Faculty Bibliography

BACKGROUND:Patients with Parkinson's disease (PD) are at higher risk of vaccine-preventable respiratory infections. However, advanced, homebound individuals may have less access to vaccinations. In light of COVID-19, understanding barriers to vaccination in PD may inform strategies to increase vaccine uptake. OBJECTIVE:To identify influenza and pneumococcal vaccination rates, including barriers and facilitators to vaccination, among homebound and ambulatory individuals with PD and related disorders. METHODS:Cross-sectional US-based study among individuals with PD, aged > 65 years, stratified as homebound or ambulatory. Participants completed semi-structured interviews on vaccination rates and barriers, and healthcare utilization. RESULTS:Among 143 participants, 9.8% had missed all influenza vaccinations in the past 5 years, and 32.2% lacked any pneumococcal vaccination, with no between-group differences. Homebound participants (n = 41) reported difficulty traveling to clinic (p < 0.01) as a vaccination barrier, and despite similar outpatient visit frequencies, had more frequent emergency department visits (31.7% vs. 9.8%, p < 0.01) and hospitalizations (14.6% vs. 2.9%, p = 0.03). Vaccine hesitancy was reported in 35% of participants, vaccine refusal in 19%, and 13.3% reported unvaccinated household members, with no between-group differences. Nearly 13% thought providers recommended against vaccines for PD patients, and 31.5% were unsure of vaccine recommendations in PD. CONCLUSION/CONCLUSIONS:Among a sample of homebound and ambulatory people with PD, many lack age-appropriate immunizations despite ample healthcare utilization. Many participants were unsure whether healthcare providers recommend vaccinations for people with PD. In light of COVID-19, neurologist reinforcement that vaccinations are indicated, safe, and recommended may be beneficial.

Objective: We report a case of concomitant Holmes' tremor (HT) and hemiparkinsonism (HP) attributable to a single structural lesion with robust clinical response to levodopa.
Background(s): HT is a low frequency (<4.5 Hz) tremor at rest that persists or increases with postural change and goal-directed action. It's believed to arise most commonly from structural lesions that disrupt the nigrostriatal pathway in conjunction with either the cerebello-thalamocortical or dentato-rubro-olivary pathway [1]. "Pure" vascular HP stems from injury to the substantia nigra and/or nigrostriatal pathway, causing contralateral rest tremor, bradykinesia, and rigidity [3]. We found only one prior case report of both HT and HP occurring in combination from a single structural lesion resulting in near absence of dopamine transporter binding in the ipsilateral striatum on DaT-SPECT imaging [3]. However, high doses of levodopa provided no clinical improvement despite prior reports of efficacy in HT [4].
Method(s): Case Report.
Result(s): A 48-year-old woman presented with insidious onset of tremor and slowness of movement. She had a known hemorrhagic midbrain cavernous malformation discovered 20 years prior in the setting of acute onset of binocular diplopia and transient left sided hemiparesis. On exam, there was isolated left facial masking, severe left arm and leg bradykinesia and rigidity, and marked reductions in stride length and arm swing when ambulating. There was a coarse, irregular 3 Hz tremor of the left arm present at rest, persisting with postural change, and increasing with goaldirected action. Brain MRI demonstrated a 2 cm cavernous malformation within the right substantia nigra with extension into the red nucleus and crus cerebri [figure 1]. She was examined following ingestion of 100 mg of levodopa. She developed dystonic dyskinesias of the left arm and leg thirty minutes after ingestion followed by resolution of HT and profound improvement of HP at sixty minutes. Symptoms gradually returned three hours after ingestion.
Conclusion(s): This represents the first reported case of concurrent HT and HP due to a single structural lesion with robust symptomatic response to levodopa, presumed secondary to disruption of both the nigrostriatal and dentato-rubro-olivary pathways. It is unclear what drives responsiveness to dopaminergic therapy, which can at times be robust and thus remains the first-line therapeutic approach. (Figure Presented)