Multiple System Atrophy: Difference between revisions

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'''Original Editors '''- [[User:Emily_Nicklies|Emily Nicklies]] from [[Pathophysiology of Complex Patient Problems|Bellarmine University's&nbsp;Pathophysiology of Complex Patient Problems project.]]  
'''Original Editors '''- [[User:Emily Nicklies|Emily Nicklies]] from [[Pathophysiology of Complex Patient Problems|Bellarmine University's&nbsp;Pathophysiology of Complex Patient Problems project.]]  


'''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}} &nbsp;  
'''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}} &nbsp;  
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== Definition/Description<br>  ==
== Introduction  ==
[[File:Parkinson's man sketches.jpg|right|frameless|209x209px]]
Multiple System Atrophy (MSA)&nbsp;is defined as a sporadic, fatal, progressive, [[Neurodegenerative Disease|neurodegenerative]] (specifically a [[synucleinopathy]]) adult-onset disorder. It is the second most common neurodegenerative movement disorder with an average annual incidence rate of 3 per 100000 person-years after [[Parkinson's|Parkinson’s disease]] (PD)<ref name=":3">Dash S, Mahale R, Netravathi M, Kamble NL, Holla V, Yadav R, Pal PK. [https://www.cureus.com/articles/83909-cognition-in-patients-with-multiple-system-atrophy-msa-and-its-neuroimaging-correlation-a-prospective-case-control-study Cognition in Patients With Multiple System Atrophy (MSA) and Its Neuroimaging Correlation: A Prospective Case-Control Study]. Cureus. 2022 Jan 29;14(1). Available:https://www.cureus.com/articles/83909-cognition-in-patients-with-multiple-system-atrophy-msa-and-its-neuroimaging-correlation-a-prospective-case-control-study (accessed 14.3.2022)</ref>. It can affect the
* Autonomic system causing autonomic failure, causing eg.fainting spells and problems with [[Heart Arrhythmias|heart rate]], erectile dysfunction, and [[Urinary Incontinence|bladder control]].
* [[Basal Ganglia|Basal ganglia]] causing [[Parkinson's|parkinsonism]], causing eg tremor, rigidity, and/or loss of muscle coordination as well as difficulties with speech and [[gait]].
* [[Cerebellum]] causing [[ataxia]] <ref name="Lundy Eckman">Lundy-Eckman, L.  Neuroscience: Fundamentals for Rehabilitation.  3rd ed. St. Louis: Saunders Elsevier, 2002.</ref>
The symptoms reflect the progressive loss of function and death of different types of nerve cells in the [[Brain Anatomy|brain]] and [[Spinal cord anatomy|spinal cord]].


Multiple System Atrophy (MSA)&nbsp;is defined as a sporadic, progressive, neurodegenerative adult-onset disorder that can affect the autonomic system causing autonomic failure, basal ganglia causing parkinsonism, and/or cerebellum causing ataxia in any combination.<ref name="Lundy Eckman">Lundy-Eckman, L.  Neuroscience: Fundamentals for Rehabilitation. 3rd ed. St. Louis: Saunders Elsevier, 2002.</ref>  
Some of these features are similar to those seen in Parkinson’s disease, and early in the disease course it often may be difficult to distinguish these disorders. This 1 minute video is titled Differentiating Multiple System Atrophy From Parkinson's Disease.
{{#ev:youtube |FZlk8a064N4|width}}<ref>MSA coalition Differentiating Multiple System Atrophy From Parkinson's Disease (PSA) Available: https://www.youtube.com/watch?v=CD7UL12GSCM<nowiki/>(accessed 14.3.2022)</ref>


[[Image:Basal ganglia.jpg|Image:Basal_ganglia.jpg]]&nbsp;&nbsp; &nbsp;
=== Etiology ===
The causes of MSA are unknown; however, as for other neurodegenerative diseases, a complex interaction of genetic and environmental mechanisms seems likely.<ref name=":1">Jellinger KA. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5870010/ Multiple system atrophy: an oligodendroglioneural synucleinopathy]. Journal of Alzheimer's Disease. 2018 Jan 1;62(3):1141-79 Available from.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5870010/ (last accessed 16.1.2020)</ref><br>Research has suggested that MSA is characterized by a progressive loss of neuronal and oligodendro[[Glial Cells|glial cells]] (myelin producing cells in CNS) in numerous sites in the CNS (basal ganglia, cerebellum). This damage is said to occur from the formation of glial cytoplasmic inclusions (GCI’s).<ref name="Diedrich">Diedrich A, Robertson D.  Multiple System Atrophy.  Vanderbilt University School of Medicine 2009. http://emedicine.medscape.com/article/1154583-overview (accessed on 24 Jan 2010).</ref>


&nbsp;&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;'''Figure 1''': Basal Gangila &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;
== Classification ==
MSA is classified by the most dominant symptom exhibited by the patient.


This disorder is considered MSA when there is a combination of symptoms arising from the components just mentioned (autonomic failure, parkinsonism, and/or ataxia). &nbsp;In order for a patient to be diagnosed with MSA, there have to be at least two components involved.&nbsp;There can be any combination of symptoms present from the three components.<ref name="Swan">Swan L, Dupont J. Multiple System Atrophy. Journal of Physical Therapy 1999;79:488-94.</ref>  
# Parkinsonian type (MSA-P): this includes symptoms similar to Parkinson's disease eg tremors at rest, rigidity of muscles, and slow movements, including gait
# Cerebellar type (MSA-C): involves difficulty walking (ataxia), issues maintaining [[balance]], and trouble [[Coordination Exercises|coordinating]] voluntary movements<ref name=":0">Very well health MSA Available: https://www.verywellhealth.com/multiple-system-atrophy-2860862<nowiki/>(accessed 14.3.2022)</ref>.


*In MSA, patients often have symptoms that are characteristic of just one component: autonomic dysfunction, parkinsonism, or cerebellar dysfunction. As the disease progresses, additional symptoms will emerge.<ref name="Swan" />
=== Epidemiology ===
*Some patients may initially have autonomic features and may be diagnosed with pure autonomic failure (PAF).<ref name="Swan" /><br>o Patients who are initially misdiagnosed with PAF may later be correctly diagnosed with MSA as the neurological symptoms of parkinsonism and/or cerebellar ataxia appear.<ref name="Swan" />
[[File:MSE Dementia pic.jpg|thumb]]
MSA is an orphan disease with an incidence of up to 2.4 cases per 100 000 persons per year, while the prevalence may reach up to 7.8 patients per 100 000 population over the age of 40. The MSA‐P variant seems to be more common in the western hemisphere, whereas MSA‐C appears to be more frequent in Asia<ref name=":4">Virtual strategy Multiple System Atrophy Epidemiology Forecast to 2030 Available: https://virtual-strategy.com/2020/07/16/multiple-system-atrophy-epidemiology-forecast-to-2030/ (accessed 14.3.2022)</ref> .


There are three different categories or types of MSA, based upon what areas of the nervous system or autonomic system are affected and to what degree:  
There is about 1 living case of MSA in the population for every 40 cases of Parkinson’s disease, but because survival in MSA is shorter than for PD, about 1 new MSA case presents every year for about every 20 who present with PD.<ref name=":4" />


*Clinically, MSA is dominated by autonomic failure (MSA-A subtype) (also referred to as ''Shy Drager Syndrome''), which may be associated with either:
=== Symptoms ===
*the movement dysfunction of parkinsonism (MSA-P subtype) (also referred to as ''Striatonigral degeneration'') in 80% of cases. 2,3<ref name="Wenning">Wenning GK, Braune S.  Multiple System Atrophy: Pathophysiology and Management.  CNS Drugs 2001;15:839-48.</ref><ref name="Wedge">Wedge F. The Impact of Resistance Training on Balance and Functional Ability of a Patient with Multiple System Atrophy.  Journal of Geriatric Physical Therapy 2008;31:79-83.</ref>
The symptoms reflect the progressive loss of function and death of different types of [[Neurone|nerve cells]] in the brain and spinal cord. The initial symptoms of MSA are often difficult to distinguish from the initial symptoms of Parkinson’s disease and include: slowness of movement, tremor, or rigidity (stiffness); clumsiness or incoordination; impaired speech, a croaky, quivering voice; fainting or lightheadedness due to [[Orthostatic Hypotension|orthostatic hypotension]]; bladder control problems, eg a sudden urge to urinate or difficulty emptying the bladder<ref name=":4" />.
*or with cerebellar ataxia (MSA-C subtype) (also referred to as ''Sporadic Olivopontocerebellar atrophy OPCA''), which will result in difficulty with postural control and coordination in 20-50% of cases. 2,3,<ref name="Wenning" /><ref name="Wedge" />


[[Image:Cerebellum1.png|center]]
The 2 minute video below gives a good introduction to MSA
{{#ev:youtube|https://www.youtube.com/watch?v=mVqiCgaLSf4&app=desktop|width}}<ref>MSA coalition.


&nbsp;&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;'''Figure 2''': Cerebellum
What is MSA available from:https://www.youtube.com/watch?v=mVqiCgaLSf4&app=desktop (last accessed 17.1.2020)</ref>
=== Cognition ===
[[File:Cerebrum animation small2.gif|thumb|150x150px|Frontal lobe red Temporal lobe green]]
[[Cognitive Impairments|Cognitive deficits]] occur in all cognitive domains. The impaired cognitive domains had a significant correlation with atrophy of frontotemporal [[Cerebral Cortex|cortical]] areas, [[Basal Ganglia|basal ganglia]], [[thalamus]], and [[cerebellum]]<ref name=":3" />. Cognitive impairment, particularly seen in executive function, may occur in up to 75% of patients The [[Mini-Mental State Examination]], or MMSE, yielded 3% of participants showing signs of cognitive decline while a test called the Frontal Assessment Battery (FAB) categorized 41% of participants as being cognitively impaired. The FAB is a cognitive test that incorporates several clinical assessments to screen for [[Frontotemporal Dementia|frontotemporal dementia]] (FTD)


== Prevalence ==
* Emotional instability may occur later in the progression of the disease
* Depression, anxiety, panic attacks, and suicidal ideation may present in MSA
* Patients with MSA can have great difficulty switching attention from one stimulus to another,<ref name="Swan">Swan L, Dupont J.  Multiple System Atrophy. Journal of Physical Therapy 1999;79:488-94.</ref>&nbsp;with a&nbsp;decrease in goal-oriented cognitive ability.


The prevalence of MSA has been estimated to be 4.4 per 100,000 people. (Diedrich).<ref name="Diedrich">Diedrich A, Robertson D. Multiple System Atrophy. Vanderbilt University School of Medicine 2009. http://emedicine.medscape.com/article/1154583-overview (accessed on 24 Jan 2010).</ref>  
== Diagnosis ==
At this time, there are no specific symptoms, blood tests or imaging studies that distinguish MSA<ref name=":2">MSA Coalition. [https://www.multiplesystematrophy.org/wp-content/uploads/2019/09/What-You-Need-to-Know-9.4.19-DSC-AM-NV-Edits2.pdf MSA what you need to know] 4.4.2019. Available from: https://www.multiplesystematrophy.org/wp-content/uploads/2019/09/What-You-Need-to-Know-9.4.19-DSC-AM-NV-Edits2.pdf (last accessed 17.1.2020)</ref>. It can take a while to receive an MSA diagnosis because of the similarities between MSA and other conditions, eg Parkinson's disease. MSA is usually diagnosed around 50 years of age and is seen in people of all ethnic backgrounds. Once symptoms begin, the disease tends to progress quite rapidly.


<br>The mean age at onset has been reported to be between 52.5 and 55 years (Diedrich).<ref name="Diedrich" />  
The Mini-Mental State Examination, or MMSE, yielded 3% of participants showing signs of cognitive decline while a test called the Frontal Assessment Battery (FAB) categorized 41% of participants as being cognitively impaired<ref>MAS coalition Depression and Cognitive Impairment in MSA Available:https://www.multiplesystematrophy.org/about-msa/depression-cognitive-impairment/ (accessed 14.3.2022)</ref>. The FAB is a cognitive test that incorporates several clinical assessments to screen for frontotemporal dementia (FTD),


<br>MSA is found more often in men than in women (Diedrich).<ref name="Diedrich" />  
'''Diagnostic Challenge''' There is no “typical” presentation for this disorder, and MSA can often be masked by other diagnoses. Patients with MSA are most commonly misdiagnosed with [[Parkinsons Disease|Parkinson’s Disease]]. About 1/3 of people with MSA die while still misdiagnosed.<ref name="Lundy Eckman" /> Only 25% of patients with MSA are correctly diagnosed at their first neurological visit. The correct diagnosis is usually established on an average of 4 to 5 years after the disease onset.<ref name="Wenning">Wenning GK, Braune S.  Multiple System Atrophy: Pathophysiology and Management.  CNS Drugs 2001;15:839-48.</ref>
=== Management ===
Currently, there is no cure for MSA, nor are there any treatments specifically designed to reverse or stop disease progression.


<br>Wenning et al. completed an analysis of 100 patients with MSA and measured their disability. Results showed that patients with MSA become disabled at a faster rate than patients with Parkinson's Disease.<ref name="Wenning" />  
* Movement disorders can be treated with levodopa and carbidopa (Sinemet), but this usually has limited results.
* Other medications such as trihexyphenidyl (Artane), benztropine mesylate (Cogentin), and amantadine (Symmetrel), may also offer some symptom relief. Several medications exist to treat orthostatic hypertension.
* Physical and occupational therapy, eg aqua therapy, can help maintain muscle function, and speech therapy can help improve any difficulties swallowing or speaking<ref name=":0" />.


<br>  
=== Physical Therapy Management ===
[[File:Man-walker dementia.jpg|thumb|Walking Aid]]
Physical therapies offer drug-free tools to maintain their function for as long as possible, by helping keep muscles strong and flexible and helping prevent [[falls]]. Encouraging mobility also lowers the risk of [[Pulmonary Embolism|pulmonary embolism]] which can be fatal<ref name=":2" />.


== Characteristics/Clinical Presentation  ==
Ideally a neurological physiotherapist will assess the client and then make a tailored program. It incorporates a combination of progressive fitness, balance, movement and strength training and stretching, as well as education on how to manage symptoms. Make PT goals realistic.  Base the goals upon current function and take into consideration the activities most important to the patient.


MSA is classified by the most dominant symptom exhibited by the patient.
[[Gait]]/Mobility Training:


'''MSA-A:'''
# Fit the patient for the most appropriate [[Walking Aids|walking aids]] in order to gain independent mobility. &nbsp;This will depend upon the patient’s level of function and safety.
# If a [[Wheelchair Assessment - Assessment Interview|wheelchair]] is most appropriate, ensure the chair is one that will best benefit their posture and mobility based upon the function of patient.&nbsp;As a PT, the need to promote independent functional mobility and optimal posture with safety in mind is most important.


*Autonomic dysfunction, primarily orthostatic hypotension, is present in approximately 75% of people with MSA.<ref name="Wedge" />  
[[File:Hip exercise 6.png|right|frameless]]
*Autonomic dysfunction commonly appears as postural/orthostatic hypotension associated with impaired or absent reflex tachycardia upon standing, bowel and bladder incontinence, thermoregulatory dysfunction, impotence, and hypohydrosis.<ref name="Swan" />,<ref name="Diedrich" />
Therapeutic Exercise/Activities:
*[[Moving and Handling|Transfer training]]
*[[Balance]] activities<ref name="Wedge">Wedge F.  The Impact of Resistance Training on Balance and Functional Ability of a Patient with Multiple System Atrophy.  Journal of Geriatric Physical Therapy 2008;31:79-83.</ref>eg [[Otago Exercise Programme|Otago balance porogram]]
*[[Strength Training|Strength training]] focusing  on  [[Knee Extensors|knee extensors]] and [[Knee Flexors|flexors]], [[Hip Abductors|hip abductors]] and [[Hip Adductors|adductors]], and ankle plantar flexors .These muscle groups are chosen because of their importance to balance.<ref name="Wedge" /> Can lead to improvements in the patient's gait pattern (better at maintaining good step height and length even) and reduces festinating gait.
*Postural muscle strengthening to improve eg head and trunk alignment in both sitting and standing).<ref name="Wedge" />


[[Image:ANS.gif]]
Education


&nbsp;&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;'''Figure 3''': Autonomic Nervous System
'''MSA-P:'''
*When a parkinson-like movement dysfunction is the prominent feature, the disease is categorized as MSA-P. [[Parkinsons_Disease|Parkinsonism]] has been identified as the initial feature in 46% of patients with MSA, but eventually over 80% of patients with MSA will develop parkinsonian features.<ref name="Wedge" />
*Characteristics of parkinsonism include bilateral involvement, bradykinesia, impaired writing, slurred speech, rigidity,<ref name="Swan" />postural and rest tremor disequilibrium, and gait unsteadiness.<ref name="Diedrich" />
'''MSA-C:'''
*When cerebellar dysfunction is more prominent, the disease is labeled as MSA-C. &nbsp;Over 50% of individuals with MSA will present with cerebellar dysfunction.<ref name="Wedge" />
*Cerebellar features that are characteristic of MSA initially manifest in the trunk and lower extremities, leading to disturbances in gait.<ref name="Swan" />. These patients also display limb kinetic ataxia and scanning dysarthria, as well as cerebella<br>
'''Additional Symptoms:'''
*Dysfunction to the pyramidal/corticospinal tracts can also occur. &nbsp;However, this symptomatic component does not own &nbsp;a subtype.<ref name="Wedge" />
*&nbsp;Signs of corticospinal tract dysfunction (hyperreflexia, impaired muscle performance, spasticity, and a positive Babinski sign) are features characteristic of MSA, but are not used as criteria for diagnosis.<ref name="Swan" />
<br>
There is no “typical” presentation of this disorder, which makes it difficult to detect, and patients often go misdiagnosed. MSA may also go misdiagnosed because the disorder may initially (as mentioned previously) manifest with S/S of only one component.<ref name="Lundy Eckman" />
*Patients with MSA are most commonly misdiagnosed with [[Parkinsons_Disease|Parkinson’s Disease]]. About 1/3 of people with MSA die while still misdiagnosed.<ref name="Lundy Eckman" />
*Only 25% of patients with MSA are correctly diagnosed at their first neurological visit. The correct diagnosis is usually established on an average of 4 to 5 years after the disease onset.<ref name="Wenning" />
<br>
It is important to differentiate MSA from PAF and pure parkinsonism.
*According to Lundy-Eckman, the distinction between MSA and parkinsonism&nbsp;is made by exclusion. &nbsp;If no autonomic or cerebellar signs are present, then the patient most likely has pure parkinsonism.<ref name="Lundy Eckman" />
*It is also important to note that up to 90% of patients with MSA-P treated with Levodopa (L-Dopa) fail to show a sustained, long-term response.<ref name="Wenning" /> This is a sign that this patient does not have pure parkinsonism, as L-Dopa is not effective.
*In addition, orthostatic hypotension, difficulty urinating, rapid progression of functional limitations, loud breathing,and impotence indicate that MSA is a more likely Dx than Parkinson’s Disease.<ref name="Wenning" />
*According to Lundy-Eckman, a patient most likely has PAF if ANS S/S (such as orthostatic hypotension) are present, but signs of parkinsonism or ataxia are not.<ref name="Lundy Eckman" /><br>
<br>
As there is no “typical” presentation for this disorder, and MSA can often be masked by other diagnoses, it is important if one has a patient with pure Parkinson’s, PAF, etc to keep a watchful eye of any suspicious S/S that are not associated with that diagnosis alone. This is pertinent so that these patients do not go misdiagnosed.<br>
== Associated Co-morbidities  ==
Level of cognition:
*While there is generally an absence of marked cognitive impairment, emotional instability may occur later in the progression of the disease.<ref name="Wedge" />
*It has been noted that patients with MSA can have great difficulty switching attention from one stimulus to another.<ref name="Swan" />&nbsp;&nbsp;A&nbsp;decrease in goal-oriented cognitive ability has also been noted in patients with MSA.<ref name="Lundy Eckman" />
*Patients with MSA may experience depression. &nbsp;In one study of 15 patients with MSA, 28.6% had moderate to severe depression compared to 3%-4% of healthy individuals.<ref name="Hemingway">Hemingway J, Franco K, Chmelik E. Shy-Drager Syndrome: Multisystem Atrophy With Comorbid Depression.  Psychosomatics.  2005;46:73-6.</ref>
<br>
Bowel and Bladder Dysfunction:
*Genitourinary dysfunctions are common symptoms of MSA. Urinary bladder dysfunction may include frequency, urgency, incontinence, and retention.<ref name="Swan" />
*Men may experience erectile difficulties early in the course of the disease.<ref name="Swan" />
*Constipation is also common problem.<ref name="Swan" />
<br>
Symptoms Occurring as the Disease Progresses:
*Dysphagia and dysarthria are symptoms that occur later in the disease<ref name="Swan" /> and should be treated by speech therapy.<br>
== Medications  ==
Since MSA is a variable disorder and can present in many different ways. &nbsp;Therefore, treatment is symptomatic.<br>
Pharmacological Treatment:
'''MSA-A'''
*To treat orthostatic hypotension: (is defined as a fall in BP on standing of more than 20mmHg in SBP or 10 mmHg in DBP)<ref name="Hardy">Hardy, Joanne.  Multiple System Atrophy: Pathophysiology, Treatment and Nursing Care.  Nursing Standard 2008;22:50-6.</ref> Drugs can be prescribed to enhance vasoconstriction and increase the blood volume, which will increase the blood pressure (''[http://www.drugs.com/pro/fludrocortisone.html Fludrocortisone]'' and ''[http://www.drugs.com/pro/midodrine.html Midodrine]'').<ref name="Lundy Eckman" />
*To treat constipation: Stool softener medications are effective.<ref name="Hardy" />
*To treat urinary dysfunction:&nbsp;Pharmacological intervention does not adequately reduce post-void residual volume in patients with MSA, but anticholinergic agents like ''[http://www.drugs.com/pro/oxybutynin.html Oxybutynin]'' can improve symptoms of hyper-reflexia.<ref name="Wenning" />
*To treat impotence:&nbsp;''Sildenafil'' (25 to 75mg) may be successful in treating erectile failure.<ref name="Wenning" />
<br>
'''MSA-C'''
*There are no currently established pharmacological treatment strategies for cerebellar ataxia and pyramidal dysfunction.<ref name="Wenning" />
<br>
'''MSA-P'''
*''Dopamimetics'' (''[http://www.drugs.com/ppa/levodopa.html Levodopa]'', ''Dopamine''&nbsp;''Agonists'') and ''[http://www.drugs.com/pro/amantadine.html Anticholinergics]''[http://www.drugs.com/pro/amantadine.html /]''[http://www.drugs.com/pro/amantadine.html Amantadine]''.<ref name="Wenning" />
<br>
== Diagnostic Tests/Lab Tests/Lab Values  ==
A definite diagnosis of MSA can only be made upon autopsy where degenerative changes characterized by cell loss, gliosis, and the presence of cytoplasmic inclusions in the oligodendrocytes are apparent on tissue examination.<ref name="Wedge" /><br>
Some atrophic changes are visible upon use of MRI. &nbsp;MRI is most useful in detecting MSA-C, as atrophic changes will occur in the cerebellum and pontine regions. &nbsp;However, due to varying data, current research is unsure of this method's ability to differentially diagnose MSA from other parkinsonian disorders.<ref name="Swan" />,<ref name="Wenning" />
[[Image:MSA.jpg]]
'''Figure 4''': MRI showing visible atrophy of the pontine (A) and cerebellar (B) regions.
<br>
Research has been done on the use of positron emission tomography (PET scan) and computed tomography (CT scan) to detect MSA against Parkinson's Disease and other associated disorders. &nbsp;Since MSA is a variable condition, many studies remain inconclusive as to whether PET or CT scans are a good sources for diagnosis of MSA.<ref name="Wenning" />,<ref name="Swan" />
While MRI and PET scans are of some use, particularly in ruling out other conditions, there is no single clinical feature or investigation that confirms MSA, which has to be diagnosed on the basis of probability (see below) from the complete clinical presentation.<ref name="Hardy" />
In order to better predict the diagnosis of MSA, the&nbsp;Consensus Committees representing the American Autonomic Society and the American Academy of Neurology developed a series of tables, which will help decipher if a patient is a possible, probable, or definite candidate for MSA.<ref name="Diedrich" />
<br>
Table I defines the diagnostic categories of MSA, which are possible, probable, and definite. &nbsp;Table II displays what clinical features (additional S/S that are often present with that particular domain) and criterion (S/S that are required to be present in order to be diagnosed under that particular domain) are required for the diagnosis of each clinical domain. Table III includes exclusion criterion for each clinical domain.<ref name="Diedrich" />
<br>
Table I. Diagnostic categories of MSA
{| width="750" cellspacing="1" cellpadding="1" border="1"
|-
| '''I. Possible MSA '''&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;
| One criterion plus two features from separate other domains. When the criterion is parkinsonism, a poor levodopa response qualifies as<br>one feature (hence only one additional feature is required)
|-
| '''II. Probable MSA'''
| Criterion for: autonomic failure/urinary dysfunction plus poorly levodopa-responsive parkinsonism or cerebellar dysfunction
|-
| '''III. Definite MSA &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;&nbsp;'''
| Pathologically confirmed by the presence of a high density of glial cytoplasmic inclusions in association with a combination of<br>degenerative changes in the nigrostriatal and olivopontocerebellar pathways
|}
<br>Table II. Clinical domains, features and criteria used in the diagnosis of MSA
{| width="750" cellspacing="1" cellpadding="1" border="1"
|-
| '''Clinical Domain'''
| '''Feature (Characteristic of the Disease)'''
| '''Criterion (Defining Feature)'''
|-
| Autonomic &nbsp; &nbsp; &nbsp; Dysfunction &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;<br>
| • Orthostatic hypotension with blood pressure falling by 20 mm Hg systolic and 10 mm Hg diastolic within 3 min of standing<br>• Urinary incontinence or incomplete bladder emptying
| Orthostatic hypotension with blood pressure falling by 30 mm Hg systolic and 15 mm Hg diastolic within 3 min of standing and/or urinary incontinence as persistent, involuntary, partial or total bladder emptying, accompanied by erectile dysfunction in men<br>
|-
| Parkinsonism &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;
| • Bradykinesia - Slowness of voluntary movement with progressive reduction in speed and amplitude during repetitive actions<br>• Rigidity<br>• Postural instability not caused by primary visual, vestibular, cerebellar, or proprioceptive dysfunction<br>• Tremor - Postural, resting, or both &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;
| Bradykinesia plus at least 1 parkinsonian feature
|-
| Cerebellar Dysfunction
| • Gait ataxia (wide-based stance with steps of irregular length and direction)<br>• Ataxic dysarthria<br>• Limb ataxia<br>• Sustained gaze-evoked nystagmus
| Gait ataxia plus at least 1 cerebellar feature
|-
| Corticospinal Tract Dysfunction &nbsp; &nbsp; &nbsp;
| • Extensor plantar response with hyperreflexia (pyramidal sign)
| Not used as criterion in defining diagnosis of MSA
|}
<br>
Table III. Exclusion criteria for the diagnosis of MSA
{| width="750" cellspacing="1" cellpadding="1" border="1"
|-
| '''Procedure'''
| '''Findings'''
|-
| History Taking &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;&nbsp;
| • Symptomatic onset at &lt;30 years<br>• Family history of similar disorder<br>• Systemic diseases or other identifiable causes for features listed in Table II&nbsp;<br>• Hallucinations unrelated to medication
|-
| Physical Examination
| • Prominent slowing of vertical saccades or vertical supranuclear gaze palsy<br>• Evidence of focal cortical dysfunction such as aphasia, alien limb syndrome, and parietal dysfunction
|-
| Laboratory Study
| • Metabolic, molecular genetic, and imaging evidence of alternative cause of features listed in Table II
|}
== Causes  ==
According to recent research, the cause of MSA is unknown.<ref name="Diedrich" />
<br>Research has suggested that MSA is characterized by a progressive loss of neuronal and oligodendroglial cells (myelin producing cells in CNS) in numerous sites in the CNS (basal ganglia, cerebellum). This damage is said to occur from the formation of glial cytoplasmic inclusions (GCI’s).<ref name="Diedrich" />
*GCI’s are thought to be similar to neurofibrillary tangles that are present in movement disorders.
*Tangles are pathological protein groups found within neurons that slowly cause damage to neurons in the CNS.
<br>
Gliosis is also a contributor to MSA:
*Once damage has occurred to the CNS (from the formation of GCI's), glial cells come in to repair the damage.<ref name="Diedrich" />
*A glial scar is then formed in order to protect and begin healing the damaged CNS. It is efficient in suppressing further damage, but it also halts neuroregeneration. Many neurological development inhibitor molecules are secreted by cells of the scar, which prevent complete physical and functional recovery of the CNS.<ref name="Diedrich" />
*This becomes a repetitive cycle of damage (from the GCI's) and ineffective healing (through gliosis), which will lead to increasingly poor control of the ANS and CNS.<ref name="Hardy" />&nbsp;<br>
[[Image:Gliosis.jpg|border]]<br>
'''Figure 5''': Gliosis
<br>
While the above process is a current thought among many researchers, the etiology of the process of the initial cell loss is still unknown.<ref name="Diedrich" />&nbsp;&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;
== Systemic Involvement  ==
Please reference the Associated Co-Morbidities Section.
== Medical Management (current best evidence)<br>  ==
As diagnostic procedures are still being researched, current literature has made it seem that neurologists turn to imaging (MRI, CT, PET scans) tools in order to rule out other possible diagnoses (Parkinson's Disease, etc.), &nbsp;making MSA more of a diagnosis of exclusion. &nbsp;As mentioned previously, there is no single feature or investigation that confirms MSA. &nbsp;Therefore MSA must be diagnosed on the basis of probability from the clinical presentation.<ref name="Hardy" />
Clinical presentation is not only important for diagnosis of MSA, but is also helpful in treatment. &nbsp;Since MSA is a variable condition, the most effective medical management is symptomatic treatment.<ref name="Hardy" /> &nbsp;Current medical management includes pharmacological treatment. &nbsp;Medication is prescribed according to the subtype of MSA and the symptoms that are present.
<br>
For more information regarding pharmacological management of MSA, please reference the Medications section.&nbsp;
== Physical Therapy Management (current best evidence)  ==
There is very little published literature on physical therapy or exercise intervention for patients with MSA.<ref name="Wedge" /><br><br>
There is the most evidence concerning patients with MSA-A.<ref name="Wedge" />
<br>
Since majority of patients with MSA-A seem to experience orthostatic hypotension, this is a main focus during a treatment session.<ref name="Swan" /><ref name="Lundy Eckman" />
*Nonpharmacological interventions include increasing the consumption of caffeine, salt, and fluids while decreasing alcohol intake and eating smaller, more frequent meals throughout the day.<ref name="Swan" />
*Mechanical interventions include elevating the head of the bed up to 20.3 cm (8 in) for sleeping and using elastic garments. &nbsp;Creating muscle tone in the calves is also helpful in regulating BP.<ref name="Swan" />
*Further patient education should include: advising the patient to refrain from quick postural changes, scheduling activities for later in the day, and avoiding motionless standing activities.<ref name="Swan" />
*Warm environmental temperatures should also be avoided.<ref name="Swan" />
*Swan suggested that swimming might be an ideal exercise, as the hydrostatic pressure of the water counteracts the hypotension the patient is experiencing.<ref name="Swan" />
*During a PT session, it will be important to monitor a patient's BP before, during, and after exercise. &nbsp;It will also be necessary to choose appropriate exercises and environment to avoid these symptoms from occurring.
<br>
Bowel and Bladder Treatment:
*Begin a urinary incontinence program if appropriate. &nbsp;Introducing exercises for the pelvic floor musculature in order to gain control/suppress urge, etc.
<br>
Gait/Mobility Training:
*Fit the patient for the most appropriate assistive device in order to gain independent mobility. &nbsp;This will depend upon the patient’s level of function and safety.
*If a wheelchair is most appropriate, ensure the chair is one that will best benefit their posture and mobility based upon the function of patient.&nbsp;
*As a PT, the need to promote independent functional mobility and optimal posture with safety in mind is most important.
<br>
Therapeutic Exercise/Activities:
*According to a study by Wedge, et al., gait training, transfer training, balance activities, and conditioning are necessary in reaching the goal of&nbsp;minimizing fatigue and risk for falling (safe transfers, etc.)<ref name="Wedge" />
*Resistance training has been proven to be effective in patients with MSA.<br>• In a case study by Wedge, knee extensors and flexors, hip abductors and adductors, and ankle plantarflexors were targeted for resistance training. &nbsp;These muscle groups were chosen because of their importance to balance.<ref name="Wedge" /><br>• Following this resistance training intervention, marked improvements were noted in the patient's gait pattern evidenced by increased consistency in maintaining good step height and length even when fatigued. &nbsp;A festinating gait was rarely evident following resistance-training. Functional changes were also evident. &nbsp;The patient improved her transfer technique and was able to maintain a more upright posture, which was evidenced by good head and trunk alignment in both sitting and standing. The most important outcome was a decreased frequency of falling.<ref name="Wedge" /><br>
*It would appear from this case study by Wedge et al. that a closely monitored, low to moderate intensity resistance training program has no adverse effects on a patient with MSA, and contributes to improvement in function and safety during mobility tasks.<ref name="Wedge" />
*Swan et al. has reported that modalities for pain are safe to use, taking the normal precautions.<ref name="Swan" />
<br>
Additional Physical Therapy Advice:
Research reinforces the fact that since MSA is a variable disorder. &nbsp;Each patient with MSA will present differently, so it is difficult to give clear PT advice.
*Based upon a patient’s level of mobility and function, PT's should use their skills and knowledge to promote a safe and optimal environment for the patient.
*As a PT, maintaining strength and physiologic fitness as long as possible will be most valuable to the patient.<ref name="Lundy Eckman" />
*Education of the patient and family on benefits of PT is important for patient/family knowledge and compliance.  
*Education of the patient and family on benefits of PT is important for patient/family knowledge and compliance.  
*Make PT goals realistic. &nbsp;Base the goals upon current function and take into consideration the activities most important to the patient.&nbsp;
*Since this is a progressive disorder, PT's must make sure to re-evaluate goals often to make sure they are appropriate.<br>


== Differential Diagnosis ==
=== Differential Diagnosis ===
 
MSA often presents as the following disorders: Pure [[Parkinson's|Parkinsonism]]<ref name="Hardy">Hardy, Joanne.  Multiple System Atrophy: Pathophysiology, Treatment and Nursing Care.  Nursing Standard 2008;22:50-6.</ref>; Pure Autonomic Failu<nowiki/>re (PAF)<ref name="Hardy" />; [[Progressive Supranuclear Palsy]]<ref name="O'Sullivan">O'Sullivan SS, Massey LA, Williams DR, Silveira-moriyama L, Kempster PA, Holton JL, Revesz T,  Lees, AJ.  Clinical Outcomes of Progressive Supranuclear Palsy and Multiple System Atrophy.  Brain.  2008;131:1362-72</ref>; Corticobasal Ganglionic Degeneration<ref name="Hain">Hain TC.  Multiple System Atrophy.  2010.  http://www.dizziness-and-balance.com/disorders/central/movement/msa.html (accessed on 5 april 2010).</ref>
MSA often presents as the following disorders:  
 
*Pure Parkinsonism<ref name="Wedge" />,<ref name="Swan" />,<ref name="Wenning" />,<ref name="Hardy" />  
*Pure Autonomic Failure<ref name="Wedge" />,<ref name="Swan" />,<ref name="Hardy" />,<ref name="Wenning" />
*Progressive Supranuclear Palsy<ref name="O'Sullivan">O'Sullivan SS, Massey LA, Williams DR, Silveira-moriyama L, Kempster PA, Holton JL, Revesz T,  Lees, AJ.  Clinical Outcomes of Progressive Supranuclear Palsy and Multiple System Atrophy.  Brain.  2008;131:1362-72</ref>  
*Corticobasal Ganglionic Degeneration<ref name="Hain">Hain TC.  Multiple System Atrophy.  2010.  http://www.dizziness-and-balance.com/disorders/central/movement/msa.html (accessed on 5 april 2010).</ref>
 
== Case Reports  ==
 
'''Wedge F. The Impact of Resistance Training on Balance and Functional Ability of a Patient with Multiple System Atrophy. Journal of Geriatric Physical Therapy 2008;31:79-83.'''<br>The following case report documents the impact of a resistance-training program on a 68 year-old-female patient with a 2-year history of MSA.&nbsp;<br>
 
'''Hemingway J, Franco K, Chmelik E. Shy-Drager Syndrome: Multisystem Atrophy With Comorbid Depression. Psychosomatics. 2005;46:73-6.'''
 
The following case report discusses the some of the struggles in the diagnostic process of a 48 year old man with MSA. &nbsp;
 
'''Mashidori T, Yamanishi T, Yoshida K, Sakakibara R ,Sakurai K, Hirata K. Continuous Urinary Incontinence Presenting as the Initial Symptoms Demonstrating Acontractile Detrusor and Intrinsic Sphincter Deficiency in Multiple System Atrophy. International Journal of Urology. 2007;14:972-74. '''<br> The following case report demonstrates how urinary incontinence can be the first symptoms of MSA in a 66-year-old female.
 
'''Goto K, Ueki A, Shimode H, Shinjo H, Miwa C, Morita, Y. Depression in Multiple System Atrophy: A Case Report. Psychiatry and Clinical Neurosciences. 2000;54:507-11.''' The following case report demonstrates how depression can be the first symptoms of MSA in a 56-year-old female.&nbsp;
 
<br>
 
== Resources <br>  ==
 
'''WE MOVE''': Worldwide Education and Awareness for Movement Disorders.
 
http://www.wemove.org
 
'''SDS/MSA Support Group'''
 
http://www.shy-drager.org/
 
== Recent Related Research&nbsp;<br>[[Adding PubMed Feed|Adding PubMed Feed]]  ==
<div class="researchbox">
<rss>http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1FgkM3o_AS6UEgbmHZIimW_QZEzyRvCgQvRN3iqdvE36UbtgD0|charset=UTF-8|short|max=10</rss>
</div>


=== Prognosis and Outlook ===
Prognosis is currently guarded, with most MSA patients passing away from the disease or its complications within 6-10 years after the onset of symptoms. Nonetheless, there is reason for hope for MSA research goes on. Since the biology of MSA may be related to other neurodegenerative diseases like Parkinson's disease, it is possible that therapies designed for other conditions will also prove helpful for patients with MSA.<ref name=":2" />
== References  ==
== References  ==


<references />  
<references />  


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Latest revision as of 11:15, 17 February 2023

Original Editors - Emily Nicklies from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Top Contributors - Emily Nicklies, Lucinda hampton, Admin, Kim Jackson, Dave Pariser, Wendy Walker, Elaine Lonnemann, Naomi O'Reilly, WikiSysop and Amrita Patro  

Introduction[edit | edit source]

Parkinson's man sketches.jpg

Multiple System Atrophy (MSA) is defined as a sporadic, fatal, progressive, neurodegenerative (specifically a synucleinopathy) adult-onset disorder. It is the second most common neurodegenerative movement disorder with an average annual incidence rate of 3 per 100000 person-years after Parkinson’s disease (PD)[1]. It can affect the

The symptoms reflect the progressive loss of function and death of different types of nerve cells in the brain and spinal cord.

Some of these features are similar to those seen in Parkinson’s disease, and early in the disease course it often may be difficult to distinguish these disorders. This 1 minute video is titled Differentiating Multiple System Atrophy From Parkinson's Disease.

[3]

Etiology[edit | edit source]

The causes of MSA are unknown; however, as for other neurodegenerative diseases, a complex interaction of genetic and environmental mechanisms seems likely.[4]
Research has suggested that MSA is characterized by a progressive loss of neuronal and oligodendroglial cells (myelin producing cells in CNS) in numerous sites in the CNS (basal ganglia, cerebellum). This damage is said to occur from the formation of glial cytoplasmic inclusions (GCI’s).[5]

Classification[edit | edit source]

MSA is classified by the most dominant symptom exhibited by the patient.

  1. Parkinsonian type (MSA-P): this includes symptoms similar to Parkinson's disease eg tremors at rest, rigidity of muscles, and slow movements, including gait
  2. Cerebellar type (MSA-C): involves difficulty walking (ataxia), issues maintaining balance, and trouble coordinating voluntary movements[6].

Epidemiology[edit | edit source]

MSE Dementia pic.jpg

MSA is an orphan disease with an incidence of up to 2.4 cases per 100 000 persons per year, while the prevalence may reach up to 7.8 patients per 100 000 population over the age of 40. The MSA‐P variant seems to be more common in the western hemisphere, whereas MSA‐C appears to be more frequent in Asia[7] .

There is about 1 living case of MSA in the population for every 40 cases of Parkinson’s disease, but because survival in MSA is shorter than for PD, about 1 new MSA case presents every year for about every 20 who present with PD.[7]

Symptoms[edit | edit source]

The symptoms reflect the progressive loss of function and death of different types of nerve cells in the brain and spinal cord. The initial symptoms of MSA are often difficult to distinguish from the initial symptoms of Parkinson’s disease and include: slowness of movement, tremor, or rigidity (stiffness); clumsiness or incoordination; impaired speech, a croaky, quivering voice; fainting or lightheadedness due to orthostatic hypotension; bladder control problems, eg a sudden urge to urinate or difficulty emptying the bladder[7].

The 2 minute video below gives a good introduction to MSA

[8]

Cognition[edit | edit source]

Frontal lobe red Temporal lobe green

Cognitive deficits occur in all cognitive domains. The impaired cognitive domains had a significant correlation with atrophy of frontotemporal cortical areas, basal ganglia, thalamus, and cerebellum[1]. Cognitive impairment, particularly seen in executive function, may occur in up to 75% of patients The Mini-Mental State Examination, or MMSE, yielded 3% of participants showing signs of cognitive decline while a test called the Frontal Assessment Battery (FAB) categorized 41% of participants as being cognitively impaired. The FAB is a cognitive test that incorporates several clinical assessments to screen for frontotemporal dementia (FTD)

  • Emotional instability may occur later in the progression of the disease
  • Depression, anxiety, panic attacks, and suicidal ideation may present in MSA
  • Patients with MSA can have great difficulty switching attention from one stimulus to another,[9] with a decrease in goal-oriented cognitive ability.

Diagnosis[edit | edit source]

At this time, there are no specific symptoms, blood tests or imaging studies that distinguish MSA[10]. It can take a while to receive an MSA diagnosis because of the similarities between MSA and other conditions, eg Parkinson's disease. MSA is usually diagnosed around 50 years of age and is seen in people of all ethnic backgrounds. Once symptoms begin, the disease tends to progress quite rapidly.

The Mini-Mental State Examination, or MMSE, yielded 3% of participants showing signs of cognitive decline while a test called the Frontal Assessment Battery (FAB) categorized 41% of participants as being cognitively impaired[11]. The FAB is a cognitive test that incorporates several clinical assessments to screen for frontotemporal dementia (FTD),

Diagnostic Challenge There is no “typical” presentation for this disorder, and MSA can often be masked by other diagnoses. Patients with MSA are most commonly misdiagnosed with Parkinson’s Disease. About 1/3 of people with MSA die while still misdiagnosed.[2] Only 25% of patients with MSA are correctly diagnosed at their first neurological visit. The correct diagnosis is usually established on an average of 4 to 5 years after the disease onset.[12]

Management[edit | edit source]

Currently, there is no cure for MSA, nor are there any treatments specifically designed to reverse or stop disease progression.

  • Movement disorders can be treated with levodopa and carbidopa (Sinemet), but this usually has limited results.
  • Other medications such as trihexyphenidyl (Artane), benztropine mesylate (Cogentin), and amantadine (Symmetrel), may also offer some symptom relief. Several medications exist to treat orthostatic hypertension.
  • Physical and occupational therapy, eg aqua therapy, can help maintain muscle function, and speech therapy can help improve any difficulties swallowing or speaking[6].

Physical Therapy Management[edit | edit source]

Walking Aid

Physical therapies offer drug-free tools to maintain their function for as long as possible, by helping keep muscles strong and flexible and helping prevent falls. Encouraging mobility also lowers the risk of pulmonary embolism which can be fatal[10].

Ideally a neurological physiotherapist will assess the client and then make a tailored program. It incorporates a combination of progressive fitness, balance, movement and strength training and stretching, as well as education on how to manage symptoms. Make PT goals realistic.  Base the goals upon current function and take into consideration the activities most important to the patient.

Gait/Mobility Training:

  1. Fit the patient for the most appropriate walking aids in order to gain independent mobility.  This will depend upon the patient’s level of function and safety.
  2. If a wheelchair is most appropriate, ensure the chair is one that will best benefit their posture and mobility based upon the function of patient. As a PT, the need to promote independent functional mobility and optimal posture with safety in mind is most important.
Hip exercise 6.png

Therapeutic Exercise/Activities:

Education

  • Education of the patient and family on benefits of PT is important for patient/family knowledge and compliance.

Differential Diagnosis[edit | edit source]

MSA often presents as the following disorders: Pure Parkinsonism[14]; Pure Autonomic Failure (PAF)[14]; Progressive Supranuclear Palsy[15]; Corticobasal Ganglionic Degeneration[16]

Prognosis and Outlook[edit | edit source]

Prognosis is currently guarded, with most MSA patients passing away from the disease or its complications within 6-10 years after the onset of symptoms. Nonetheless, there is reason for hope for MSA research goes on. Since the biology of MSA may be related to other neurodegenerative diseases like Parkinson's disease, it is possible that therapies designed for other conditions will also prove helpful for patients with MSA.[10]

References[edit | edit source]

  1. ↑ 1.0 1.1 Dash S, Mahale R, Netravathi M, Kamble NL, Holla V, Yadav R, Pal PK. Cognition in Patients With Multiple System Atrophy (MSA) and Its Neuroimaging Correlation: A Prospective Case-Control Study. Cureus. 2022 Jan 29;14(1). Available:https://www.cureus.com/articles/83909-cognition-in-patients-with-multiple-system-atrophy-msa-and-its-neuroimaging-correlation-a-prospective-case-control-study (accessed 14.3.2022)
  2. ↑ 2.0 2.1 Lundy-Eckman, L. Neuroscience: Fundamentals for Rehabilitation. 3rd ed. St. Louis: Saunders Elsevier, 2002.
  3. ↑ MSA coalition Differentiating Multiple System Atrophy From Parkinson's Disease (PSA) Available: https://www.youtube.com/watch?v=CD7UL12GSCM(accessed 14.3.2022)
  4. ↑ Jellinger KA. Multiple system atrophy: an oligodendroglioneural synucleinopathy. Journal of Alzheimer's Disease. 2018 Jan 1;62(3):1141-79 Available from.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5870010/ (last accessed 16.1.2020)
  5. ↑ Diedrich A, Robertson D. Multiple System Atrophy. Vanderbilt University School of Medicine 2009. http://emedicine.medscape.com/article/1154583-overview (accessed on 24 Jan 2010).
  6. ↑ 6.0 6.1 Very well health MSA Available: https://www.verywellhealth.com/multiple-system-atrophy-2860862(accessed 14.3.2022)
  7. ↑ 7.0 7.1 7.2 Virtual strategy Multiple System Atrophy Epidemiology Forecast to 2030 Available: https://virtual-strategy.com/2020/07/16/multiple-system-atrophy-epidemiology-forecast-to-2030/ (accessed 14.3.2022)
  8. ↑ MSA coalition. What is MSA available from:https://www.youtube.com/watch?v=mVqiCgaLSf4&app=desktop (last accessed 17.1.2020)
  9. ↑ Swan L, Dupont J. Multiple System Atrophy. Journal of Physical Therapy 1999;79:488-94.
  10. ↑ 10.0 10.1 10.2 MSA Coalition. MSA what you need to know 4.4.2019. Available from: https://www.multiplesystematrophy.org/wp-content/uploads/2019/09/What-You-Need-to-Know-9.4.19-DSC-AM-NV-Edits2.pdf (last accessed 17.1.2020)
  11. ↑ MAS coalition Depression and Cognitive Impairment in MSA Available:https://www.multiplesystematrophy.org/about-msa/depression-cognitive-impairment/ (accessed 14.3.2022)
  12. ↑ Wenning GK, Braune S. Multiple System Atrophy: Pathophysiology and Management. CNS Drugs 2001;15:839-48.
  13. ↑ 13.0 13.1 13.2 Wedge F. The Impact of Resistance Training on Balance and Functional Ability of a Patient with Multiple System Atrophy. Journal of Geriatric Physical Therapy 2008;31:79-83.
  14. ↑ 14.0 14.1 Hardy, Joanne. Multiple System Atrophy: Pathophysiology, Treatment and Nursing Care. Nursing Standard 2008;22:50-6.
  15. ↑ O'Sullivan SS, Massey LA, Williams DR, Silveira-moriyama L, Kempster PA, Holton JL, Revesz T, Lees, AJ. Clinical Outcomes of Progressive Supranuclear Palsy and Multiple System Atrophy. Brain. 2008;131:1362-72
  16. ↑ Hain TC. Multiple System Atrophy. 2010. http://www.dizziness-and-balance.com/disorders/central/movement/msa.html (accessed on 5 april 2010).
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