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Multiple system atrophy

Multiple system atrophy (MSA) is a rare
neurodegenerative disorder[1] characterized by Multiple system atrophy
tremors, slow movement, muscle rigidity, postural
instability (collectively known as parkinsonism),
autonomic dysfunction and ataxia. This is caused by
progressive degeneration of neurons in several parts
of the brain including the basal ganglia, inferior
olivary nucleus, and cerebellum. MSA was first
described in 1960 by Milton Shy and Glen Drager
and was then known as Shy–Drager syndrome.[2]

Many people affected by MSA experience Alpha-synuclein immunohistochemistry of the

dysfunction of the autonomic nervous system, which brain showing many glial inclusion bodies
commonly manifests as orthostatic hypotension, Specialty Neurology
impotence, loss of sweating, dry mouth and urinary
Symptoms Parkinsonism, xerostomia,
retention and incontinence. Palsy of the vocal cords
dysautonomia, ataxia
is an important and sometimes initial clinical
manifestation of the disorder. Complications Cardiac arrest, infections,
aspiration pneumonia
A prion of the alpha-synuclein protein within Usual onset 50–60 years
affected neurons may cause MSA.[3] About 55% of Duration Long term
MSA cases occur in men, with those affected first
Types MSA-P · MSA-C
showing symptoms at the age of 50–60 years.[4]
MSA often presents with some of the same Causes Unknown
symptoms as Parkinson's disease. However, those Diagnostic MRI, CT scan, autopsy
with MSA generally show little response to the method
dopamine agonists used to treat Parkinson's disease Treatment Physical therapy, hospice
and only about 9% of MSA patients with tremor care
exhibit a true parkinsonian pill-rolling tremor.[5]
Medication L-DOPA, fludrocortisone,
midodrine
MSA is distinct from multisystem proteinopathy, a
more common muscle-wasting syndrome. MSA is Prognosis Life expectancy 6–12 years
also different from multiple organ dysfunction after onset of symptoms
syndrome, sometimes referred to as multiple organ Frequency 5 per 100,000 people
failure, and from multiple organ system failures, an
often-fatal complication of septic shock and other severe illnesses or injuries.

Signs and symptoms

MSA is characterized by the following: Autonomic and at least one Motor (clinically
established MSA criteria 2022)[6][7]

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autonomic dysfunction: Post-void urinary residual volume ≥100 mL (usually by ultrasound);

Unexplained urinary urge incontinence; or Neurogenic orthostatic hypotension (≥20/10 mmHg
blood pressure drop) within 3 minutes (usually by head‐up tilt)
parkinsonism (muscle rigidity +/ tremor and slow movement: MSA-P)
cerebellar ataxia (Poor coordination/unsteady walking: MSA-C)
A variant with combined features of MSA and dementia with Lewy bodies may also exist.[8] There
have also been occasional instances of frontotemporal lobar degeneration associated with MSA.[9]

Initial presentation
The most common first sign of MSA is the appearance of an "akinetic-rigid syndrome" (i.e.
slowness of initiation of movement resembling Parkinson's disease) found in 62% at first
presentation. Other common signs at onset include problems with balance (cerebellar ataxia)
found in 22% at first presentation, followed by genito-urinary symptoms (9%): both men and
women often experience urgency, frequency, incomplete bladder emptying, or an inability to pass
urine (retention). About 1 in 5 MSA patients experience a fall in their first year of disease.[10]

For men, the first sign can be erectile dysfunction. Women have also reported reduced genital
sensitivity.[11]

Progression
As the disease progresses, one of three groups of symptoms predominates. These are:[12]

1. Parkinsonism - slow, stiff movement, writing becomes small and spidery[13][14]

2. Cerebellar dysfunction - difficulty coordinating movement and balance[15]
3. Autonomic nervous system dysfunction - impaired automatic body functions, including one,
some, or all of the following:[16]

postural or orthostatic hypotension, resulting in dizziness or fainting upon standing

up[17]
urinary incontinence or urinary retention[18][19][20]
impotence[21]
constipation[22]
vocal cord paralysis
dry mouth and skin
trouble regulating body temperature due to sweating deficiency in all parts of the
body
loud snoring, abnormal breathing or inspiratory stridor during sleep
other sleep disorders including sleep apnea, REM behavior disorder[23]
double vision[24]
muscle twitches[24]
Cognitive impairment[25]

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Genetics
One study found a correlation between the deletion of genes in a specific genetic region and the
development of MSA in a group of Japanese patients. The region in question includes the SHC2
gene which, in mice and rats, appears to have some function in the nervous system. The authors of
this study hypothesized that there may be a link between the deletion of the SHC2 and the
development of MSA.[26]

A follow-up study was unable to replicate this finding in American MSA patients.[27] The authors
of the study concluded that "Our results indicate that SHC2 gene deletions underlie few, if any,
cases of well-characterized MSA in the US population. This is in contrast to the Japanese
experience reported by Sasaki et al., likely reflecting heterogeneity of the disease in different
genetic backgrounds."

Another study investigated the frequency of RFC1 intronic repeat expansions, a phenomenon
implicated in CANVAS; a disease with a diagnostic overlap with MSA.[28][29] The study concluded
that these repeats were absent in pathologically confirmed MSA, suggesting an alternative genetic
cause.[28]

Pathophysiology
Multiple system atrophy can be explained as cell loss and gliosis or a proliferation of astrocytes in
damaged areas of the central nervous system. This damage forms a scar which is then termed a
glial scar.[30] The presence of inclusion bodies known as Papp–Lantos bodies, in the movement,
balance, and autonomic-control centres of the brain are the defining histopathologic hallmark of
MSA.[31]

The major filamentous component of Papp-Lantos bodies, glial and neuronal cytoplasmic
inclusions, is alpha-synuclein.[32] Mutations in this substance may play a role in the disease.[33]
The conformation of the alpha-synuclein is different from that of alpha-synuclein in Lewy
bodies.[3] The disease probably starts with an oligodendrogliopathy.[34] It has been proposed that
the α-synuclein inclusions found in Oligodendrocytes result from the pruning and the engulfment
of diseased axonal segments containing aggregated α-synuclein, i.e., of Lewy neurites [35]

Tau proteins have been found in some glial cytoplasmic inclusion bodies.[36]

Diagnosis

Clinical
Clinical diagnostic criteria were defined in 1998[37] and updated in 2007[38] and in 2022.[39]
Certain signs and symptoms of MSA also occur with other disorders, such as Parkinson's disease,
making the diagnosis more difficult.[40][41][42]

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Features characteristic of OPCA include progressive cerebellar ataxia, leading to clumsiness in

body movements, veering from midline when walking, wide-based stance, and falls without signs
of paralysis or weakness.[43][44] Clinical presentation can vary greatly between patients, but mostly
affects speech, balance and walking.[45] Other possible neurological problems include spasmodic
dysphonia, hypertonia, hyperreflexia, rigidity, dysarthria, dysphagia and neck dystonic posture.[44]
Dysarthria is characterized by increased pauses of irregular duration, impaired coordination of
vocal pitch, prolonged syllables and an overall irregular speech rhythm.[46] Diagnosis may be
based on a thorough medical exam; the presence of signs and symptoms; imaging studies; various
laboratory tests; and an evaluation of the family history.[47]

Radiologic
Both MRI and CT scanning may show a decrease in the size of
the cerebellum and pons in those with cerebellar features
(MSA-C). The putamen is hypointense on T2-weighted MRI
and may show an increased deposition of iron in the
Parkinsonian (MSA-P) form. In MSA-C, a "hot cross bun"
sign is sometimes found; it reflects atrophy of the
pontocerebellar tracts that give T2 hyper intense signal
intensity in the atrophic pons.

MRI changes are not required to diagnose the disease as these

features are often absent, especially early in the course of the
disease. Additionally, the changes can be quite subtle and are
usually missed by examiners who are not experienced with The "Hot Cross Bun" sign, found in
MSA. MSA with MRI

Pathologic
Pathological diagnosis can only be made at autopsy by finding abundant glial cytoplasmic
inclusions (GCIs) on histological specimens of the central nervous system.[48]

Olivopontocerebellar atrophy can be used as a pathological term to describe degeneration of

neurons in specific areas of the brain – the cerebellum, pons, and inferior olivary nucleus.[49]
OPCA is present in several neurodegenerative syndromes, including inherited and non-inherited
forms of ataxia (such as the hereditary spinocerebellar ataxia known as Machado–Joseph disease)
and MSA, with which it is primarily associated.[49]

Contrary to most other synucleinopathies, which develop α-synuclein inclusions primarily in

neuronal cell populations,[50] MSA presents with extensive pathological α-synuclein inclusions in
the cytosol of oligodendrocytes (glial cytoplasmic inclusions), with limited pathology in
neurons.[51] MSA also differs from other synucleinopathies in its regional pathological
presentation, with α-synuclein positive inclusions detected predominantly in the striatum,
midbrain, pons, medulla and cerebellum,[52][53] rather than the brainstem, limbic and cortical
regions typically effected in Lewy inclusion diseases.[53] However, recent studies using novel,
monoclonal antibodies specific for C-terminally truncated α-synuclein (αSynΔC) have now shown
that neuronal α-synuclein pathology is more abundant than previously thought.[54][55] One group
revealed robust α-synuclein pathology in the pontine nuclei and medullary inferior olivary nucleus
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upon histological analysis of neurological tissue from MSA patients.[54] Histopathological

investigation on six cases of pathologically confirmed MSA, using antibodies directed at a variety of
α-synuclein epitopes, revealed substantial variation in α-synuclein protein deposition across both
cases and brain regions within cases, providing evidence for 'strains' of aggregated conformers that
may differentially promote pathological prion-like spread.[56]

In 2020, researchers at The University of Texas Health Science Center at Houston concluded that
protein misfolding cyclic amplification could be used to distinguish between two progressive
neurodegenerative diseases, Parkinson's disease and multiple system atrophy, being the first
process to give an objective diagnosis of Multiple System Atrophy instead of just a differential
diagnosis.[57][58]

Classification
MSA is one of several neurodegenerative diseases known as synucleinopathies: they have in
common an abnormal accumulation of alpha-synuclein protein in various parts of the brain. Other
synucleinopathies include Parkinson's disease, the Lewy body dementias, and other more rare
conditions.[59]

Old terminology
Historically, many terms were used to refer to this
Olivopontocerebellar atrophy
disorder, based on the predominant systems
Other Multiple system atrophy –
presented. These terms were discontinued by
names cerebellar subtype[60]
consensus in 1996 and replaced with MSA and its
subtypes,[61] but awareness of these older terms and
their definitions is helpful to understanding the
relevant literature prior to 1996. These include
striatonigral degeneration (SND),
olivopontocerebellar atrophy (OPCA), and Shy–
Drager syndrome.[62] A table describing the
characteristics and modern names of these
conditions follows:

Sagittal section through right cerebellar

hemisphere. The right olive has also been cut
sagittally.
Specialty Neurology

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Historical Name Characteristics Modern name and abbreviation

Striatonigral predominating Parkinson's-like

MSA-P, "p" = parkinsonian subtype
degeneration symptoms

characterized by progressive ataxia

Sporadic (an inability to coordinate voluntary
olivopontocerebellar muscular movements) of the gait and MSA-C, "c" = cerebellar dysfunction subtype
atrophy (OPCA) arms and dysarthria (difficulty in
articulating words)
No modern equivalent – this terminology fell
out of favour[64] and was not specified in the
characterized by Parkinsonism plus a
Shy-Drager syndrome more pronounced failure of the 2007 consensus paper.[38] The earlier
autonomic nervous system.[63] consensus of 1998[37] referred to MSA-A, "a" =
autonomic dysfunction subtype but this subtype
is no longer used.

The term olivopontocerebellar atrophy was originally coined by Joseph Jules Dejerine and André
Thomas.[65][66] It was subdivided as:

Number OMIM Alt. name Inheritance

OPCA type 258300 (https://omim.org/entry/25 autosomal
2 8300) Fickler[67]-Winkler[68] type OPCA recessive

OPCA type 164700 (https://omim.org/entry/16 OPCA with dementia and extrapyramidal autosomal
5 4700) signs dominant

Non-hereditary diseases formerly categorized as olivopontocerebellar atrophy have were

reclassified as forms of MSA[69] as well as to four hereditary types, that have been currently
reclassified as four different forms of spinocerebellar ataxia:

SCA
Hereditary OPCA type OPCA name Gene OMIM
#

164400 (https://omim.org/entry/
OPCA type 1 "Menzel type OPCA" SCA1 ATXN1
164400)

OPCA type 2, autosomal 183090 (https://omim.org/entry/

"Holguin type OPCA" SCA2 ATXN2
dominant 183090)
"OPCA with retinal 164500 (https://omim.org/entry/
OPCA type 3 SCA7 ATXN7
degeneration" 164500)

"Schut-Haymaker type 164400 (https://omim.org/entry/

OPCA type 4 SCA1 ATXN1
OPCA" 164400)

Current terminology
The current terminology and diagnostic criteria for the disease were established at a 2007
conference of experts and set forth in a position paper.[38] This Second Consensus Statement
defines two categories of MSA, based on the predominant symptoms of the disease at the time of
evaluation. These are:

MSA with predominant parkinsonism (MSA-P) - defined as MSA where extrapyramidal features
predominate. It is sometimes termed striatonigral degeneration, a parkinsonian variant.
MSA with cerebellar features (MSA-C) - defined as MSA in which cerebellar ataxia
predominates. It is sometimes termed sporadic olivopontocerebellar atrophy.

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Management

Supervision
Ongoing care from a neurologist specializing in movement disorders is recommended, because the
complex symptoms of MSA are often not familiar to less-specialized neurologists.
Hospice/homecare services can be very useful as disability progresses.

Drug therapy
Levodopa (L-Dopa), a drug used in the treatment of Parkinson's disease, improves parkinsonian
symptoms in a small percentage of MSA patients. A recent trial reported that only 1.5% of MSA
patients experienced any improvement at all when taking levodopa, their improvement was less
than 50%, and even that improvement was a transient effect lasting less than one year. Poor
response to L-Dopa has been suggested as a possible element in the differential diagnosis of MSA
from Parkinson's disease.[70]

The drug riluzole is ineffective in treating MSA or PSP.[10]

Rehabilitation
Management by rehabilitation professionals including physiatrists, physiotherapists, occupational
therapists, speech therapists, and others for difficulties with walking/movement, daily tasks, and
speech problems is essential.

Physiotherapists can help to maintain the patient's mobility and will help to prevent
contractures.[30] Instructing patients in gait training will help to improve their mobility and
decrease their risk of falls.[71] A physiotherapist may also prescribe mobility aids such as a cane or
a walker to increase the patient's safety.[71]

Speech therapists may assist in assessing, treating and supporting speech (dysarthria) and
swallowing difficulties (dysphagia). Speech changes mean that alternative communication may be
needed, for example, communication aids or word charts.

Early intervention of swallowing difficulties is particularly useful to allow for discussion around
tube feeding further in the disease progression. At some point in the progression of the disease,
fluid and food modification may be implemented.

Avoidance of postural hypotension

One particularly serious problem, the drop in blood pressure upon standing up (with risk of
fainting and thus injury from falling), often responds to fludrocortisone, a synthetic
mineralocorticoid.[72][73] Another common drug treatment is the alpha-agonist midodrine.[72]

Non-drug treatments include "head-up tilt" (elevating the head of the whole bed by about 10
degrees), salt tablets or increasing salt in the diet, generous intake of fluids, and pressure (elastic)
stockings. Avoidance of triggers of low blood pressure, such as hot weather, alcohol, and
dehydration, are crucial.[73] The patient can be taught to move and transfer from sitting to

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standing slowly to decrease risk of falls and limit the effect of postural hypotension.[71] Instruction
in ankle pumping helps to return blood in the legs to the systemic circulation.[71] Other
preventative measures are raising the head of the bed by 8 in (20.3 cm), and the use of
compression stockings and abdominal binders.[6]

Supine hypertension
In addition to orthostatic hypotension, supine hypertension, where the BP is excessively high lying
down, is a frequent problem in multiple system atrophy. Treatment of one symptom can easily
aggravate the other, and supine hypertension in such patients has been linked to the same
cardiovascular complications as essential hypertension.[74]

Support
Social workers and occupational therapists can also help with coping with disability through the
provision of equipment and home adaptations, services for caregivers and access to healthcare
services, both for the person with MSA as well as family caregivers.

Prognosis
The average lifespan after the onset of symptoms in patients with MSA is 6–10 years.[4]
Approximately 60% of patients require a wheelchair within five years of onset of the motor
symptoms, and few patients survive beyond 12 years.[4] The disease progresses without remission
at a variable rate. Those who present at an older age, those with parkinsonian features, and those
with severe autonomic dysfunction have a poorer prognosis.[4] Those with predominantly
cerebellar features and those who display autonomic dysfunction later have a better prognosis.[4]

Causes of death
The most common causes of death are sudden death and death caused by infections, which include
urinary catheterization infections, feeding tube infections, and aspiration pneumonia. Some deaths
are caused by cachexia, also known as wasting syndrome.[75]

Epidemiology
Multiple system atrophy is estimated to affect approximately 5 per 100,000 people. At autopsy,
many patients diagnosed during life with Parkinson's disease are found actually to have MSA,
suggesting that the actual incidence of MSA is higher than that estimate.[4] While some suggest
that MSA affects slightly more men than women (1.3:1), others suggest that the two sexes are
equally likely to be affected.[4][6][30] The condition most commonly presents in persons aged 50–
60.[4]

Research
Mesenchymal stem cell therapy may delay the progression of neurological deficits in patients with
MSA-cerebellar type.[76]

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Notable cases
Nikolai Andrianov was a Soviet/Russian gymnast who held the record for men for the most
Olympic medals at 15 (7 gold medals, 5 silver medals, 3 bronze medals) until Michael Phelps
surpassed him at the 2008 Beijing Summer Olympics.[77]
Todd J. Campbell (1956–2021), United States district judge and counsel to former Vice
President Al Gore.[78]
Singer and songwriter Johnny Cash wrote in his autobiography that he was diagnosed with
Shy–Drager in 1997.[79]
Ronald Green (1944–2012), American-Israeli basketball player[80]
Joseph C. Howard Sr. (1922-2000) was the first African American to serve as a United States
district judge of the United States District Court for the District of Maryland.[81]
Kenneth More British actor, originally diagnosed with Parkinson's disease.
Chef Kerry Simon died from complications of MSA.[82]
David Colin Sherrington FRS (1945–2014), noted polymer chemist, who was diagnosed in
2012 and died from pneumonia two years later.
Karsten Heuer (1968-2024) Canadian Biologist, Conservationist, Filmmaker and Author.

See also
Olivopontocerebellar atrophy-deafness syndrome

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External links
Medical Textbook: "Multiple System Atrophy" (https://www.springer.com/medicine/neurology/bo
ok/978-3-7091-0686-0) edited by Gregor Wenning and Alessandra Fanciulli
Olivopontocerebellar atrophy (https://www.ninds.nih.gov/health-information/disorders/Olivopont
ocerebellar-Atrophy) at NINDS

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