilateral)
minimal or absent relaxation of the UES
Wallenberg Syndrome Nutritional Support
often requires temporary or long-term supplemental nutrition/hydration via PEG
TBI Pathophysiology
direct head trauma, coup-contrecoup impact, puncture, or brainstem twisting forces
causes diffuse neural damage rather than single focal lesions
TBI Disease Course & Prognosis
non-progressive trajectory, overall recovery expected
voluntary oral control improves alongside attention and concentration recovery
cognitive-communication deficits typically outlast swallowing impairments
TBI Specific Dysphagia Features
no two cases are the same
driven heavily by cognitive-behavioral factors (impulsivity, awareness, impaired sensation and comprehension) and iatrogenic factors (tracheostomy, medications)
Dementia Pathophysiology
impairment in cognition or cognitive-communication skills that interfere with everyday life
dependent on the type (Alzheimer's, Frontotemporal, Vascular, Lewy Body)
Dementia Dysphagia Causes
stems from reduced muscle strength, oral sensation, motor planning, cognitive dysfunction, and oral lubrication
Dementia Disease Course & Prognosis
progressive, degenerative trajectory with variable rates of decline
managed primarily in SNFs and long-term care facilities
Dementia Dysphagia Features
agnosia = loss of food recognition
slow oral manipulation, lingual searching, and oral holding
slow/delayed pharyngeal swallow trigger
What types of support do people with dementia need for feeding?
increased verbal/physical cues for self-feeding
direct assistance with utensil setup
imitation of feeding behavior from meal partner
Motor Neuron Disease/ALS Pathophysiology
rapidly progressive
fatal neurodegenerative disease of motor neurons (UMN/LMN)
Motor Neuron Disease/ALS Risk Factors
smoking
extreme physical activity
infectious disease
genetics
military service/trauma
Motor Neuron Disease/ALS Disease Course & Prognosis
rapid continuous decline; post-onset lifespan typically 3-6 years
supportive care planned early (tube feeding, non-invasive ventilation, AAC)
co-occurs with progressive dysarthria and generalized weakness
Motor Neuron Disease/ALS Specific Dysphagia Features
weakness in oral structures, delayed swallow reflex, nasal regurgitation, wet/gurgly voice, coughing, aspiration, gagging
Parkinson's Disease Pathophysiology
basal ganglia degeneration causes dopamine depletion that affects many body functions (resting tremor, bradykinesia/hypokinesia, and rigidity)
Parkinson's Disease Course & Prognosis
slowly progressive neurodegenerative trajectory
symptoms fluctuate and temporarily improve with treatment (deep brain stimulation) and meds (carbidopa-levodopa)
Parkinson's Disease Oral Stage Dysphagia Features
repetitive lingual rolling/pumping
lingual/velar tremor
ramplike tongue posture
piecemeal deglutition
buccal retention
Parkinson's Disease Pharyngeal Stage Dysphagia Features
delayed trigger
reduced pharyngeal constriction/elevation
vallecular/pyriform sinus residue
penetration/aspiration
Parkinson's Disease Sensory & Esophageal Dysphagia Features
elevated sensory thresholds (reduced sensation)
PE segment dysfunction
T/F: dysphagia from neurological disorders reflects the underlying sensorimotor characteristics of the neurological deficit
true
Treatment of neurogenic dysphagia relies heavily on understanding the _________ process
neurologic
In the absence of an overt neurological disease, how should we go about dysphagia that seems neurogenic?
it should be considered reflective of an underlying neurological cause until proven otherwise
Many forms of neurogenic dysphagia can change over time, and we need to pivot according to…
recovery
degeneration and decline in function