Contents 1 Pinyin 2 English reference 3 Overview 4 Disease name 5 English name 6 Alias ??of multiple system atrophy 7 Classification 8 ICD number 9 Epidemiology 10 Cause 11 Pathogenesis 11.1 In the cytoplasm of oligodendrocytes Inclusion bodies 11.2 Neuronal apoptosis 11.3 Abnormal enzyme metabolism 11.4 Pathological changes 11.4.1 Nigrostriatal and locus coeruleus lesions 11.4.2 Pontine nucleus and cerebellar Purkinje cell lesions 11.4.3 Autonomic neuropathy 11.4.4 Oligodendrocytes Intracytoplasmic inclusions in plasma cells 12 Clinical manifestations of multiple system atrophy 13 Complications of multiple system atrophy 14 Laboratory examinations 14.1 Upright test 14.2 Blood biochemical examination 14.3 Cerebrospinal fluid examination 15 Auxiliary examination 15.1 Electromyography examination 15.2 Electroencephalography examination 15.3 Nerve Psychological examination 15.4 Imaging examination 16 Diagnosis 16.1 Clinical features 16.2 Diagnostic criteria 17 Differential diagnosis 17.1 Orthostatic hypotension 17.2 Parkinson's disease 17.3 Others 18 Treatment of multiple system atrophy 18.1 Treatment of orthostatic hypotension 18.1.1 Physical therapy 18.1.2 Drugs Treatment 18.1.3 Pacemaker 18.1.4 Water intake 18.2 Treatment of Parkinson's syndrome 18.3 Symptomatic treatment 18.4 Others 19 Prognosis 20 Prevention of multiple system atrophy 21 Related drugs 22 Related examinations 1 Pinyin
duō xì tǒng wěi suō 2 English reference
MSA
multiple system atrophy 3 Overview
Multiple system atrophy (MSA) was proposed by Graham and Oppenheimer in 1969 A group of sporadic adult-onset progressive neurodegenerative diseases of unknown origin that were first named in 2001 and mainly involve the extrapyramidal system, cerebellum, autonomic nervous system, brainstem and spinal cord.
This syndrome involves multiple systems, including the striatum nigral system, olivopontocerebellar system, spinal autonomic nervous center and even the anterior horn of the spinal cord, lateral cords and peripheral nervous system. Clinically, it manifests as parkinsonism, different combinations of cerebellar, autonomic nervous system, pyramidal tract and other dysfunctions, so it can be clinically classified into three syndromes: striatonigral degeneration, which mainly manifests as extrapyramidal system dysfunction. (SND), ShyDrager syndrome (SDS), which mainly manifests as autonomic nervous dysfunction, and sporadic olivopontocerebellar atrophy (OPCA), which mainly manifests as ataxia.
In fact, it is often difficult to clearly distinguish between these diseases. Graham and Oppenheimer summarized cases with similar clinical symptoms and signs in the literature and proposed that these three syndromes are separate descriptions and names of independent degenerative diseases of the nervous system by different authors. They only differ in the location and severity of involvement. The clinical difference is that symptoms of a certain system appear earlier or are severely affected, while symptoms of other systems appear later or are relatively mildly affected.
Neuropathological examination results confirmed that the degree of involvement of each system was completely consistent with the characteristics of clinical manifestations. Currently, in the MEDLINE database, sporadic OPCA, SDS, and SND are classified in MSA.
The age of onset of multiple system atrophy is mostly in middle age or early old age (32 to 74 years old), 90% of which are between 40 and 64 years old, which is significantly earlier than idiopathic Parkinson's disease, and the course of the disease is 3 to 9 years. ? years, there is no specific treatment, generally supportive and symptomatic treatment. 4 Disease name
Multiple system atrophy 5 English name
multiple system atrophy 6 Alias ??of multiple system atrophy
Multiple system atrophy 7 Classification
< p> Neurology> Nervous system degenerative diseases 8 ICD numberG31.8 9 Epidemiology
At present, no authoritative and comprehensive incidence statistics have been found. However, experts believe that the incidence and prevalence of the disease in my country are low.
The age of onset of MSA is mostly in middle age or early old age (32 to 74 years old), and 90% of them are between 40 and 64 years old, which is significantly earlier than idiopathic Parkinson's disease, and the course of the disease is 3 to 9 years. 10 Causes
The cause of multiple system atrophy is unknown. Currently involved are lipid peroxidative damage, abnormal enzyme metabolism, lentiviral infection, neuronal apoptosis, oligodendrocyte intracytoplasmic inclusions, etc., resulting in progressive multi-system degeneration of the nervous system. 11 Pathogenesis 11.1 Oligodendrocyte intracytoplasmic inclusions
Oligodendrocyte intracytoplasmic inclusions (oligodendroglial cytoplasmic inclusions) are the histological characteristics of MSA. Plasma cells play an important role in pathogenesis. In the past, it was believed that among the pathological changes in MSA, neuron degeneration and loss were primary and were the basis of pathological changes, while demyelination was secondary. Since the discovery of oligodendrocyte intracytoplasmic inclusions, some authors have put forward new perspectives on the pathogenesis of MSA, believing that oligodendrocytes play an equally important role in the pathogenesis of neuronal degeneration. The reason is Silver staining and immunohistochemistry showed that abnormal intracellular changes in oligodendrocytes were more obvious and characteristic than changes in neurons themselves. The distribution location and density of intracytoplasmic inclusions in oligodendrocytes observed by Nakazato Yoichi et al. are consistent with the severity of disease degeneration. However, some authors believe that the number of inclusions in the cytoplasm of oligodendrocytes has no significant correlation with the severity of MSA lesions. Papp et al. observed that areas with higher density of oligodendrocytes are in the primary motor cortex, pyramidal and extrapyramidal systems, corticocerebellar projection fibers, and autonomic nervous network centers in the brainstem. The main function of oligodendrocytes is to maintain the integrity of the myelin sheath of myelinated fibers. When the structure of oligodendrocytes is abnormal, its function will inevitably be affected, which may be an important cause of myelin loss. 11.2 Neuronal apoptosis
Some people believe that its pathogenesis is related to neuronal apoptosis. There are two types of neuronal death in the nervous system: necrosis and apoptosis. When apoptosis occurs, the integrity of the cell membrane is maintained, and the only manifestations are that the cell size becomes smaller, the structure and shape of organelles are present, lysosomal components are preserved, nuclear chromatin is condensed, and endogenous DNA endonuclease is activated, which degrades DNA to produce DNA. fragments and apoptotic bodies. 11.3 Abnormal enzyme metabolism
See olivopontocerebellar atrophy. 11.4 Pathological changes
Gross specimens show atrophy and thinning of the cerebellum, brainstem and spinal cord; under the microscope, there is degeneration and loss of nerve cells in the above-mentioned specific parts, gliosis and demyelination of myelinated fibers. The main locations of pathological changes are the transverse pontine fibers, the basal pontine nucleus, the inferior olivary nucleus of the medulla oblongata, the dorsal nucleus of the vagus nerve, the locus coeruleus, the middle and inferior cerebellar peduncles, the dentate nucleus and hemispheres of the cerebellum, and the globus pallidus of the substantia nigra and basal nucleus of the midbrain. Neuron loss and gliosis in the caudate nucleus, putamen, mediolateral column cells, anterior horn cells and other parts of the spinal cord; degeneration of the corticospinal tract and loss of sheaths. Peripheral nerves are mainly demyelinating lesions. 11.4.1 (1) Nigrostriatal and locus coeruleus lesions
are the main causes of Parkinson's disease in patients. Neuron loss is mainly in the outer 1/3 of the substantia nigra zone compacta. The pigment cells disappear; the neurons in the striatum are reduced early, with the dorsal 2/3 of the putamen being the most severe; the globus pallidus is extensively involved, and the locus coeruleus neurons are reduced; the above pathological changes are completely consistent with idiopathic Parkinson's disease. consistent. 11.4.2 (2) Purkinje cell lesions of the pontine nucleus and cerebellum
OPCA is the most prominent clinical symptom. The areas with significant neuronal loss include the pontine nucleus, cerebellar Purkinje cells, and inferior olivary nucleus. The middle cerebellar peduncle is more obviously affected, but the cerebellar granule cells, dentate nucleus, and superior cerebellar peduncle usually have no obvious changes. 11.4.3 (3) Autonomic neuropathy
The pathological changes of autonomic nervous failure are mainly located in the mediolateral cell columns of the spinal cord and the dorsal nucleus of the vagus nerve. The lesions involve both the sympathetic and parasympathetic systems. Other cells affected are monoaminergic neurons and cells of the arcuate nucleus in the ventrolateral reticular formation of the brainstem. Onuf’s nuclei in the ventral anterior horn cells of the sacral segments 2 and 3 of the spinal cord, which regulate the autonomic nerve centers of the bladder and rectal sphincter, are also significantly damaged. Mild neuronal loss is seen in the hypothalamus. 11.4.4 (4) Oligodendrocyte intracytoplasmic inclusions
The most common and characteristic pathological changes are the presence of intracytoplasmic inclusions in white matter using Gallyas staining, immunohistochemical staining or modified Bielschowsky silver staining. Widespread oligodendrocyte intracytoplasmic inclusions, also known as "oligodendroglial tanglelike inclusions" or "glial cytoplasmic inclusions" ** *ic inclusion (GCI)", "oligodendrocyte microtubular tangle (oligodendroglial microtubular tangle)".
Predominantly found as a half-moon/sickle shape around the small round nucleus, or as a flame-argyrophilic structure immediately adjacent to the nucleus, these structures are primarily composed of altered microtubules. Under an electron microscope, such inclusions are 10 to 25 nm in diameter and are a network structure composed of fine granular materials. They are mainly distributed in the white matter of the brainstem, basal ganglia, cerebellum and cerebral cortex. Their number varies from person to person. Polyacrylamide gel electrophoresis can separate a variety of protein bands from the cytoplasmic inclusions in oligodendrocytes, which mainly contain α-synuclein, αB crystallin, and tubulin. tubulin) and ubiquitin. These proteins are all cytoskeletal proteins. Some authors believe that intracytoplasmic inclusions in oligodendrocytes may represent synchronized degeneration of neurons, or may be a phenomenon before neuronal degeneration, and can be used as a special pathological sign for the diagnosis of MSA, because these inclusions are seen in pathologically confirmed cases. Almost all MSA patients were not present in the control group. These structures support the concept that OPCA, SDS, and SND are variants of the same disease process. Most reports currently suggest that oligodendrocyte intracytoplasmic inclusions are only found in the white matter of the brain and spinal cord in sporadic MSA cases, but not in the central nervous system white matter of simple or hereditary spinocerebellar degeneration. This pathological feature is helpful for distinguishing MSA from hereditary spinocerebellar degenerative diseases. Some authors also believe that oligodendrocyte intracytoplasmic inclusions, like inclusions in other neurological degenerative diseases, are neurobiological changes related to α-synuclein gene mutations that lead to changes in the coding and structure of α-synuclein. Chemically abnormal synucleinopathies.
Pathological diagnosis of MSA requires at least three lesions including the putamen and substantia nigra. The pathological changes of SDS, SND and OPCA often overlap with each other. For example, SDS cases show obvious loss of lateral horn cells in the spinal cord, but the latter is not completely consistent with clinical autonomic nervous system dysfunction, and some cases of OPCA also have the same damage. The characteristic pathological manifestations of SND are loss of putamen neurons, deposition of haematin and lipofuscin, and degeneration of the substantia nigra. The basic lesions of OPCA are atrophy of the cerebellar cortex, pons, and inferior olivary nucleus, reduction of neurons and transverse fibers, and severe neuronal loss and significant gliosis in the olivary nucleus. Cerebellar Purkinje cells are lost and the granular layer is thinned, especially in the vermis.
Mcleod and Ben et al. reported that the pathological changes in peripheral nerves include a decrease in myelinated fibers, axonal degeneration in the dorsal root ganglion, and no changes in unmyelinated fibers. However, Guo Yupu et al. performed sural nerve biopsy on 7 patients with MSA combined with peripheral neuropathy, which showed mild to moderate loss of myelinated fibers. The morphological findings were mainly myelinated and thin myelin sheaths, and there were also hypertrophic nerve changes and regenerated fibers. No axonal degeneration was seen. Under the electron microscope, some cases of unmyelinated fibers decreased, but Schwann cells and collagen fibers proliferated, and collagen capsules were formed, which was consistent with chronic demyelinated lesions. No evidence of primary degeneration of posterior root ganglion cells in MSA could be demonstrated. 12 Clinical manifestations of multiple system atrophy
The age of onset of MSA is mostly in middle age or early old age (32 to 74 years old), and 90% of them are significantly earlier than idiopathic Parkinson's disease between the ages of 40 and 64. 3 to 9 years.
There are three main clinical symptoms: cerebellar symptoms, extrapyramidal symptoms, and autonomic nervous system symptoms. 89% of them developed Parkinson's syndrome; 78% developed autonomic nervous system failure; 50% developed cerebellar ataxia. The most common combinations are parkinsonism and autonomic failure or cerebellar dystaxia and autonomic failure. In addition, a considerable number of patients may have pyramidal tract signs, brainstem damage (extraocular muscle paralysis), cognitive dysfunction, etc.
The clinical characteristics are:
1. Insidious onset, slow progression, and gradual aggravation.
2. From a single system to multiple systems, each group of symptoms may appear one after another, overlapping and combining with each other.
SND and OPCA are easier to evolve into MSA. Xu Xiaoxiang reported that clinical symptoms of invasion of other parts of the nervous system appeared on average 3 years after the onset of the first symptoms. Comparing the degree of damage: autonomic symptoms SDS>OPCA>SND, cerebellar symptoms OPCA>SDS>SND, extrapyramidal symptoms SND>SDS >OPCA, pyramidal tract sign SND≥SDS>OPCA, brainstem damage OPCA>SDS.
3. Clinical manifestations are separated from pathological findings. Pathological findings often involve a wider range of lesions than clinical findings. In addition to complex compensatory mechanisms, this separation phenomenon may also be related to clinical examination. Roughness or clinical manifestations lag behind pathological damage.
In a group of 188 pathologically confirmed MSA patients, 28% of the patients had four signs of the cerebellum, extrapyramidal system, autonomic nervous system and pyramidal system at the same time; another 29% of the patients also had Parkinson's syndrome. There are three signs: signs, signs of impaired autonomic nervous function, and cerebellar signs or pyramidal tract signs; 11% of patients have parkinsonian syndrome and signs of impaired autonomic nerve function; 10% of patients only show parkinsonian syndrome.
Sakakibara conducted a questionnaire survey on 121 MSA patients (48 OPCA, 17 SND, 56 SDS). The results showed that urinary system symptoms (96%) in MSA patients were significantly more common than orthostatic hypotension symptoms ( 43%) (P<0.01), especially OPCA and SND. 53 patients had both urinary and orthostatic hypotension symptoms. 48% had urinary system symptoms as the first symptom, which was more common than orthostatic hypotension as the first symptom (29%). 23% of patients had both symptoms at the same time. The authors concluded that urinary system dysfunction is more common in MSA patients than orthostatic hypotension and often appears earlier. 13 Complications of Multiple System Atrophy
Common complications in MSA patients include syncope, concurrent head or systemic trauma, depression, mental and behavioral abnormalities, varying degrees of dementia, and seborrheic dermatitis.
In addition, attention should be paid to secondary lung infections, urinary tract infections, etc. 14 Laboratory examinations 14.1 Upright test
Measure blood pressure in supine, sitting and upright positions respectively. If the blood pressure drops within 2 to 3 minutes of standing, the systolic blood pressure is more than 30mmHg, the diastolic blood pressure is more than 20mmHg, but the heart rate does not change. is positive. 14.2 Blood biochemical examination
The plasma noradrenaline norepinephrine content and the 24-hour urine catecholamine content were significantly reduced. 14.3 Cerebrospinal fluid examination
Except for individual reports of reduced acetylcholinesterase in the cerebrospinal fluid, the cerebrospinal fluid of most patients is normal. 15 Auxiliary examination 15.1 Electromyography examination
Fibrillation potential may appear in the muscles being examined. 15.2 Electroencephalogram examination
The background is mostly slow wave rhythm. 15.3 Neuropsychological examination
Mild cognitive impairment, depression and anxiety factor scores were increased. 15.4 Imaging examination
Head CT and MRI examination showed atrophy of the pons and cerebellum. It manifests as atrophy of the cerebellar vermis, hemispheres and the whole cerebellum, and the cerebellar sulci become deeper and more numerous. The superior cerebellar cistern, cerebellopontine angle cistern, cerebellomedullary cistern, and cerebellar subarachnoid space were all enlarged. The midbrain atrophies, the cerebral peduncles become thinner, the quadrigeminal cisterns, circumferential cisterns and basal cisterns enlarge, the pons and middle cerebellar peduncles atrophy, and the fourth ventricle enlarges. In severe cases, there may be extensive brain atrophy changes such as bilateral lateral ventricle and third ventricle enlargement, lateral sulcus widening, and cerebral hemisphere atrophy such as the frontal and parietal lobes.
Brain MRI is the most valuable diagnostic method. Pathological iron deposition is often found on MRI T2-weighted images, which is manifested by decreased signal in the posterolateral side of the bilateral putamen and narrowing of the normal high-signal area between the red nucleus and substantia nigra. These changes are seen in all pathologically confirmed MSA patients. These changes can be present long before a patient's symptoms appear. Patients with Parkinson's disease do not have these changes. In addition, T1-weighted images show reduced signal in the atrophic putamen and atrophy of the cerebellum and brainstem.
PET shows that the basal metabolic rate is reduced in the frontal lobe, striatum, cerebellum and brainstem, and the uptake of fluorodopa in the striatum is reduced; the uptake of 123I3 iodine 6 methoxy in the striatum Formamide (123IIIBZM) reduces. 16 Diagnosis
Due to the low incidence and prevalence of the disease, the clinical manifestations of involvement of different parts of the nervous system are the first symptoms in the course of the disease, and damage to one system is often the most prominent manifestation, while damage to other systems is often the most prominent symptom. The clinical symptoms of systemic damage are relatively mild or do not appear until late, making early clinical diagnosis difficult.
In 1999, Gilman et al. of the University of Michigan proposed 4 groups of clinical characteristics and diagnostic criteria for MSA 16.1 Clinical characteristics
(1) Autonomic nervous system failure and/or urinary function obstacle.
(2) Parkinson’s syndrome.
(3) Cerebellar dystaxia.
(4) Corticospinal dysfunction. 16.2 Diagnostic criteria
(1) Possible MSA: 1st clinical feature plus 2 other features.
(2) Probable MSA: 1 clinical feature plus parkinsonism or cerebellar dystaxia with poor response to dopamine.
(3) Confirmed MSA: Confirmed by neuropathological examination. 17 Differential diagnosis
If it overlaps with other degenerative diseases, pay attention to the differential diagnosis. 17.1 Orthostatic hypotension
When the human body is in an upright posture, due to dysfunction of the nervous or cardiovascular system that regulates and maintains normal blood pressure, the blood pressure cannot change accordingly with the posture. hypotensive state. Clinical features: Blood pressure suddenly drops to greater than 15mmHg within 7 minutes after standing upright, accompanied by symptoms of insufficient blood supply to the brain. The incidence of orthostatic hypotension is 4% in the general population and 33% in elderly patients.
Mainly divided into: idiopathic (combined with autonomic nervous system symptoms); secondary (secondary to various neurological diseases); and *** adjustment disorder (vasoinhibitory syncope), general There is no associated bladder and rectal dysfunction. 17.2 Parkinson's disease
Based on past autopsy results, 5.1% to 11% of patients clinically diagnosed with primary Parkinson's disease were confirmed to have MSA at autopsy. In 1995, Wenning reported that among 370 brain specimens with clinical manifestations of Parkinson's syndrome in the UK Parkinson's Disease Brain Bank, 35 cases (9.5%) were consistent with the pathological diagnosis of MSA after neuropathological examination. The average age of onset of these patients was 55. Years old, all showed parkinsonism syndrome during their lifetime; 97% of those with autonomic nervous system involvement; 34% of those with cerebellar ataxia; 54% of those with pyramidal tract signs; the average survival was 7.3 years (2.1 to 11.5 years) ). It is suggested that among patients clinically diagnosed with idiopathic Parkinson's disease, nearly 10% of patients have pathological examination results confirmed to meet the diagnostic criteria of MSA. 17.3 Others
Also pay attention to the differentiation from familial OPCA, progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, etc. 18 Treatment of multiple system atrophy
There is no specific treatment for multiple system atrophy. Supportive and symptomatic treatment is generally used. 18.1 Treatment of orthostatic hypotension 18.1.1 Physical therapy
Among various measures, physical therapy should be used first, because these therapies are simple and practical and can often control symptoms. For example, the head should be kept in the recumbent position. The body and trunk are 15° to 20° higher than the lower limbs. Tights and elastic stockings are often worn, and daily tilt exercise is performed. 18.1.2 Drug treatment
There is currently no specific drug. Patients should be supplemented with sodium chloride (2 to 4 g/d) to increase plasma volume and increase salt and water retention as needed.
The peripheral α1-adrenoceptor agonist midodrine (midodrine hydrochloride) is an effective drug that can increase peripheral vascular resistance and increase systolic blood pressure in patients with orthostatic hypotension , improve dizziness and orthostatic hypotension caused by insufficient circulating blood volume; 2.5 mg can be given orally, twice a day; it has good physiological tolerance. The main adverse reactions are slowed heart rate, piloerection reaction, urinary retention and increased blood pressure in the recumbent position.
Fludrocortisone (9α fludrocortisone), 0.1mg per day for the first few days, gradually increased to 0.3mg ~ 1.0mg, according to changes in blood pressure and plasma volume Change to adjust dosage. Patients should be carefully monitored to avoid water retention and elevated blood pressure. L-Threo-3,4-dihydrophenylserine (DOPS) may also be effective in orthostatic hypotension.
Diamond et al. gave tyramine-rich foods (such as dry yeast 9-18g/d and beer 500ml/d) and oral monoamine oxidase inhibitors (such as isoniazid, 0.6g/d , oral or intravenous infusion; or furazolidone 0.3g/d), promotes the release of norepinephrine from the sympathetic nerve terminals and inhibits the reabsorption of sympathetic nerve terminals to treat this disease.
In recent years, treatment with Xamoterol has reduced episodes of orthostatic hypotension by 67% and can especially increase diastolic blood pressure. It is worth a try. Medications such as indomethacin (indomethacin) and beta-adrenergic blockers such as propranolol (propranolol) may also be tried. 18.1.3 Pacemaker
Installing a pacemaker can increase blood pressure appropriately if the heart rate is adjusted to greater than 100 beats/min. 18.1.4 Water intake
Recent studies believe that water intake can effectively constrict blood vessels and increase blood pressure, which cannot be explained by currently understood physiological and pathophysiological mechanisms. In some patients, water intake can increase blood pressure by 50% and is more effective than existing vasoconstrictor drugs. By carefully combining the vasoconstrictive effects of water with the inhibitory effects of sugar-rich foods, many MSA patients can now control their blood pressure without the interference of medications (Robertson, 2001). 18.2 Treatment of Parkinson’s syndrome
Dopamine replacement therapy, monoamine oxidase B inhibitors or dopamine receptor agonists can be given, but most patients do not respond well, or the effect can only be maintained for a short period of time. . Human body surface area calculator BMI index calculation and evaluation Female safe period calculator Pregnancy date calculator Normal weight gain during pregnancy Safety classification of medication during pregnancy (FDA) Five elements and eight characters Adult blood pressure evaluation Body temperature level evaluation Diabetes diet recommendations Clinical biochemistry common units conversion basal metabolic rate Calculate sodium supplementation calculator Iron supplementation calculator Commonly used Latin abbreviations for prescription Quick check Common symbols for pharmacokinetics Quick check Effective plasma osmolality calculator Ethanol intake calculator
Medical encyclopedia, calculate now! 18.3 Symptomatic treatment
Control infection; for patients with symptoms such as nocturnal apnea, try to improve ventilation, and tracheotomy surgery is possible for severe patients.
18.4 Others
Vitamin E, adenosine triphosphate (ATP), citicoline (citicoline), physostigmine, etc. may relieve symptoms. 19 Prognosis
As of 1995, there were 300 cases of MSA patients confirmed by neuropathological examination in foreign literature, of which 200 had a survival time of 5 to 6 years, with the longest survival being 10 years.
1. It is often complicated by syncope and head or body trauma, depression, mental and behavioral abnormalities, varying degrees of dementia and seborrheic dermatitis.
2. During the course of the disease, Parkinson's syndrome causes limitations in limb movement and the inability to take care of oneself in daily life.
3. Late-stage patients develop aspiration or aspiration pneumonia due to laryngeal muscle paralysis causing choking on drinking water and difficulty swallowing. Those who have been bedridden for a long time are complicated by bedsores, lung infections and urinary system infections.
4. In the late stage of the disease, sleep apnea, stridor at night, and cyanosis and respiratory obstruction may occur at any time due to paralysis of throat muscles. Sudden central breathing, cardiac arrest, or chronic central breathing may also occur. Exhaustion affects life.
5. Arrhythmia or cardiac arrest occurred due to cardiovascular dysfunction, and all patients died due to comorbidities or accidents. 20 Prevention of multiple system atrophy
There is no effective prevention method for multiple system atrophy, and symptomatic treatment is an important part of clinical medical care.
21 Related drugs
Oxygen, collagen, norepinephrine, epinephrine, dopamine, sodium chloride, midodrine, fludrocortisone, cortisone, dry yeast, isoniazid, furazolidone , Zamotero, indomethacin, propranolol, vitamin E, adenosine, citicoline, physostigmine 22 related examinations