A 72-year-old woman with a history of hypertension, hyperlipidemia, smoking, and depression presented on early April 2020 with delirium and fever. A cranial CT scan was normal. A chest X-ray showed bilateral interstitial pneumonia, and nasopharyngeal exudate polymerase chain reaction (PCR) testing was positive to SARS-CoV-2. Cerebrospinal fluid (CSF) was normal. She was admitted and started on hydroxychloroquine, azithromycin, ceftriaxone, and IV methylprednisolone. A few days later she was transferred to the intensive care unit due to a cardiogenic shock caused by a myocardial infarction. Further hemodynamic and respiratory evolution was good, and she was discharged without delirium or cognitive impairment on day 22 after admission. She was readmitted eight days later due to a 48-h history of dizziness, oscillopsia, and unsteadiness. Her vital signs were normal, and she was afebrile. Systemic examination was unremarkable. She was conscious, and her language and speech were normal, but slight inattention and disorientation were present. A downbeat nystagmus in all gaze positions and impairment of smooth pursuit eye movements were present. Horizontal and vertical eye movements showed no limitation. Motor and sensory examinations were normal, and deep tendon reflexes were all present and symmetrical. The left plantar response was extensor. There was no limb dysmetria, but severe truncal ataxia was present. Reflex
The frequency of five cytochrome P450IID6 allelic variants was studied in deoxyribonucleic acid from 123 patients with Parkinson's disease and 150 healthy volunteers. This was achieved by the use of mutation-specific polymerase chain reaction and restriction fragment length polymorphism. The analyses of the CYP2D6 genotype revealed no evidence for a higher prevalence of poor metabolizers among patients with Parkinson's disease. However, increased frequency of patients with Parkinson's disease with the genotype CYP2D6wt/CYP2D6B was observed. This is attributable exclusively to subjects with early onset of the disease (28 to 49 years), with a relative risk ratio of 4.16 (95% confidence limits, 2.0 to 8.3; p < 0.0005). The subjects who had late-onset Parkinson's disease (> or = 50 years) had genotypes and CYP2D6 allele frequencies similar to the healthy subjects. This indicates that the oxidative polymorphism is related to early-onset but not to late-onset Parkinson's disease. A different influence of CYP2D6 genotype on the risk of development of Parkinson's disease is observed in Spaniards, compared with previous findings in British subjects. These results suggest the combined effect of environmental toxins and CYP2D6 in the cause of Parkinson's disease.
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