Tag Archives: SLP

Amyotrophic Lateral Sclerosis Info & Sources (Anatomy Paper) [Again and Sorry]

17 Jul

Excuse me for posting this one again.  And no pictures even–what a gyp for you!  I’m sort of at a stopping point on this paper until I go to the campus library.  And who knows when that will be.  It seems something (tiredness, weather, holidays, other fun stuff to do, running, laziness, everything) is always stopping me.  But I am determined to get it finished BEFORE the semester begins.  I want to get some legit (physical) journals in their entirety and use those.  Then, once I have those sources–the easy part–writing the facts in a cohesive order.  It’s the works-cited page that I think is the most difficult.  That, and the in-text citations.  USING the information in the paper will be easy.  So this is more for me, then you, my readers.  If you’re totally bored and tired of my Anatomy class ALS paper’s sources–you can always check out my blog archives.  There is plenty of interesting material there. . .

ALS (9,620 results) {note to self:  type out full name to get more and better results}

bilateral degeneration of the upper motor neuron in the primary motor areas also impairs further adjusted motor areas, which leads to a strong reduction of ‘swallowing related’ cortical activation. While both hemispheres are affected by the degeneration a relatively stronger activation is seen in the right hemisphere.

Source 1:  http://www.springerlink.com/content/w7fd9x9b1a2v1ew1/

-Dysphagia severity tended to be particularly influenced by dysfunction of the posterior tongue.

-early stage of dysphagia in ALS was mainly caused by oral dysfunction, and the oral phase disorders began in some cases with a decreased function of bolus transport at the anterior part of the tongue, and in other cases with a deteriorated function of holding the bolus at the posterior part of the tongue.

Source 2:  http://www.ncbi.nlm.nih.gov/pubmed/11681400

-abnormal lingual movement may result in pharyngeal residue that is aspirated after the swallow is completed and respiration is resumed. ALS patients with bulbar involvement demonstrate more severe swallowing problems (such as aspiration)

Source 3:  http://jama.jamanetwork.com/article.aspx?volume=234&issue=7&page=715

-Until a definitive treatment is found for amyotrophic lateral sclerosis, there will continue to be a need to provide symptomatic care.

Using amyotrophic lateral sclerosis as the search term:

Source 4:  http://www.ajcn.org/content/63/1/130.short

-fatal neurodegenerative disease characterized by progressive muscle atrophy and weakness.

-Although dysphagia is a universal feature of this illness, the nutritional and metabolic status of ALS patients has received little attention.  Regression analysis demonstrated progressive decreases in body fat, lean body mass, muscle power, and nitrogen balance and an increase in resting energy expenditure as death approached.

-We conclude that ALS patients have a chronically deficient intake of energy and recommended augmentation of energy intake rather than the consumption of high-protein nutritional supplements.

Source 5:  http://www.nejm.org/doi/full/10.1056/NEJM200105313442207

–  no cut & paste allowed

-good overview/history

Source 6:  http://ukpmc.ac.uk/abstract/MED/11854102

Amyotrophic lateral sclerosis (ALS) is the most common degenerative motor neuron disease in adults.

-The clinical picture consists of generalized fasciculations, progressive atrophy and weakness of the skeletal muscles, spasticity and pyramidal tract signs, dysarthria, dysphagia, and dyspnea. Pseudobulbar affect is common.

Nutritional deficiency caused by dysphagia can be relieved by a percutaneous endoscopic gastrostomy. Respiratory insufficiency can be effectively treated by non-invasive home mechanical ventilation. The terminal phase of the disease should be discussed at the latest when symptoms of dyspnea appear, in order to prevent unwarranted fears of “choking to death.” Psychological and spiritual care of patients and families are important. Collaboration with hospice institutions and completion of advance directives can be of invaluable help in the terminal phase.

Source 7:  http://www.ojrd.com/content/4/1/3/abstract

-whole abstract is good info for entire overview of DZ

Source 8:  http://www.ncbi.nlm.nih.gov/pubmed/9562665

-Amyotrophic lateral sclerosis (ALS) is a motor neuron disease with evidence of both anterior horn cell and corticospinal tract degeneration. The incidence of ALS is 1 to 2.5 cases per 100,000 population and the disease occurs primarily in adult life. The etiology of sporadic ALS remains unknown, although 5 to 10% of cases are familial. The diagnosis of ALS requires the presence of both upper and lower motor neuron findings and progressive motor dysfunction. Several theories regarding the pathogenesis of ALS have emerged including glutamate excitotoxicity, free radical oxidative stress, neurofilament accumulation, and autoimmunity. Clinical trials involving antiglutamate agents, antioxidants, immunosuppressants, and growth factors have shown no substantial benefit in slowing progression, with death usually occurring 2 to 5 years following the onset of symptoms. The management of ALS patients requires a multidisciplinary team that can provide the numerous medical and physical interventions necessary to treat weakness and fatigue, bulbar dysfunction, spasticity and pain, depression, and respiratory failure.

Source 9:  http://ukpmc.ac.uk/abstract/MED/7952238

-Therapeutic trials for amyotrophic lateral sclerosis have attracted much attention, but no drug tested has been effective yet. Three major theories of pathogenesis form the basis for these trials: autoimmunity, chronic excitotoxic stimulation due to accumulation of glutamate, and, in the familial form, peroxidation due to subnormal activity of superoxide dismutase. In striking contrast to the negative results of all of the other drug trials, riluzole (a glutamate antagonist) was said to benefit patients with bulbar onset but not those with spinal onset. Problems with the original trial may be clarified by other studies now in progress.

Source 10:  http://www.sciencedirect.com/science/article/pii/S0140673696916803

-In an initial study, riluzole decreased mortality and slowed muscle-strength deterioration in ALS patients. We have carried out a double-blind, placebo-controlled, multicentre study to confirm those findings and to assess drug efficacy at different doses.

-959 patients with clinically probable or definite ALS of less than 5 years’ duration were randomly assigned treatment with placebo or 50 mg, 100 mg, or 200 mg riluzole daily; randomisation was stratified by centre and site of disease onset (bulbar or limb).

-primary outcome was survival without a tracheostomy. Secondary outcomes were rates of change in functional measures (muscle strength, functional status, respiratory function, patient’s assessments of fasciculation, cramps, stiffness, and tiredness).

-The most common adverse reactions were asthenia, dizziness, gastrointestinal disorders, and rises in liver enzyme activities; they were commonest with the 200 mg dose

-Overall, efficacy and safety results suggest that the 100 mg dose of riluzole has the best benefit-to-risk ratio. This study confirms that riluzole is well tolerated and lengthens survival of patients with ALS.

Source 11:  http://www.sciencedirect.com/science/article/pii/S0140673610611567

-Substantial wasting of the tongue muscles in bulbar-onset ALS. Note the absence of palatal elevation present on vocalisation. Difficulty with mouth opening and dysphagia might require supplementary feeding through a percutaneous endoscopic gastrostomy. In further support of a corticomotoneuronal hypothesis, the tongue is often disproportionately affected in comparison to other oropharyngeal musculature in patients with bulbar-onset ALS. As with the thenar muscles in the hand, the tongue receives more extensive cortical input than other muscle groups in the oropharyngeal area.

-neurodegeneration in ALS might result from a complex interaction of glutamate excitoxicity, generation of free radicals, cytoplasmic protein aggregates, SOD1 enzymes, combined with mitochondrial dysfunction, and disruption of axonal transport processes through accumulation of neurofilament intracellular aggregates. Mutations in TARDBP andFUS result in formation of intracellular aggregates, which are harmful to neurons. Activation of microglia results in secretion of proinflammatory cytokines, resulting in further toxicity. Ultimately, motor neuron degeneration occurs through activation of calcium-dependent enzymatic pathways

 

ALS Anatomy Paper: Unsuitable (for citations) Internet Database

14 Jun

Are you getting tired of reading about this?  Maybe you are, but it’s very helpful for me to do all the prep work on a blog.  It links up to the rest and I can use the stages to write the actual paper.  And I’m getting finished with the most difficult part:  Finding and formatting appropriate citations.  Trouble is–you can never have too many good sources of information in a paper.  A secondary concern is that good sources don’t always convey the basic information that I want to include in the paper.

Reading the “facts” on Wiki seems to much easier and complete, then wading through research jargon and trying to put together their results in some sort of comprehensive and conclusive statement.  When is research conclusive, anyway?  You always need more.  That’s the trouble.

At any rate, that’s why this ALS info keeps popping up on the blog.  Sorry if it’s disruptive to your entertainment needs.  Maybe a post about alcohol tomorrow. . .

I can’t really use these quotes or sources, but I CAN use the information to find legit sources on Google Scholar.

Pub-Med:  http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001708/

-ALS is also known as Lou Gehrig’s disease.

-In about 10% of cases, ALS is caused by a genetic defect. In the remaining cases, the cause is unknown.

-In ALS, nerve cells (neurons) waste away or die, and can no longer send messages to muscles. This eventually leads to muscle weakening, twitching, and an inability to move the arms, legs, and body. The condition slowly gets worse. When the muscles in the chest area stop working, it becomes hard or impossible to breathe on one’s own.

-ALS affects approximately 5 out of every 100,000 people worldwide.

-Symptoms usually do not develop until after age 50.

-Breathing or swallowing muscles may be the first muscles affected. As the disease gets worse, more muscle groups develop problems.

–>refer to long symptoms list

–>refer to diagnostic list

-There is no known cure for ALS.

-first drug treatment for the disease is a medicine called riluzoleRiluzole slows the disease progression and prolongs life.

–>refer to management of symptoms

-Death often occurs within 3 – 5 years of diagnosis. About 25% of patients survive for more than 5 years after diagnosis.

–>refer to DZ complications

Wiki:  http://en.wikipedia.org/wiki/Amyotrophic_lateral_sclerosis

-The condition is sometimes called Lou Gehrig‘s disease in North America, after the New York Yankees baseball player who was diagnosed with the disease in 1939.

-bladder and bowel sphincters and the muscles responsible for eye movement are usually, but not always, spared.

-Cognitive function is generally spared for most patients although some (~5%) also have frontotemporal dementia.[1] A higher proportion of patients (~30-50%) also have more subtle cognitive changes which may go unnoticed but are revealed by detailed neuropsychological testing. Sensory nerves and the autonomic nervous system, are generally unaffected meaning the majority of people with ALS will maintain sight, hearing, touch, smell, and taste.

-presenting symptoms include muscle fasciculation (twitching), cramping, or stiffness of affected muscles; muscle weakness affecting an arm or a leg; and/or slurred and nasal speech.

-About 75% of people contracting the disease experience “limb onset” ALS i.e. first symptoms in the arms or legs. Patients with the leg onset form may experience awkwardness when walking or running or notice that they are tripping or stumbling, often with a “dropped foot” which drags gently along the ground. Arm-onset patients may experience difficulty with tasks requiring manual dexterity such as buttoning a shirt, writing, or turning a key in a lock.

-About 25% of cases are “bulbar onset” ALS. These patients first notice difficulty speaking clearly or swallowing.

-A smaller proportion of patients experience “respiratory onset” ALS where theintercostal muscles that support breathing are affected first.

-Symptoms of upper motor neuron involvement include tight and stiff muscles (spasticity) and exaggerated reflexes (hyperreflexia) including an overactive gag reflex.

-An abnormal reflex commonly calledBabinski’s sign also indicates upper motor neuron damage.

-Symptoms of lower motor neuron degeneration include muscle weakness and atrophy, muscle cramps, and fleeting twitches of muscles that can be seen under the skin (fasciculations).

-Around 15–45% of patients experience pseudobulbar affect, also known as “emotional lability”, which consists of uncontrollable laughter, crying or smiling, attributable to degeneration of bulbar upper motor neurons resulting in exaggeration of motor expressions of emotion.

-To be diagnosed with ALS, patients must have signs and symptoms of both upper and lower motor neuron damage that cannot be attributed to other causes.

-rate of progression can be measured using an outcome measure called the “ALS Functional Rating Scale (Revised)”, a 12-item instrument administered as a clinical interview or patient-reported questionnaire that produces a score between 48 (normal function) and 0 (severe disability). Though there is a high degree of variability and a small percentage of patients have much slower disease, on average, patients lose about 1 FRS point per month.

-Most people with ALS die from respiratory failure, usually within three to five years from the onset of symptoms. The median survival time from onset to death is around 39 months, and only 4% survive longer than 10 years. [6] The best-known person with ALS, Stephen Hawking, has lived with the disease for more than 50 years, though his is an unusual case.

-Recently, a genetic abnormality known as a hexanucleotide repeat was found in a region called C9ORF72, which is associated with ALS combined with frontotemporal dementia ALS-FTD [9], and accounts for some 6% of cases of ALS among white Europeans. [10]

-A defect on chromosome 21 (coding for superoxide dismutase) is associated with approximately 20% of familial cases of ALS, or about 2% of ALS cases overall.[11][12][13] This mutation is believed to be autosomal dominant, and has over a hundred different forms of mutation. The most common ALS-causing SOD1 mutation in North American patients is A4V, characterized by an exceptionally rapid progression from onset to death.

-The defining feature of ALS is the death of both upper and lower motor neurons in the motor cortex of the brain, the brain stem, and the spinal cord. Prior to their destruction, motor neurons develop proteinaceous inclusions in their cell bodies and axons. This may be partly due to defects in protein degradation.[15] These inclusions often contain ubiquitin, and generally incorporate one of the ALS-associated proteins: SOD1TAR DNA binding protein (TDP-43, or TARDBP), or FUS.

-important step toward determining the cause came in 1993 when scientists discovered that mutations in the gene that produces the Cu/Zn superoxide dismutase (SOD1) enzyme were associated with some cases (approximately 20%) of familial ALS. This enzyme is a powerfulantioxidant that protects the body from damage caused by superoxide, a toxic free radical generated in the mitochondria.

-It is speculated that aggregate accumulation of mutant SOD1 plays a role in disrupting cellular functions by damaging mitochondriaproteasomes, protein folding chaperones, or other proteins.

-Scientists have found that, compared to healthy people, ALS patients have higher levels of glutamate in the serum and spinal fluid.[12] Riluzole is currently the only FDA approved drug for ALS and targets glutamate transporters. It only has a modest effect on survival, however, suggesting that excess glutamate is not the sole cause of the disease.

-diagnosis of ALS is primarily based on the symptoms and signs the physician observes in the patient and a series of tests to rule out other diseases.

-Certain EMG findings can support the diagnosis of ALS.

Riluzole (Rilutek) as of 2011 is the only treatment that has been found to improve survival but only to a modest extent.[23] It lengthens survival by several months, and may have a greater survival benefit for those with a bulbar onset. It also extends the time before a person needs ventilation support. Riluzole does not reverse the damage already done to motor neurons, and people taking it must be monitored for liver damage (occurring in ~10% of people taking the drug).[24] It is approved byFood and Drug Administration (FDA) and recommended by the National Institute for Clinical Excellence (NICE).

-supportive care:

–Medical professionals can prescribe medications to help reduce fatigue, ease muscle cramps, control spasticity, and reduce excess saliva and phlegm. Drugs also are available to help patients with pain, depression, sleep disturbances, dysphagia, and constipationBaclofen and diazepam are often prescribed to control the spasticity caused by ALS, and trihexyphenidyl or amitriptyline may be prescribed when ALS patients begin having trouble swallowing their saliva.

–physical and occupational therapists can set goals and promote benefits for individuals with ALS by delaying loss of strength, maintaining endurance, limiting pain, preventing complications, and promoting functional independence.[25]

–Gentle, low-impact aerobic exercise such as performing activities of daily living (ADL’s), walking, swimming, and stationary bicycling can strengthen unaffected muscles, improve cardiovascular health, and help patients fight fatigue and depression.

–Range of motion and stretching exercises can help prevent painful spasticity and shortening (contracture) of muscles. Physical and occupational therapists can recommend exercises that provide these benefits without overworking muscles.

–Physical and occupational therapists can recommend exercises that provide these benefits without overworking muscles. They can suggest devices such as ramps, braces, walkers, bathroom equipment (shower chairs, toilet risers, etc.) and wheelchairs that help patients remain mobile.

–Occupational therapists can provide or recommend equipment and adaptations to enable people to retain as much safety and independence in activities of daily living as possible.

–speech-language pathologists can recommend the use ofaugmentative and alternative communication such as voice amplifiers, speech-generating devices (or voice output communication devices) and/or low tech communication techniques such as alphabet boards or yes/no signals.

-ALS is one of the most common neuromuscular diseases worldwide, and people of all races and ethnic backgrounds are affected. One or two out of 100,000 people develop ALS each year.[30] ALS most commonly strikes people between 40 and 60 years of age, but younger and older people can also develop the disease. Men are affected slightly more often than women.

Amyotrophic comes from the Greek languageA- means “no”, myo refers to “muscle”, and trophic means “nourishment”; amyotrophic therefore means “no muscle nourishment,” which describes the characteristic atrophication of the sufferer’s disused muscle tissue. Lateral identifies the areas in a person’s spinal cord where portions of the nerve cells that are affected are located. As this area degenerates it leads to scarring or hardening (“sclerosis“) in the region.

–>refer to history

KNS-760704 (Dexpramipexole) is under clinical investigation in ALS patients. It is hoped that the drug will have a neuroprotective effect.

Talampanel is being tested in ALS

–>explore Wiki’s resources list

Audiology Essay Outline–Maybe

9 Jun

This has been sitting in my drafts for so long, that I can’t remember how much it is or isn’t updated.  So I’m going to publish it.  Again.

Outline:

Intro about non-direct path

vet story of non-verbal communication [short, short, short]


Cat Cues:

Squishing to the back of the carrier or kennel

big, dilated eyes

pinned ears

swatting with paws

turning head or body quickly

becoming stiff

scrunching head close to the body (neck disappears)

hunching to counter

grabbing with paws (looking to climb)

eyes darting around

trying to hide head

edging off exam table

hair standing up

shaking

rolling over

kicking with back feet

snapping jaws

shopping with my dad

finish vet vitals [short, short, shorter!]

talk about what audiology avenue I want to pursue [spend most time here]

I never did anything the easy way. Following my own path and taking my own, meandering route is just what I do. My journey to audiology was not a direct one. I veered through pre-veterinary studies before coming back around to my initial interest of helping people like my father.

This path was not time wasted though.

Every weekend of my childhood, my dad and I would go do the grocery shopping.  It was our special time together.  We went to a few stores, but the check-out process at each was always the same.  The friendly cashier would be pleased to see a father-daughter duo obviously enjoying each other’s company.  Maybe she would recognize us from weekends past and smile.  Seeing genuine affection and helpfulness was probably a welcome break from the normlacy of screaming and tantrums the employee encountered during the majority of the weekend.  My dad would proudly say “This is my good helper-girl.”

Then, the part I hated would arrive.  The checker would read out the total.  I didn’t hate this part because we couldn’t afford the items or even because my dad fussed at the price.  Neither of those things ever occurred.  What did happen was my Dad’s inevitable, “What?”  The checker would repeat the number, and I would be so embarrassed, knowing what was to come.  My dad still didn’t hear what amount he should write on his check.  My face would flush, and the poor cashier, desperate to get her lines moving, would eventually just turn the written numbers toward my dad so he could see his total for himself.  It is from that mortification that I felt, that I want to help people with hearing loss.  My compassion for my beloved dad motivates me to help others like him.

Growing up, I had no idea audiology existed.  Like most little girls, I was determined to be a veterinarian and work with animals.  Unknowingly, I was honing my communication skills especially non-verbal ones as my career trajectory led me toward veterinary medicine.  In my current job as an animal assistant at a feline exclusive veterinary hospital, I have to quickly asses cat temperaments so I can collect vitals and help with medical procedures.

The owners set the green cat carrier on the exam table and I announced I would be taking some vitals, in a cheery voice.  With my right hand I unlatched the door, and peered inside the cave.  Behind the worn towel was a crunched ball of orange and white fur.  Despite his large frame, Scrappy was trying to become as small as possible in order to evade the uncomfortable veterinary visit he was about to endure.  Unpreturbed, I reached in and scruffed Scrappy with confidence, tugging him toward the door and asking the owners to provide resistance by holding the kennel in place.  I joked that Scrappy was doing the “kitty splits” as he splayed his legs in all directions in a final attempt to remain in the safety of the box, which I’m sure he fought tooth and nail to not enter at home.

Finally extricated from the box, I suggested the owners take away temptation by putting the carrier on the exam room floor.  Scrappy, hunched to the counter, was still trying to be invisible to my probing hands.  His ears were pinned and his eyes were darting wildly searching for any escape route.  He tried to creep toward the edge of the counter and settled for burrowing his head under the crook of his mom’s arm as I fitted the stethoscope to my ears and took Scrappy’s heart rate–as expected it was accelerated.

Next, I needed to get Scrappy’s weight.  While asking the owners about the brand of food he ate, and his eating habits, I picked him up to get the number of pounds we were dealing with.  I could feel Scrappy’s body stiffen.  He was shaking with fear, and I knew if I did not leave him alone, which I couldn’t just yet, that given the chance, he would scratch or bite to get away from me.  While maintaining the conversation about Scrappy’s water consumption, I tried to scruff the chubby cat, but he defensively scrunched his head, making his neck disappear entirely.  I held him close to my body and well away from my face then kept my hand on him when I put him on the scale.

“15 pounds!” I announced as I carefully placed Scrappy back on the exam table.  He whipped around and I yanked my hands out of potential harm’s way.  Scrappy had a mind to bite me to get away, but after I gave him a moment held himself together.  I gave his ears a pet and he relaxed somewhat.  His owners cooed at him and gave him lovins and he settled down further.  I was pretty certain I could obtain a rectal temperature without him flying off the table in a fury.  As his owners were distracting him I eased up his tail and planted the thermometer.  Nine seconds can be so long!  At first, oblivious to what was going on behind him Scrappy soaked up the attention.  Then, he gave me a sideways glance, stiffened his posture, and I could see his hair begin to stand up.  He turned and swatted at me with his claws just as I removed the instrument.  “100.5, right in the normal range!”  I sang out.  “I’ll have the doctor in as soon as she is available.”

Using both verbal communication with the owners and non-verbal cues from the kitty I was able to obtain a history on the patient, collect quantitative data for the veterinarian, and soothe both people and pet.

Potential (Internet) Sources for Dysphagia Pathology Anatomy Paper

7 Jun

I found at least 3 reputable sources from Google Scholar and copy/pasted verbatim just to see which pathology would be easiest to research.

eosinophillic esphogitis (3,230 results)

Decreases the ability of the esophagus to stretch and accommodate mouthfuls of swallowed food probably as a result of the presence of so many eosinophils but also, perhaps as a result of some scaring that occurs in the wall of the esophagus.

source 1:  http://www.nature.com/ajg/journal/v95/n6/abs/ajg2000372a.html

-previously confused with esophageal inflammation due to gastroesophageal reflux, has recently begun to be distinguished from it.

-Presenting symptoms encompass vomiting, pain, and dysphagia (some with impactions or strictures). Allergy, particularly food allergy, is an associated finding in most patients, and many have concomitant asthma or other chronic respiratory disease.

-Differentiation from gastroesophageal reflux disease is approached by analyzing eosinophil density and response to therapeutic trials.

-Therapy encompasses dietary elimination and anti-inflammatory pharmacotherapy.

Source 2:  http://www.nature.com/modpathol/journal/v19/n1/abs/3800498a.html

-raw data

-Eosinophilic esophagitis is a disease with a predilection for young males with dysphagia and rings on endoscopy.

-Biopsies in eosinophilic esophagitis have high epithelial eosinophil counts, averaging nearly 40/hpf.

-Increased awareness of eosinophilic esophagitis is necessary, since treatment with allergen elimination or anti-inflammatory therapy may be more effective than acid suppression.

Source 3:  http://www.nejm.org/doi/full/10.1056/NEJM200408263510924

-This disease is differentiated from reflux esophagitis on the basis of the magnitude of mucosal eosinophilia and a lack of response to acid suppression.

-Approximately 71 percent were male, with a mean (±SD) age of 10.5±5.4 years. The patients presented with the typical symptoms and atopic history that have been described previously (Table 1TABLE 1Presenting Symptoms among 103 Pediatric Patients with Eosinophilic Esophagitis. and Table 2TABLE 2History of Atopy in the 103 Pediatric Patients.).1-4 However, our demographic analysis revealed a strong familial pattern

-first, a genetic predisposition and, second, a cause related to an unknown environmental exposure (e.g., infection or allergen). Both these possibilities now warrant pursuit.

schleroderma (6,550 results)

Can cause wasting of the esophageal muscle and poor contraction of the lower esophageal sphincter (LES). Often accompanied by heartburn.

Source 1:  http://ukpmc.ac.uk/abstract/MED/3491774/reload=0;jsessionid=KJfKOvTIjtnroRTv3GyC.0

-Abnormal motility characterized by loss of peristalsis in the distal esophagus was present in all patients with erosive esophagitis, including the 5 who were asymptomatic.

-The patients with erosive esophagitis also had significantly diminished lower esophageal sphincter pressures and increased frequency and duration ofgastroesophageal reflux episodes.

-The duration of disease, rate of gastric emptying, and fungal smear and culture were not significantly different in those with or without esophagitis.

Source 2:  http://www.annals.org/content/40/1/92.short

-Scleroderma is a systemic disease involving the collagenous tissues. The skin, gastrointestinal tract, and the cardiovascular, musculoskeletal, genitourinary and pulmonary systems may be involved. Dysphagia is a common complaint with esophageal involvement.

Source 3:  http://www.sciencedirect.com/science/article/pii/S0003497510639720

Source 3 (full text online):  http://ats.ctsnetjournals.org/cgi/reprint/22/2/120

-raw data

-Gastroesophageal reflux, not impaired motility, is the major cause of esophageal symptoms in scleroderma.

-The most common esophageal symptoms were heartburn and dysphagia.

ALS (9,620 results) {note to self:  type out full name to get more and better results}

bilateral degeneration of the upper motor neuron in the primary motor areas also impairs further adjusted motor areas, which leads to a strong reduction of ‘swallowing related’ cortical activation. While both hemispheres are affected by the degeneration a relatively stronger activation is seen in the right hemisphere.

Source 1:  http://www.springerlink.com/content/w7fd9x9b1a2v1ew1/

-Dysphagia severity tended to be particularly influenced by dysfunction of the posterior tongue.

-early stage of dysphagia in ALS was mainly caused by oral dysfunction, and the oral phase disorders began in some cases with a decreased function of bolus transport at the anterior part of the tongue, and in other cases with a deteriorated function of holding the bolus at the posterior part of the tongue.

Source 2:  http://www.ncbi.nlm.nih.gov/pubmed/11681400

-abnormal lingual movement may result in pharyngeal residue that is aspirated after the swallow is completed and respiration is resumed. ALS patients with bulbar involvement demonstrate more severe swallowing problems (such as aspiration)

Source 3:  http://jama.jamanetwork.com/article.aspx?volume=234&issue=7&page=715

-Until a definitive treatment is found for amyotrophic lateral sclerosis, there will continue to be a need to provide symptomatic care.

Using amyotrophic lateral sclerosis as the search term:

Source 4:  http://www.ajcn.org/content/63/1/130.short [abstract]

http://www.ajcn.org/content/63/1/130.full.pdf+html [full text]

-fatal neurodegenerative disease characterized by progressive muscle atrophy and weakness.

-Although dysphagia is a universal feature of this illness, the nutritional and metabolic status of ALS patients has received little attention.  Regression analysis demonstrated progressive decreases in body fat, lean body mass, muscle power, and nitrogen balance and an increase in resting energy expenditure as death approached.

-We conclude that ALS patients have a chronically deficient intake of energy and recommended augmentation of energy intake rather than the consumption of high-protein nutritional supplements.

Source 5:  http://www.nejm.org/doi/full/10.1056/NEJM200105313442207

–  no cut & paste allowed

-good overview/history

Source 6:  http://ukpmc.ac.uk/abstract/MED/11854102

Amyotrophic lateral sclerosis (ALS) is the most common degenerative motor neuron disease in adults.

-The clinical picture consists of generalized fasciculations, progressive atrophy and weakness of the skeletal muscles, spasticity and pyramidal tract signs, dysarthria, dysphagia, and dyspnea. Pseudobulbar affect is common.

Nutritional deficiency caused by dysphagia can be relieved by a percutaneous endoscopic gastrostomy. Respiratory insufficiency can be effectively treated by non-invasive home mechanical ventilation. The terminal phase of the disease should be discussed at the latest when symptoms of dyspnea appear, in order to prevent unwarranted fears of “choking to death.” Psychological and spiritual care of patients and families are important. Collaboration with hospice institutions and completion of advance directives can be of invaluable help in the terminal phase.

mysthenia gravis (7,320 results)

Antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder.

Source 1:  http://jnnp.bmj.com/content/76/9/1297.short

-Oesophageal manometry was carried out in two patients and showed generalised weakness of peristaltic contractions which included the smooth muscle part of the oesophagus. These disturbances worsened with repeated swallows.

-They were partly reversed by intravenous edrophonium and by rest

Source 2:  http://jnnp.bmj.com/content/65/6/848.short

-In patients with myasthenia gravis with dysphagia, it was found that the time necessary for the larynx to remain in its superior position during swallowing and swallowing variability in successive swallows increased significantly compared with normal subjects and with patients with myasthenia gravis without dysphagia.

-a coordination disorder between normal CP sphincter muscle and the affected striated muscles of the laryngeal elevators may be one of the reasons for dysphagia in myasthenia gravis.

Source 3:  http://www.ncbi.nlm.nih.gov/pubmed/8017368

-Myasthenia gravis is an autoimmune disorder of the neuromuscular junction that causes muscle weakness. Involvement of oropharyngeal musculature is not uncommon, which leads to dysphagia. Timely consideration of myasthenia gravis in evaluating dysphagia is crucial to prevent complications and to improve the quality of life of these patients. We report four patients who underwent extensive investigations for dysphagia, by gastroenterologists as well as otolaryngologists, before the diagnosis of myasthenia gravis was established.

Source 4:  http://jama.jamanetwork.com/article.aspx?volume=134&issue=12&page=987

-some difficulty in swallowing being the first sign of abnormal muscular fatigue. The defect in the swallowing reflex is due to weakness of the buccopharyngeal muscles, usually with relaxation of the constrictors.

-Both the feeble power of the reflex act, as shown by the slowness of movement, and the relaxation, with dilation of the pharyngeal tube, are easily demonstrated by roentgenoscopic examination.

-The tightening of these muscles and the increased rate of swallowing, after stimulation by an appropriate amount of neostigmine (“prostigmine”) methylsulfate, was observed and recorded in cases of myasthenia gravis

Dysphagia Cookbook

2 Jun

I am trying to get some anatomy finished now to alleviate some stress in the fall.  As part of that plan, I ordered my Anatomy textbook two Saturdays ago.  I wanted to at least have the reading finished by the time the school year began.  And I didn’t pay for expedited shipping to save money.  The company, stupid TextbooksRUs.com, sent me an e-mail confirming my order and saying the book would be processed within 3 days, and the order would arrive in 7-14 days.  So I waited.

After about 13 days, I thought my order should certainly be here by now.  I tried to check the status, but my account had a password on it.  And I couldn’t for the life of me remember the password.  For another 2 days, I typed in every possible option.  Of course I had requested my password my password be e-mailed to me first thing.  But it was slow to arrive.  Maybe my spam-blocker got it?

Finally, I signed in using Facebook–which is really creepy to me.  That makes me afraid.  Facebook rules the world.  Anyway, my “password” was just a jumble of letters and numbers that I never would have arrived at by guessing.  The status of my order said “processed.”  So I thought–uh oh, they mailed it to the wrong place somehow. . .  Or someone stole it. . .

Then, I clicked my order number, trying to find out ANY information.  And the next screen said, “back-ordered/cancelled.”  What?!  Thanks for telling me, TextbooksRUs!  When you cannot deliver an expected order, you use my e-mail address and TELL me!!!!!!!  So I have been wasting precious study time, waiting for a book that was never going to arrive.  Jerks!  It infuriated me.  So much so, that I will never use that textbook site again.

I went ahead and re-ordered the book through Amazon.  So the point of that story, is I’m hungry to get ahead, but still without the all-important book.  So here’s another assignment:

This one is not so easy to get ahead on, because some things are left to chance.  There are a variety of nationalities and specific pathology represented.  So Maybe I’ll just brainstorm some multi-cultural options for myself.

Cultures + Food:

Traditional American–twice baked potatoes

Native American (feather)–http://www.myrecipes.com/recipe/pumpkin-maple-pie-10000000223442/

German–potato salad–mashed

Dutch-corn chowder

Italian-cheese & bacon frittata

pg 25 in MY cookbook:

Grease a muffin tin (only fill each half full of mixture–will rise) with butter/margarine (to add calories).  Use Southwest liquid eggs and substitute bacon grease for bacon (about 1 George Foreman catcher-full, or grease from 8 pieces).  Use 1 C whipping cream instead of milk to get the right calories and consistancy.  +/- small sprinkle of cheese after baking.

English-duff

Middle Eastern–http://www.yummly.com/recipe/Curry-Butternut-Squash-Soup-Recipezaar_1

Indian (dot)–http://www.foodnetwork.com/recipes/alton-brown/indian-rice-pudding-recipe/index.html

Switzerland-cheese fondue

Jewish-http://www.myjewishlearning.com/culture/2/Food/Ashkenazic_Cuisine/Israel/Hummus.shtml

Australian–http://www.taste.com.au/recipes/21611/mango+and+passionfruit+australian+mess

http://australianfood.about.com/od/bakingdesserts/r/Pavlova.htm

Vegetarian–http://www.food.com/recipe/vegan-vegetable-cream-cheese-mashed-potatoes-295819

-Shred the cauliflower florets in tiny pieces before putting in the blender.

-put glops of chip dip, butter, cream cheese, sour cream, liquid eggs, garlic salt, and half & half in the blender.

-blend

-shred broccoli and carrots to desired thickness.

-Once the mixture is blended, pour into cupcake tin.

-Bake for about 30 min.

Russian–http://www.tastebook.com/recipes/1168091-Russian-Mushroom-and-Potato-Soup

New England, America-clam chowder

African–http://allrecipes.com/recipe/african-sweet-potato-and-peanut-soup/

South American–http://veganfeastkitchen.blogspot.com/2010/05/delicious-latin-american-fruit-and-oat.html

Asian–tapioca

French–mousse, omelet

Thai–http://www.food.com/recipe/thai-pumpkin-soup-88347

Hispanic/Mexican–bean dip

Spanish-guacamole

Irish-potato soup

Food Options:

Dips

smoothies

fondue

pudding

Gosh–some of these looked so good that I want to make some for ME!  I’ll have to practice these over the summer, so I’ll be cool as a cucumber when this assignment comes up toward the end of the semester.

Enhanced by Zemanta

Narrowing Anatomy Topics

29 May

I’ll get rid of the super-obvious ones b/c everyone will pick those.  So Down Syndrome, Parkinson’s, M.S., stroke, and cleft palate are out.

I should also see how much information is available on the rest of these.  I don’t want something too obscure that doesn’t have very strong sources.

CHARGE syndrome (4,780 results)

Neonatal brain stem dysfunction causes poor suck swallow mech.  Facial palsy, hyposemia, anatomical problems in structures for sucking, swallowing, and breathing.  Symptoms can also be secondary to exogenious factors such as hospitalization time or dyspnea.

velopharyngeal insufficiency (1,200 results)

is the inadequate closing of the velopharyngeal sphincter often due to a congenital abnormality, can result in problems such as hypernasal speech or regurgitation of fluids through the nose when swallowing.

dystonia (oromandibular or cranial) (7,020 results)

Disorder of neurological movement.  Muscle spasms.

Wilson’s Disease (1,619 results)

Impaired coordination of chewing and swallowing.  Weakness of lips, tongue, and throat muscles.

achalasia (11,200 results)

This sphincter muscle is normally contracted to close the esophagus. When the sphincter is closed, the contents of the stomach cannot flow back into the esophagus. Backward flow of stomach contents (reflux) can irritate and inflame the esophagus, causing symptoms such as heartburn. The act of swallowing causes a wave of esophageal contraction called peristalsis. Peristalsis pushes food along the esophagus. Normally, peristalsis causes the esophageal sphincter to relax and allow food into the stomach. In achalasia, which means “failure to relax,” the esophageal sphincter remains contracted. Normal peristalsis is interrupted and food cannot enter the stomach.

GERD–>esphogeal stricture (3,070 results)

When the lining of the esophagus is damaged, scarring develops. When scarring occurs, the lining of the esophagus becomes stiff. In time, as this scar tissue continues to build up, the esophagus begins to narrow in that area. The result then is swallowing difficulties.

eosinophillic esphogitis (3,230 results)

Decreases the ability of the esophagus to stretch and accommodate mouthfuls of swallowed food probably as a result of the presence of so many eosinophils but also, perhaps as a result of some scaring that occurs in the wall of the esophagus.

post-polio syndrome (537 results)

swallowing abnormalities due to weakness of the bulbar muscles of the tongue, mouth, and throat that increase the risk of choking

schleroderma (6,550 results)

Can cause wasting of the esophageal muscle and poor contraction of the lower esophageal sphincter (LES). Often accompanied by heartburn.

diverticula (6,720 results)

May be responsible for the dysphagia, particularly if it is very large and filled with food or a bezoar.

cervical osteophytes (1,750 results)

Mechanical mass narrows esophagus or creates scar tissue.  Inflammatory reaction may produce muscle spasms as well.

ALS (9,620 results)

bilateral degeneration of the upper motor neuron in the primary motor areas also impairs further adjusted motor areas, which leads to a strong reduction of ‘swallowing related’ cortical activation. While both hemispheres are affected by the degeneration a relatively stronger activation is seen in the right hemisphere.

mysthenia gravis (7,320 results)

Antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder.

myotonic dystrophy (2,460 results)

Mouth, tongue, throat muscle weakness.  Esophageal sphincter laxity causes reflux.

Sjogren’s syndrome (2,680 results)

may be related to a combination of lack of saliva and oesophageal dysmotility. As well as reducing lubrication and hence prolonging pharyngeal transit time, absence of saliva predisposes to dental caries and to oral Candida, both of which may impair mastication [17]; it also diminishes the acid clearance capacity of the oesophagus

Anatomy Essay–>More DZ Details

24 May

down syndrome

low muscle tone, small mouths which make tongue appear large, tongue thrust, teeth can appear at a late age & be abnormally shaped

CHARGE syndrome

Neonatal brain stem dysfunction causes poor suck swallow mech.  Facial palsy, hyposemia, anatomical problems in structures for sucking, swallowing, and breathing.  Symptoms can also be secondary to exogenious factors such as hospitalization time or dyspnea.

velopharyngeal insufficiency

is the inadequate closing of the velopharyngeal sphincter often due to a congenital abnormality, can result in problems such as hypernasal speech or regurgitation of fluids through the nose when swallowing.

dystonia (oromandibular or cranial)

Disorder of neurological movement.  Muscle spasms.

Wilson’s Disease

Impaired coordination of chewing and swallowing.  Weakness of lips, tongue, and throat muscles.

Parkinson’s Disease

Progressive loss of muscle control.  Weak tongue or cheek muscles can impair chewing & moving food around mouth.  Motor impairment of throat.  Medications can cause lack of saliva.

M.S.

Damage to brain and brain stem can cause in-coordination of swallowing.  Medications can cause lack of saliva.

achalasia

This sphincter muscle is normally contracted to close the esophagus. When the sphincter is closed, the contents of the stomach cannot flow back into the esophagus. Backward flow of stomach contents (reflux) can irritate and inflame the esophagus, causing symptoms such as heartburn. The act of swallowing causes a wave of esophageal contraction called peristalsis. Peristalsis pushes food along the esophagus. Normally, peristalsis causes the esophageal sphincter to relax and allow food into the stomach. In achalasia, which means “failure to relax,” the esophageal sphincter remains contracted. Normal peristalsis is interrupted and food cannot enter the stomach.

GERD–>esphogeal stricture

When the lining of the esophagus is damaged, scarring develops. When scarring occurs, the lining of the esophagus becomes stiff. In time, as this scar tissue continues to build up, the esophagus begins to narrow in that area. The result then is swallowing difficulties.

eosinophillic esphogitis

Decreases the ability of the esophagus to stretch and accommodate mouthfuls of swallowed food probably as a result of the presence of so many eosinophils but also, perhaps as a result of some scaring that occurs in the wall of the esophagus.

stroke

Injury to the central and periphery nervous system causes difficulty.

meningitis

cleft palate

A cleft palate can preclude an infant from creating appropriate intraoral negative pressure during suckling.

post-polio syndrome

swallowing abnormalities due to weakness of the bulbar muscles of the tongue, mouth, and throat that increase the risk of choking

schleroderma

Can cause wasting of the esophageal muscle and poor contraction of the lower esophageal sphincter (LES). Often accompanied by heartburn.

diverticula

May be responsible for the dysphagia, particularly if it is very large and filled with food or a bezoar.

cervical osteophytes

Mechanical mass narrows esophagus or creates scar tissue.  Inflammatory reaction may produce muscle spasms as well.

ALS

bilateral degeneration of the upper motor neuron in the primary motor areas also impairs further adjusted motor areas, which leads to a strong reduction of ‘swallowing related’ cortical activation. While both hemispheres are affected by the degeneration a relatively stronger activation is seen in the right hemisphere.

mysthenia gravis

Antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder.

myotonic dystrophy

Mouth, tongue, throat muscle weakness.  Esophageal sphincter laxity causes reflux.

Sjogren’s syndrome

may be related to a combination of lack of saliva and oesophageal dysmotility. As well as reducing lubrication and hence prolonging pharyngeal transit time, absence of saliva predisposes to dental caries and to oral Candida, both of which may impair mastication [17]; it also diminishes the acid clearance capacity of the oesophagus

And Some Good

12 Apr

After such a bad, ugly, and annoying start to the day, I wanted to write a quick update to the afternoon.

It went well-I LOVE school!

My semster long, huge project was due today.  It was this resource notebook which included handouts for the significant others of patients with speech sound problems.  As sort of interactive homework ideas.  Another part was the articulation tool summaries.  And we had to include typed pages outlining every step of the comprehensive intervention hierarchy for both children and adults.  We had to summarize, outline, type, and include examples of three different types of therapy approaches, and we had to write details of a diverse lingusitic population, dialect, or bilingual population (mine was Appalachian and Ozark English) with descriptions of their speech characteristics, ways to approach intervention, and a works cited page.

Anyway, I probably didn’t have to go into that much detail just now–but since I typed it, just go with it.  The point is–I worked really, really hard on mine.  My instructor told me I was a very conscientious student!  And when I saw what the rest of the class turned in I suspect my resource notebook is one of the best!  Hopefully, the content is worthy of an A+

Now, I just have one more BIG project and a TBA comprehensive final.  So I’m still stressed, but everything is coming to an end.  And Right now I have a 95.6% in the class–which is JUST an A+.  Now, to keep it.

And I just talked to my (nice) adviser, and she said I was a highly motivated student and had excellent work ethic.  She was trying to convince me to go for the SLP masters at Riverpoint, and said I’m officially part of “the cohort” and I’ll be all set up for the grad program.  She was telling me I could use my medical background to work with some sort of barium-swallowing-radiology kinds of studies, or work with adults with motor impairment, or go in a number of different directions.  Then, I could go for the AuD.  There’s no reason I can’t do both.  Or apply to both simultaneously and see which pans out.  I also turned in all my overabundance of financial aid paperwork to my adviser today, which also took a lot of running about, copying, and headache, but THAT’S finished too.  And I’m about to sign up for fall classes.

Everything school-related is good 😀