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Disorders of the Nervous System Program Transcript
Disorders of the Nervous System Program Transcript
[MUSIC PLAYING] NORBERT MYSLINSKI: In the year 2000, Alvin Toffler, who was the author of Future Shock back in the 1960s, was asked this question. What do you think is the most important question facing mankind in the new millennium? He answered by saying, “What does it mean to be human?”
FEMALE SPEAKER: This week, Dr. Norbert Myslinski takes an in-depth look at the human brain and how it is affected by disorders of the nervous system.
NORBERT MYSLINSKI: The most human part of the body is the brain. This is the human brain. It doesn’t look like very much. It’s only about three pounds, and it’s kind of wrinkled. But if you think about it, this is the product of 3 and 1/2 billion years of evolution. It is probably the most complicated machine, or organ, or article that we know of in the universe, and it is composed of a hundred billion neurons, a hundred billion neurons. And if you look at the supporting cells, the glia, there’s about a trillion. And if you look at one of the most important parts, the connections between all of these cells, the connections that are responsible for memory and for all of our activities, there’s about a quadrillion, a quadrillion with this individual brain. And I’m sure that through the centuries, through the millions of years of our existence on this planet, this brain has evolved, and this brain has had pathologies of different kinds, and changes of many kinds. Initially, we only had this part of the brain.
The dinosaurs, for instance, had this basic brain. And this is the basic brain that controls our breathing, controls our respiration, controls our heart rate, controls of all the other autonomic or vegetative functions of the body. And so sometimes, we call this part of the brain the reptilian brain. It’s the vegetative part. And then as the brain evolved through the centuries, through the millennia, another big step in the evolution was the development of this part of the brain. That’s the limbic system. And the limbic system is responsible for emotion, the wagging of the tail of a dog, the purring of a cat. This big step occurred mainly with the mammals, and so we call this the mammalian brain or the emotional brain. And the next big step in the evolution of the brain was the cerebral cortex, this part. This is the flower of the human brain. That big step occurred with the development of the homo sapiens, and it involves cognition, and so we call this the human brain. And so we have this triune brain. It’s a brain that’s developed over the years through time in that order. But we see this development in that order everyday.
We see it inside every woman who is pregnant, because every fetus who’s developing a brain develops it exactly the same way. We first have the vegetative reptilian brain. And then months later, we have the development of the limbic part of the brain. And then we have the development of the human or cognitive part of the brain. And the cognitive part of the brain continues developing after birth. It continues developing through childhood, through adulthood. And hopefully, it’ll continue until the day we die. So we have this development not only through the years, but also in utero. It’s very interesting that one of the major diseases that we have of the elderly is Alzheimer’s disease.
Alzheimer’s disease is very dehumanizing because it attacks that part of the brain that is one of our main humanistic parts, and that is our memory. It attacks who we are, and it’s a progressive degenerative disease. And what’s interesting is that it destroys the brain in the reverse order of its development. And what happens first, there is a group of cells down here, nucleus of Meynert. And they have a neurotransmitter called acetylcholine. And it preferentially, this group of cells preferentially degenerates, and it has pathways to all different parts of the brain. But one of the parts is over here, the hippocampus, which has to do with memory, long-term memory. And so this is what happens first. And as it progresses, there are all these plaques and tangles, we call them, that develop and choke different cells of the brain. And it continues to increase through all parts of the brain until you get many different cognitive deficits. And after that, then it attacks the mammalian brain, the emotional part of the brain. After that, it attacks the reptilian brain, the vegetative brain, and then you lose your vital functions, and then you die about 10 to 12 years, usually, after first diagnosis.
So you have this reversal. Now, it’s very interesting because a lot of people are afraid of losing their memory, of getting Alzheimer’s disease. And rightfully so, because as our population ages and more and more people are older, more and more people are going to get Alzheimer’s disease. There’s about 4 million in the United States right now. And if you are lucky enough to live to the age of 85, half— half of the people will have Alzheimer’s disease. So it’s going to be pretty prevalent, and it’s going to increase in leaps and bounds as we get older, and it’s going to be a more and more important disease for the nursing profession and the health professionals. 65% of the dementias are of the Alzheimer’s type, but there are others that are not. And it’s important to be diagnosed, and to be examined, and tested, because if it’s a dementia not of Alzheimer’s, then it may be cured, even though Alzheimer’s itself is not curable, nowadays.
Now, there’s another idea that I mentioned earlier, and that is that the human brain keeps on developing after we’re born until the day we die. And one of the reasons for that is because of the plasticity of the brain. That means the malleability. That means the changeability of the brain. The brain can adapt to challenges put to it, to experiences, to our needs, and our wants. It can keep changing. All of these connections, these quadrillion connections among the different parts of the brain do change, increase and decrease. As a matter of fact, the more we challenge the brain, the more we learn, the more we experience, the more connections you have, all right? If you take two animals and put one in insipid sort of adult environment and one in a rich environment and examine their brains at the end of their lives, the one in the rich environment has many more connections, many more synapses between the different— and that is the basis of memory. That is the basis of intelligence, not the number of your cells, not inside of your brain. It’s the number of synapses that we have, the number of engrams that we have withing the brain. So we have this plasticity, this growth developing.
So your brain is continuously changing. Hopefully, the brain that you had before I started talking is not going to be the same brain as when I finish talking, OK? So it’s important not to traumatize the brain, and to protect it. And we’ve been giving many different protections for the brain. Unlike other organs and parts of the body, the brain has a skull to protect it. The brain has cerebral spinal fluid in it to protect it. The brain has a barrier between it and the blood that no other organ has. It’s called the blood-brain barrier to keep the toxins and bad materials of blood from getting into the brain. Before the golden age of pharmacology in the late ’50s, and they did everything they can, and they did a lot of experimentation with the brain. For instance, they were doing the frontal lobotomies that they thought would help individuals decrease agitation, as we know how terrible that was now.
So they tried this stimulation of this pathway for people that are pathologically depressed, and there would be wires from there all the way down to a little box on their belt, and they’d press a button, and they feel good. And if you ask how they felt, they’d say, oh, I feel contentment, and joy, and so forth, and they feel good. But it didn’t last very long because that would destroy the pathway, and it would become refractory, and it wouldn’t work. And also, right after that, the pharmacology started, and the antipsychotic drugs came in, and so that was a lot less invasive, and a lot more effective. This dichotomy between the right and left sides of the brain is very important in understanding our perception of the world.
I mentioned earlier that there are a quadrillion synapses within the brain, and this is the essential unit of memory, and it’s the essential unit of functioning of the brain. And when there is a disorder of the brain, more often than not, it has to do with the synapse. The synapse is that point of communication between two different neurons. And when you have this dysfunction or when the neuron itself dies, you have a decrease in a neurotransmitter. A neurotransmitter is a chemical that is essential for the communication. And so a lot of diseases are characterized and identified by the fact that they don’t have a certain neurotransmitter. There are many different types of neurotransmitters throughout the brain. An ideal way to study pathopharmacology is to look at a disease like Parkinson’s disease.
Now, Parkinson’s disease was first analyzed back in the 1950s, when they looked at the brains of dead patients, and they did autopsies, and found that a small part of the basal ganglia called the nigostriatal pathway preferentially degenerates in these patients. And then the biochemists came along, and they analyzed the pathway, and they found that dopamine was the vital chemical, the neurotransmitter, within that pathway. And then the pharmacologists came along, and they said, you know what? I wonder if we can replace that dopamine, if we can alleviate some of the symptoms. And so they tried it. They gave dopamine. It didn’t work because it couldn’t cross the blood-brain barrier. But eventually, they gave a precursor that did cross the blood-brain barrier. And eventually, it did work, and it was called L-DOPA, and it was one of the big breakthroughs. And so patients with Parkinson’s disease then found out that their symptoms can be alleviated by taking this drug. And that’s because we replaced the neurotransmitter that is being depleted with an exogenous neurotransmitter of a similar type, and it alleviated the symptoms.
If we look at Alzheimer’s disease, they thought that they could do the same thing. They looked at the Parkinson’s story, and they said, hey, if they can do it, we can do it with Alzheimer’s. Because in Alzheimer’s, we also have a small pathway that degenerates, but that has acetylcholine as its neurotransmitter. So they tried to give a drug to exacerbate the acetylcholine in the brain, and it did not work. Then they tried some other drugs, but it seemed to work, but they had a big side effect of liver toxicity. And so they put that drug aside. And so they kept studying, and studying, and studying. So by 10, 20, 30 years later, they bring that drug out again which had the big liver toxicity. They were able to find a way to minimize the liver toxicity, and they found that it does work in some Alzheimer’s patients. and that this drug is Aricept. It was the first drugs used to treat Alzheimer’s disease. So that’s one way in which pharmacology can be used to alleviate the symptoms of neurodegenerative disorders. You have similar ideas with Huntington’s chora, Huntington’s disease.
You have a similar situation with epilepsy in the sense that you’re not really replacing something, but you’re exacerbating the pathway that can actively inhibit these epileptic foci that I talked about before from spontaneously discharging, and causing that epileptic seizure. So you can give drugs to exacerbate certain pathways, stimulate certain pathways, just like drugs [INAUDIBLE] stimulate the positive reinforcement area, and make us feel good. Now, you can have drugs that can stimulate other pathways in the brain pharmacologically so that you can alleviate symptoms, inhibit certain things, stimulate certain things, and so forth.
Now, besides chemically doing it, some of the more recent therapies are going back 50 years, and they’re trying to electrically stimulate certain parts of the brain. Yeah, you have certain therapies now based on new technological developments where you have, for instance, deep brain stimulation, where they actually take an electrode, and stimulate, and implant it in the brain semi-permanently so that if you stimulate it, then you can alleviate the movements of somebody with Parkinson’s disease, and they can control their movements, and they have an actual electrode in there being stimulated in a certain part of the brain. So you can do it physically as well as chemically. Sometimes, you surgically can remove a certain part of the brain to alleviate symptoms, like in Parkinson’s disease. So there’s a lot of avenues of approach that we can use to treat the brain, whether surgically or pharmacologically.
The case study concerns a 43-year-old man with a history of chronic pain for several years after sustaining a fall and now ambulates with crutches. He has been referred for a psychiatric evaluation by his family physician after suspecting his pain is psychological, and he has been exaggerating the pain to get a narcotic prescription to get high. He complains of cooling and intense cramping in the right leg. He has been diagnosed with complex regional pain syndrome (CRPS). The purpose of this paper is to explain the interventions for each decision and if they are backed by evidence-based literature.
Decisions Recommended For the Patient Case Study
The first decision was to start Amitriptyline 25 mg PO QHS and increase it by 25 mg every week to a maximum of 200 mg daily. The decision is supported by the study by Shim et al. (2019), which found that Amitriptyline is an effective evidence-based treatment for neuropathic pain disorder and peripheral diabetic neuropathic pain. In decision two, I maintained Amitriptyline and increased the dose to 125 mg with a maximum target of 200 mg. The patient was to take the medication an hour earlier than usual. Increasing the dose is supported by the article by Eldufani et al. (2020), which recommends slow titration of the Amitriptyline dose if a patient exhibits a positive response to the initial dose. It also recommends taking the bedtime dose an hour earlier to minimize morning sleepiness.
In decision three, I continued Amitriptyline at 125 mg and referred the patient to a life coach for counseling on nutrition and exercise. Weight gain is a documented side effect of Amitriptyline. Brueckle (2020) backs this intervention by asserting that patients on medications associated with weight gain should be counseled on lifestyle modification in diet and exercise for a healthy weight.
What I Was Hoping To Achieve With the Decisions I Recommended For the Patient Case Study
By initiating the patient on Amitriptyline, I hoped it would help improve the client’s mood swings, alleviate pain to 4/10, and ambulate without crutches within four weeks. Komoly (2019) established that Amitriptyline helps alleviate pain and autonomic and motor symptoms in CRPS cases. I hoped that increasing Amitriptyline to 125 mg would alleviate the limb to 3/10, and taking the drug an hour earlier would prevent morning sleepiness. Taking the medication an hour earlier decreases morning sleepiness (Rosenthal & Burchum, 2021). In decision three, I hoped that referring the client for lifestyle modification counseling would guide him in practicing a healthy lifestyle in dietary and physical exercise habits that would prevent unhealthy weight gain. Aguilar-Latorre et al. (2022) recommend counseling on lifestyle modification to enable patients on TCAs to manage their weight and avoid being overweight/obese.
Difference between What You Expected To Achieve With Each of the Decisions and the Results of the Decision in the Exercise
In the first decision, the pain decreased to a 6/10, and the patient ambulated without crutches. The pain severity was not as anticipated, probably because of the low Amitriptyline dose and duration it takes to have maximum effect. In the second decision, the patient’s pain was reduced to 4/10, comparable to the expected outcome of a pain severity of 3/10.
Conclusion
The PMHNP started the patient on an initial dose of Amitriptyline of 25 mg QHS, which was to be increased by 25 mg weekly to 200 mg. The drug led to a positive response and was increased to 125 mg QHS to improve the patient’s pain. The medication led to weight gain, and the PMHNP referred the client to a life coach for counseling on a healthy lifestyle.
References
Aguilar-Latorre, A., Pérez Algorta, G., Navarro-Guzmán, C., Serrano-Ripoll, M. J., & Oliván-Blázquez, B. (2022). Effectiveness of a lifestyle modification programme in the treatment of depression symptoms in primary care. Frontiers in medicine, 9, 954644. /orders/doi.org/10.3389/fmed.2022.954644
Brueckle, M. S., Thomas, E. T., Seide, S. E., Pilz, M., Gonzalez-Gonzalez, A. I., Nguyen, T. S., … & Muth, C. (2020). Adverse drug reactions associated with Amitriptyline—protocol for a systematic multiple-indication review and meta-analysis. Systematic reviews, 9(1), 1-8. /orders/doi.org/10.1186/s13643-020-01296-8
Eldufani, J., Elahmer, N., & Blaise, G. (2020). A medical mystery of complex regional pain syndrome. Heliyon, 6(2), e03329. /orders/doi.org/10.1016/j.heliyon.2020.e03329
Komoly, S. (2019). Treatment of complex regional pain syndrome with Amitriptyline. Ideggyogyaszati szemle, 72(7-8), 279-281. /orders/doi.org/10.18071/isz.72.0279
Rosenthal, L. D., & Burchum, J. R. (2021). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.) St. Louis, MO: Elsevier.
Shim, H., Rose, J., Halle, S., & Shekane, P. (2019). Complex regional pain syndrome: a narrative review for the practicing clinician. British Journal of Anaesthesia, 123(2), e424–e433. /orders/doi.org/10.1016/j.bja.2019.03.030
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