Neurogenic Dysphagia Pt. 1

Neurogenic Dysphagia often concurrent with…

dysarthria, dysphonia, and/or cognitive-linguistic disorders

Neurogenic dysphagia occurs when there is damage to the…

CNS (brainstem/spinal cord) and/or PNS (efferents, cranial nerves, neuromuscular junction)

Neurogenic =

originating from/controlled by nervous system

How many individuals are affected by neurogenic dysphagia each year

between 300,000 and 600,000

Neurogenic dysphagia results in…

• sensory-motor changes; changes to both sensory and motor

• sensory and motor generally occur together, but can be separate

i.e. aspiration (sensory in trachea not responsive, inadequate muscular function)

Central Etiologies (brainstem/spinal cord)

Non-degenerative

• CVA (Stroke)

• brain injury

• medication

• neoplasm

• Congential CP syringobulbia, arnold chiari malformation)

• Psychogenic

Degenerative

• dementia/AD

• PD and PD+

• MS

• HD

• ALS

Peripheral Etiologies (cranial nerves/ efferent muscular junction)

Myopathy

• polymyositis, dermatomyositis

• Muscular dystrophies

  • OPMD, MD, DMD

Neuropathy

• Guillain-Barre

Latrogenic

• Post-surgery or RT of H&N

Neuromuscular

• MG

• Polio, Post-polio syndrome

Neurogenic dysphagia: Evaluations

• best completed in a multidisciplinary environment (multidisciplinary team; neurologists, nurses, PA etc)

• Sensitivity of BCES ranges from 40-80%; specificity ranges from 59-91%

• Instrumental assessment is invaluable; most often VFS or FEES

• Bedside swallow can tell us that someone has a swallowing issue, but it doesn’t account for sensory issues, so we need to use an MBS or FEES to see if there is any “silent aspiration” occurring etc.

Evaluation

• get a good/thorough case history

• do oral mech exam

• then pick an evaluation technique (MBS/FEES)

• no treatment = no deficit, patient doesn’t want treatment

• From evaluation, then decide on treatment

Compensatory Treatment

• diet modifications

• postural changes

• prothetics

• sensory input

Rehabilitative/ Restorative Treatment

• range of motion

• strength

• coordination

• endurance

Combined Modality Treatment

compensation + rehab strategies

Normal Oral Prep stage

• food to mouth (sensory and motor)

• lips seal- Orbicularis Oris

• keep bolus from spilling into pharynx- palatalglossus

• bolus formation (mix with saliva)

• Chewing- masseter, temporalis, pterygoids, submentals

Oral prep stage: Disordered

• lack of interest in food following sensory impairments, depression, reduced alertness/consciousness

  • hyperphagia (overeating/over fill the oral cavity)

  • feeding aversion

  • reduced appetite

• motor problems may lead to reduced ability to maintain appropriate position for feeding or difficulty bringing food to the mouth

  • i.e. tremor, drooling, impaired chewing

  • infants may have difficulties in breast feeding

Oral transit: Normal

• posterior movement of bolus

• tip of tongue contracts to touch alveolar ridge (superior longitudinal)

• bolus squeezed back

  • anterior to posterior; squeezing action through groove

• faucial arches

• back of tongue depresses (hyoglossus)

• bolus held between tongue and soft palate (palatalglossus)

• pharyngeal stage is triggered

Oral Transit: disordered

• tongue pumping

• lingual paralysis

• pre-swallow spill

• impaired movement of bolus from front to back of oral cavity

  • residue

  • weak propulsion of bolus into pharynx

  • i.e. spills into valleculae

Pharyngeal stage: Normal

• base of tongue- PPW contact (PG, SG, superior constrictor)

• soft palate closure (LVP)

• hyolaryngeal elevation/excursion

• laryngeal closure

• VF closed (LCA, IA, TA)

• Vestibule closes

• epiglottis inverts

• stripping action by constrictors

• UES relaxes/pulled open

• about 1 second long

Pharyngeal stage: disordered

• nasal regurgitation

• improper airway closure: penetration/aspiration

• slow movement of the bolus through the pharynx

• late triggering of swallow

• reduced extent and/or duration of cricopharyngeal opening

• residue in valleculae

• residue in pyriform sinuses

• lack of paristalsis

Esophageal stage: Normal

• UES-LES-STOMACH

• timely manner

• peristalsis

• 8-20 seconds

Esophageal: disordered

• esophageal strictures

• diverticulum (pocketing of tissue)

• lack of peristaltic movements: residual food in the esophagus

• GERD

• Tertiary contractions

• you miss 100% of esophageal causes you don’t look for!

Achalasia =

no peristalsis

Non-degenerative CNS Etiologies =

• one time incident (like a stroke)

• we expect them to get better over time/with therapy (for the most part)

• damage to brain/brainstem, or spinal cord

Cerebrovascular Accident (CVA)— stroke

• dysphagia will occur in 29-80% of individuals following an acute stroke

  • 50% will aspirate

  • 35% will develop aspiration pneumonia

• many cases 50-90% will resolve rapidly (spontaneous recovery)

• 20-50% of patients maintain persistent chronic dysphagia

• aspiration pneumonia is the most common cause of re-hospitalization and the LEADING cause of death in this population

  • possibly related to depressed immune system post-stroke

• UMN is resilient to CN X; cortical stroke won’t expect damage to pharyngeal

CVA timing of evaluation

• EARLY SLP assessment is required within the first week to assess appropriateness of PO (by mouth intake)

  • follow-up at bedside if any concerns

  • can give diet mods

  • recommend instrumental (MBS, FEES) if concerned.

Prolonged dysphagia =

symptoms > 2 weeks; anything more than 2 weeks

VFS exposes patient to radiation, therefore..

• you want to complete VFS when stability is reached

• or when it is clear PO intake compromises airway protection

CVA: Neuropathophysiology

• swallowing function has bilateral cortical and brainstem representation

  • resilient

  • however, diffuse nature also can be the cause of dysfunction

• Brainstem - will be more impacted than cortex

  • nucleus ambiguous often impacted by stroke- provides motor output to pharynx and esophagus

    • reduced pharyngeal peristalsis

    • slow pharyngeal transit

    • penetration/aspiration

    • UES dysfunction

    • esophageal dysmotility

  • hypoglossal nucleus involvement - lingual dysfunction

• Cortex- less impacted

  • reduced facial symmetry

  • oral incompetence

  • poor bolus control

Brain Injury

• reports vary, but 20-70% of patients who experience brain injury will demonstrate dysphagia

  • surgery/radiotherapy

  • TBI

  • vascular insult

  • metabolic disorders

• impacts children (68%-76%) and adults

• typically onset of dysphagia is acute and then resolves after initial injury

  • makes re-assessment vital to monitory ongoing dietary recommendations and modifications

• Tracheostomy and mechanical ventilation increased dysphagia risks

Brain injury & swallowing impairments:

• impairments often involve VOLUNTARY phases of swallowing and dyscoordination of oME

• level of cognition also a factor

• VFS may show:

  • tongue pumping

  • residue

  • pre-swallow spill

  • delayed initiation of swallow

  • primitive reflexes (suckle, tongue protrusions)

• One study showed that one month post injury, 17% of 18 participants aspirated during VFS, about 2/3 of those were silent

Cerebral Palsy

• non-progressive neurological motor and processing disorder

  • arises following injury to the fetal or infant brain

  • >85% of individuals will survive well into adulthood

  • causes sensory, motor, cognitive-linguistic dysfunction

• Increased spasticity may result in:

  • unusual posturing (contraction of neck etc)

  • difficulty transferring food and fluids to the oral cavity

  • penetration/aspiration

  • increased coughing/choking

• Severity of dysphagia is related to presence of other disabilities

  • non-ambulatory

  • intellectual disability

  • gastrostomies

Psychogenic Dysphagia

• Physiology/mechanism is okay; patient still experiences dysphagia; some part of brain is causing it

• AKA: conversion dysphagia, functional, hysterical, hyperfunction etc

• medically unexplained (anatomy and phys are okay)

• always use imaging to rule out organic causes

• current research: investigating personality link

• may be aphagic (inability to swallow); however, manage saliva efficiently - generally embarrassed and desire help

Conversion dysphagia

unexplained symptoms or deficits affecting voluntary motor function suggest a neurologic or medical condition