"Lemon and glycerine swabs stimulate production of saliva initially but are acidic, causing irritation and decalcification of the teeth and resulting in rebound xerostomia." from Mary Jo Grap et al., “Oral Care Interventions in Critical Care: Frequency and Documentation,” Am J Crit Care 12, no. 2 (March 1, 2003): 113-118. (free full text at http://ajcc.aacnjournals.org/cgi/reprint/12/2/113)
J H Meurman et al., “Hospital mouth-cleaning aids may cause dental erosion,” Special Care in Dentistry: Official Publication of the American Association of Hospital Dentists, the Academy of Dentistry for the Handicapped, and the American Society for Geriatric Dentistry 16, no. 6 (December 1996): 247-250.
Patricia Coleman PhD et al., “Improving oral health care for the frail elderly: A review of widespread problems and best practices,” Geriatric Nursing 23, no. 4 (July 2002): 189-199.
Friday, September 18, 2009
Monday, September 14, 2009
Three Good Dysphagia References
Eisenhuber, E., Schima, W., Schober, E., Pokieser, P., Stadler, A., Scharitzer, M., et al. (2002). Videofluoroscopic assessment of patients with dysphagia: pharyngeal retention is a predictive factor for aspiration. American Journal of Roentgenology, 178(2), 393-398.
Perlman, A. L., Booth, B. M., & Grayhack, J. P. (1994). Videofluoroscopic predictors of aspiration in patients with oropharyngeal dysphagia. Dysphagia, 9 (2), 90-95.
Rosenbek, J. C., Robbins, J. A., Roecker, E. B., Coyle, J. L., & Wood, J. L. (1996). A penetration-aspiration scale. Dysphagia, 11(2), 93-98.
Perlman, A. L., Booth, B. M., & Grayhack, J. P. (1994). Videofluoroscopic predictors of aspiration in patients with oropharyngeal dysphagia. Dysphagia, 9 (2), 90-95.
Rosenbek, J. C., Robbins, J. A., Roecker, E. B., Coyle, J. L., & Wood, J. L. (1996). A penetration-aspiration scale. Dysphagia, 11(2), 93-98.
Thursday, June 25, 2009
Student Presentations
Date: July 7th at 8am-9am. You will have 10 minutes to present on a topic of interest to seasoned SLPs like me. Location: TBA.
Search this blog for more information on previous years. Type in "Student Presentations." See what comes up.
Good luck!
Search this blog for more information on previous years. Type in "Student Presentations." See what comes up.
Good luck!
Friday, June 19, 2009
Wednesday, June 10, 2009
VRE, MRSA -- What Else Is New!
Look 'em up! Know why we in healthcare need to be concerned and careful!
Tracheal Stenois and Tracheomalacia - Samantha Conner CSD Graduate Student
Two conditions affecting the trachea include tracheomalacia and tracheal stenosis. Tracheal stenosis is a narrowing or constriction of the tracheal cartilage that can cause shortness of breath, coughing, wheezing, stridor, dyspnea, (and pneumonia - are you sure there is a direct cause-effect relationship?) Tracheal stenosis consists of two types, including congenital and acquired. Congenital stenosis occurs at birth. Acquired stenosis can be secondary to tracheostomy, radiation treatment, surgery, and cancer. Also, stenosis can be caused by bacterial infection, external injury, and autoimmune conditions such as polychondritis and sarcoidosis that cause inflammation. However, the majority of cases are due to prolonged intubation.The most common treatments for tracheal stenosis include endoscopic surgery, open surgery and medical treatment. The treatment varies according to the etiology of the stenosis. For example, if the condition is secondary to an infection, it may be treated using antibiotics or antifungals. Also, if it is secondary to a malignant growth, chemotherapy or corticosteroids may be used for treatment. Although surgery is not necessary in most cases, some stenosis requires surgery. Minimally invasive surgery such as endoscopic surgery can be an effective treatment, as well as open surgery such as a tracheal resection. Tracheal stenosis also can be treated by dilation, either performed by a health care provider or at home by savvy patients.
In contrast to tracheal stenosis, tracheomalacia is a condition characterized by weakness of tracheal cartilage. Symptoms of malacia include stridor, dypnea, upper respiratory infections, and pneumonia. Tracheal malacia can be congenital or acquired. Congenital tracheal malacia occurs when the tracheal cartilage is not properly formed. It is often associated with fistulas. Congenital malacia can be treated with humidified air, physical therapy, careful feeding and monitoring, and antibiotics for infections associated with malacia. Acquired stenosis can occur as type II malacia from pressure on the trachea from an outside force such as a tumor. Another acquired malacia, type III, occurs from prolonged intubation or chronic infections. Acquired tracheomalacia can be treated through CPAP (continuos positive airway pressure), or surgery sometimes followed by the placement of a stint.
In contrast to tracheal stenosis, tracheomalacia is a condition characterized by weakness of tracheal cartilage. Symptoms of malacia include stridor, dypnea, upper respiratory infections, and pneumonia. Tracheal malacia can be congenital or acquired. Congenital tracheal malacia occurs when the tracheal cartilage is not properly formed. It is often associated with fistulas. Congenital malacia can be treated with humidified air, physical therapy, careful feeding and monitoring, and antibiotics for infections associated with malacia. Acquired stenosis can occur as type II malacia from pressure on the trachea from an outside force such as a tumor. Another acquired malacia, type III, occurs from prolonged intubation or chronic infections. Acquired tracheomalacia can be treated through CPAP (continuos positive airway pressure), or surgery sometimes followed by the placement of a stint.
Wednesday, June 3, 2009
June, July Practicum Schedule
No practicum on these dates:
Friday, June 12th
Monday, June 15th
Wednesday, June 24th
Tuesday, June 30th
Thursday, July 9th
Wednesday, July 15th
Monday, July 21st
Friday, July 31st
Friday, June 12th
Monday, June 15th
Wednesday, June 24th
Tuesday, June 30th
Thursday, July 9th
Wednesday, July 15th
Monday, July 21st
Friday, July 31st
Assignment
Look up tracheomalacia and tracheal stenosis, description and etiology. Treatment options.
Tuesday, May 26, 2009
Thursday, May 14, 2009
CHF and Aspiration Pneumonia
The explanation takes a little time to set up so I hope it is worth the wait. This is very condensed from what usually takes a couple of hours to properly describe so I apologize in advance if it is overly simplified. There are some great textbooks that explain this stuff clearly and with good detail.
Congestive heart failure is the inability of the heart to pump blood with adequate pressure to maintain the physiologic demands of organs. It occurs when the myocardium (heart muscle) becomes weak. There are several causes of this progressive weakening of the myocardium. One is disease of the heart muscle itself (cardiomyopathy). Another is arterial hypertension which forces the left ventricle to pump blood against too much resistance for a long period of time, until the muscle itself is overcome by the excessive workload. (The heart muscle first becomes thickened or hypertrophic just as your skeletal muscles get larger when you exercise but heart exercise is good only up to a point.). Likewise, pulmonary hypertension can cause right sided heart failure because the right ventricle is pumping blood through the pulmonary circulation against excessive resistance.
It is this last example that might partially answer your question. Diseases of the lungs such as some forms of COPD (emphysema in particular) can destroy portions of the respiratory membrane which is formed by the alveolar membrane plus the pulmonary capillaries. When the capillaries are destroyed the blood flow into the lungs (to pick up oxygen and get rid of CO2) is blocked so the right ventricle is pumping some blood into a dead end, the pressure in these vessels becomes very high. The result of this pulmonary hypertension is the leakage of material from the blood (that should not leak out of the circulatory system) into the lung. This example is one way that patients develop pulmonary edema (this fluid leakage into the lung is defined as pulmonary edema caused by congestive heart failure). Similarly this heart failure causes fluid to accumulate in the pleural cavity (the space outside of the lungs between the inner and outer pleural membranes that line the lungs and chest cavity).
OK so now we have COPD as a source of CHF. Patients with COPD have reduced mucociliary clearance, reduced expiratory capacity, both of which increase the patient’s resistance to infection (i.e. pneumonia) which are some reasons that COPD patients have a higher risk of any type of pneumonia. These patients also have a different pattern of breathing/swallowing coordination than normals that disrupts the typical “swallow at the onset of exhalation” pattern that predominates in normals, and also increases the respiratory rate above a normal (12-20 or so breaths per minute) further discoordinating (I don’t know if that is a real word) swallow-breathing. Likewise COPD patients exhibit more frequent laryngeal penetration than normals (Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Good-Fratturelli, Curlee, & Holle, 2000)
CHF itself and the associated pulmonary edema and pleural effusions, reduce respiratory surface area by restricting inflation of the lungs (effusions) or by obstructing air from the respiratory membrane (edema). The result of either is the patient has to breathe more times per minute (increased respiratory rate- see above).
There are some good studies that show the association between COPD and dysphagia, and CHF and dysphagia, (see below) but the link between these conditions and dysphagia, as well as the link to subsequent pneumonia risk, is based on the understanding of the pathophysiology of those diseases and mostly based on animal studies, though the inferences are very strong. For example, we know the above processes take place in these diseases, and we know that these patients have increased respiratory rate, swallow-respiratory coordination abnormalities, higher incidence of pneumonia, etc., so we infer that the diseases’ properties explain some if not all of the association between them and dysphagia, increased pneumonia risk, etc. (Langmore, Skarupski, Park, & Fries, 2002).
Cricopharyngeal dysfunction is also seen in some patients with COPD and this can contribute to prandial aspiration and increased likelihood of inoculating thelungs with pathogens ((Good-Fratturelli, Curlee, & Holle, 2000; Langmore, Skarupski, Park, & Fries, 2002; Mokhlesi, 2003; Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Stein, Williams, Grossman, Weinberg, & Zuckerbraun, 1990).
Cheers,
James L. Coyle, Ph.D., CCC-SLP, BRS-S
Assistant Professor, Communication Science and Disorders
University of Pittsburgh
Confidential University of Pittsburgh information. Any unauthorized or improper disclosure, copying, distribution, or use of the contents of this e-mail or attached documents is prohibited. The information contained in this e-mail message is intended only for the personal and confidential use of the recipient(s) named above. If you have received this communication in error, please notify the sender immediately by e-mail and delete the original message.
Good-Fratturelli, M. D., Curlee, R. F., & Holle, J. L. (2000). Prevalence and nature of dysphagia in VA patients with COPD referred for videofluoroscopic swallow examination. Journal of Communication Disorders, 33(2), 93-110.
Langmore, S. E., Skarupski, K. A., Park, P. S., & Fries, B. E. (2002). Predictors of aspiration pneumonia in nursing home residents. Dysphagia, 17(4), 298-307.
Mokhlesi, B. (2003). Clinical implications of gastroesophageal reflux disease and swallowing dysfunction in COPD. American Journal of Respiratory Medicine, 2(2), 117-121.
Mokhlesi, B., Logemann, J. A., Rademaker, A. W., Stangl, C. A., & Corbridge, T. C. (2002). Oropharyngeal deglutition in stable COPD. Chest., 121(2), 361-369.
Stein, M., Williams, A. J., Grossman, F., Weinberg, A. S., & Zuckerbraun, L. (1990). Cricopharyngeal dysfunction in chronic obstructive pulmonary disease. Chest.97(2):347-52.
Congestive heart failure is the inability of the heart to pump blood with adequate pressure to maintain the physiologic demands of organs. It occurs when the myocardium (heart muscle) becomes weak. There are several causes of this progressive weakening of the myocardium. One is disease of the heart muscle itself (cardiomyopathy). Another is arterial hypertension which forces the left ventricle to pump blood against too much resistance for a long period of time, until the muscle itself is overcome by the excessive workload. (The heart muscle first becomes thickened or hypertrophic just as your skeletal muscles get larger when you exercise but heart exercise is good only up to a point.). Likewise, pulmonary hypertension can cause right sided heart failure because the right ventricle is pumping blood through the pulmonary circulation against excessive resistance.
It is this last example that might partially answer your question. Diseases of the lungs such as some forms of COPD (emphysema in particular) can destroy portions of the respiratory membrane which is formed by the alveolar membrane plus the pulmonary capillaries. When the capillaries are destroyed the blood flow into the lungs (to pick up oxygen and get rid of CO2) is blocked so the right ventricle is pumping some blood into a dead end, the pressure in these vessels becomes very high. The result of this pulmonary hypertension is the leakage of material from the blood (that should not leak out of the circulatory system) into the lung. This example is one way that patients develop pulmonary edema (this fluid leakage into the lung is defined as pulmonary edema caused by congestive heart failure). Similarly this heart failure causes fluid to accumulate in the pleural cavity (the space outside of the lungs between the inner and outer pleural membranes that line the lungs and chest cavity).
OK so now we have COPD as a source of CHF. Patients with COPD have reduced mucociliary clearance, reduced expiratory capacity, both of which increase the patient’s resistance to infection (i.e. pneumonia) which are some reasons that COPD patients have a higher risk of any type of pneumonia. These patients also have a different pattern of breathing/swallowing coordination than normals that disrupts the typical “swallow at the onset of exhalation” pattern that predominates in normals, and also increases the respiratory rate above a normal (12-20 or so breaths per minute) further discoordinating (I don’t know if that is a real word) swallow-breathing. Likewise COPD patients exhibit more frequent laryngeal penetration than normals (Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Good-Fratturelli, Curlee, & Holle, 2000)
CHF itself and the associated pulmonary edema and pleural effusions, reduce respiratory surface area by restricting inflation of the lungs (effusions) or by obstructing air from the respiratory membrane (edema). The result of either is the patient has to breathe more times per minute (increased respiratory rate- see above).
There are some good studies that show the association between COPD and dysphagia, and CHF and dysphagia, (see below) but the link between these conditions and dysphagia, as well as the link to subsequent pneumonia risk, is based on the understanding of the pathophysiology of those diseases and mostly based on animal studies, though the inferences are very strong. For example, we know the above processes take place in these diseases, and we know that these patients have increased respiratory rate, swallow-respiratory coordination abnormalities, higher incidence of pneumonia, etc., so we infer that the diseases’ properties explain some if not all of the association between them and dysphagia, increased pneumonia risk, etc. (Langmore, Skarupski, Park, & Fries, 2002).
Cricopharyngeal dysfunction is also seen in some patients with COPD and this can contribute to prandial aspiration and increased likelihood of inoculating thelungs with pathogens ((Good-Fratturelli, Curlee, & Holle, 2000; Langmore, Skarupski, Park, & Fries, 2002; Mokhlesi, 2003; Mokhlesi, Logemann, Rademaker, Stangl, & Corbridge, 2002; Stein, Williams, Grossman, Weinberg, & Zuckerbraun, 1990).
Cheers,
James L. Coyle, Ph.D., CCC-SLP, BRS-S
Assistant Professor, Communication Science and Disorders
University of Pittsburgh
Confidential University of Pittsburgh information. Any unauthorized or improper disclosure, copying, distribution, or use of the contents of this e-mail or attached documents is prohibited. The information contained in this e-mail message is intended only for the personal and confidential use of the recipient(s) named above. If you have received this communication in error, please notify the sender immediately by e-mail and delete the original message.
Good-Fratturelli, M. D., Curlee, R. F., & Holle, J. L. (2000). Prevalence and nature of dysphagia in VA patients with COPD referred for videofluoroscopic swallow examination. Journal of Communication Disorders, 33(2), 93-110.
Langmore, S. E., Skarupski, K. A., Park, P. S., & Fries, B. E. (2002). Predictors of aspiration pneumonia in nursing home residents. Dysphagia, 17(4), 298-307.
Mokhlesi, B. (2003). Clinical implications of gastroesophageal reflux disease and swallowing dysfunction in COPD. American Journal of Respiratory Medicine, 2(2), 117-121.
Mokhlesi, B., Logemann, J. A., Rademaker, A. W., Stangl, C. A., & Corbridge, T. C. (2002). Oropharyngeal deglutition in stable COPD. Chest., 121(2), 361-369.
Stein, M., Williams, A. J., Grossman, F., Weinberg, A. S., & Zuckerbraun, L. (1990). Cricopharyngeal dysfunction in chronic obstructive pulmonary disease. Chest.97(2):347-52.
Wednesday, April 1, 2009
Thursday Rounds: Student Presentation
In order to keep things moving on time for rounds on Thursday I would ask that you have your students be there 10-15 minutes early to preload their presentations and test any visuals prior to beginning. Please have your student email their topics and I will have an agenda printed. Thank you!
Tuesday, March 17, 2009
Adult Clinical Rotations: Student Presentation Guidelines Fresh Off the Press!
Adult Clinical Rotations
Student Presentation Guidelines
Description: Students will be required to present a clinical topic to the adult speech pathologists. Oral and written components are required.
Topics: Teach us something new! Keep in mind, the point of the presentation is to enhance the staff’s knowledge. Maybe a disorder you had an experience with during your rotation (something we could learn more about); patient and/or family information packets; or a treatment strategy. If you decide to present a treatment strategy, please include the following information: treatment efficacy, cost efficiency, availability, reliability, etc.
If you have difficulty choosing a topic, ask your supervisor for suggestions.
Written requirement: Please prepare a summarized handout for clinicians (1-2 pages) or a packet for patients/families. Include references. Do not print something directly from a website. You should organize this information on your own. If creating a Pt/family packet, provide helpful web sites, phone numbers, support groups, etc.
Oral requirement: You will be given less than 10 minutes including a brief question-answer period. This is not a great deal of time, so plan accordingly.
Date: Presentations will be Thursday, April 2nd from 8:00-9:00am during rounds.
Location: 202 Basic Science Building (rounds location)
Student Presentation Guidelines
Description: Students will be required to present a clinical topic to the adult speech pathologists. Oral and written components are required.
Topics: Teach us something new! Keep in mind, the point of the presentation is to enhance the staff’s knowledge. Maybe a disorder you had an experience with during your rotation (something we could learn more about); patient and/or family information packets; or a treatment strategy. If you decide to present a treatment strategy, please include the following information: treatment efficacy, cost efficiency, availability, reliability, etc.
If you have difficulty choosing a topic, ask your supervisor for suggestions.
Written requirement: Please prepare a summarized handout for clinicians (1-2 pages) or a packet for patients/families. Include references. Do not print something directly from a website. You should organize this information on your own. If creating a Pt/family packet, provide helpful web sites, phone numbers, support groups, etc.
Oral requirement: You will be given less than 10 minutes including a brief question-answer period. This is not a great deal of time, so plan accordingly.
Date: Presentations will be Thursday, April 2nd from 8:00-9:00am during rounds.
Location: 202 Basic Science Building (rounds location)
Friday, March 13, 2009
Reduction of Risk for Aspiration Pneumonia
...why the goal of "reducing the risk of pneumonia caused by aspiration of colonized oral secretions" (should) not be considered a legitimate therapeutic goal. I use it as one of my goals in the acute care setting. Patients known to aspirate (as so many have cited in this thread) are already at increased pneumonia risk due to dysphagia, and have a greater risk due to colonized oral secretions. As we all know Langmore et al. (1998) concluded that dysphagia alone was insufficient to predict risk of morbidity and mortality but when combined with other risk factors including periodontal disease and dependency for feeding (odds ratio of almost 20 - that is a twenty-fold increase in risk) and oral care, dysphagia became an important risk factor for pneumonia.
Some additional evidence to support this include the recommendation from the Centers for Disease Control and Prevention that secretions lying above an endotracheal tube cuff should be removed prior to extubation, to reduce risk of health-care associated pneumonia - a category II recommendations (Category II. Suggested for implementation and supported by suggestive clinical or epidemiologic studies or by strong theoretical rationale) (CDC, 2003), as well as the natural history of oral colonization and biofilm development seen in a number of studies in the oral health literature.
Adachi et al, (2007) found a high prevalence of oral pathogens (staph. aureus, pseudomonas species, and yeast (candida albicans) in nursing home patients, and showed a significant decrease in incidence of "fatal aspiration pneumonia" in patients receiving professional oral hygiene (by dental hygienists) than in those that did not (I cannot get the actual article so this is cited only from their abstract; the methods are not detailed enough in the abstract to allow critical appraisal. Likewise Azarpazhooh et al. (2006) conducted a systematic review that is well designed, on the association between oral health and respiratory infections. This study identified "fair evidence (II-2, grade B recommendation) of an association of pneumonia with oral health", and "good evidence (I, grade A recommendation) that improved oral hygiene and frequent professional oral health care reduces the progression or occurrence of respiratory diseases among high-risk elderly adults living in nursing homes and especially those in intensive care units". This evidence might help justify these clinical procedures by SLP's however appropriate training should precede such programs.
In the School in which I teach, faculty in the Clinical Dietetics program (and I understand this is an institutionalized professional initiative in their field) are teaching their students to conduct "physical examinations" including oral inspections to identify risks associated with oral intake. Dental hygienists are not ordinarily seen in nursing homes yet SLP's are, so perhaps as front-line observers of oral condition in these patients, SLP's are justified in performing at least screenings. Either we need dental hygienists in nursing homes or SLP's need to learn this important skill (or at least advocate for support to train (on an ongoing basis) the CNA's in these facilities).
Adachi, M., Ishihara, K., Abe, S., & Okuda, K. (2007). Professional oral health care by dental hygienists reduced respiratory infections in elderly persons requiring nursing care. International Journal of Dental Hygiene, 5(2), 69-74.
Azarpazhooh, A., & Leake, J. L. (2006). Systematic review of the association between respiratory diseases and oral health. Journal of Periodontology, 77(9), 1465-1482.
Centers for Disease, C., & Prevention (2003). Guidelines for preventing health-care associated pneumonia, 2003 (No. MMWR, 53 (RR-3)).
Langmore, S. E., Terpenning, M. S., Schork, A., Chen, Y., Murray, J. T., Lopatin, D., et al. (1998). Predictors of aspiration pneumonia: how important is dysphagia? Dysphagia, 13(2), 69-81.
Cheers,
James L. Coyle, Ph.D., CCC-SLP; BRS-S
Assistant Professor, Communication Science and Disorders University of Pittsburgh
Some additional evidence to support this include the recommendation from the Centers for Disease Control and Prevention that secretions lying above an endotracheal tube cuff should be removed prior to extubation, to reduce risk of health-care associated pneumonia - a category II recommendations (Category II. Suggested for implementation and supported by suggestive clinical or epidemiologic studies or by strong theoretical rationale) (CDC, 2003), as well as the natural history of oral colonization and biofilm development seen in a number of studies in the oral health literature.
Adachi et al, (2007) found a high prevalence of oral pathogens (staph. aureus, pseudomonas species, and yeast (candida albicans) in nursing home patients, and showed a significant decrease in incidence of "fatal aspiration pneumonia" in patients receiving professional oral hygiene (by dental hygienists) than in those that did not (I cannot get the actual article so this is cited only from their abstract; the methods are not detailed enough in the abstract to allow critical appraisal. Likewise Azarpazhooh et al. (2006) conducted a systematic review that is well designed, on the association between oral health and respiratory infections. This study identified "fair evidence (II-2, grade B recommendation) of an association of pneumonia with oral health", and "good evidence (I, grade A recommendation) that improved oral hygiene and frequent professional oral health care reduces the progression or occurrence of respiratory diseases among high-risk elderly adults living in nursing homes and especially those in intensive care units". This evidence might help justify these clinical procedures by SLP's however appropriate training should precede such programs.
In the School in which I teach, faculty in the Clinical Dietetics program (and I understand this is an institutionalized professional initiative in their field) are teaching their students to conduct "physical examinations" including oral inspections to identify risks associated with oral intake. Dental hygienists are not ordinarily seen in nursing homes yet SLP's are, so perhaps as front-line observers of oral condition in these patients, SLP's are justified in performing at least screenings. Either we need dental hygienists in nursing homes or SLP's need to learn this important skill (or at least advocate for support to train (on an ongoing basis) the CNA's in these facilities).
Adachi, M., Ishihara, K., Abe, S., & Okuda, K. (2007). Professional oral health care by dental hygienists reduced respiratory infections in elderly persons requiring nursing care. International Journal of Dental Hygiene, 5(2), 69-74.
Azarpazhooh, A., & Leake, J. L. (2006). Systematic review of the association between respiratory diseases and oral health. Journal of Periodontology, 77(9), 1465-1482.
Centers for Disease, C., & Prevention (2003). Guidelines for preventing health-care associated pneumonia, 2003 (No. MMWR, 53 (RR-3)).
Langmore, S. E., Terpenning, M. S., Schork, A., Chen, Y., Murray, J. T., Lopatin, D., et al. (1998). Predictors of aspiration pneumonia: how important is dysphagia? Dysphagia, 13(2), 69-81.
Cheers,
James L. Coyle, Ph.D., CCC-SLP; BRS-S
Assistant Professor, Communication Science and Disorders University of Pittsburgh
Tuesday, March 3, 2009
Schedule, Wednesday, March 4th, 2009
Tomorrow, rather than meet me at ART, plan to come to 7N as usual because Caroline's student, Annie is following us to ART. Also, my lab coat is in the main hospital.
Thanks!
Thanks!
Tuesday, February 24, 2009
Thursday, February 12, 2009
What is Devic's Disease?
What is Devic's disease? In what manner might it lead to speech and language difficulties?
"Certificates... Do We Really Need 'Em?"
You do not need to pay for a certification course to become competent to perform FEES, MBS’s or other techniques. As I stated in my earlier post, you do need “Training, yes (does it need to be training by a specific entity, I would argue “not necessarily”). Sound and evidence based decision making capabilities, yes. The ability to produce an objective and defensible rationale for the proposed treatment, yes.”
Holding a piece of paper only means that the certificate holder attended a meeting. It does not convey competence or evidence based decision making. You state that you are not trained to perform FEES or MBS’s, but that training is possible without paying for a “certificate”.
True SLP’s pay to receive a certificate for certain kinds of training such as FEES (as you have cited). However many facilities “certify” clinician competence of SLP’s to perform FEES after they have performed 25 (or a specific number of) exams under supervision or other clinicians with more than that level of experience/competence. They do not have to pay for a piece of paper. Similarly, physicians that perform many surgical procedures do not necessarily receive a certificate stating they have attended a meeting to train them to perform the procedure. They learn from each other, in much the same way that we train and educate our students and supervisees.
Isn’t a clinician who is “certified” in lsvt qualified to train others to perform lsvt? If not, what would qualify him or her to train others? I attended a Jeri Logemann conference in 1987 and received a piece of paper, but was completely unqualified to perform the MBS procedure until I had received mentoring, experience and extensive training after the conference.
Cheers,
James L. Coyle, Ph.D., CCC-SLP, BRS-S
Assistant Professor, Communication Science and Disorders
University of Pittsburgh
Holding a piece of paper only means that the certificate holder attended a meeting. It does not convey competence or evidence based decision making. You state that you are not trained to perform FEES or MBS’s, but that training is possible without paying for a “certificate”.
True SLP’s pay to receive a certificate for certain kinds of training such as FEES (as you have cited). However many facilities “certify” clinician competence of SLP’s to perform FEES after they have performed 25 (or a specific number of) exams under supervision or other clinicians with more than that level of experience/competence. They do not have to pay for a piece of paper. Similarly, physicians that perform many surgical procedures do not necessarily receive a certificate stating they have attended a meeting to train them to perform the procedure. They learn from each other, in much the same way that we train and educate our students and supervisees.
Isn’t a clinician who is “certified” in lsvt qualified to train others to perform lsvt? If not, what would qualify him or her to train others? I attended a Jeri Logemann conference in 1987 and received a piece of paper, but was completely unqualified to perform the MBS procedure until I had received mentoring, experience and extensive training after the conference.
Cheers,
James L. Coyle, Ph.D., CCC-SLP, BRS-S
Assistant Professor, Communication Science and Disorders
University of Pittsburgh
Wednesday, February 11, 2009
Parkinson's Disease
"I don’t see anything in the description suspicious for a CN V3 (mandibular nerve) injury (was there a sensory impairment on the right side? V3 carries sensory fibers to the lower 1/3 of the face) except the jaw droop at rest which may just be his posture. Tongue to right would be right XII and palate paresis with hypernasality would be X. Also you would have to figure out what type of lesion would selectively affect these nerves/brainstem nuclei on both sides of the patient.
The most likely explanation for your observations is the rigidity associated with parkinsonism. The inability to initiate motion is one property of rigidity in which both agonist muscles (those that perform the intended movement) and their antagonists (those that resist the intended movement) are activated at the same time the patient wants to move (antagonist inhibition is disrupted in parkinsonism). Of course a MRI of his brain would help you to sort this out because certainly, apraxia after an undiagnosed stroke could cause motor planning problems (but the same stroke should not cause the bilateral cranial nerve lower motor neuron pattern observations.
If rigidity it might help to ask the patient whether he notes any improvement in the inability to initiate movement shortly after taking his Parkinson medications. Some patients (probably about 25%) notice a distinct “on” phase after medications in which they move much more easily for a short time. In those cases we ask the attending or neurologist to consider whether trying timing the medication to precede the intended activity (eating) by one-half hour or so is not contraindicated.
This article is an interesting as it relates to treatment of Parkinsons patients by using a motor pre-cue.
Johnson, A. M., Vernon, P. A., Almeida, Q. J., Grantier, L. L., & Jog, M. S. (2003). A role of the basal ganglia in movement: the effect of precues on discrete bi-directional movements in Parkinson's disease. Motor Control., 7, 71-81."
The most likely explanation for your observations is the rigidity associated with parkinsonism. The inability to initiate motion is one property of rigidity in which both agonist muscles (those that perform the intended movement) and their antagonists (those that resist the intended movement) are activated at the same time the patient wants to move (antagonist inhibition is disrupted in parkinsonism). Of course a MRI of his brain would help you to sort this out because certainly, apraxia after an undiagnosed stroke could cause motor planning problems (but the same stroke should not cause the bilateral cranial nerve lower motor neuron pattern observations.
If rigidity it might help to ask the patient whether he notes any improvement in the inability to initiate movement shortly after taking his Parkinson medications. Some patients (probably about 25%) notice a distinct “on” phase after medications in which they move much more easily for a short time. In those cases we ask the attending or neurologist to consider whether trying timing the medication to precede the intended activity (eating) by one-half hour or so is not contraindicated.
This article is an interesting as it relates to treatment of Parkinsons patients by using a motor pre-cue.
Johnson, A. M., Vernon, P. A., Almeida, Q. J., Grantier, L. L., & Jog, M. S. (2003). A role of the basal ganglia in movement: the effect of precues on discrete bi-directional movements in Parkinson's disease. Motor Control., 7, 71-81."
Friday, February 6, 2009
Measuring Attention: Digit Span Forward
Please check out post dated October 23rd, 2008 on digit span and attention in testing.
MBS Protocol
One of the issues in performing a modified barium swallow study with a radiologist is time-constraints.
The radiologist is generally attempting to perform the study as quickly and efficiently as possible. This, of course, should be our goal as well.
Arranging your presentation items is key to improving efficiency.
Sometimes, the radiologist will begin to "take over" your study if you are not fully in control. Try not to allow this to make you nervous.
As you (as a student) perform more and more MBSes, you will gain confidence and all will fall into place.
The radiologist is generally attempting to perform the study as quickly and efficiently as possible. This, of course, should be our goal as well.
Arranging your presentation items is key to improving efficiency.
Sometimes, the radiologist will begin to "take over" your study if you are not fully in control. Try not to allow this to make you nervous.
As you (as a student) perform more and more MBSes, you will gain confidence and all will fall into place.
Tuesday, January 27, 2009
Self-Mediation and Requests for Repetition
Self-mediation is a compensatory technique used by persons who are having some sort of difficulty processing information. It may be a full repetition of the stimulus question or a sub-vocalization of part of that stimulus message.
A request for repetition is another compensatory technique used for the same purpose except that it tends to occur less frequently and needs to be encouraged and reinforced when it does occur.
A request for repetition is another compensatory technique used for the same purpose except that it tends to occur less frequently and needs to be encouraged and reinforced when it does occur.
Therapy Tidbits: Expansion and Elaboration
Expansion/Elaboration:
Basically, the response you have obtained from the patient is correct but not perfect; so, you expand the response or ask the person to elaborate.
For example, you ask: "How are shoes and boots alike?" and the person responds, "You wear them." You say, "That's right. Shoes and boots are worn." You can continue to expand the response by saying "Yes, they are worn on your feet. What kind of clothing are they?" or you may ask them to elaborate, "On what part of the body do you wear shoes and boots?" and/or "What kind of clothing are shoes and boots?"
The "perfect" response you are trying to elicit is "footwear."
Basically, the response you have obtained from the patient is correct but not perfect; so, you expand the response or ask the person to elaborate.
For example, you ask: "How are shoes and boots alike?" and the person responds, "You wear them." You say, "That's right. Shoes and boots are worn." You can continue to expand the response by saying "Yes, they are worn on your feet. What kind of clothing are they?" or you may ask them to elaborate, "On what part of the body do you wear shoes and boots?" and/or "What kind of clothing are shoes and boots?"
The "perfect" response you are trying to elicit is "footwear."
Thursday, January 22, 2009
January/February/March 2009 Practicum Schedule
No practicum on the following dates:
Wednesday, January 28th
Tuesday, February 3rd
Tuesday, February 17th
Monday, February 23rd
Wednesday, March 4th
Monday, March 9th
Thursday, March 19th
Wednesday, March 25th
Tuesday, March 31st
Wednesday, January 28th
Tuesday, February 3rd
Tuesday, February 17th
Monday, February 23rd
Wednesday, March 4th
Monday, March 9th
Thursday, March 19th
Wednesday, March 25th
Tuesday, March 31st
Tuesday, January 6, 2009
Spring Practicum - January 13th, 2009
Hello!
Welcome to your MUSC speech practicum with Carley. Please refer to this blog throughout the semester for valuable information and feedback. When you visit, please comment so that I will know you stopped by.
Please note that I will not be here on Monday, January 12th. Therefore, your practicum will begin on Tuesday, January 13th at 9 a.m. in Main Hospital North Tower Room 741.
Thank you so much.
Welcome to your MUSC speech practicum with Carley. Please refer to this blog throughout the semester for valuable information and feedback. When you visit, please comment so that I will know you stopped by.
Please note that I will not be here on Monday, January 12th. Therefore, your practicum will begin on Tuesday, January 13th at 9 a.m. in Main Hospital North Tower Room 741.
Thank you so much.
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