Exam 1 Review - PDF
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This document is a thorough review of the phases of swallowing involving discussions of the cranial nerves involved, and the neurologic control of swallowing. It covers signs, symptoms of dysphagia, intervention strategies for adults and children, and the goals of intervention. It is likely intended for medical professionals or students in the field of speech-language pathology or a related discipline.
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Exam 1 review Phases of swallowing Swallowing is a complex process Saliva, liquids, and foods are transported from the mouth into the stomach Swallowing commonly divided into four phases1: 1. Oral preparatory Food or liquid manipulated in the mouth to form a cohesive bolus (include...
Exam 1 review Phases of swallowing Swallowing is a complex process Saliva, liquids, and foods are transported from the mouth into the stomach Swallowing commonly divided into four phases1: 1. Oral preparatory Food or liquid manipulated in the mouth to form a cohesive bolus (includes sucking liquids, chewing solid food, manipulating soft bolus ) 2. Oral (transit) Begins with the posterior propulsion of the bolus by the tongue Ends with the initiation of the pharyngeal swallow 3. Pharyngeal Involuntary and reflexive (begins with voluntary pharyngeal swallow) Propels the bolus through the pharynx via an involuntary contraction of the pharyngeal constrictor muscles 4. Esophageal Bolus is carried to the stomach through the process of esophageal peristalsis Four phases of swallowing – Cranial nerves Oral preparatory Oral transport Pharyngeal Esophageal Mastication - CN V Labial seal: CN VII Soft palate closure: Esophageal opening and Gland secretion Tongue retraction: CN V CN V, CN IX, X constriction: CN X CN VII and IX Post bolus movement: Laryngeal closure: CN X CN XII CN involvement in oral preparation Cranial nerve and neurophysiology review Saliva production o Submandibular (submaxillary) glands (CN VII) o Parotid gland (CN IX) Taste sensation o Anterior 2/3 of the tongue, hard palate, soft palate (CN VII) o Posterior 1/3 of the tongue, tonsils, pharynx (CN IX) o Back of the oral cavity, 1/3 of esophagus (CN X) Gag reflex and nasal regurgitation depend on the function of the glossopharyngeal (CN IX) and the vagus (CN X) nerves Peripheral and medullary controls Muscles of the oropharynx: CN V, X, XII Muscles of the hypopharynx: CN X Extrinsic muscles of the larynx: CN V and CN XII Intrinsic muscles of the larynx: CN X Esophagus: CN X Neurologic controls of swallowing Neuroregulation of swallowing involves the activation of multiple levels of afferent and efferent pathways at different levels of the nervous system This process involves: cranial nerves, brainstem, cerebellum, cortex Swallowing does not represent a truly reflexive, brainstem-mediated response We don’t swallow food the same way each time regardless of similarity in bolus type and size Swallowing represents a more patterned type of neurologic response that can be influenced by control centers above the level of the brainstem o Peripheral muscles of swallowing contract sequentially but can be altered to accommodate different feeding activity o (e.g.) Typical eating and drinking vs. when trying to swallow a pill Signs and symptoms: Adult dysphagia Drooling and poor oral management of secretions and/or bolus Inability to maintain lip closure → food/liquids leaking from the oral cavity (anterior loss of bolus) Ineffective chewing (e.g., extra time needed to chew or swallow) Food or liquid remaining in the oral cavity after the swallow (oral residue) Food and/or liquids leaking from the nasal cavity (nasopharyngeal regurgitation) Complaints of food “sticking” or complaints of a “fullness” in the neck (globus sensation) Complaints of pain when swallowing (odynophagia) Changes in vocal quality (e.g., wet or gurgly sounding voice) Coughing or throat clearing Difficulty coordinating breathing and swallowing Acute or recurring aspiration pneumonia, respiratory infection, fever Changes in eating habits (e.g., avoidance of certain foods/drinks) Weight loss, malnutrition, or dehydration from not being able to eat enough Primary goals of feeding/swallowing intervention For adults For children Support adequate nutrition and hydration Support safe and adequate nutrition and Return to oral intake hydration Incorporating patient’s dietary preferences Determine optimum feeding techniques to and consulting with caregivers to ensure maximize swallowing safety and feeding efficiency that the patient’s daily living activities are being considered Collaborate with family to incorporate dietary Determine the optimum supports (e.g., preferences posture, or assistance) to reduce patient Attain age-appropriate eating skills in the and caregiver burden while maximizing the most normal setting and manner possible patient’s quality of life Minimize the risk of pulmonary complications Develop a treatment plan to improve the Maximize the quality of life safety and efficiency of the swallow Prevent future feeding issues with positive feeding-related experiences to the extent possible, given the child’s medical situation Anatomy of head and neck (swallowing) Esophageal sphincters Esophagus: Muscular tube connecting the pharynx with the stomach Approximately 8 inches long, lined by mucosa Runs behind the trachea and heart, in front of the spine Just before entering the stomach, the esophagus passes through the diaphragm UES (upper esophageal sphincter) – also PES Muscles at the top of the esophagus Major component of UES is cricopharyngeus muscle Keep food and secretions from going down the trachea LES (lower esophageal sphincter) Muscles at the low end of the esophagus When closed, prevents acid and stomach contents from traveling backwards from the stomach Valleculae and Piriform sinuses Valleculae: Lateral recesses at the base of the tongue on each side of the epiglottis Piriform sinuses: Lateral recesses between the larynx and the anterior hypopharyngeal wall These recesses serve as important anatomic landmarks in the assessment of pharyngeal swallow Phases of swallowing: (2) Oral transit 1. Moving upward and forward, the tip of the tongue comes into contact with the hard palate. 2. The area of tongue-palate contact expands posteriorly, which pushes food into the oropharynx. 3. The area of tongue-palate contact continues to increase as a portion of the food collects in the valleculae. 4. The jaw reaches its maximum downward position and the tongue drops away from the palate. (A portion of food may remain in the valleculae.) Phases of swallowing: (2) Oral transit Once bolus is prepared, the tongue tip is elevated to occlude the anterior oral cavity at the alveolar ridge, and the bolus is held against the hard palate o Posterior tongue is responsible for delivering the bolus into the pharynx Before (but almost simultaneous with) the first posterior movement of the tongue, respiration ceases, followed by arytenoid cartilage approximation Retraction of the tongue is accomplished by extrinsic tongue muscles Tongue base applies positive pressure to the tail of the bolus by its contact with the velum and posterior pharyngeal wall → Allows the bolus to move rapidly through the pharynx into an open UES The velum is elevated by levator veli palatini to seal the nasopharyngeal opening Phases of swallowing: (3) Pharyngeal phase Pharyngeal stage begins when the bolus arrives at the level of valleculae and ends when the UES closes When the bolus enters the pharynx, the hyoid bone continues its superior and anterior excursion toward the edge of the mandible o Tilts the larynx under the tongue base o Protect the bolus from entering the upper airway As the bolus enters the pharynx, the pharyngeal constrictor muscles are activated to narrow and shorten the pharynx Contributes to peristalsis-like movements in the posterior pharyngeal wall that aid in bolus propulsion into the esophagus Pharyngeal phase By the tongue’s connection to the hyoid bone, and the hyoid bone’s connection to the thyroid and cricoid cartilages, the larynx is pulled up and forward, resting under the tongue base that now partially covers the opening to the airway As the larynx rises ((2-3cm on average), the epiglottis descends over the top of the airway → Airway protection allows for bolus to be directed toward the esophagus rather than into the trachea As the bolus enters the pharynx, it is divided by the vallecular spaces, helping deflect it away from the airway as an additional component of airway protection Phases of swallowing: (4) Esophageal Esophageal swallowing tasks require an ordered pattern of function Coordinated activities in three distinctive zones: 1. Cervical: Proximal, striated muscle zone 2. Thoracic: Body 3. Abdominal: Specialized smooth muscles of the distal zone As the bolus enters the esophagus, primary peristalsis (primary contraction wave) triggered in the proximal, striated portion (CN X) The motor activity of cervical esophagus is rapid Gradually slows as it approaches the mid and distal esophageal regions The contraction force in the cervical esophagus is the strongest Accompanied by a drop in pressure (relaxation) in the LES to allow the bolus to enter the stomach Phases of swallowing: (4) Esophageal phase The primary peristalsis is followed by secondary peristalsis o Propagated by the bolus distending the esophagus Second wave propagation may begin at any point in the esophageal body and often assist in primary transport of solid food boluses o Primary wave may fail to push the bolus to the level of the LES Primary and secondary peristalsis are accompanied by longitudinal muscle contraction, resulting in shortening of the esophagus by its proximal attachments to the hypopharynx and distal attachment to the stomach Phases of swallowing: (4) Esophageal phase Tertiary contractions of the esophagus are random contractions Not peristaltic (orderly) in nature Inefficient in assisting in bolus transport They occur independent of swallowing activity but have been reported to occur more frequently in older adults Tertiary contractions may be the result of air trapped in the esophagus, or they may result from irritation of the esophageal lumen such as from gastroesophageal reflux Respiration during swallowing: Relevant anatomy Respiratory system is protected during pharyngeal swallow by occlusive muscular constriction of the laryngeal vestibule and downward displacement of the epiglottis True vocal folds: at the inferior margin of the laryngeal ventricles Attached-- anteriorly at the thyroid cartilage posteriorly at the arytenoid cartilages False vocal folds (vestibular vocal folds) separate the ventricle and the vestibule Epiglottis extends from the base of the tongue into the pharyngeal cavity Respiration during swallowing Respiration and swallowing are linked by their anatomy (mouth and pharynx) and their neuroanatomic relations in the medulla of the brainstem Respiration is inhibited by swallowing, and disorders of respiration affect swallow safety Airflow inhibition in normal adults begin before the onset of the oral phase o During mastication, respiratory patterns are modified o Respiratory pause occurs only after the bolus collects at the vallecular level o A short exhalation cycle precedes the cessation of respiration As the tail of the bolus passes through the UES, the larynx descends o Respiration on the exhalation cycle until slightly before the UES closes Exhalation-swallow-exhalation pattern changes with normal aging and disease Exhalation accompanied by a buildup of subglottic pressure that separates the vocal folds Burst of exhalation: protective feature, expel any swallowed material lodge in the upper airway* *This explosion of exhaled air is encouraged with the Heimlich maneuver. Swallow and normal aging 65 years+*, some changes in swallowing performance are attributable to age. o May be due to sensory perception changes, decreased muscle strength, structural changes (changes in mass and contractility): tongue, lips, jaw, velum, and lungs Loss of muscle strength and speed results in increased swallow durations Loss of elasticity in lung tissue + reduced respiratory capacity and control Hospitalization: Normal swallowing biomechanics may change under stress How do the different phases of swallowing change with normal aging? Dysphagia risk factors for CDE Community dwelling elders (CDE) in the US ~12 million Three factors in the CDE that increased the risk for dysphagia and its complications: 1. History of a clinical disease 2. Advancing age (> 70) 3. Frailty + reduction in activities of daily living Terminology Frailty: Loss of physical strength with accompanying loss of ability to compensate for weakness Presbyphagia: Old yet healthy swallow (changes in swallowing mech of otherwise healthy adults) Those with normal age-related changes in the aerodigestive tract that may be associated with frailty Sarcopenia: Reduction of lean skeletal muscle mass with loss of strength/speed of movement Symptoms: low muscle mass or gradual loss, overall weakness, lower stamina Terminology: Undernutrition Poor nutritional status may complicate dysphagia Loss of muscle mass + loss of strength and speed of motor performance may impact swallow safety and result in dysphagic symptomology Contributing factors: Loss of masticatory force, lip and tongue strength, loss of dentition Reduction in tongue pressure generation associated with low body mass index, risk of dysphagia Diminution of tongue thickness also associated with undernutrition (and risk for dysphagia) Loss of dentition: particularly important! Sources of protein found in meat too difficult to masticate, eventually become absent from dietary intake Dysphagic symptomology may lead to negative changes in dietary preferences, impacting nutritional integrity. Introduction to adult neurologic disorders Cortical functions Where is swallowing function represented in the human cortex? Lateral frontal cortex, inferior frontal lobule, insula found to be associated with various motor acts of feeding and swallowing Sensorimotor cortex and basal ganglia (e.g., Internal capsule) frequently associated with the presence of dysphagia in stroke patients Cortical hemispheric lesions that impair sensory functions? Stroke patients with dysphagia can have damage to the parietal lobe with associated sensory deficits Primary sensory areas have extensive interconnections with motor areas Sensory function important in the control of voluntary movement Hemispheric contribution to swallowing control Swallowing motor functions are bilaterally represented in the hemispheres If the dominant hemisphere is impaired, a contralateral backup may be available to facilitate recovery Cortical plasticity may occur over time, increasing the utility of the intact, non-dominant hemisphere to control swallowing motor functions (many patients with unilateral strokes often recover the ability to swallow after a period of dysphagia) Bilateral stroke would result in the most severe dysphagias Subcortical functions: Basal ganglia Basal ganglia: Regulate tone (resting tension level of muscles) and steadiness of movement Impairment of basal ganglia functions may create: Excessive tone - create delays in the initiation of movements, slow movements, or a reduced amount of movement Extra, unintended movements - disrupt the smooth, coordinated nature of voluntary movement attempts Movement disruptions may be seen as tremor, regular clonic movements, slow, sustained postural interruptions (dystonias), or other unintentional movements (e.g.) Parkinson’s disease Hemispheric stroke Two general considerations: 1. Location and extent of damage - important in understanding sensory and motor impairments, and the severity and potential for recovery 2. Functional consequences of the damage - may be the best “road map” to understanding and predicting dysphagia characteristics Acute stoke patients (~50% with dysphagia) at greatest risk for dysphagia Early screening important Patients at risk for respiratory abnormalities: Respiratory functions should be part of comprehensive swallowing evaluation Majority recover functional swallowing ability within 1-6 months after stroke Prolonged swallowing recovery was associated with poor stroke outcomes: Five predictive variables: age, stroke severity on submission, lesion location, initial risk of aspiration, impairment in ora l intake As patient’s condition improves, dysphagia treatment strategies may also change Spontaneous resolution of dysphagia Many stroke patients have some degree of recovery in swallowing ability However, persisting dysphagia 11-50% 6 months after stroke (chronic) Dementia Hallmark of dementia: Progressive deterioration in cognitive abilities (memory, judgment, abstract reasoning, personality changes) Persistent weight loss may be the first indication of significant swallowing problem Pneumonia is a common cause of death in patients with dementia Generalized cognitive impairments in dementia may contribute to deficits in volitional motor control → oral stage dysfunction Dysphagia in mild-stage dementia: SLOW; Oral rinsing ability significantly associated with dysphagia Treatment consideration: Dysphagia intervention for persons with dementia should incorporate basic principles of quality of life, dignity, and comfort [FYI] AGE (American Geriatrics Society): feeding tubes not recommended for older adults with advanced dementia TBI (Traumatic Brain Injury) TBI typically results in diffuse neurologic deficits affecting behavioral control Prevalence of dysphagia in acute-subacute TBI: 60-90% (Oral phase and pharyngeal phase deficits evenly distributed) Severity of neurotrauma assessed by clinical scales = Primary factor related to the presence of dysphagia in TBI (also, time to recovery of functional swallowing ability) Various scales to assess severity of neurotrauma: Glasgow Coma Scale (GCS), Rancho Los Amigos Scale (RLAS), Functional Independence Measure (FIM), Functional Oral Intake Scale (FOIS) Pneumonia frequently seen in patients with TBI: Early in the post-traumatic course of treatment Clinical factors associated with presences of pneumonia: Severity of neurotrauma (GCS, RLAS) No oral intake on admission Presence of tracheostomy tube or feeding tube Prolonged intubation time (Patients with mechanical ventilator) each additional day on the ventilator associated with 7% increase in risk of pneumonia Swallowing deficits in TBI Other considerations Tracheostomy tube Communicative or cognitive deficits Physical deficits Severe injury with widespread comorbid conditions, alternate feeding routes may be indicated (e.g., early post-injury course) The good news: With appropriate clinical intervention, many patients with dysphagia after TBI do regain the ability to eat by mouth. Subcortical functions and swallowing impairment: Parkinson’s disease (PD) Parkinson’s disease (PD): slowly progressive disease of the basal ganglia Classic features of PD: Resting tremor, bradykinesia, rigidity Swallowing deficits are common in patients with PD Motor deficits: Oropharyngeal deficits resulting from poor bolus control– inefficient, weakened swallow Sensory deficits: abnormal airway somatosensory functions, increased oropharyngeal residue → contribute to aspiration of saliva and other liquids Sensory limitations may contribute to underreporting of dysphagia symptoms by patients with PD Other considerations Drooling (sialorrhea): common problem in patients with PD Increased risk for silent aspiration and respiratory infection Impaired coordination between swallowing and respiration Esophageal abnormalities (e.g.) Delayed transport through the esophagus, esophageal stasis, abnormal contraction Gastroparesis Daily problems (e.g.) food shopping, preparation of meals, self-feeding activities (caregiver burden) Brainstem Damage to the brainstem typically results in sensory deficits to the head and neck regions + motor deficits associated with UMN and LMN damage o UMN damage → spastic weakness o LMN damage → flaccid weakness Alternating hemiplegia = flaccid weakness on one side of the body (head) + spastic weakness on contralateral side (body) (e.g.) Facial alternating hemiplegia = flaccid weakness in face (7th CN) + spastic weakness in contralateral upper or lower (or both) extremities Home to a ”swallowing center” - rostral brainstem o Nucleus tractus solitaries, nucleus ambiguous: Facilitate coordination among various components of swallowing, coordinate swallowing functions with respiration o Damage to this area of brainstem → severe dysphagia Swallowing impairment: Brainstem Dysphagia in brainstem stroke involve two aspects: 1. Incoordination related to disruption of the swallowing center 2. Weakness from damage to corticobulbar system (sensory deficits may be present) “Incomplete swallow” o Incoordination among stages of swallowing and between swallowing and respiration o Weakness in one or more of the muscle groups (velum, pharynx, larynx, pharyngoesophageal segment) Cerebellum Role of cerebellum in swallowing is poorly understood, however: Imaging studies – bilateral cerebellar activation during volitional swallowing Clinically, cerebellar damage results in: Ataxia (unsteadiness) Intention tremor (tremor that is exaggerated at the initiation of movement) Hypotonia (low muscular tone) →Impairment in coordination of swallowing functions (e.g.) difficulty in controlling bolus, oral residue from reduced swallowing effort LMN: Amyotrophic Lateral Sclerosis (ALS) Clinical presentation: Progressive weakness ALS is progressive and terminal: Patients may survive over 5 years, the majority do not Respiratory failure = Common cause of death in patients with ALS Movement difficulties with arms and legs, dysarthria, respiratory decline from chest muscle weakness, cognitive changes Impact of disease on all aspects of daily functions is severe → consider this in planning any rehabilitative efforts Neurologic deficits of ALS involve both central and peripheral nervous system structures → motor deficits “mixed” Typically, flaccid (LMN) + spastic (UMN) weakness Mixture of effects can be seen in the musculature of the swallowing mechanism, respiratory musculature, and throughout the remainder of the body Muscle disease and swallowing impairment Disease processes that might impair peripheral muscle function: (weaken muscles, contribute to dysarthria) Polyneuropathy Myasthenia gravis Inflammatory muscle diseases Muscular dystrophy We do not typically encounter patients with these disorders or diseases For the exam: general understanding of what each disease is, what type of muscles are affected (skeletal, smooth muscles, etc.), think about how it impacts swallowing functions LMN and muscle diseases: Treatment considerations Swallowing intervention generally symptomatic react to specific set of clinical circumstances presented Various strategies may be used: Diet modification to behavioral interventions Strengthening exercises may be questionable in some cases exercise may exaggerate underlying weakness Remember that patients are receiving ongoing medical care Patients taking multiple medications (and dosage changes) Understand the effects of various medications to make optimum decisions