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. Approximately 60% of patients require a wheelchair within five years of onset of the motor symptoms, and few patients survive beyond 12 years. 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. Those with predominantly cerebellar features and those who display autonomic dysfunction later have a better prognosis. 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. 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. 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. The condition most commonly presents in persons aged 50–60. Research
Mesenchymal stem cell therapy may delay the progression of neurological deficits in patients with MSA-cerebellar type.
Benedikt syndrome, also called Benedikts syndrome or paramedian midbrain syndrome, is a rare type of posterior circulation stroke of the brain, with a range of neurological symptoms affecting the midbrain, cerebellum and other related structures. Signs and symptoms
It is characterized by the presence of an  oculomotor nerve (CN III) palsy and cerebellar ataxia including tremor and involuntary choreoathetotic movements. Neuroanatomical structures affected include the oculomotor nucleus, red nucleus, corticospinal tracts and superior cerebellar peduncle decussation. It has a similar cause, morphology, signs and symptoms to Webers syndrome; the main difference between the two being that Webers is more associated with hemiplegia (i.e. paralysis), and Benedikts with hemiataxia (i.e. disturbed coordination of movements). It is also similar to Claudes syndrome, but is distinguishable in that Benedikts has more predominant tremor and choreoathetotic movements while Claudes is more marked by the ataxia. Causes
Benedikt syndrome is caused by a lesion (infarction, hemorrhage, tumor, or tuberculosis) in the tegmentum of the midbrain and cerebellum. Specifically, the median zone is impaired. It can result from occlusion of the posterior cerebral artery or paramedian penetrating branches of the basilar artery. Diagnosis
Oculomotor nerve palsy: eyeball gazing downward and outward position, diplopia, miosis, mydriasis, and loss of accommodation reflex. Contralateral loss of proprioception and vibration sensations. Cerebellar ataxia: involuntary movements. Treatment
Deep brain stimulation may provide relief from some symptoms of Benedikt syndrome, particularly the tremors associated with the disorder. See also
Claudes syndrome
Wallenberg syndrome

References


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