Kramer, Neha M.

Abstract Background Compared to Parkinson's disease, atypical parkinsonian disorders (APD) are characterized by a more rapidly progressive course, often leading to profound disability. Effective communication between clinicians, patients, and care partners is essential to support patient‐centered care and shared decision‐making. However, most neurologists lack formal training in serious illness conversations (SIC). Objective To develop a practical SIC guide tailored to the needs of individuals with APD. Methods Members of the CurePSP Centers of Care Palliative Care Working Group, in collaboration with a SIC education expert (TC), developed a SIC guide for APD. A literature review was conducted, followed by online consensus‐building rounds. Results Applying core communication principles—such as active listening, pausing, naming and validating emotions, assessing understanding, and reframing—can foster alignment between clinicians, patients, and their care partners. Navigating the balance between maintaining hope and providing realistic, anticipatory guidance remains challenging but best achieved by honest, compassionate dialogue. Four practical guides were developed, addressing common and often challenging scenarios: delivering an APD diagnosis, eliciting patient goals in the context of changing clinical status, addressing safety concerns, and discussing quality of life and end‐of‐life considerations. Conclusions Patients and their care partners living with APD benefit greatly from individualized guidance, and honest, empathic communication is a vital part of patient‐centered care. While existing SIC frameworks offer valuable foundations, further research is needed to optimize their adaptation for APD—identifying best timing, specific frameworks, relevant outcome measures, and education strategies to build team‐wide competency.

Background: Seizures are a known complication of ischemic stroke. Some studies have reported a higher risk of post-stroke seizure with cardioembolic strokes, whereas others have not. The risk of post-stroke seizure for different stroke mechanisms is unclear. Objective: To compare different stroke etiologies and the risk of post-stroke seizure in a population-based study. Methods: Utilizing the Rochester Epidemiology Project medical records linkage system, we ascertained all first ischemic strokes occurring among Rochester, MN residents from 1990-1994, and followed the patients in the comprehensive medical record through March 2014 for occurrence of seizure. TOAST stroke subtype classification was determined by a consensus of cerebrovascular neurologists. New post-stroke seizure was identified by physician diagnosis and/or EEG report. Patients with a seizure before the index stroke were not included. Pre-morbid stroke risk factors were recorded. Associations between seizure after index ischemic stroke as outcome and other variables of interest were assessed using univariate logistic regression. Results: A total of 490 patients met inclusion criteria, with median follow-up of 6.5 years. Out of 490 patients, 35 had new onset seizures (7.1%). Median age was significantly lower at index stroke for patients with seizures (73 v. 77 years, p=0.017). The most common TOAST stroke subtype was cryptogenic (46.8%) followed by cardioembolic (24.9%). There was no significant difference in TOAST stroke subtypes between patients with post-stroke seizure and those without (p=0.35). There was also no difference between the two groups when comparing combined cardioembolic and large-vessel to small-vessel (p=0.28) or cryptogenic to small-vessel (p=0.9) mechanisms. There was also no difference in pre-morbid stroke risk factors between the two groups, including hypertension (p=0.22), total cholesterol (p=0.95), type 2 diabetes mellitus (p=0.13), tobacco use (p=0.27), atrial fibrillation (p=0.9), or previous myocardial infarction (p=0.67). Conclusion: This study suggests that the long-term risk of post-stroke seizures does not differ by ischemic stroke etiology.

Background: Coronary artery disease (CAD) is a significant cause of morbidity and mortality in ischemic stroke (IS) patients. IS and CAD often coexist and share common risk factors. Absolute risk and predictors of myocardial infarction (MI) in IS and by IS etiology subtype is not well known. We determined the risk of MI and its predictors in patients with incident IS in a population based cohort. Methods: Using the Rochester Epidemiology Project (REP) medical records linkage system we identified all residents with incident IS in a 5-year period between January 1, 1990, and December 31, 1994. Comprehensive medical records were reviewed and variables of interest were retrieved and analyzed. Univariate Cox proportional hazard regression models were constructed to assess hazard ratios and 95% CI for predictors of MI occurrence after IS. Results: We identified 490 persons with IS, mean age at IS was 76.6 (SD 12.9) years, mean follow up to death or final follow-up was 6.5 (SD 6.3, range 0.0-23.8) years. There were 126 recurrent strokes and 93 MIs during followup. The 1-year actuarial risk of MI was 3.6% (95% CI, 2.2% - 5.9%), and 5-year actuarial risk of MI was 11.4% (95% CI, 8.4% - 15.3%). Univariate predictors of MI included (HR; 95% CI): age (1.02;1.0-1.04), pre-IS history of MI (1.37;1.13-1.65), CHF (1.85;1.06-3.23), CABG (2.11;1.19-3.75), left ventricular dyskinesia (2.14;1.32-3.4), peripheral vascular disease (1.32;1.18-1.49), diabetes mellitus (1.54;1.21-1.96), elevated creatinine (1.93;1.44-2.59), LDL level (1.01;1.00-1.01). Conclusion: MI is common after first IS. Several factors predicted an increased risk of MI after stroke, and should be taken into account in determining CAD screening strategies at the time of IS. Recurrent stroke was more common than MI during long-term followup.

Introduction: Studies have suggested a high incidence of dementia after stroke; however data regarding risk factors are conflicting and few studies are population-based. The aims of this population-based study are to determine the frequency of diagnosis and predictors of clinical dementia after ischemic stroke. Methods: The Rochester Epidemiology Project medical records linkage system was used to ascertain all first ischemic strokes (IS) occurring among Rochester, MN residents between 1990 -1994. Comprehensive medical records were reviewed. Patient and stroke characteristics, medical comorbidities, and the development of clinical dementia any time after IS were recorded. Dementia was defined as any reflection in the chart by a clinician of memory loss resulting in functional impairment. Patients with a pre-stroke diagnosis of dementia were excluded. Associations between new dementia after the index IS and other variables of interest were analyzed using univariate logistic regression. Results: First IS was detected in 490 people, 82 of whom had a prior history of dementia, and 119 (29%) of whom developed dementia during a mean follow-up of 6.5 years (range 0-23.8). The mean age at index stroke was 76.6 years (SD 12.9). Those who developed dementia were a mean 4 years older at the time of IS (p = 0.003). The odds of developing dementia were 1.7 higher in those who had at least one recurrent stroke. There was no effect of sex, stroke location (cortical, subcortical, brainstem), stroke mechanism, or premorbid stroke risk factors (coronary artery disease, atrial fibrillation/flutter, hypertension, diabetes mellitus, left-sided valvular disease) on the occurrence of dementia. Conclusions: Dementia is commonly diagnosed following ischemic stroke. While stroke risk factors did not impact the risk of diagnosis of dementia, recurrent stroke increased this risk. Stroke risk factors may indirectly increase the risk of dementia by increasing the risk of recurrent IS. This suggests that aggressive secondary stroke prevention measures may significantly decrease the risk of being diagnosed with dementia following IS.

Background & Purpose: Seizures are a recognized complication of stroke. However, available data are conflicting in terms of incidence, risk factors for occurrence, and impact on functional outcome and mortality. The aim of this study was to assess the incidence and characteristics of seizures following ischemic stroke in a well-defined population, and their effect on long-term patient outcome. Methodology: Utilizing the Rochester Epidemiology Project medical record linkage system, we identified all incident cases of ischemic stroke (IS) that occurred between January 1, 1990, and December 31, 1994. We identified all patients who developed seizures following first IS. Detailed data regarding stroke (including TOAST subtype, anatomic location, functional outcome), seizures (date, type, functional outcome, recurrence, presence of status epilepticus, complications, treatment, EEG findings), and patient status at the last follow-up were recorded and analyzed. Results: We identified 490 patients with first IS. Mean follow-up was 6.5 years (range 0.0 - 23.8). Of these, 35 (7.1%) developed seizures. Early seizures (occurring within 14 days of stroke) were present in 13 (37.1%), of which 9 (69.2%) had their seizure within the first 24 hours. Partial seizures were the most common type (23 patients, 65.7%). Status epilepticus occurred in two cases (5.7%). Tongue biting was the most common complication of poststroke seizures (4 patients, 11.4%). Treatment with antiepileptic drugs (AEDs) was initiated in 32 cases (91.4%). Only one drug was necessary for seizure control in all treated patients. The mean modified Rankin Scale score was 2.9 (SD 1.48) after the first IS, and worsened to 3.3 (SD 1.43) after the first seizure. Mortality at the last follow-up was higher in the seizure group compared to the non-seizure group, even after adjusting for TOAST subtype (HR 1.52; 95% CI 1.07 - 2.16; P = 0.02). Conclusion: Seizures are mostly a late complication of IS. They do not bear a high risk of life-threatening complications and are readily controllable by a single AED. However, patients who developed poststroke seizures tended to have a worse functional outcome and an increased mortality.

Nonhemorrhagic neurological deficits are underrecognized symptoms of intracranial dural arteriovenous fistulas (dAVFs) having cortical venous drainage. These symptoms are the consequence of cortical venous hypertension and portend a clinical course with increased risk of neurological morbidity and mortality. One rarely documented and easily misinterpreted type of nonhemorrhagic neurological deficit is progressive dementia, which can result from venous hypertension in the cortex or in bilateral thalami. The latter, which is due to dAVF drainage into the deep venous system, is the less common of these 2 dementia syndromes. Herein, the authors report 4 cases of dAVF with venous drainage into the vein of Galen causing bithalamic edema and rapidly progressive dementia. Two patients were treated successfully with endovascular embolization, and the other 2 patients were treated successfully with endovascular embolization followed by surgery. The radiographic abnormalities and presenting symptoms rapidly resolved after dAVF obliteration in all 4 cases. Detailed descriptions of these 4 cases are presented along with a critical review of 15 previously reported cases. In our analysis of these 19 published cases, the following were emphasized: 1) the clinical and radiographic differences between dAVF-induced thalamic versus cortical dementia syndromes; 2) the differential diagnosis and necessary radiographic workup for patients presenting with a rapidly progressive thalamic dementia syndrome; 3) the frequency at which delays in diagnosis occurred and potentially dangerous and avoidable diagnostic procedures were used; and 4) the rapidity and completeness of symptom resolution following dAVF treatment.

We present the case of a 34-year-old woman with Klippel-Feil syndrome who developed progressive generalized dystonia of unclear etiology, resulting in intractable pain despite aggressive medical and surgical interventions. Ultimately, palliative sedation was required to relieve suffering. Herein, we describe ethical considerations including defining sedation, determining prognosis in the setting of an undefined neurodegenerative condition, and use of treatments that concurrently might prolong or alter end-of-life trajectory. We highlight pertinent literature and how it may be applied in challenging and unique clinical situations. Finally, we discuss the need for expert multidisciplinary involvement when implementing palliative sedation and illustrate that procedures and rules need to be interpreted to deliver optimal patient-centered plan of care.