3. Results
Of the thirty-six cases identified with COVID-19 (Table 1), twenty-three (64%) were men and thirteen (36%) were women. The median age was 74.5 (range 33 to 90 years old), with majority (89%) being over 60 years old. The patients in this cohort carried the following diagnoses (n; %): idiopathic Parkinson disease without dementia (n = 8; 22%), idiopathic Parkinson disease with dementia (n = 14, 39%), atypical parkinsonism (n = 7; 19%), vascular parkinsonism (n = 1; 3%), Tourette syndrome (n = 2; 5%), neurodegeneration with brain iron accumulation type 5 (n = 1; 3%), multifactorial gait disorder (n = 1; 3%), essential tremor (n = 1; 3%), and post-COVID-19 cerebellar ataxia (n = 1; 3%).
This last patient (patient 21) did not have a prior diagnosis of a movement disorder, but rather was referred to our program for new-onset cerebellar ataxia. He presented one month prior to our evaluation, with fever, cough, shortness of breath, and fatigue, but was not tested for COVID-19 at that time. His wife developed similar symptoms two days later, and she tested positive for SARS-CoV-2. He recovered after 11 days and returned to work. About a week later, he developed symptoms of cerebellar dysfunction, including disabling tremors, gait instability, dysarthria, and vertigo. He also complained of mild short-term memory impairment. On presentation to our center, he had notable gait and left upper extremity ataxia, but vertigo had resolved, and tremors were mild. He tested positive on both the rt-PCR and antibody testing for SARS-CoV-2. Electrophysiologic testing was negative for evidence of an acute inflammatory demyelinating polyradiculopathy. He declined a spinal tap. Possible autoimmune, paraneoplastic and metabolic causes of subacute ataxia were negative on laboratory testing. Cranial MRI showed mild prominence of cerebellar vasculature at the surface, which was described as nonspecific, but possibly seen with an inflammatory etiology. A diagnosis of post-viral cerebellitis related to COVID-19 was proposed. He continued to improve, without any further intervention, over the next few weeks. By the time of this reporting, most symptoms had almost completely resolved.
Twenty-eight patients (78%) had at least one of six comorbidities associated with more severe COVID-19 (hypertension, cardiovascular disease, renal disease, diabetes, chronic lung disease, or immunosuppression), with the majority having more than one risk factor. Thirteen patients (36%) lived in their own home, while twenty-three (64%) were at extended care facilities: nursing home (n = 17), assisted living facility (n = 5), and group home (n = 1). Their presentation, clinical course, management, and outcome are also presented in Table 1. Of interest, twenty-seven patients (75%) exhibited alteration in mental status (including lethargy, confusion, delirium, hallucinations, or bradyphrenia), and in twenty-two (61%), it was the presenting symptom. Of these, only fifteen (56%) had a pre-existing diagnosis of dementia. Thirteen patients (36%) were documented to have hypotension, and fifteen (42%) were noted to have abnormalities of movement. Worsening of their movement disorder was reported by seven patients (19%), and generalized weakness or worsening mobility were noted as the presenting symptom by eleven patients (31%). Twenty-four patients (67%) required hospitalization. Nine patients received hydroxychloroquine and two received oseltamivir. Six patients were receiving an adamantane as part of their neurologic management (three on amantadine, three on memantine).
Mortality in this series was thirteen out of thirty-six patients (36%). Of the patients who died, twelve (92%) were greater than 60 years old, eleven (85%) had parkinsonism, eleven (85%) were from an extended care facility, nine (69%) had comorbid dementia, nine (69%) had at least one high-risk comorbid condition, eight (62%) had alteration in mental status as a presenting symptom, and eight (62%) received a medication with antiviral properties (hydroxychloroquine, oseltamivir, amantadine, and memantine), including three who were on an adamantane prior to contracting COVID-19. Looking specifically at the patients in our cohort with parkinsonism, versus those without parkinsonism, their outcomes are separated out and shown in Figure 1.
Lastly, upon review of the inpatient database of Hartford HealthCare’s six affiliate hospitals throughout the state, we found that of 2028 patients admitted for COVID-19 within the same 90-day period of our study, forty-two patients (2%) carried a diagnosis of PD or a parkinsonism. Only sixteen of these forty-two patients (38%) admitted to the HHC hospital network were patients of the Chase Family Movement Disorders Center.