A Case of Probable Parkinson Disease After COVID-19
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- This is a case presentation of a patient who developed acute-onset parkinsonism following SARS-CoV-2 infection. The patient had no history of Parkinson disease, parkinsonism, or known premotor findings, and did not have known major genetic or environmental risk factors. Approximately 2 months after COVID-19 onset, he displayed relatively severe parkinsonism, which was bradykinetic-rigid dominant, and 18F-fluorodopa PET scanning showed asymmetric reduction in uptake in both putamina.
- Although this is, for now, an isolated case, it is important for the community to be aware of and vigilant about this possibility of postinfectious parkinsonism.
– Codrin I. Lungu, MD
abstract
This abstract is available on the publisher's site.
Access this abstract now Full Text Available for ClinicalKey SubscribersParkinson's disease or parkinsonism have been described after infections by viruses, such as influenza A, Epstein-Barr virus, varicella zoster, hepatitis C virus, HIV, Japanese encephalitis virus, or West Nile virus. We report a patient with probable Parkinson's disease, who was diagnosed after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
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A Case of Probable Parkinson's Disease After SARS-Cov-2 Infection
Lancet Neurol 2020 Oct 01;19(10)804-805, ME Cohen, R Eichel, B Steiner-Birmanns, A Janah, M Ioshpa, R Bar-Shalom, JJ Paul, H Gaber, V Skrahina, NM Bornstein, G YahalomFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
COVID-19 Related Parkinson’s Disease: True-True-Unrelated?
COVID-19 has been associated with a variety of acute neurological complications, including anosmia, headaches, myalgia/myositis, encephalopathy, stroke, meningitis/encephalitis, seizures, peripheral neuropathy, and post-viral chronic neurological manifestations, such as disseminated encephalomyelitis, necrotizing hemorrhagic encephalopathy, transverse myelitis, Guillain-Barré syndrome, multisystem inflammatory syndrome (Kawasaki’s disease), dysautonomia, and chronic fatigue syndrome.1-3 In some patients, referred to as “long-haulers,” symptoms (such as low-grade fever, clouding of mentation, sleep disturbances, and various other somatic symptoms) persist for months.4 Encephalitis lethargica and postencephalitic parkinsonism, such as that reported after the 1916–1919 pandemic,5 has not yet been reported.
Cohen et al6 recently described a 45-year-old Ashkenazi Jewish man who noticed loss of smell followed by cough and myalgias after returning to Israel from the USA. He was diagnosed with COVID-19, and, while in the hospital, he experienced fatigue, shortness of breath, and chest pain but no fever. After a 3-day hospitalization, he was isolated for 3 weeks. During that time, he apparently first noticed micrographia, dysarthria, hand incoordination, and right-hand tremor. On examination, about 2 months after he initially tested positive for SARS-CoV-2, he was noted to have hypomimia, hypophonia, cogwheel rigidity in the left arm, bradykinesia in the right extremities, slow gait, and absent right arm swing. There was no cognitive decline, and his gait and balance were apparently normal. His laboratory tests, including an autoimmune and genetic panel, MRI, and EEG, were essentially normal. F-DOPA PET scan, however, showed decreased uptake in the left more than right putamen. He improved with 0.375 mg of extended-release pramipexol. Because of tremor in the right more than left leg, biperiden was added and increased to 4 mg per day with marked improvement in the tremor.
Although his genetic tests, including next-generation sequencing, were negative, the authors suggested that “a susceptible genetic makeup” made the patient vulnerable to some immunologic or mitochondrial injury. They proposed other hypotheses but do not mention the possibility of a prodromal (presymptomatic) Parkinson’s disease (PD) that became symptomatic as a result of stress related to the COVID-19.7 This explanation is supported by the normal MRI, which is typically abnormal in postencephalitic parkinsonism. Furthermore, the abnormal F-DOPA PET scan, which is consistent with moderate nigrostriatal damage, would be an unlikely finding a few days from the reported onset of COVID-19 symptoms to the onset of parkinsonian manifestations, and is more consistent with idiopathic PD. Although it is possible, indeed likely, that the patient’s PD-like disorder is not related to his COVID-19, it is critical to continue screening the survivors of COVID-19 for emerging symptoms of parkinsonism. We recently published a new screening instrument that may be well-suited for this purpose.8 Finally, patients with an established diagnosis of PD should be carefully monitored when they become affected with COVID-19 as they have a significantly higher risk of dying from COVID-19 compared with patients without PD.9
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