Faculty Bibliography

OBJECTIVE:Presenting the diagnosis of psychogenic nonepileptic seizures (PNES) can be a difficult task, but disclosing this information effectively is important to optimize patient outcomes. We sought to develop a standardized method to teach neurology residents how to introduce the diagnosis of PNES via an objective structured clinical examination (OSCE) with a standardized patient (SP). METHODS:In conjunction with the New York University School of Medicine Simulation Center (NYSIM), we designed an OSCE in which a resident had to inform a SP of her diagnosis of PNES and discuss a treatment plan. The SP was provided with details to gradually disclose depending on what the resident said about the history of her episodes, triggers for her episodes and her history of sexual abuse. Each encounter was observed by an attending physician who provided real-time feedback to the resident after the session. Additionally, the SP completed an objective written checklist of items the resident should have covered in the session and gave them verbal feedback. RESULTS:Twenty-six adult neurology (n = 22), child neurology (n = 3), and neuropsychiatry (n = 1) residents participated in this OSCE in 2018 and 2019, with full data available for 25 participants. Residents reported the OSCE was very useful (mean Likert score of 4.9/5). They felt moderately prepared (mean Likert score 3.8/5) and rated their performance as a mean of 3.3/5. On the SP's checklist, most residents were rated as Well Done in the domains of information gathering, relationship development, and education and counseling. Only in the domain of psychosocial assessment were most residents rated as Not Done (only 7/25 inquired about past trauma as a risk factor for PNES). SIGNIFICANCE/CONCLUSIONS:The OSCEs are a feasible and useful way to teach neurology residents about discussing PNES, as they allow for provision of real-time practice and feedback in a safe environment without real patients.

BACKGROUND AND PURPOSE/OBJECTIVE:Patients with intracerebral hemorrhage (ICH) frequently present with hypertension, but it is unclear if this is due to pre-existing hypertension (prHTN) or to the bleed itself or associated pain. We sought to assess the relationship between prHTN and admission systolic blood pressure (aBP) and bleed severity. METHODS:We retrospectively assessed the relationship between prHTN and aBP and NIHSS in patients with ICH at 3 institutions. RESULTS:Of 251 patients, 170 (68%) had prHTN based on history of hypertension/antihypertensive use. Median aBP was significantly higher in those with prHTN (155 mm Hg (IQR 135-181) versus 139 mm Hg (IQR 124-158), P < .001). Patients with left ventricular hypertrophy (LVH) on electrocardiogram (ECG) or transthoracic echocardiogram (TTE) had significantly higher aBP than those without LVH (median aBP 195 mm Hg (IQR 155-216) for patients with LVH on ECG versus 147 mm Hg (IQR 129-163) for patients with no LVH on ECG, P < .001; median aBP 181 mm Hg (IQR 153-214) for patients with LVH on TTE versus 152 mm Hg (IQR 137-169) for patients with no LVH on TTE, P = .01). prHTN was associated with a higher median NIHSS (11 (IQR 3-20) for patients with history of hypertension/antihypertensive use versus 6 (IQR 1-14) for patients without this history (P = .02); 9 (IQR 3-19) versus 5 (IQR 2-13) for patients with/without LVH on ECG (P = .085); and 10 (IQR 5-18) versus 5 (IQR 1-13) for patients with/without LVH on TTE (P = .046). CONCLUSIONS:Patients with ICH who have prHTN have higher aBP and NIHSS, suggesting that prHTN may worsen reactive hypertension in the setting of ICH.

Objective: To present clinical and radiographic descriptions of conditions that may feature corticospinal tract abnormalities observed on magnetic resonance imaging (MRI). Background: Corticospinal tract lesions have a broad differential diagnosis, including neurodegenerative diseases, toxic/metabolic derangements, malignancies, autoimmune diseases, infectious diseases, and neurogenetic conditions. Design/Methods: Review of clinical presentations and brain MRIs. Results: Conditions that have been associated with corticospinal tract hyperintensities on brain MRI include: amyotrophic lateral sclerosis, primary lateral sclerosis, heroin leukoencephalopathy, brainstem glioma, neuroBehcets, HIV infection, neuromyelitis optica, Krabbe A disease, adult polyglucosan body disorder, Xlinked Charcot-Marie-Tooth disease, Behr syndrome, Whipple disease, and sequela of liver transplantation. We present representative images and discuss clinical and radiographic features that distinguishing these conditions. Conclusions: Corticospinal tract lesions have a heterogenous etiology, with widely different treatments and prognoses. An understanding of these potential etiologies will assist neurologists confronted with this imaging finding

Introduction Patients with intracerebral hemorrhage (ICH) frequently present with hypertension. It is unclear whether this is due to preexisting hypertension (prHTN) causing the bleed, an effect of the bleed, or both. Methods We retrospectively analyzed a single-institution cohort of ICH patients presenting between 2013 and 2016. Data included home antihypertensive use; aSBP; TTE, and EKG and imaging results; and nicardipine administration. The primary objective was to assess the relationship between prHTN and aSBP, while the secondary objectives were to assess the relationship between prHTN, imaging and acute antihypertensive requirements. Results 112 ICH patients met inclusion criteria. In our assessment for prHTN, we found that 46% of patients were on antihypertensives, 16% had LVH on EKG, and 15% had LVH on TTE. There was a significant relationship between LVH on TTE and LVH on EKG (p<0.001), but not between home antihypertensive use and presence of LVH using either modality. aSBP was higher for all patients with markers of pHTN, but this was only significant for patients with LVH on TTE (181mmHg, IQR 153-214 vs. 152mmHg, IQR 137-169, p < 0.001) and patients with LVH on EKG (195 mm Hg, IQR 155-216 vs. 147 mm Hg, IQR 129- 163, p<0.001). All patients with markers of prHTN were more likely to require nicardipine, but this was only significant for patients with LVH on TTE (94% vs. 64%, p=0.016) and patients with LVH on EKG (83% vs. 52%, p=0.018). All patients with markers of prHTN were more likely to have deep bleeds (p=0.017 for patients with LVH on EKG vs. those without LVH on EKG). There was no relationship between any markers of prHTN and the presence of a spot sign. Conclusions In patients with ICH, prHTN is related to higher aSBP, deep bleed location, and increased acute antihypertensive requirements