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Cerebellar Lesions and Dysphagia

Sue Curfman, M.A.,CCC

June 12, 2006

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Question

In our facility we have a 50 year old patient suffering from dysphagia as a result of a cerebellar stroke. He has been in the facility for 2 weeks on a kaofeed but has shown no real progress with his swallow function. To date, he is unable to initiate a

Answer

A brief clinical review of the cerebellar circuitry is beneficial in understanding the effects of lesions in the cerebellum. The cerebellum is located in the posterior fossa and is attached to the brainstem by the superior, middle, and inferior cerebellar peduncles, which contain the input and output fibers of the cerebellum. It integrates massive sensory and other inputs from many regions of the brain and spinal cord, which is used by the cerebellum to smoothly coordinate ongoing movements and to participate in motor planning. The cerebellum has no direct connections to lower motor neurons, but instead exerts its influence through connections to the motor systems of the cortex and brainstem. In addition, cerebellar pathways participate in several other functions including articulation of speech, respiratory movements, motor learning, and certain higher-order cognitive processes.

Effects of lesions on the cerebellum typically result in dysphagia ranging from mild to profound impairment. The degree of impairment is influenced by etiology/type of stroke (vascular, hemorrhagic, and ischemic), site and extent of lesion, clinical course of intervention, and other physical problems and biographical variables. Impaired function is frequently manifested in the pharyngeal phase swallowing affection salivation, swallow integrity, and upper esophageal sphincter function.

Symptoms of impaired salivation function may include pooled oral secretions, reduced frequency of saliva swallows, and excessive copious (mucoidal) secretions. Symptoms of impaired swallow function may include reduced/absent elevation of the hyoid and thyroid cartilage, reduced pharyngeal swallow, patient appears unable to protect airway, aspiration risk, reduced pharyngeal peristalsis, and laryngeal penetration aspiration. Oral stage symptoms may be present including impaired lips protrusion/closure, slow initiation of oral bolus transit, reduced/absent ability to draw tongue base up/back, and insufficient recollection of food bolus following mastication. The presence of pharyngeal stage dysphagia symptoms would indicate further instrumental assessment to evaluate the pharyngeal swallow and risk of aspiration. In addition, information gained from instrumental assessment would guide the selection of intervention techniques.

The patient profile described in the question indicates a severe-profound impairment of dysphagia. Given the absence of a volitional swallow, review of the literature indicates the following intervention techniques, some of which remain controversial in terms of efficacy and research validity, to trigger swallow initiation:

  1. Deep pharyngeal neuromuscular stimulation (DPNS) is a systematized therapeutic method for pharyngeal dysphagia which utilizes eleven specific stimulation techniques within the oral/pharyngeal areas.

  2. Vital Stimulation Therapy, which uses small electrical currents to stimulate the muscles responsible for swallowing, is reported to activate key swallowing muscles. Clinicians then implement an active regimen of therapy to create or re-learn functional muscle use patterns necessary to initiate or re-establish swallowing

  3. Thermal/tactile stimulation of the anterior facial arches using a cold medium may help stimulate the onset of the swallow. A laryngeal mirror has traditionally been used to stimulate the arches ten times on each arch prior to introducing a bolus or series of boluses. The swallow reflex should be triggered when the head of the bolus reaches the anterior facial arches, so theory states that this when a bolus passes the arches, the swallow will be stimulated in a timely manner following thermal stimulation. Often lemon is added to the ice and mirror as sour boluses tend to initiate a more rapid reflexive response
Once the patient has regained volitional swallow initiation, the following intervention techniques based on the dysphagia symptom may be of benefit:
  • Symptom - Reduced frequency of saliva swallows: Patient reliance on oral suctioning: Intervention - Patient reliance on oral suctioning: Facilitate frequency of dry swallows; Cold liquid/food stimuli

  • Symptom - Slow initiation of oral bolus transit: Intervention - Verbal cueing; Optimize liquid/food texture; Sufficient bolus volumes; Cold liquid/food stimuli

  • Symptom - Immediate cough or throat clearing due to delayed pharyngeal swallow: Intervention - Cold stimulus; Thickened liquids; Controlled bolus volume; Thermal stimulation; Bolus hold exercises; Chin tuck; Supraglottic swallow

  • Symptom - Immediate cough or throat clearing; wet vocal quality; Throat clearing after swallows; multiple effortful swallows per bolus due to delayed laryngeal elevation & closure: Intervention - Controlled bolus volume; Slightly thickened liquids and thinned semi-solids; Chin tuck; Mendelsohn maneuver; Laryngeal valving exercises; Supraglottic swallow

  • Symptom: Delayed cough or throat clearing; wet vocal quality due to laryngeal penetration/aspiration after the swallow or bilateral pyriform residue: Intervention: Liquids and semi or soft solids; Controlled bolus volume; Head/trunk @ 45-60 degrees Hard swallow; Double wallow; Mendelsohn maneuver.
Absence of additional information from the neurologic exam and neuroimaging makes it is difficult to formulate a prognostic statement for recovery. Rate and extent of recovery are dependent to a large extent on the site and size of structural damage. Clinical research has identified general patterns of recovery that indicate change in function began most frequently at two weeks post onset with the greatest change evolving in the first month. Given the profound nature of the impairment at two weeks post-onset, clinical research would indicate the next weeks are significant in determining further recovery.

Sue Curfman, MA, CCC, has been in the field of healthcare for 24 years with experience across the continuum of care including acute hospital, home health, outpatient and skilled nursing. She works as a Clinical Program Consultant with RehabCare Group. She holds a certificate in Case Management and Quality Management
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sue curfman

Sue Curfman, M.A.,CCC


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