Friday, April 26, 2024

Ms Vs Parkinson’s Disease

Multiple Sclerosis Vs Parkinsons Disease: Risk Factors And Complications

Neurological Disorders: Parkinson’s, MS, MG, ALS

Risk factors for multiple sclerosis include being female, having afamily history of multiple sclerosis, having certain infections, being white of European descent, living furthest from the equator, living in temperate climate regions, already having an autoimmune disease, and smoking.

Complications resulting from multiple sclerosis include muscle stiffness and spasms, paralysis, problems with bladder, bowel, and sexual function, as well as forgetfulness, mood changes, depression, and epilepsy.

Risk factors for Parkinsons disease include being over the age of 50, being male, having a family history of Parkinsons disease, carrying gene variations, experiencing a head injury, being exposed to environmental toxins, and taking certain medications such as anti-anxiety medications or sleeping pills.

Complications associated with Parkinsons disease include difficulty thinking, depression, emotional changes, swallowing problems, sleep problems and disorders, bladder issues, constipation, changes in blood pressure, smell dysfunction, fatigue, pain, and sexual dysfunction.

What Is Parkinsons Disease

Parkinsons disease is a neurodegenerative disorder that affects predominately dopamine-producing neurons in a specific area of the brain called substantia nigra. Dopamine is a neurotransmitter that is primarily responsible for controlling movement, emotional responses and the ability to feel pleasure and pain.

The cells that make dopamine are impaired and as the disease progresses, the more dopamine-producing brain cells die. Once a person develops motor symptoms, the amount of dopamine loss is already substantial. The brain eventually reaches a point where it stops producing dopamine in any significant amount, thus increasing problems with movement.

Sonda Is Clinically Relevant

The SONDA paradigm allows for a comprehensive examination of eye-movements that provides detailed information on the dynamics and statistical properties of saccades, as well as a novel set of spatio-temporal properties that quantify both smooth and saccadic pursuit behavior. Given the large number of parameters, our technique also opens up possibilities for machine-learning-aided diagnosis of neuro-ophthalmic and neurological impairment based on eye movements. We and others have previously demonstrated the feasibility of such an approach for identifying ophthalmic disorders , and for neurological conditions . Compared to other high-throughput eye-tracking tests, SONDA has two main advantages. First, excluding calibration , the whole assessment takes only 4 min . Second, our task and stimulus were designed to be as intuitive and simple as possible to avoid confounding factors that may be caused by natural or more complex stimuli, or complicated instructions resulting in a higher cognitive load.

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Ms Vs Als: How Do They Differ

Although multiple sclerosis and amyotrophic lateral sclerosis share some similarities, there are key differences between the two disorders in terms of progression, treatment, and outlook.

MSis an immune-mediated disorder in which the patients own immune system mistakenly attacks the protective covering around nerve cells called the myelin sheath. As myelin is destroyed, nerve signals that travel along nerve cell extensions called axons are delayed or lost.

ALS, also known as Lou Gehrigs disease, is a progressive disorder in which the nerve cells that control muscles become damaged and die. Without these cells, nerve signals cannot get from the brain to the muscles. With time, they begin to waste away, or atrophy.

Pool Therapy For Multiple Sclerosis Patients

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Multiple Sclerosis is a condition that weakens muscles and movements over time. Thus, strength training early and often is one of the key ways to keeping the muscles from weakening. However, this can be understandably difficult for someone who has difficulty walking, picking up a fork to eat or simply waving hello. For Multiple Sclerosis sufferers, the HydroWorx therapy pool can be a place for them to more easily build lean muscle mass than would ever be possible on land. Even if they cannot walk down the street comfortably or safely, they can walk on a treadmill in the water without fear. Not only are they protected by the innate buoyancy of the water, but they are given a psychological boost because they arent afraid to fall.

In a case study that was recently done in Great Britain, a woman with Multiple Sclerosis was treated in the HydroWorx pool. She had complained of progressive weakness in her upper and lower left limbs during a two-year period. She had to walk with a cane, and tended to favor one of her legs over the other. This was causing serious gait problems.

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Is It Possible To Have Ms And Parkinsons Disease

Unfortunately, yes it is possible to have co-existing MS and Parkinsons disease. Given their similarities, you would think that they are too similar for them to co-exist together. They both affect the CNS, they are degenerative neurologic conditions, and it just wouldnt be fair.

However, MS is an autoimmune disease. Parkinsons is not. Given this fact alone, it is entirely possible for them to co-exist.

In 2015, a team of researchers set out to determine if co-existing MS and Parkinsons disease was coincidental or were a cause-effect situation meaning, in this particular study, did the presence of Parkinsons increase the likelihood of developing MS?

The researchers studied 8947 MS cases with 44735 control cases. According to the study, Our results suggest a causal effect of MS on PD in MS whether this can be explained by the localization of lesions alone is not clear.

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Multiple Sclerosis And Parkinsons Disease

ABSTRACT

REFERENCES

  • Friese, M.A. Schattling, B. Fugger, L. Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. Nature Reviews Neurology 10, 225.

  • Thompson, A.J. Banwell, B.L. Barkhof, F. Carroll, W.M. Coetzee, T. Comi, G. Correale, J. Fazekas, F. Filippi, M. Freedman, M.S. Diagnosis of multiple sclerosis: 2017 revisions of the mcdonald criteria. The Lancet Neurology 2018, 17, 162-173.

  • Mehanna, R. Jankovic, J. Movement disorders in multiple sclerosis and other demyelinating diseases. Journal of the neurological sciences 2013, 328, 1-8.

  • Etemadifar, M. Afshar, F. Nasr, Z. Kheradmand, M. Parkinsonism associated with multiple sclerosis: A report of eight new cases and a review on the literature. Iranian journal of neurology 2014, 13, 88.

  • Moccia, M. Erro, R. Montella, S. Carotenuto, A. Pappatà, S. Orefice, G. Diagnostic challenges of parkinsonism occurring in multiple sclerosis. Acta Neurologica Belgica 2015, 115, 513-515.

  • Daroff, R.B. Jankovic, J. Mazziotta, J.C. Pomeroy, S.L. Bradleys neurology in clinical practice seven edition ed. Elsevier Health Sciences: 2016.

  • Andersen, A.D. Binzer, M. Stenager, E. Gramsbergen, J.B. Cerebrospinal fluid biomarkers for Parkinsons disease: A systematic review Acta Neurologica Scandinavica 2016, 135, 34-56.

  • Gibb, W. Lees, A. The relevance of the lewy body to the pathogenesis of idiopathic Parkinsons disease. Journal of Neurology, Neurosurgery & Psychiatry 1988, 51, 745-752.

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    Autism: No Link To Lyme Disease

    In 2013, scientists analyzed serum samples of 120 children, including 70 with autism and 50 without autism. None of the 120 children tested positive for anti-bodies to Lyme using well established two-tier testing.

    The scientists concluded:

    The studys sample size is large enough to effectively rule out the suggested high rates of Lyme disease or associated seroprevalence among affected children.

    NIH scientists performed a similar study by looking at 183 children: 104 with autism, 24 with developmental delays, and 55 neurotypical controls. All 183 children tested negative for Lyme antibodies and had no history of Lyme disease.

    The NIH scientists concluded:

    There was no evidence of an association between Lyme disease and autism.

    Thankfully, the Lyme-Induced Autism Foundation is now defunct. Sadly, many of the doctors who spoke at Lyme-Induced Autism conferences are still practicing.

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    Parkinsons Vs Multiple Sclerosis: How Are These Conditions Different

    Tremor Disorder or Parkinson’s?

    Parkinson’s Disease and Multiple Sclerosis are two medical conditions that are frequently confused with each other since they are both progressive and have similar symptoms, but there are some significant differences between the two.

    Here we will discuss the difference and similarities between the two.

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    What Is The Difference Between Parkinsons And Myasthenia Gravis

    Parkinsons disease is a movement disorder characterized by a decline in the dopamine level of the brain whereas myasthenia gravis is an autoimmune disorder characterized by the production of antibodies that block the transmission of impulses across the neuromuscular junction. Myasthenia gravis is an autoimmune disease but Parkinsons is not considered as an autoimmune disease. This is the main difference between Parkinsons and myasthenia gravis. The appearance of Lewy bodies and loss of dopaminergic neurons in pars compacta of the substantia nigra region of midbrain are the hallmark morphological changes in Parkinsons disease. In contrast, the block of the transmission of nervous impulses at the neuromuscular junction due to the action of autoantibodies is the pathological basis of myasthenia gravis.

    In addition, there is no laboratory test for the exact identification of Parkinsons disease. However, investigations such as Anti ACh receptor antibodies in the serum, tensilon test, imaging studies, ESR and CRP can help to diagnose myasthenia gravis. Furthermore, anticholinesterases such as pyridostigmine, immunosuppressants such as corticosteroids, Thymectomy, Plasmapheresis and intravenous immunoglobulins can help to manage myasthenia gravis. On the other hand, drugs such as dopamine receptor agonists and levodopa, which restore the dopamine activity of the brain, can alleviate motor symptoms in Parkinsons.

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    Ethics Approval And Consent To Participate

    The study was carried out in accordance with the recommendations of the Oregon Health & Science University institutional review board with written informed consent from all subjects. All subjects gave written informed consent in accordance with the Declaration of Helsinki. The protocols were approved by the OHSU IRB .

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    Is There A Link Between Parkinsons And Multiple Sclerosis

    The chances of developing both multiple sclerosis and Parkinsons disease is less than

    where a formal diagnosis can be made clinically based on your signs and symptoms during a physical and neurological exam. For your doctor to make a diagnosis, you need to have 2 out of 3 of the following:

    • shaking or tremors
    • slowness of movement
    • muscle stiffness

    One of the clearest signs of Parkinsons is a positive response to the medication Levodopa.

    Imaging techniques such as single photon emission computed tomography scans and magnetic resonance imaging may help rule out other conditions.

    A dopamine transporter scan may be used to identify loss of dopaminergic uptake in a part of your brain called the basal ganglia. However, interpreting the results can be difficult, and it isnt routinely used.

    Neither Parkinsons nor multiple sclerosis currently have a cure. Treatment aims to slow progression and minimize symptoms.

    Multiple Sclerosis Vs Parkinsons Disease: Treatment And Therapies

    1668 best Neuro Assessment, Diseases and Disorders images on Pinterest ...

    Treatment for multiple sclerosis is lifelong, and although it cannot cure the condition, it aims to minimize symptoms and allow the patients to live as normal of a life as possible. Some treatment methods include corticosteroids and plasma exchange, beta interferons, Glatiramer acetate, Dimethyl fumarate, Fingolimod, Teriflunomide, Natalizumab, Alemtuzumab, and Mitoxantrone, which all help to reduce the likelihood of relapses.

    Other treatment methods include physical therapy to improve mobility, muscle relaxants, medications to reduce fatigue, and other medications like antidepressants, medications to control the bowels and bladder, and medications to improve sexual function.

    Exercise, meditation, yoga, and acupuncture are also recommended as a means to reduce stress and improve overall mental and physical well-being.

    There is no cure for Parkinsons disease as well, but treatments are available to manage the symptoms and slow down the disease progression as much as possible. Alongside traditional treatments, supportive therapies are also used to improve different aspects of a persons health.

    Common medications prescribed in Parkinsons disease include dopamine replacement therapy, dopamine agonists, anticholinergics, amantadine, monomine oxidase type B inhibitors, and catechol-o-methyl transferase inhibitors.

    You can work closely with your doctor to create a specific treatment plan for you.

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    Does Lesion Location Predict Post

    There has been a lively debate on the subject of lesion location in relation to post-stroke depression. Data from the early 1980s first suggested that there was a relation between proximity of the lesion to the frontal pole and depression. This appeared to have been contradicted by a meta-analysis published in the Lancet in 2000. This analysis was further criticised by others on the grounds that the hypothesis was not specific enough and that some relevant studies had been omitted. When a similar methodology was used but the data looked at separately for each hemisphere, there was a clear relation between proximity of the lesion to the left frontal pole and depression, especially in the first few months after stroke. The results of this second meta-analysis were given further weight by a Finnish study published earlier this year. This study also found that a brain infarct affecting the pallidum was a strong predictive factor for post-stroke depression . This finding also fits with case reports of dysphoria in relation to insertion of deep brain stimulating electrodes in the same area.

    Posttranslational Modifications That Inactivate Parkin

    The reports summarized above raise the intriguing possibility that idiopathic PD pathogenesis or disease risk may arise by processes whereby neuronal stress might inactivate parkin via insolubility and aggregation. As a biochemical phenocopy of PARK2-associated familial PD, a severe loss of active, soluble parkin could compromise the viability of nigral neurons in the sporadic disease.

    The one problem with this model is that Lewy bodies have generally not been observed in PARK2-associated familial PD brains, whereas they are almost always present to some extent in postmortem analyses of sporadic PD patients. No biochemical or genetic evidence has yet conclusively tied parkin into -synuclein aggregation, raising the possibility that neither protein is the direct cause of any form of PD, but that each may act independently through either the same or different downstream initiators of cell death. Of course, the other possibility is that macroscopic -synuclein aggregates are not involved in pathogenesis, and that loss of parkin function causes disease by producing whatever the actual toxic -synuclein species is.

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    The Impact Of Disease

    The clinical mutations in Parkin associated with disease span from genomic deletions to premature truncations and subtle missense mutations in the coding sequence. For this reason, it has been widely accepted that the pathogenicity of these PARK2 mutations derives from a critical loss-of-function. Despite the predicted loss of E3 ligase activity of these parkin mutants, biochemical evidence of parkin E3 ligase activity and the impact of parkin deficiency has been notoriously difficult to establish. Although numerous putative substrates have been reported, many have failed to withstand independent confirmation. The lack of well-founded substrates has also made it difficult to examine the degree to which each mutation alters activity, precluding an analysis of the correlation between the biochemical impact of a given parkin mutation and the severity of the resultant disease in patients. Nonetheless, there have been many valuable observations made regarding the novel PD-associated parkin variants.

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    What Is Multiple Sclerosis

    4 Goals for Neuro Patients *Part 5* (Parkinsons vs. M.S. vs. MG vs. A

    Multiple sclerosis is a progressive and debilitating disease of the central nervous system that disables the communication between the brain and other parts of the body. It involves an immune-mediated process in which an abnormal response of the bodys immune system is directed against the central nervous system.

    Within the central nervous system , the immune system causes inflammation that damages myelinthe fatty substance that surrounds and insulates the nerve fibersas well as the nerve fibers themselves, and even the specialized cells that make myelin. When the nerve fibers are destroyed, messages within the CNS are altered or halted completely. Then, the damaged areas produce neurological symptoms that can vary among people in type and severity. These areas develop scar tissue, giving the disease its namemultiple areas of scarring or multiple sclerosis.

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    Comparison Of Static Sway Performance Between Groups Within One Balance Task

    During side-by-side stance, significant differences between the groups were found for sway area , velocity in ML direction , acceleration in ML direction and jerk in ML direction . Post hoc tests revealed that PD patients showed significantly higher velocity in ML direction , compared to healthy adults . MS patients showed a significantly higher acceleration and jerk in ML direction, and a tendency toward a larger sway area , compared to the healthy adults .

    Figure 3. Sway parameters of healthy adults , Parkinson’s disease and multiple sclerosis patients. sway area, velocity in antero-posterior direction, velocity in medio-lateral direction, acceleration in AP direction, acceleration in ML direction, jerk in AP direction and jerk in ML direction. The black horizontal lines indicate a significant difference between the groups, the grey horizontal lines indicate a tendency toward a difference between the groups. * indicates a significant difference compared to the side-by-side stance, # indicates a significant difference compared to the semi-tandem stance.

    There were no significant differences between PD and MS patients in any of the three tasks .

    Parkinsons Disease Vs Multiple Sclerosis: Differences

    Some of the differences between Parkinsons disease and multiple sclerosis include:

    • Parkinson’s symptoms usually appear at the age of 60 and beyond, whereas multiple sclerosis commonly affects individuals between the age group of 20 and 50.
    • According to several research, having multiple sclerosis may increase your chance of developing Parkinsons disease later in life. This is due to inflammation caused by multiple sclerosis, which can cause lesions in the brain, affecting how dopamine is produced. However, the reverse has yet to be confirmed.
    • Parkinson’s disease develops when the brain generates tiny levels of dopamine, a hormone that regulates movement, whereas multiple sclerosis is an autoimmune illness in which the immune system attacks and destroys the myelin sheath around nerve axons.
    • Parkinson’s disease involves a few unique symptoms, such as foot-dragging, slowness of movement , poor posture, lack of control over motions such as blinking or smiling, and others. Dizziness, double vision, tingling feelings throughout the body, hearing loss, and seizures.

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