Objective To describe the spectrum of neurological complications observed in a hospital‐based cohort of COVID‐19 patients who required a neurological assessment. Methods We conducted an observational, monocentric, prospective study of patients with a COVID‐19 diagnosis hospitalized during the 3‐month period of the first wave of the COVID‐19 pandemic in a tertiary hospital in Madrid (Spain). We describe the neurological diagnoses that arose after the onset of COVID‐19 symptoms. These diagnoses could be divided into different groups. Results Only 71 (2.6%) of 2750 hospitalized patients suffered at least one neurological complication (77 different neurological diagnoses in total) during the timeframe of the study. The most common diagnoses were neuromuscular disorders (33.7%), cerebrovascular diseases (CVDs) (27.3%), acute encephalopathy (19.4%), seizures (7.8%), and miscellanea (11.6%) comprising hiccups, myoclonic tremor, Horner syndrome and transverse myelitis. CVDs and encephalopathy were common in the early phase of the COVID‐19 pandemic compared to neuromuscular disorders, which usually appeared later on ( p = 0.005). Cerebrospinal fluid severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) polymerase chain reaction was negative in 15/15 samples. The mortality was higher in the CVD group (38.1% vs. 8.9%; p = 0.05). Conclusions The prevalence of neurological complications is low in patients hospitalized for COVID‐19. Different mechanisms appear to be involved in these complications, and there was no evidence of direct invasion of the nervous system in our cohort. Some of the neurological complications can be classified into early and late neurological complications of COVID‐19, as they occurred at different times following the onset of COVID‐19 symptoms.

Guillain-Barré syndrome (GBS) in spinal nerves and we read their previous studies with great interest. 3 Gallardo et al showed involvement of spinal nerves with electrophysiologic, ultrasonographic, and pathologic findings in patients with early GBS. 3 Correspondingly, magnetic resonance imaging (MRI) of our patient using short-tau inversion recovery (STIR) sequences showed edema of the spinal nerves and corresponding rami, demonstrating proximal demyelination. MRI using post-contrast T1 sequences helps to demonstrate the topography of nerve root enhancement in GBS, but it is not applicable to patients with kidney failure or contrast allergies. 4 We think that adding coronal STIR sequences to the imaging protocol is a useful method for the detection inflammatory edema of nerve roots and plexus. In STIR sequences, all structures with short T1 relaxation times are suppressed, whereas structures with high water content show a bright signal on a dark background and demonstrate the swollen spinal nerves and corresponding rami. The coronal plane is the most valuable plane in STIR images, because it demonstrates anatomic structures including proximal nerve segments in a familiar perspective. 5 Late-response alterations (F wave and H reflex) are the most common early electrophysiologic findings supporting proximal demyelination in early GBS. 6,7 In our case, the increased chronodispersion and decreased persistence of F waves in the median and ulnar nerves can be caused by demyelination in any segment of the peripheral nerve, because nerve conduction studies revealed conduction blocks of median and ulnar nerves in the wrist-elbow segment, and STIR images showed involvement of proximal nerve segments. More investigations with electrophysiologic, radiologic, and pathologic studies will help further our understanding of the pathophysiologic mechanisms of GBS and elucidate therapeutic strategies.

Introduction: We analyzed whether the coronavirus disease 2019 (COVID-19) crisis affected acute stroke care in our center during the first 2 months of lockdown in Spain. Methods: This is a single-center, retrospective study. We collected demographic, clinical, and radiological data; time course; and treatment of patients meeting the stroke unit admission criteria from March 14 to May 14, 2020 (COVID-19 period group). Data were compared with the same period in 2019 (pre-COVID-19 period group). Results: 195 patients were analyzed; 83 in the COVID-19 period group, resulting in a 26% decline of acute strokes and transient ischemic attacks (TIAs) admitted to our center compared with the previous year (p = 0.038). Ten patients (12%) tested positive for PCR SARS-CoV-2. The proportion of patients aged 65 years and over was lower in the COVID-19 period group (53 vs. 68.8%, p = 0.025). During the pandemic period, analyzed patients were more frequently smokers (27.7 vs. 10.7%, p = 0.002) and had less frequently history of prior stroke (13.3 vs. 25%, p = 0.043) or atrial fibrillation (9.6 vs. 25%, p = 0.006). ASPECTS score was lower (9 [7–10] vs. 10 [8–10], p = 0.032), NIHSS score was slightly higher (5 [2–14] vs. 4 [2–8], p = 0.122), onset-to-door time was higher (304 [93–760] vs. 197 [91.25–645] min, p = 0.104), and a lower proportion arrived within 4.5 h from onset of symptoms (43.4 vs. 58%, p = 0.043) during the CO­VID-19 period. There were no differences between proportion of patients receiving recanalization treatment (intravenous thrombolysis and/or mechanical thrombectomy) and in-hospital delays. Conclusion: We observed a reduction in the number of acute strokes and TIAs admitted during the COVID-19 period. This drop affected especially elderly patients, and despite a delay in their arrival to the emergency department, the proportion of patients treated with recanalization therapies was preserved.

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Background: Comprehensive clinicopathological studies of neuropsychiatric symptoms (NPS) in dementia are lacking. Objective: To describe the pathological correlations of NPS in a sample of institutionalized people with dementia. Methods: We studied 59 people who were consecutively admitted to a nursing home and donated their brain. Correlations between pathological variables and NPS upon admission (n = 59) and at one-year follow-up assessment (n = 46) were explored and confirmed using bivariate and multivariate statistical methods. Results: Mean (SD) age at admission was 83.2 (6.4) years and mean (SD) age at demise was 85.4 (6.6); 73% of the subjects were female and 98% presented advanced dementia. The most frequent etiological diagnosis was Alzheimer’s disease (AD; 74.6% clinical diagnosis, 67.8% pathological diagnosis). The pathological diagnosis of AD was associated with aggression (β est 0.31), depression (β est 0.31), anxiety (β est 0.38), and irritability (β est 0.28). Tau stage correlated with aggressive symptoms (β est 0.32) and anxiety (βest 0.33). Coexistence of AD and Lewy body pathology was associated with depression (β est 0.32), while argyrophilic grains were associated with eating symptoms (β est 0.29). Predictive models were achieved for apathy, including cognitive performance, basal ganglia ischemic lesions, and sex as predictors (R2 0.38) and for sleep disorders, including pathological diagnosis of AD and age at demise (R2 0.18) (all p-values <0.05, unadjusted). Conclusion: AD was the main pathological substrate of NPS in our sample of very elderly people with advanced dementia. However, correlations were mild, supporting a model of focal/asymmetric rather than diffuse brain damage, along with relevance of environmental and other personal factors, in the genesis of those symptoms.