Once an MCC diagnosis is made, a sentinel lymph node biopsy as well as other imaging is recommended as a part of the staging work-up needed to determine prognosis and subsequent treatment options. Prevention
Sunlight exposure is thought to be one of the causes of Merkel cell carcinoma (MCC). The World Health Organization, American Academy of Dermatology, and Skin Cancer Foundation recommend the following measures to prevent excessive UV exposure and skin cancer:
Limiting sun exposure between the hours of 10am and 4pm, when UV rays are the strongest
Seeking shade when UV rays are most intense
Wearing sun-protective clothing including a wide brim hat, sunglasses, and tightly woven, loose-fitting clothing
Using sunscreen
Avoiding tanning beds and artificial UV exposure

Treatment
MCC is rare and expedient referral to radiation oncology is critical. MCC will quickly relapse following any attempted excisional biopsy. Surgery
The first step and primary goal of surgical treatment is to obtain negative histologic margins with 1-cm to 2-cm margins. Retrospective analyses of data from the National Comprehensive Database (NCDB) suggest no difference in the overall and relative survival of patients with stage I to II MCC who were treated with wide local excision versus MMS. Radiation
Radiation therapy is the primary management of Merkel cell carcinoma (MCC). The largest series we have are from Australia and have demonstrated that radiotherapy alone achieves equal outcomes with upfront or neoadjuvant surgery followed by radiation therapy. The role of surgery is largely historical and relegated to biopsy.
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 MSA. Pathologic
Pathological diagnosis can only be made at autopsy by finding abundant GCIs on histological specimens of the central nervous system.Contrary to most other synucleinopathies, which develop α-synuclein inclusions primarily in neuronal cell populations, MSA presents with extensive pathological α-synuclein inclusions in the cytosol of oligodendrocytes (glial cytoplasmic inclusions), with limited pathology in neurons. 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, rather than the brainstem, limbic and cortical regions typically effected in Lewy inclusion diseases. 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. One group revealed robust α-synuclein pathology in the pontine nuclei and medullary inferior olivary nucleus upon histological analysis of neurological tissue from MSA patients.