Swallowing

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Swallowing

  1. 1. Normal Swallowing • Complicated and intricate phenomenon • Mixture of voluntary and reflex, or automatic, actions • Total number of swallows per day is about 600: – 200 while eating and drinking – 350 while awake without food – 50 while sleeping 'empty' swallows primarily to the clearance of saliva from the mouth
  2. 2. Anatomy of swallowing • 55 muscles of the oropharyngeal, laryngeal, and esophageal regions • Five cranial nerves – V, VII, IX, X, XII • Two cervical nerve roots • Centers within the central nervous system
  3. 3. Anatomy of swallowing A. Oral cavity – Separated from the pharynx by the faucial pillars B. Pharynx C. Esophagus
  4. 4. Anatomy of swallowing • Laryngeal aditus (upper end of the larynx) opens into the lower portion of the pharynx • Epiglottis – Originates in the larynx and is angled upward and backward – Attached to the hyoid bone anteriorly
  5. 5. Anatomy of swallowing Hyoid bone • Mechanical connections to the cranial base, mandible, sternum, and thyroid cartilage via the suprahyoid and infrahyoid muscles • Important role in controlling the movements of the jaw and tongue.
  6. 6. Anatomy of swallowing Valleculae • Space between the pharyngeal surface of the tongue and the epiglottis Pyriform recesses • Two spaces in the pharynx lateral to the larynx
  7. 7. Anatomy of swallowing Constrictor muscles • Flattens and contracts the pharynx in swallowing Cricopharyngeus muscle •Closes the UES by compressing it against the back of the cricoid cartilage
  8. 8. Innervation of major muscles related to swallowing Cranial nerves Muscles Masticatory muscles Mylohyoid Trigeminal Nerve (V) Tensor veli palatini Anterior belly of digastrics Facial muscle Facial nerve (VII) Stylohyoid Posterior belly of digastrics
  9. 9. Innervation of major muscles related to swallowing Cranial nerves Muscles Glossopharyngeal Nerve (IX) Stylopharyngeus Levator veli palatine Palatopharyngeous Salpingopharyngeous Vagus nerve (X) Intrinsic laryngeal muscles Cricopharyngeus Pharyngeal constrictors
  10. 10. Innervation of major muscles related to swallowing Cranial nerves Muscles Intrinsic tongue muscles Hyoglossus Geniohyoid Hypoglossal nerve (XII) Genioglossus Styloglossus Thyrohyoid
  11. 11. Sensory afferents I. Trigeminal – Teeth and gums, palate and roof of the pharynx II. Glossopharyngeal – Posterior third of the tongue, pharynx, area of the tonsil III. Vagus – Pharynx, larynx
  12. 12. Brainstem centers • Central pattern generators – Dorsomedial & Ventrolateral • Mainly involves nucleus of the tractus solitarius and the nucleus ambiguous • Programs directing the sequential movements of the various muscles involved
  13. 13. Brainstem centers • Activated by – Descending pathways from the motor cortex (cortico bulbar tracts) – Ascending pathways from sensory structures within the oropharynx and esophagus Nucleus of the tractus solitarius receives the descending and peripheral afferent influences
  14. 14. Dorsomedial pattern generator • Resides in the medial reticular formation of the rostral medulla and the reticulum adjacent to the nucleus tractus solitarius • Initiation and organization of the swallowing sequence
  15. 15. Ventrolateral pattern generator • Lies near the nucleus ambiguous and its surrounding reticular formation • Serves primarily as a connecting pathway to motor nuclei such as the nucleus ambiguus and the dorsal motor nucleus of the vagus, which directly control motor output to the pharyngeal musculature and proximal esophagus
  16. 16. Cortical control to brainstem structures Inferior precentral gyrus • Cortical representations of tongue and face • Bilaterally symmetrical activation
  17. 17. Other cortical areas involved in swallowing Supplementary motor area • Preparation for volitional swallowing Anterior cingulate cortex • Monitoring autonomic and vegetative functions.
  18. 18. Other cortical areas involved in swallowing Anterior insula, particularly on the right • Activation during volitional swallowing • Allows gustatory and other intraoral sensations to modulate swallowing. • Lesions increase the swallowing threshold and delay the pharyngeal phase of swallowing
  19. 19. Other higher centers in swallowing Cerebellum • Esp left-sided activation • Coordination, timing, and sequencing of swallowing • controls output for the motor nuclei of cranial nerves V, VII, and XII Putamen • Activated during volitional swallowing
  20. 20. Stages of Swallowing Initiated reflexly when food or liquid stimulates sensory nerves in the oropharynx Three distinct stages or phases: • Oral Horizontal subsystem Volitional in character • Pharyngeal • Esophageal Vertical subsystem Primarily under reflex control
  21. 21. ORAL PHASE • Oral preparatory and oral propulsive stages • Food bolus is formed and pushed to pharynx
  22. 22. Oral preparatory stage Chewing • Cyclic movement of the jaw coordinated with the movements of the tongue, cheek, soft palate and hyoid bone • Food particles are reduced in size and softened by salivation until the food consistency is optimal for swallowing • Movements of the jaw and tongue pump air into the nasal cavity through the pharynx, delivering the food's aroma to chemoreceptors in the nose
  23. 23. Oral propulsive stage Shallow midline gutter in tongue to accommodate bolus Styloglossi and genioglossi Emptying of the longitudinal gutter posteriorly Hyoglossus and some intrinsic lingual muscles Elevation of anterior and mid tongue, hyoid bone and floor of the mouth Mylohyoid, geniohyoid and stylohyoid Relaxation of the posterior oral seal and a forward movement of the posterior tongue Palatoglossi. Overall effect is sweeps or squeezes the bolus towards the fauces to pharynx
  24. 24. ORAL PHASE • Transported food accumulates on the pharyngeal surface of the tongue and in the valleculae • Duration of bolus aggregation in the oropharynx ranges from a fraction of a second to about ten seconds in normal individuals eating solid food
  25. 25. PHARYNGEAL PHASE • Rapid sequential activity, occurring within a second • Pharynx changes from being an air channel to food channel Two crucial biological features: 1. Food passage 2. Airway protection
  26. 26. Airway protection Closing the nasopharynx • Superior Pharyngeal Constrictor + Palatopharyngeal forming a variable, ridge-like, structure (Passavant's Ridge) to which the soft palate is elevated. • Occurs at same time the bolus head comes into the pharynx • Prevents bolus regurgitation into the nasal cavity
  27. 27. Airway protection Closure at lower level a) Vocal folds close to seal the glottis b) hyoid bone and larynx are pulled upward and forward – Tucks the larynx under the base of the tongue Suprahyoid and Thyrohyoid c) Epiglottis tilts backward to seal the laryngeal vestibule
  28. 28. Food passage • Sequential contraction of three pharyngeal constrictor muscles • Driving force which propels the bolus towards the oesophagus
  29. 29. OESOPHAGEAL PHASE Involves • Relaxation of UES • Propulsion of food bolus to stomach
  30. 30. Relaxation of UES 3 factors UES consists of the inferior pharyngeal constrictor, cricopharyngeous and most proximal part of the esophagus 1) Relaxation of the cricopharyngeous muscle – Precedes arrival of the bolus 2) Contraction of the suprahyoid and thyrohyoid muscles – Pull the hyo-laryngeal complex forward, opening the sphincter – Active opening process 3) Pressure of the descending bolus
  31. 31. OESOPHAGEAL PHASE Once in the oesophagus, the bolus is propelled by peristaltic contractions down to the lower oesophageal sphincter, which opens momentarily to allow the bolus to enter the stomach
  32. 32. Synchronization of swallowing with respiration • Breathing ceases briefly during swallowing – Physical closure by elevation of the soft palate and tilting of the epiglottis – Neural suppression of respiration in the brainstem • Respiratory pause continues for 0.5 to 1.5 s • Expiration immediately follows a swallow, thus reducing the risk of aspiration
  33. 33. Dysphagia • Impaired swallowing can originate from disturbances in the mouth, pharynx, or esophagus • Can involve mechanical, musculoskeletal, or neurogenic mechanisms
  34. 34. Consequences of dysphagia • Inadequate nutrition • Dehydration • Recurrent upper respiratory infections • Frank aspiration with consequent pneumonia and even asphyxia
  35. 35. Approach to a case of Dysphagia Good history will accurately identify the location and cause of dysphagia in 80% of cases
  36. 36. Approach to a case of Dysphagia • Dysphagia for solid food but not liquids Mechanical obstruction • Equal dysphagia for both solids and liquids Esophageal dysmotility
  37. 37. Mechanical Dysphagia • Structural abnormalities, both within and adjacent to the mouth, pharynx, and esophagus Oral Pharyngeal Esophageal Congenital abnormalities Cervical anterior Esophageal carcinoma Intraoral tumors osteophytes Esophageal diverticulum Burns Diphtheria Esophageal infection: Trauma Thyromegaly Esophageal stricture Temporomandibular joint Retropharyngeal abscess Esophageal webs or rings dysfunction Retropharyngeal tumor GERD Zenker diverticulum Thoracic aortic aneurysm
  38. 38. Neurogenic dysphagia Oropharyngeal Or Esophageal Perception of the bolus “sticking” in the neck may indicate either pharyngeal or esophageal localization
  39. 39. Oropharyngeal source for the dysphagia • Difficulty initiating swallowing • Need for repeated attempts to succeed at swallowing • Presence of nasal regurgitation during swallowing • Coughing or choking immediately after attempted swallowing
  40. 40. If Oropharyngeal Phase Dysfunction Suspected Screening tests: • Clinical examination Complementary tests: • Cervical auscultation •Pharyngeal videoendoscopy • 3-oz water swallow •Pharyngeal manometry Primary test: •Electromyography • Modified barium swallow •Videomanofluorometry
  41. 41. Oral stage dysfunction Clinical examination of CN V, VII, XII Weakness of the buccal or labial muscles • Food trapped in the buccal or labial sulci (between the lower teeth and the cheeks or gums, respectively)
  42. 42. Oral stage dysfunction Tongue dysfunction • impaired mastication and bolus formation, and bolus transport Sensory impairments • excessive retention of food in the oral cavity after eating and swallowing
  43. 43. Pharyngeal stage dysfunction • Clinical examination of CN IX and X • Cervical ausculatation
  44. 44. Cranial nerve IX • Examine pain and touch sensation of the pharynx, tonsilar region and soft palate • Only muscle with innervation purely from CN IX is stylopharyngeus • Only deficit detectable is a slight lowering of the palatal arch at rest on the involved side. • Gag reflex
  45. 45. VAGUS NERVE • With a contribution from the bulbar portion of CN XI, supplies all the striated muscles of the soft palate, pharynx, and larynx except for the stylopharyngeus (CN IX) and tensor veli palatini (CN V) • Sensory from the pharynx, larynx
  46. 46. CN X lesions • Speech may have a nasal quality • Dysphagia more marked for liquids than solids with a tendency to nasal regurgitation • Droop of the palate and flattening of the palatal arch – Preserved tensor veli palatini (CN V) may prevent marked drooping of the palate • Gag reflex lost on the involved side
  47. 47. CN X lesions Vernet's rideau phenomenon • Due to unilateral weakness of the superior pharyngeal constrictor • “curtain movement”, with motion of the pharyngeal wall toward the nonparalyzed side on testing the gag reflex or at the beginning of phonation
  48. 48. Gag reflex • Elicited by touching the lateral oropharynx in the region of the anterior faucial pillar (pharyngeal reflex) • Or by touching one side of the soft palate or uvula (palatal reflex) Pharyngeal reflex is the more active of the two
  49. 49. Gag reflex Three motor components 1) Elevation of the soft palate to seal off the nasopharynx 2) Closure of the glottis to protect the airway 3) Constriction of the pharynx to prevent entry of the substance.
  50. 50. Gag reflex Afferent limb - CN IX Reflex center - medulla Efferent limb - CNs IX and X • Constriction and elevation of the oropharynx • Midline raphe of the palate and the uvula elevate • Pharyngeal constrictors contract
  51. 51. Gag reflex • Unilateral weakness – Raphe will deviate away from the weak side and toward the normal side • May be bilaterally absent in some normal individuals • Unilateral absence signifies a lower motor neuron lesion
  52. 52. Significance of gag reflex • Poor gag reflex in an awake patient with an acute deficit may be a predictor of swallowing difficulties Useful but limited in assessing airway protection • Patients with an apparently intact gag reflex may still aspirate • Absent in ~ 37% of normals - low predictive value in the assessment of aspiration risk
  53. 53. Cervical auscultation • Assess coordination between respiration and swallowing • In the normal situation, swallowing occurs during exhalation • Discoordinated swallowing in the midst of inhalation increases aspiration possibility
  54. 54. Standardized 3 oz water swallow test • Simple bedside evaluation for oropharyngeal dysphagia. • Presence of cough on swallowing – Positive predictive value of 84% with regard to the presence of aspiration – Negative predictive value of 78%. • After the swallow, observe the patient for 1 minute or more to see if a delayed cough response is present
  55. 55. Dysphagia limit • Normal subjects can swallow a 20-ml bolus of water in a single attempt • With dysphagia must divide the bolus into two or more parts in order to complete the swallow
  56. 56. Dysphagia limit • Individuals are administered stepwise increases in bolus volume, the volume of fluid at which the division of the bolus first occurs is labeled the dysphagia limit Dysphagia limit of less than 20 ml as abnormal and indicative of dysphagia
  57. 57. Modified barium swallow test • Swallowing barium impregnated food of differing consistencies (thin liquid, pudding, cookie) • Observed via videofluoroscopy
  58. 58. Modified barium swallow test • Oral and pharyngeal function can be characterized • Presence of aspiration accurately documented • Response to corrective measures such as positioning techniques can also be evaluated • Increasing bolus viscosity typically improves swallowing function in individuals with neurogenic dysphagia
  59. 59. Modified barium swallow test Laryngeal penetration • passage of the food into the larynx but above the vocal folds • sometimes observed in normal individuals Aspiration • passage of material through the vocal folds
  60. 60. Videoendoscopy of the pharynx • Via the nasal passageway • Allows direct visualization of the pharyngeal component of swallowing before and after passage of the food bolus • Primary value is to demonstrate the presence of residual material in the pharynx after a swallow, indicative of increased risk of aspiration
  61. 61. Swallowing Electromyography • Mechanical upward-downward movement of the larynx is detected by using a piezoelectric sensor while submental integrated electromyography (EMG) activity is recorded during dry and wet swallowing • EMG activity of the cricopharyngeal muscle also can be recorded.
  62. 62. Swallowing Electromyography • In muscular disorders, laryngeal elevators are involved, whereas the cricopharyngeal sphincter is intact • In pyramidal lesions, discoordination between paretic laryngeal elevators and the hyperreflexic cricopharyngeal sphincter is present. EMG can be used for muscle selection and for performing injections of botulinum toxin in patients with dysphagia
  63. 63. Esophageal dysfunction • Sensation of food “hanging up” in a retrosternal location • Main concern with esophageal dysphagia is to exclude malignancy
  64. 64. Esophageal dysfunction Malignancy is likely if there is: • Short duration (< 4 months) • Disease progression • Dysphagia more for solids than for liquids • Weight loss
  65. 65. If Esophageal Dysfunction Suspected: Primary tests: • Videofluoroscopy • Endoscopy Complementary test: • Esophageal manometry
  66. 66. Oculopharyngeal Muscular Dystrophy • Rare autosomal dominant disorder • GCG trinucleotide repeat on chromosome 14 • First appearing between ages 40 and 60 • Slowly progressive ptosis, dysphagia, and proximal limb weakness • Evolves slowly over many years
  67. 67. Oculopharyngeal Muscular Dystrophy • Dysphagia due to impaired function of the oropharyngeal musculature • No specific treatment • Cricopharyngeal myotomy affords relief in over 80% • Botulinum toxin injections have been successfully used
  68. 68. Myotonic Dystrophy • autosomal dominant disorder • cardiac, ophthalmological, and endocrinological involvement • Subjective dysphagia in 37% to 56% of patients • Objective measures demonstrating disturbances in swallowing in 70% to 80%
  69. 69. Myotonic Dystrophy • Dysphagia due to – Abnormal cricopharyngeal muscle activity is present in 40% – Impaired esophageal peristalsis – incomplete relaxation of the UES and esophageal hypotonia Both muscle weakness and myotonia play a role in the development of dysphagia
  70. 70. Inflammatory Myopathies • Dysphagia more frequently is present in dermatomyositis and when present is more severe • Indicator of poor prognosis Dysphagia in inclusion body myositis • May even be the presenting symptom • In late stages of the disorder, the frequency exceed that seen in dermatomyositis and polymyositis
  71. 71. Inflammatory Myopathies Treatment • May respond to corticosteroids and other immunosuppressive drugs Unresponsive to steroids • IVIG therapy has produced dramatic improvement Inclusion-body myositis • Typically responds poorly • Myotomy is often necessary
  72. 72. Mitochondrial Disorders Dysphagia due to • Severe abnormalities of pharyngeal and upperesophageal peristalsis • Cricopharyngeal dysfunction • Impaired deglutitive coordination
  73. 73. Myasthenia Gravis • In ~ 6% to 30%, bulbar involvement is evident from the beginning • with disease progression, most eventually develop • major precipitant of myasthenic crisis in 56% of patients • Bedside speech pathology assessment is not a reliable predictor of aspiration
  74. 74. Myasthenia Gravis Dysphagia due to Dysfunction at oral, pharyngeal, or even esophageal levels • Oral phase involvement due to fatigue and weakness of the tongue or masticatory muscles • Decreased amplitude and prolongation of the peristaltic wave in esophagus • Cricopharyngeal sphincter pressure reduced
  75. 75. Stroke • Dysphagia in 45% to 57% • Aspiration in – 30% to 55% of stroke patients – 36% of patients with unilateral cerebral stroke – 46% with bilateral cerebral stroke – brainstem strokes - more than 80% Associated with increased likelihood of severe disability or death
  76. 76. Warning signs of post-stroke dysphagia • Drooling • Excessive tongue movement • Spitting food out of the mouth • Poor tongue control • Pocketing of food in the mouth • Facial weakness • Slurred speech • Coughing or choking when eating
  77. 77. Warning signs of post-stroke dysphagia • Regurgitation of food through the nose • Wet or “gurgly” voice after eating • Hoarse or breathy voice • Complaints of food sticking in the throat • Absence or delay of laryngeal elevation • Prolonged chewing • Prolonged time to eat or reluctance to eat • Recurrent pneumonia
  78. 78. Dysphagia and site of stroke Brainstem infarction • Pharyngeal phase is primarily impaired Hemispheric strokes • Delay in initiation of voluntary swallowing • Bilateral hemispheric damage is more likely to produce dysphagia
  79. 79. Dysphagia and site of stroke Can also occur in the setting of unilateral damage Right hemisphere • More impairment of pharyngeal motility Left hemisphere • Greater effect on oral stage function
  80. 80. Dysphagia and site of stroke Subcortical strokes • higher incidence of dysphagia and aspiration than those with cortical damage • delayed initiation of the pharyngeal stage of swallowing
  81. 81. Dysphagia and site of stroke Foix- Chavany-Marie syndrome (anterior operculum syndrome) • Bilateral infarction of the frontoparietal operculum • inability to perform voluntary movements of the face, jaw, tongue, and pharynx but fully preserved involuntary movements of the same muscles • Impairment of volitional swallowing
  82. 82. Tongue deviation & dysphagia • Classically associated with medullary lesions damaging the hypoglossal nucleus • In almost 30% of persons with hemispheric infarctions • Dysphagia is present in 43% of affected patients
  83. 83. Stepwise assessment of swallowing in stroke patients • Modified swallowing assessment on the day of admission • Clinical swallowing examination performed within 72 hours • Performance of flexible transnasal swallowing endoscopy within 5 days • Appropriate diet and treatment determined after each step • Significant reduction in the rate of pneumonia and in antibiotic consumption (ickenstein et al., 2010)
  84. 84. Prognosis • Swallowing often improves spontaneously in the days and weeks after stroke • more likely to occur after cortical strokes, compared with those of brainstem origin
  85. 85. Dysphagia in other cerebrovascular processes • Carotid artery aneurysms • Elongation and dilatation of the basilar artery • Posterior inferior cerebellar artery aneurysm • Intracranial vertebral artery dissections • Giant dissecting vertebrobasilar aneurysms
  86. 86. Dysphagia in Multiple Sclerosis • Frequent but often overlooked (24% to 34% ) • Prevalence rises with increasing disability • Individuals with severe brainstem involvement as part of their MS are especially likely to experience dysphagia. Mild disability • Abnormalities in the oral phase of swallowing More severe disability • Additional pharyngeal phase abnormalities develop
  87. 87. Dysphagia in Parkinson Disease • Frequent phenomenon - 30% to 82% • More likely to swallow during inspiration and also to inhale post swallow • Both increase the risk of aspiration Oral phase • Difficulty with bolus formation • Delayed initiation of swallowing • Repeated tongue pumping, and other abnormalities
  88. 88. Dysphagia in Parkinson Disease Pharyngeal phase • Pharyngeal dysmotility and impaired relaxation of the cricopharyngeal muscle Esophageal phase • Slowed esophageal transit • Both segmental and diffuse esophageal spasm • Ineffective or tertiary contractions, and even aperistalsis • Lower-esophageal sphincter dysfunction - reflux as well as dysphagia.
  89. 89. Dysphagia in Parkinson Disease Management • Inconsistent response to levodopa or dopamine agonist therapy • Cricopharyngeal muscle dysfunction cricopharyngeal myotomy and botulinum toxin injections • Behavioral swallowing therapy • PEG tube placement rarely necessary
  90. 90. Other Basal Ganglia Disorders Parkinsonism-plus syndromes- PSP, MSA, CBD, DLB • Dysphagia is a frequent problem • Develops relatively early in the course of the illness Appearance of dysphagia within 1 year of symptom onset virtually eliminates PD as a diagnostic possibility
  91. 91. Amyotrophic Lateral Sclerosis • Dysphagia eventually develops in most individuals • Presenting feature in approximately 25% • Sensation of solid food sticking in the esophagus may provide the initial clue to emerging dysphagia
  92. 92. Amyotrophic Lateral Sclerosis • Impaired function of the lips and tongue (particularly the posterior portion of the tongue) due to evolving muscle weakness typically appears first • Next involvement of jaw and suprahyoid musculature • Finally weakness of pharyngeal and laryngeal muscles • Delay in, and eventual abolishment of, triggering of the swallowing reflex for voluntarily initiated swallows, with relative preservation of spontaneous reflexive swallows until the terminal stages of the disease
  93. 93. Cranial Neuropathies • Extramedullary, intracranial involvement in processes involving the meninges, extramedullary tumors, aneurysms, and skull fractures • Lesions at the jugular foramen or in the retroparotid space some combination of IX, X, XI, XII, and the cervical sympathetic • Prominent in the miller fisher variant of AIDP • Herpes zoster infection - attributed to cranial ganglionic involvement • Charcot-marie-tooth disease
  94. 94. Nuclear lesions • Brain stem stroke and MS • Brainstem tumors, both primary and metastatic, • Central pontine myelinolysis • Progressive multifocal leukoencephalopathy • Leukoencephalopathy due to cyclosporin toxicity • Brainstem encephalitis – Listeria and Epstein-barr Virus
  95. 95. Cervical Spinal Cord lesions • Especially if associated with respiratory insufficiency • With higher spinal cord injury • With treatment and time, most patients demonstrate improvement
  96. 96. Management of dysphagia • Dietary modification • Exercises • Facilitation techniques • Compensatory mechanisms • Enteral feeding • Surgical methods • Botulinum toxin therapy
  97. 97. Dietary Modification • Difficulties with the oral preparatory phase – Diet of pureed foods • As patients' swallowing function improves – Soft and semisolid foods with regular consistencies • Recommend to patients that they alternate bites with sips, bite or sip size, and the number of swallows per size • Good oral hygiene and dental care
  98. 98. Viscosity and texture of food Oropharyngeal neurogenic dysphagia • Thickened liquids – Liquids can be thickened with starch-based food thickeners Difficulties with mastication • Chopped or pureed foods Uniform and viscous bolus of food or beverage - less risk of aspirating
  99. 99. Exercises Indirect – Strengthen swallowing muscles Direct – Performed while swallowing • Designed to facilitate oral motor strength, range of motion (ROM), and coordination • Usually are performed 5-10 times per day
  100. 100. Exercises Lip exercises • facilitate the patient's ability to prevent food or liquid from leaking out of the oral cavity Tongue exercises • facilitate manipulation of the bolus and its propulsion through the oral cavity or to facilitate retraction of the tongue base Jaw exercises • facilitate the rotatory movements of mastication
  101. 101. Exercises Respiratory exercises • improve respiratory strength Vocal cord adduction exercises • promote strengthening of weak vocal cords.
  102. 102. Exercises Head-lift (Shaker) exercise • to increase anterior movement of the hyolaryngeal complex and opening of the upper esophageal sphincter • lie flat and with shoulders on the floor and raise their head high enough to see their toes, maintaining this position for 1 minute
  103. 103. Facilitation techniques Somatosensory stimulation (electrical current )applied to the pharynx • Change the excitability of the corticobulbar projection • Induce cortical reorganization in patients with poststroke dysphagia Repetitive transcranial magnetic stimulation (RTMS)
  104. 104. Facilitation techniques Deep pharyngeal neuromuscular stimulation (DPNS) • To improve pharyngeal swallow • On stimulating 3 reflex sites 1) Bitter taste buds and tongue base -improve tongue-base retraction 2) Soft palate - improve palatal elevation 3) Superior and medial pharyngeal constrictor - improve pharyngeal peristalsis and cricopharyngeal opening
  105. 105. Compensatory Techniques Chin-tuck position • decreases the space between the base of the tongue and the posterior pharyngeal wall • creating increased pharyngeal pressure to move the bolus through the pharyngeal region
  106. 106. Compensatory Techniques Rotation of the head to the affected side • closes the pyriform sinus on the affected side and directs food down the opposite or stronger side • also adds external pressure on the damaged vocal cord and moves it toward the midline, improving airway closure.
  107. 107. Compensatory Techniques Tilting the head to the strong side • bolus tends to be directed down the stronger side in the oral cavity and in the pharynx • effective for patients who have unilateral tongue dysfunction or a unilateral pharyngeal disorder.
  108. 108. Compensatory Techniques Supraglottic swallow • Close the airway voluntarily before and during the swallow • Take a deep breath and hold your breath • Keep holding your breath while you swallow • Cough immediately after the swallow
  109. 109. Compensatory Techniques Mendelsohn maneuver • mimics the upward movement of the larynx voluntarily • increase the duration of the cricopharyngeal opening
  110. 110. Enteral Feeding • Unable to achieve adequate alimentation and hydration by mouth • Impaired level of consciousness, massive aspiration, silent aspiration, esophageal obstruction, or recurrent respiratory infections
  111. 111. Enteral Feeding Nasogastric tube feeding • In post stroke dysphagia temporarily provide adequate nutrition and buy time until swallowing improves • prolonged use can lead to lesions to the nasal wing, chronic sinusitis, gastroesophageal reflux, and aspiration pneumonia
  112. 112. Enteral Feeding Percutaneous endoscopic gastrostomy Oroesophageal tube feeding • patient is taught to insert the 14F urethral tube into the mouth and past the side of the tongue, pushing slowly until the catheter end reaches the lips • Food supplements and liquid are administered by means of a 500-mL syringe at a rate of approximately 50 mL/min
  113. 113. Other methods Cricopharyngeal Myotomy • to decrease pressure on the pharyngoesophageal sphincter Botulinum toxin injection into the UES
  114. 114. Thank you

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