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More definitions:
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Dysphagia and Related Disorders: Management
Lecture Three: Rehabilitation Techniques
Rehabilitative Manoeuvres • Oral Motor Exercises • Vocal Adduction Exercises • Modified Valsalva Swallow or Effortful Swallow (Logemann, et al.) • Mendelsohn Manoeuvre (Mendelsohn) • Tongue Holding Manoeuvre or Masako Manoeuvre (Fujui, et al.) • Head Lifting Manoeuvre (Shakir, et al.)
Oral Motor Exercises • What we know: • Lazarus (1999): Controlled trial (no OM exercise, resistance with tongue blade, exercise with IOPI). • 31 young healthy subjects…..ie…no tongue weakness to start with. • Demonstrated increased lingual pressure measurements in exercise groups, but not in control group. No increase in endurance reported.
MLHuckabee
Compensation: Strategies that provide an immediate but typically transient effect on the efficiency or safety of swallowing. As a rule, if the strategy is not consistently executed, swallowing will return to the prior dysfunctional status. May include but are not necessarily limited to posturing, adaptations in rate, route or nature of oral intake. Rehabilitation: Interventions that when provided over the course of time and are thought to result in permanent changes in the substrates underlying deglutition; ie...changing the physiology of swallowing mechanisms. May include, but not limited to oral/facial exercises, vocal adduction exercises, breathing exercises, pharyngeal strengthening exercises.
Oral Motor Exercises • What they are: • Exercises designed to increase strength and/or control of oral musculature with an assumed carryover to functional tasks. • Can address issues of hyperfunction, hypofunction or dyscoordination • Range of motion, resistance exercises, icing, stretching
Oral Motor Exercises • What we don't know: • Lots! • Very little empirical data to support efficacy despite enormous amounts of clinical belief • Do rote exercises focusing on completion of volitional movements carry over to functional swallowing?
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Effortful Swallow
Oral Motor Exercises • What we hope to be true: • Lots! • Oral motor training programs to improve oral lingual control of the bolus during functional swallowing tasks.
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What it is: • •
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Effortful Swallow • What we know: • First introduced by Logemann, et al (1990, 1991,1992) as a compensatory technique • Early research suggested that increased effort in swallowing will results in immediate increased pressure on the bolus and thus decreased pharyngeal residual
• Bülow (1999): Effortful swallow results in decreased hyomandibular distance before the swallow; but actually reduced laryngeal excursion/decreased overall hyoid movement during the swallow in normal.
“Swallow hard” Generally thought to be appropriate for the physiologic abnormality of decreased pharyngeal stripping, and or pharyngeal weakness. Increased pressure on the bolus is generated by effortful swallow
Effortful Swallow • Bülow (2001): – In Patients with mod to severe pharyngeal phase dysphagia, effortful swallow results in: • No change in aspiration/penetration, although depth of penetrated material higher • No change in pharyngeal retention • Does not improve weak pharyngeal contraction
• Bülow (2002): extension of above study – Same patient group • No change in peak amplitude or duration of intra-bolus pharyngeal pressures at the level of UES
Effortful Swallow • Hind, Nicosia, Roecker, Carnes, Robbins (2001) – Another study to evaluate effortful swallow with videofluoro and oral pressure – Increased oral pressure with effortful swallow – Increased duration of • Maximal anterior hyoid excursion • Laryngeal vestibule closure • UES opening
– Increased superior hyoid movement – Trend toward increased oral bolus clearance
MLHuckabee
• Huckabee, Hiss, Barclay & Jit 2002 – Manoendoscopic evaluation of normal and effortful swallowing – PHaryngeal catheter measured upper and middle pharyngeal pressures and UES pressure during swallowing – sEMG measured submental muscle contraction – RESULTS • Effortful swallow results in significantly increased amplitude of all measures. • But sEMG was not highly correlated with phharyngeal pressure.
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Huckabee, Hiss, Barclay & Jit 2002
Effortful Swallow • What we don’t know? • Are thre two effortful swallows that accomplish two distinct goals?
140 120 100 80 60 40 20 0 -20
effortful peak semg
sensor 1
sensor 2
• What is effect of effortful swallow on physiology? Only increased BOT? Increased pharyngeal contraction? • Compensatory -vs- rehabilitative?
normal UES
rest
Mendelsohn Manoeuvre • What we really hope to be true? • Long term repetitive execution of this technique improves overall underlying physiology of swallowing. • Muscle strengthening of striated pharyngeal musculature
Mendelsohn Manoeuvre • What we know: • Logemann & Kahrilas (1990) Case report • 45 year old medullary infarct; studies over 60 month period. Mendelsohn improved swallowing efficiency greater than two-fold over other techniques. • Kahrilas et al. (1991) Manofluorographic study • Mendelsohn results in prolonged UES opening but not increased diameter of the UES. Increases hyolaryngeal superior displacement but not anterior displacement.
MLHuckabee
• What is it: • First identified by Mendelsohn as suggested as a compensatory technique. • Swallow---at height of laryngeal excursion maintain suprahyoid contraction to prolong the swallow---relax/complete the swallow. • Prolonging the swallow prolong UES opening • Thought to be effective for addressing inadequate UES opening, or 2nd weak hyolaryngeal excursion or pharyngeal contraction.
Mendelsohn Manoevre • Kahrilas, Logemann, Krugler, Flanagan (1991) – Manofluorography evaluation of mendelsohn in normals – Increased anterior superior excursion of the larynx and hyoid – Thereby delayed UES closure – No comment in this study on bolus flow
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Mendelsohn Manoevre • Miller and Watkins (1997) – Real Time Ultrasound study of lateral pharyngeal wall movement during mendelsohn – Increased duration of lateral pharyngeal wall movement compared to normal swallow during mendelsohn
Mendelsohn Manoeuvre •What we don't know:
•What effect on other aspects of swallowing? Recall Bülow study •What effect on bolus flow? •With or without a bolus?
•What we really hope with all our hearts to be true: •Repetitive ‘stretching’ of UES ultimately results in more function UES opening •Neuromuscular re-ed training programs
Masako Manoeuvre • What it is: • First identified by Fujui (199 ) • Tongue holding manoeuvre….Swallow with tongue stabilized anteriorly between teeth. • Designed specifically to address inadequate BOT to PPW approximation
Masako Manoeuvre • What we don't know: • What effect on other aspects of swallowing? Recall Bülow study
• What we really hope with all our hearts to be true: • Repetitive execution of manoeuvre ultimately results in greater activation of the posterior pharyngeal wall thus improving pharyngeal swallowing function • Neuromuscular re-ed training programs
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Masako Manoeuvre • What we know: • Fujiu et al (1995). Radiographic documentation of patients with BOT resection to have greater PPW anterior movement. • Fujiu et al (1996).Radiographic evaluation • 10 non-resected individuals. Technique results in significantly increased anterior bulging of the posterior pharyngeal wall. Recruits greater activation of the pharyngeal constrictors as a compensation. • Increased aspiration risk with a bolus…. not a compensatory technique (except….)
Head-lifting Manoeuvre • What it is: • First identified by Shaker (1997) • Lying in bed, raise head from level repetitively, raise and hold. • Not a direct swallowing task • Intended for use in patients with inadequate opening of the UES.
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Head-lifting Manoeuvre • What we know: • Shaker et al (1997). Manofluorographic analysis • Two groups elders: sham exercise, head lift exercise performed for 6 months. • No change in group with sham; Those with head lift exercise demonstrated increased laryngeal excursion, increased width and duration of UES opening, decreased intra-bolus pressure. • Nicely done cross over design
Head-lifting Manoeuvre, cont... • Shaker et al (1999): • 17 dysphagic patients; videofluoroscopic assess. • Two groups (sham & Shaker exercise) then crossover • Aspiration resolved in 15/17 patients with Shaker ex. • Follow up 4-12 mos later…no decline.
Emerging modalities • Neuromuscular electrical stimulation – Defined as "the external control of innervated, but paretic or paralytic, muscles by electrical stimulation of the corresponding intact peripheral nerves" (Baker, et al., 1993). – Achieved through the carefully regulated administration of pulsed electrical current at predetermined frequencies and amplitudes to nerves, myoneural junctions or muscles (Ragnarrson, 1994).
MLHuckabee
Head-lifting Manoeuvre, cont... • Jurell (1996): EMG study • EMG evidence of fatigue in submental muscles suggestnig increased work with manoeuvre
• Alfonzo,et al. (1998): EMG study • Increased amplitude in supra- and infra-hyoid muscles with this technique.
Head-lifting Manoeuvre, cont... • What we don't know: • How does this work? Other effects on swallowing? Spontaneous recovery effects? Head rotation as an option?
• What we really hope with all our hearts to be true:
Effects of NMES • Alternations range from changes in permeability of the cell membrane at the cellular level, to systemic changes such as analgesia secondary to neurotransmitter release, circulatory changes secondary to vasoactive polypeptide release, and kidney and cardiac changes secondary to modulation of internal organ activity • The therapeutic benefit is a consequence of tissue level changes which are manifested in part by skeletal muscle contraction and subsequent effects on strength, reaction time and stamina (Alon, 1991). • Very simply stated, the current administered during electrical stimulation changes the ionic composition of the neural or muscular cell membrane and if of adequate intensity, triggers transmission of a motor unit action potential with a subsequent motor response.
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The complexity of stimulation • The conduction of an action potential and the chemical synaptic transmission created by artificial electrical stimulation involves the same processes of neurosecretion and chemoreception as a naturally occurring excitation. • However, the externally stimulated contraction differs from physiologic muscle activity in the ordering of muscle fiber recruitment, the synchronicity of individual motor units and the intensity of stimuli required to produce these changes.
• Therapeutic application of this stimulation is not a simple process and requires knowledge of neural transmission, electrophysiology, biologic impedance and muscle physiology. • The effectiveness of the treatment is dependent on precisely chosen stimulation parameters for a selected therapeutic goal. These parameters are critical for treatment effectiveness but also to ensure patient safety. – – – – –
Type of current applied Pulse amplitude Duration Repetition rate Duty cycle
Indications
Contraindications
• The US FDA documents present indications for electrical stimulation to include the therapeutic goals of muscle re-education, prevention of disuse atrophy, and maintenance of range of motion • The literature in physical medicine and rehabilitation reports numerous applications of electrical stimulation, including increasing muscle strength and range of motion, correcting contractures from spasticity, increasing sensory awareness and volitional muscle control and decreasing antagonistic spasticity (Kasman, 1994).
• Since electrical stimulators introduce active current into biologic tissue, and at much higher intensity levels than endogenous current, there are contraindications related to patient safety. • NMES is contraindicated in patients with: – – – – – – –
demand type pacemakers superficial metal implants or orthotics skin breakdown Cancer history of cardiac or seizure disorder impaired peripheral nerve conduction systems pregnancy.
So what do we know about NMES applications to swallowing? • May also be specific contraindications for use around head and neck "Severe spasm of the laryngeal and pharyngeal muscles may occur when the electrodes are positioned over the neck or mouth. The contractions may be strong enough to close the airway or cause difficulty in breathing" (FDA, 1985).
MLHuckabee
• Freed et al. (2002) – Methods: • Stroke patients with swallowing disorder were alternatelyassigned to one of the two treatment groups (Thermal Simulation or NMES). • NMES was administeredwith a modified hand-held battery-powered electrical stimulator connected to a pair of electrodes positioned on the neck. • Daily treatments of TS or ES lasted 1hour. • Swallow function before and after the treatment regimen was scored from 0(aspirates own saliva) to 6 (normal swallow) based on substances the patientscould swallow during a modified barium swallow.
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– RESULTS: • Both treatment groups showed improvement in swallow score, but the final swallow scores were higher in the ES group (p >0.0001). • In addition, 98% of ES patients showed some improvement, whereas 27% of TS patients remained at initial swallow score and 11% got worse. • These results are based on similar numbers of treatments (average of 5.5 for ES and 6.0 forTS, p = 0.36). – ?? NMES paired with dilitation of UES
Alon, in a chapter on neuromuscular electrical stimulation, comments: “The present disarray, and the natural tendency to accept nonscientific, subjective and commercially motivated claims….may threaten the substantive potential that electrical stimulation can offer as an objective clinical modality” (1991).
Basic Research • Power et al (2002) – Evaluated 15 healthy subjects – 10 minutes of electrical stim applied to anterior faucial pillars at two frequencies (0.2 and 5 Hz), 75% max tolerated intensity. – TCMS used immediately after and 30, 60 minutes after stimulation. – Results: • At 5 Hz, faciaul pillar stimulation induced inhibition of swallowing motor cortex, whereas at 0.2 Hz stimulation there was excitation. • On VFSS eval, 5 Hz lengthened pharyngeal delay time, whereas 0.2 Hz produced no change. • Maximal response seen 30 min after stim
– Results: frequency • Stimulation at 1 or 5 Hz increased excitability, wtihout altering latency as determined by greater response amplitude of TMS potentials • Stimulation at 10, 20 and 40 Hz actually decreased excitability of neural transmission. Presented an inhibitory effect on neural conduction. • Overall 5 Hz stimulation had greatest effect with maximum effect at 30 and 60 minutes after stimulation.
MLHuckabee
• Fraser et al (2002) – Methods: • 8 healthy subjects received NMES at different frequencies, intensities and duration through bipolar pharyngeal electrode inserted transorally or nasally. • E stim provided for 10 min at frequencies of 1, 5 10, 20 & 40 Hz. Intensity set at 75% of max tolerated. • EMG responses evoked in the pharynx by TMS were tested before stimulation, immediately after, 30 and 60 minutes afterwards.
– Results: Intensity • Higher the intensity of tolerated stimulation, the larger the effect on corticobulbar excitability. • Increasing effect over time….with larger response at 60 minutes compared with immediately after stimulation.
– Results: Duration • Stimulation for 5 or 20 minutes facilitated motor evoked potentials less than stimulation for 10 minutes.
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• Fraser, cont… – Three subjects underwent detailed bihemispheric topographic mapping before and after stim. • Increase in the size of pharyngeal area of response occurred in all subjects, with the effect largest in the pharyngeal dominant hemisphere. • Confirmed by fMRI studies
• Fraser, cont…. – 16 dysphagic patients • 10 randomised to estim group; 6 to no tx. • Stim group: 10 min stim at 5 Hz. • All had videofluro before and 1 hour after stim – Pharyngeal stimulation resultsed in reduction in pharyngeal transit time, swallowing response time and aspiration score, compared to pre-stim values. – No treatment group had no change in swallowing – Highly signirficant correlation within patients between total change in excitability after stim and the change in aspiration. – Establishes causal relationship between increased cortical exccitability and improvement in swallowing function across individuals.
Basic Research • Burnett et al. (2002) – Goal: to develop intramuscular stimulation device to imporve hyolaryngeal elevation – Methods: • Evaluated kinematic and pressure effectives of stimulating select extrinsic laryngeal muscles in normals using manofluoroscopy • Hooked wire electrodes in mylohyhoid, geniohyoid and thyrohyoid regions bilaterally • Stimulation in 1 sec trains of 0.2 ms pulses at 30 hz. Amplitude to max effect without pain
Current approach to rehab • State of the art in swallowing rehab typically views recovery of muscle function through a very narrow lens…muscle weakness. • However, neuromuscular deficits can be classified into three categories of physiologic impairment: – Flaccidity or hypofunction – Spasticity or hyperfunction – Muscle dyscoordination or apraxia (wow…fascinating issue in terms of dysphagia!)
MLHuckabee
– Results: • Equivalent degrees of laryngeal elevation were achieved by stimulation fo all muscle pairs • Hyoid elevation was greatest with bilateral MH or ipsilateral MH + GH stimulation. • Anterior hyoid movementn during bilateral GH stimulation was greater than that seen in normal swallowing • Ipsilateral combined stimulation of GH and MH or TH produced marked anterior hyoid movement • Increassed anterior hyoid movement resulted in decreased UES pressure
Flaccidity or hypotonicity • Characteristic of patients with cranial nerve lesions or isolated pyramidal tract lesions from cortical stroke – Typically presents unilaterally – Weakness is the cardinal feature
• Typical approach to rehab – Strengthening exercises – Effortful swallows, mendelsohns, masakos, OM
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Spasticity, cont...
Spasticity or hypertonicity • Typically characterized by increased tone that is variable within an individual muscle and across muscles.
• Typical approach to rehab – Relaxation – Inhibition of spasticity – Emergence of voluntary activity upon the backdrop of relaxation – Mendelsohns & head lift for UES impairment?
– movement is imprecise and difficult to initiate. – Rigidity is characterized by consistent muscle tension across muscles, which inhibits range of motion.
• Caused typically by lesions to the UMN or extrapyramidal system and involves disordered input from basal ganglia, cerebellum, red nucleus & other structures
Limitation in our approach to rehabilitation
Dyscoordination/apraxia • Considered to result from damage to supplemental motor area, premotor areas, inferior parietal lobe – Disorder of voluntary movement; inability to execute purposeful movement
• Parkinsonism with extraneous movement (tremor?) • Typical approach to rehab – Patterning of the motor response – Maximizing external cues
• We don’t understand the extent or mechanisms of cortical control of swallowing. • Preliminary data suggest that it is significant in establishing a “preparatory set” for swallowing, maximizing neural control • Thus, enhancing cognitive awareness of oral intake will likely improve efficiency in swallowing • What do we know about neural recovery mechanisms …..nuttin! • If we understood more about how patients get better, ie…what happens in the brain, we may be much more effective in developing rehab techniques that focus directly on those recovery mechanisms. • Current practice focuses on addressing physiology and biomechanics. But it is relatively hit and miss. Greater information yields more precision in rehab development.
MLHuckabee
• Theoretical understanding of why they work at a biomechanical level. • But no understanding of how rehabilitative efforts influence neuronal recovery. • Brute force vs neuronal reorganization • Peripheral vs central processes
Effects of Neural Injury • Centrally, symptoms of insult caused by – Cell death resulting from the event – Secondary physiologic shutdown of associated neurons • “Diaschisis: functional standstill or abolition of electrical excitability transmitted to neuronal areas that are related to damaged part of system
• Peripherally, when an axon is cut, the two ends close, swell and retract from each other. – Axons and myelin sheath degenerate, macrophages absorb and destroy the debris – Glial cells proliferate and form a scar around the trauma – Degeneration proceeds in both directions – As it approaches the cell body, cell death occurs. .
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What do we know about neural recovery • • • • • •
Recovery of synaptic effectiveness Synaptic hypereffectiveness Denervation supersensitivity Recruitment of silent synapses Collateral sprouting Vicarious function
• Denervation supersensitivity: – A mechanism similar to that above, denervation supersensitivity holds that residual neurons near the site of injury will increase the number of receptor sites for neurotransmitter released by residual incoming axons.
• Recruitment of silent synapses: – Normally quiescent neurons, typically not needed for function, become activated in response to injury.
Mechanisms of neural recovery • Recovery of synaptic effectiveness: – Neural injury results in edema from retained fluid in the brain. Very simply put, after the swelling resolves, injured neurons can recover some degree of function. – Resolution of diaschisis
• Synaptic hypereffectiveness: – This theory holds that post injury, residual neurons near the site of injury will increase the amount of neurotransmitter released into the post synaptic threshold, to increase the likelihood of synaptic connections to other residual neurons.
• Collateral sprouting: – Injury produces a change in the dendritic aborization of remaining neurons and collateral sprouting of spared axons to supply innervation to targeted denervated neurons.
• Vicarious function or Redundancy: – This simply means that there may be more than one region of the brain for a single function which initiates greater activity following injury.
Stimulation Studies • Hamdy, Aziz, Rothwell, Power, Singh, Nicholson, Tallis & Thompson, 1998 – 22 stroke patients underwent cortical brain mapping at one week, one month and three months post onset using the transcranial magnetic stimulation protocol. – Of those patients who were initially dysphagic but recovered swallowing function by three months, there was a statistically significant increase in the area of pharyngeal representation at both the 1and 3-months studies as compared to representation at onset.
MLHuckabee
• Hamdy et al., cont… – However, dysphagic patients who did not recover and those patients who were not dysphagic at onset did not demonstrate this change in pharyngeal representation. – This study demonstrates that swallowing recovery is related to increased cortical excitability of the unimpaired hemisphere, or a shifting of cortical representation for swallowing, and is the first documentation of cortical plasticity as an identified contributor to swallowing recovery.
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Hamdy et al.
A=not dysphagic; b=dysphagic and recovered; c=dysphagic and not recovered
But these are all considered to be mechanisms of spontaneous recovery (within minutes, hours,days or weeks after insult). What about latent recovery mechanisms; rehabilitative recovery mechanisms?
Keefe, cont.. • Structural changes in the nervous system (collateral sprouting). – dendritic branching of non-injured axons occurs not only in the regions immediately adjacent to the injury, but in areas remote to the injury as well, such as the contralateral cortex, providing evidence for both injury related and experientially related changes. – degree and pattern of dendritic branching has shown to be clearly related, both positively and negatively, to behavioural influences.
MLHuckabee
• Further work by Hamdy in an extended series of studies suggests that overall pharyngeal representation in the undamaged hemisphere increased remarkably as a function of recovery, whereas no change in representation was seen in those that did not recover or those without dysphagia. • Additionally, no changes were seen in the damaged hemsiphere of any group • Thus suggests that recovery of swallowing is purely issue of hemispheric cortical shifting, rather than intra-hemispheric reorganisation
Keefe, 1995 • Changes in synaptic functions of the nervous system. – Keefe describes the theories of long term and associative potentiation in which stimulation of a neural input pathway produces a sustained increase in neural transmission at a given synapse (synaptic hypereffectiveness and denervation supersensitivity). – This further potentiate the synaptic response of temporally related, but convergent, neural input. Keefe speculates that optimising the temporal relationship between stimulus presentation of impaired and nonimpaired modalities may facilitate this neural mechanism.
The last bit of Keefe • Changes in neural networks, or cortical reorganization (vicarious function). – three additional features that may influence cortical reorganization as a result of intervention: • intensive repetition of tasks may be required to facilitate this shift, • cortical shifting may return to pre-treatment status if tasks are discontinued, suggesting the need for rigorous carryover, • cortical shifting appears only to be effected for the modality which is directly trained, thus implying the need for focused attention to the treatment task.
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What is the role of rehabilitation in swallowing? Many more questions than answers. • Hamdy documents spontaneous recovery • Can we facilitate neural change (neural reorganisation) – Are we re-organising and restructuring the neurophysiological basis of swallowing?
• Can we facilitate peripheral change? (muscle changes) • Central vs peripheral process – The quandry of oral motor exercises, Head Lift exercise
• Can we make these changes happen? • How do we make these changes happen? • How much required to make changes?
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