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The diagnosis is frequently made, particular with things like MR, CT myelography, imaging modalities very clear again because of technological advances. The rest is the main stay of treatment, go to bed for six weeks, that kind of thing which was in text books until fairly recently, that surgical indications are very clear and the prognosis is poor. Well, actually, this last part may be a little bit truer than we would like to believe, but with the exception of that, as I mentioned a moment ago, all these things are false, and in fact, as you know from treating this in your own practices, that you seldom make the diagnosis of low back pain. There are a number of diagnostic codes that can be used for low back pain, most of which have very little clinical or anatomic significance, and the problem with that is that back pain is a symptom, it’s not a disease; so what does cause it? If we go back to the medical model where we actually want to make a diagnosis and then create a disease specific treatment plan, how can we do that with back pain, more on that in just a little bit.
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Part of the problem for low back pain, is the etiology is not clear, and the primary cause as identified by an expert, usually to be something within that expert’s realm of interest or clinical specialty.
If you talk to most surgeons, it’s a disc, ever since Mixter and Bard described disc herniations in 1934. If you talk to physiotherapists, it’s fascia and if you talk to just about any body else, it’s psychological, and that of course, is a real danger. There is a problem when you are dealing with a disease, you are giving a patient good care and they are not getting better, it’s easy to sit back and say the patient has psychological problems, what it really means is we haven’t approached it in a very intelligent manner. Well, the anatomy, and I promise this will be mercifully brief or your postprandial somnolence will take over, the slide on the right is from Frank Netter, the things I would like you to keep in mind from this, are the supporting structures of the spinal column.
TREATMENT
Attempted therapies for dyslexia include educational remediation, medications, and psychosocial interventions. It appears that the most effective therapy is remedial education involving direct instruction in reading. Such remediation should include instruction and practice with letter-sound associations (phonics), word recognition tasks, and reading comprehension. That treatment approach is considered effective whether used in settings such as Head Start programs, pull-out programs or resource rooms, small classroom settings, or individual tutoring.
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Various types of cognitive-perceptual skills training (for example, sensory integration training, perceptual-motor training, occupational therapy, auditory memory training, vestibular stimulation, hemispheric stimulation, optometric training) have been used with reading disabled children. The effectiveness of those methods in improving dyslexia and reading disorder in the majority of children has not been convincingly demonstrated.
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Medical approaches to treating dyslexia include stimulant medications, antianxiety medications, motion sickness medication, vitamins, and special diets. The most promising are stimulants and piracetam. Both methylphenidate (Ritalin) and piracetam have been studied in double-blind trials. Although methylphenidate does not appear specifically beneficial to reading skills, there is some indication that piracetam may facilitate reading performance.
Psychosocial approaches to dyslexia include supportive psychotherapy, parent guidance and training, social skills training, relaxation training, and behavioral modification approaches. The effectiveness of such approaches for dyslexia has not been proved, although they are likely to be helpful for associated behavioral and emotional problems. Similarly, the benefits of speech or language therapy for reading are not known, although it may prove helpful for associated speech and language deficits.
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An overall treatment program should include attention to associated disorders such as language disorders or psychiatric disorders. In addition, it is likely that individual characteristics of the child–motivation, learning style, attentional abilities, and responses to instructional strategies or to curriculum materials – may be significant to treatment selection and outcome.
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This disorder of phonologic processing and decoding of words is the most common developmental language disorder. It is estimated that as many as 30% of the American urban population has reading problems. Dyslexia frequently is familial, occurring more often in sons (35% to 40% risk of occurrence) than in daughters (17% to 18% risk). The underlying deficit is impaired recognition and processing of phonemes – the most discrete elements of sound in language. Those who have dyslexia do not appreciate that speech is composed of sounds that join together to form segments, syllables, morphemes, and words. The processing of language in the course of reading or writing is constantly compromised by the struggle to decode or encode words. Preschool children who have dyslexia manifest delays in acquisition of speech, poor articulation, difficulty with learning the names of letters and colors, and persistent missequencing of syllables (eg, “aminals” for “animals”). These children experience difficulty following multistep directions. They are unable to express frustration by “using their words” and, therefore, are prone to develop secondary behaviors such as hitting, kicking, or throwing tantrums.
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Dyslexia can be diagnosed confidently by the end of the second grade. Children will be slow and halting in their oral reading and have difficulty in reading comprehension. They have poor word retrieval and frequently use more fillers (”um,” “like,” “you know”) in their narratives. They experience markedly increased difficulties in the fourth grade when there is a shift from “learning to read” to “reading to learn.” Children must be taught to break down, or segment, syllables into phonemes. Some children whose overall cognitive abilities are high may compensate for their dyslexia and not be identified by the schools because they can maintain average grades. However, they will have persistent difficulties with spelling and written language into adulthood.
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Abnormal development of the left hemisphere (planum temporale) has been postulated to have taken place in adults who have dyslexia. This theory is supported by autopsy studies of five adults who had dyslexia in which multiple areas of microdysgenesis or “brain warts” were present in the left perisylvian cortex, as well as by recent neuroimaging studies.
The successful management of inborn errors has many components to it. Early detection is the key. You can’t treat these diseases until you diagnose them. So you must have an index of suspicion. You have to educate the family, especially if there is a special diet involved or special medications involved, they must be compliant. The need financial and social support. If the medications or the formulas are expensive and if the family has to bear that burden, they may not be as compliant as you’d like. You have to anticipate that they may get very sick with trivial illnesses, colds, flu. Kids with urea cycle disorders or some of the organic acidurias can really go into a tailspin with just a very simple classroom illness. So these kids are admitted frequently to the hospital for acute management. You have to institute the treatment early, whether it is dietary or pharmacologic or both. Then they need to be followed periodically in a referral center to get complete nutritional assessment. To make sure that they have the right amount of protein for growing or to make sure that they are compliant with their medication.
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In terms of Hurler’s, the diagnostic test is to measure the enzyme iduronidase, which can be measured in blood as well as from a skin fibroblast cell line. The clinical features: progressive, coarse facial features. So-called gargoylism. Corneal clouding, loss of milestones, severe mental retardation, hepatosplenomegaly, hirsutism, hernias and these multiple bony changes. So dysostosis multiplex. Complications include recurrent pneumonia because of thick secretions, congestive heart failure because of valvular involvement, and in the case of Hurler’s, usually death by the age of ten. Note that there is a milder form of MPS-1, iduronidase deficiency, called Scheie syndrome which shares the same enzyme defect but does not present with mental retardation. Now biochemically you can’t distinguish between Hurler’s and Scheie’s because in both you have a gross deficit of iduronidase. But clinically they are different because Scheie’s is milder.
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The mucopolysaccharidoses present sometimes with growth delay, with organomegaly, corneal clouding, joint stiffness. The more severe manifestations include hirsutism or increased body hair, loss of milestones and these gargoyle-like coarsening features.
There was a treatment touted a few years ago, something called Lorenzo’s oil, which is a dietary supplement consisting of monounsaturated long chain fatty acids. The theory here was to decrease the amount of very long chain fatty acids by putting in not quite so long chain fatty acids into the diet and making them monounsaturated so they have a single double bond here. This was thought to decrease the amount of saturated very long chains. Taking viagra super active before the planned date will make you invincible. The problem with Lorenzo’s oil is it doesn’t cross the blood-brain barrier. So although if you measure in plasma, the very long chains, you may see an improvement. You really don’t have much affect on the CNS and that’s very often the case in many of these metabolic disorders which affect the central nervous system. You can make them look better on paper if you are measuring blood, but that’s not what’s going on in the brain. Also bear in mind that palliative treatment of course is to replace the corticosteroids which are deficient. Now there is also a neonatal form of adrenoleukodystrophy, which is autosomal recessively inherited, and it resembles Zellweger’s. Zellweger’s is not as common as ALD so in the interests of time, I chose to illustrate this case rather than a case of Zellweger’s. Although we’ve seen two cases of Zellweger’s in the last six months at Vanderbilt. Not a good thing to have.
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There are some metabolic diseases we can do something about: PKU and a low phenylalanine, low-protein diets. You give them just enough proteins so that these patients can grow. Homocystinuria: we used to decrease their protein restriction a little bit but now betaine has sort of taken care of all of that, and we usually don’t restrict the diet in kids with homocystinuria. However, in the urea cycle disorders, regardless of which one it is, all those kids need protein restriction to decrease their ammonia load. In the more rare disorders, like maple-syrup urine disease there are a whole series of special formulas which you can buy, at great expense – which are usually covered by insurance – which are fine-tuned to the particular metabolic requirements of those patients. So for example, in maple-syrup urine disease the infant formulas have decreased branch chain amino acids, valine, leucine and isoleucine. The problem comes when these kids grow out of the formula age and you have to look at table foods, and keep them happy. So this usually requires the services of a well-trained nutritionist. And we have one that works part time in our metabolic clinic and she is very very useful. The advantages of Lorenzo’s oil are over-touted.
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We also have some pharmacologic weaponry to fight some of these disorders: betaine in homocystinuria, the ammonia scavengers, sodium benzoate and phenyl acetate, phenylbutyrate for urea cycle disorders. Many patients with MSUD are responsive to thiamin. Some of the organic acidemias are responsive to vitamin B-12. Biotinidase kids obviously need biotin. The MCAD kids benefit from carnitine, which aids in medium chain fatty acid oxidation.
How do we treat urea cycle disorders, without going through all five of them? Three key points. First of all, we need to prevent protein catabolism because these infants, if they don’t get enough calories they break down their own muscle protein, and in the process of doing that generate more ammonia. That’s the last thing you want to happen. So you have to pump these kids full of calories in the form of fat and carbohydrates. If the urea cycle is impaired, arginine then becomes an essential amino acid and if you don’t supply the arginine they are going to break down their own protein to make new proteins. So that’s why you have to supplement them with arginine. You have to decrease the ammonia load going in. So again, you have to restrict the amount of protein in their diet to a reasonable amount. Lastly, we can utilize these pharmacologic ammonia scavengers – which were discovered serendipitously about 15, 20 years ago – in the form of sodium benzoate and sodium phenyl acetate. Canadian aciphex online 20 mg. Benzoate actually binds to glycine, which is the smallest amino acid that has ammonia as part of it – nitrogen is part of it as do all amino acids – and conjugates with that and excretes it into the urine.
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Tay-Sachs. The incidence used to be about 1:4,000 among Ashkenazi Jews because the carrier frequency is quite high. The screening test is to measure hexosaminidase A in the serum, and the clinical features you must be familiar with. Hyperacusis, or increased startle reflex, progressive weakness or hypotonia, visual loss, the cherry red macula, macrocephaly and usually early death, because this is untreatable. Primary defect we know is in the alpha and hexosaminidase A, and if you have a defect in the beta sub-unit, that knocks out both hex-A and hex-B and results in Sandhoff’s disease, which is another gangliosidosis. It used to be that Tay-Sachs was only seen in the Ashkenazi Jewish population, but in the late 1960s and early 1970s screening programs were set up which were centered in synagogues. The Jewish community and the leaders embraced this screening program and engaged in pre-conceptual counseling, prenuptial counseling, to the point where it was very successful. Because the Jewish community has embraced the screening program – and has even consented to terminating affected pregnancies, which was quite surprising – that we seldom see Tay-Sachs in the Ashkenazi Jews anymore because the screening program is so effective. So we see it in these other unusual populations. We see it in Hispanics, we see it in blacks, because there is a much lower carrier frequency in other populations. Probably in order of magnitude or two less than this. But there is still that chance that two carriers will get together.
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