Neurologist最新文献

Background and objective: West Nile neuroinvasive disease (WNND) displays a wide range of clinical manifestations due to its involvement of various structures within the central nervous system and peripheral nervous system, often including prolonged unresponsiveness as the presenting symptom.

Methods and results: We describe 2 patients presenting with coma and bilateral thalamic lesions on brain magnetic resonance imaging, found to have WNND after extensive workup. These cases illustrate some of the challenges associated with evaluating coma in general and specifically in diagnosing WNND.

Conclusion: The clinical diagnosis of WNND requires a high index of suspicion, particularly in immunocompromised and elderly patients. Brain and spine magnetic resonance imaging findings can help narrow down the differential diagnosis, although other diseases may manifest similarly. Serological studies on the cerebrospinal fluid are essential to confirm the diagnosis but have inherent limitations. Given these challenges, WNND should be considered in all patients living in endemic areas who present with unexplained altered mental status during the late summer and early fall seasons.

Objectives: Whether patients with infarct volume ≥150 mL could benefit from endovascular thrombectomy (EVT) remains unclear.

Methods: Patients (n=104) with anterior circulation Alberta Stroke Program Early Computed Tomography Score <6 were screened for infarct volume ≥150 mL using the Pullicino formula × (1-22%). The following were compared with the baseline at 90 days: the modified Rankin scale score (mRS) ≤3, mortality rate, symptomatic intracranial hemorrhage and any intracranial hemorrhage within 48 hours, and modified Thrombolysis in Cerebral Infarction (mTICI) ≥2b between the EVT and drug therapy (DT) groups.

Results: In patients with infarct volumes ≥150 mL, mRS≤3 at 90 days was higher in the EVT group than in the DT group [adjusted odds risk (aOR), 5.52; 95% CI: 1.10-28.24, P =0.04), and mTICI ≥2b at 82.8%. Intracranial hemorrhage within 48 hours occurred in 7 (24.1%) patients in the EVT group and 5 (14.7%) in the DT group (aOR, 0.75; 95% CI: 0.16-3.46; P =0.71). Older age (aOR, 0.94; 95% CI: 0.90-0.99, P =0.01), EVT treatment (aOR, 4.51; 95% CI: 1.60-12.78, P =0.01), and infarct volume ≥150 mL (aOR, 0.11; 95% CI: 0.04-0.31, P <0.01) were significantly associated with patient prognosis.

Conclusions: Patients with infarct volume ≥150 mL who received EVT had a higher proportion of mRS≤3 compared with those who received DT. However, there was no statistically significant difference in intracranial hemorrhage and death between the groups. EVT, smaller infarct volume, and younger age were associated with a good prognosis. The findings require large sample data verification.

Background: Subarachnoid hemorrhage (SAH) refers to bleeding in the subarachnoid space, which is a serious neurologic emergency. However, the treatment effects of SAH are limited. In recent years, stem cell (SC) therapy has gradually become a very promising therapeutic method and advanced scientific research area for SAH.

Review summary: The SCs used for SAH treatment are mainly bone marrow mesenchymal stem cells (BMSCs), umbilical cord mesenchymal stem cells (hUC-MSCs), dental pulp stem cells (DPSCs), neural stem cells (NSCs)/neural progenitor cell (NPC), and endothelial progenitor cell (EPC). The mechanisms mainly included differentiation and migration of SCs for tissue repair; alleviating neuronal apoptosis; anti-inflammatory effects; and blood-brain barrier (BBB) protection. The dosage of SCs was generally 106 orders of magnitude. The administration methods included intravenous injection, nasal, occipital foramen magnum, and intraventricular administration. The administration time is generally 1 hour after SAH modeling, but it may be as late as 24 hours or 6 days. Existing studies have confirmed the neuroprotective effect of SCs in the treatment of SAH.

Conclusions: SC has great potential application value in SAH treatment, a few case reports have provided support for this. However, the relevant research is still insufficient and there is still a lack of clinical research on the SC treatment for SAH to further evaluate the effectiveness and safety before it can go from experiment to clinical application.

Introduction: Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode (MELAS) is one of the most common maternally inherited mitochondrial diseases. The stroke-like episode affecting the cortical cortex is the hallmark of MELAS; however, it rarely presents as simultaneously bilateral symmetric cortices lesions.

Case report: We reported a case of MELAS in a 46-year-old female patient with bilateral symmetric occipital and internal temporal cortices involvements on brain magnetic resonance imaging (MRI). A literature review of MELAS patients and a retrospective analysis were performed. She had a family history of diabetes. Although she denied a history of diabetes, elevated blood glucose was noted after admission, and diabetes was diagnosed. Laboratory examination revealed elevated lactate acid and creatine kinase levels in blood. Cranial computed tomography (CT) image demonstrated basal ganglia calcification, as well as subtle decreased attenuation in bilateral symmetric occipital and internal temporal cortices. Brain magnetic resonance imaging (MRI) demonstrated symmetric gyriform hyperintensity in bilateral occipital lobes and internal temporal lobes in both grey and white matter on fluid-attenuated inversion recovery (FLAIR) images with restricted diffusion on diffusion weighted images (DWI). A genetic test revealed a point mutation in the mtDNA(3243A > G) by blood examination. Literature review showed that there were 231 eligible patients with MELAS identified from 212 published papers. Symmetric cortical involvements were seen in 15 (6.5%) patients on brain MRI.

Conclusions: MELAS should be considered as a potential diagnosis in the patients with bilateral symmetric stroke-like cortices lesions.

Introduction: Rocky Mountain Spotted Fever (RMSF) is a tick-borne disease caused by Rickettsia rickettsii (R. rickettsii). RMSF presents after a tick bite with fever, rash, and headache but can also cause more serious neurological manifestations. We report a case of RMSF encephalitis presenting with altered sensorium and rapid progression to coma, fever, and petechial rash, and an magnetic resonance imaging (MRI) brain notable for a "starry sky" pattern.

Case report: A 61-year-old woman presented with confusion and fever and was diagnosed with a urinary tract infection. Two days later, she became comatose. MRI brain revealed lacunar infarcts in the right centrum semiovale and splenium of the corpus callosum. Lumbar puncture was notable for neutrophilic pleocytosis and elevated protein with negative bacterial and viral cultures. Empiric meningitis therapy was initiated, and she was transferred to our institution. On transfer, she was febrile, comatose, and had a diffuse petechial rash. Repeat MRI brain demonstrated diffuse, innumerable punctate foci of diffusion restriction with susceptibility-weighted signal attenuation throughout cerebral hemispheres in a "starry sky" pattern. Skin biopsy revealed perivascular lymphocytic infiltrates. Serologic RSMF antibody titers were obtained, and doxycycline was initiated for presumed RMSF encephalitis. The family opted to pursue palliative measures, given no clinical improvement. RSMF titers and postmortem PCR from brain tissue were positive for R. rickettsii.

Conclusions: This case report highlights the clinical presentation of RMSF encephalitis. RMSF encephalitis should be suspected in a patient presenting with encephalopathy, fever, petechial rash, and MRI brain findings of diffuse punctate foci of diffusion restriction and susceptibility-weighted signal attenuation in a "starry-sky" pattern.

Background: The concept of wake-up stroke (WUS) as a distinct subtype of acute ischaemic stroke, characterized by an uncertain onset time, traditionally resulted in the exclusion of patients from intravenous thrombolysis treatment.

Review summary: Advancements in neuroimaging have prompted a shift in the approach to intravenous thrombolysis treatment, moving away from a strict focus on the onset time window toward consideration of the tissue time window. This paradigm shift has expanded the opportunity for a larger cohort of patients with WUS to receive timely and effective treatment, ultimately leading to improved prognosis.

Conclusions: This study reviews the WUS pathogenesis and the progress of various imaging diagnostic techniques to clarify the WUS onset time and select the optimal treatment plan.

Introduction: The C9orf72 mutation can manifest in diverse clinical ways, including rapid cognitive decline, parkinsonism, or late-life neuropsychiatric symptoms, sometimes mimicking autoimmune encephalitis.

Case report: A 64-year-old female presented to the autoimmune neurology clinic with rapidly progressive dementia (RPD) associated with episodes of headache, confusion, auditory hallucinations, and abnormal electroencephalogram. She was treated empirically at an outside hospital for possible autoimmune encephalitis with intravenous methylprednisolone, but there was no improvement, and rapid cognitive decline continued. Family history was notable for RPD with akinetic mutism in her sister, sudden severe depression followed by parkinsonism with progressive dementia in her father in his 60s, and late-life gradually progressive dementia in her mother. Additional testing revealed a low titer positive contactin-associated protein-like 2 (CASPR2) immunoglobulin G (IgG) in the serum and elevated CSF 14-3-3 protein. CSF CASPR2 IgG and real-time quaking-induced conversion for Creutzfeldt-Jakob disease were negative. Brain MRI showed normal parenchymal volume. Genetic testing was conducted, which identified a heterozygous pathogenic hexanucleotide tandem repeat expansion in the C9orf72 gene.

Conclusion: This case underscores the phenotypic variability of C9orf72 mutation and the importance of a detailed family history exploring young or atypical deaths and neuropsychiatric symptoms or behavioral changes. Genetic etiologies are crucial to consider in those with a family history concerning autosomal dominant inheritance patterns of early-onset dementia, parkinsonism, or late-onset psychiatric disease. Emphasis is placed on considering alternative etiologies early, particularly when there is no response to first-line immunomodulation for suspected autoimmune dementia.

Objectives: To draw attention to acute positional vertigo and central positional nystagmus (CPN) developing as the sole features of cerebellar nodulus infarction.

Background: The cerebellar nodulus is vascularized by the medial branch of the posterior inferior cerebellar artery, which also supplies the uvula, tonsil, tuber, and pyramid of the vermis, and the inferior part of the cerebellar hemisphere, making isolated cerebellar nodulus infarction extremely rare. CPN occurs after a change in head position with respect to gravity and is caused by pathologies involving the vestibulo-cerebellar pathways. CPN is rarely seen in isolation. Additional neurological signs and ocular motor abnormalities are generally present.

Methods: A 62-year-old man was admitted to the emergency department with acute-onset positional vertigo and CPN as the sole finding on examination. Cranial magnetic resonance imaging revealed an acute infarction involving the nodulus. Results: Infarcts restricted to nodulus can cause positional vertigo and CPN without any associated neurological signs or ocul ar motor abnormalities.

Conclusion: Though very rare, cerebellar nodulus stroke must be searched in patients with positional vertigo of acute onset and isolated CPN on examination.

Objectives: To investigate the safety of administering low-dose aspirin (81 mg) 18 hours after intravenous thrombolytic therapy.

Methods: This is a retrospective cohort investigation. Individuals received either alteplase or tenecteplase for acute ischemic stroke followed by aspirin 81 mg (after follow-up imaging). An institutional change moved follow-up post-thrombolytic CT scans to 18 hours, and qualifying patients were grouped based on whether they received aspirin ≤24 hours or >24 hours. Chart reviews were conducted to assess the primary outcome of new or worsening intracranial hemorrhage, as well as secondary outcomes of change in stroke scale scores at discharge and 3 months, lengths of stay, favorable outcomes at 3 months, hospital readmission, and mortality.

Results: Out of 350 patients screened, 130 qualified for inclusion-50 of whom received aspirin ≤24 hours (mean 21.1 hours, SD±6.2), and 80 who received aspirin >24 hours (mean 34 hours, SD±8.2). Only 1 new intracranial bleed occurred following aspirin administration in the >24-hour group. No statistically significant differences were observed in any of the secondary outcomes, although there was higher mortality (3/50 vs. 2/80, P =0.372) and shorter hospital length of stay (median difference -1.0 day, P =0.0336) in the <24 hours group.

Conclusions: Low-dose aspirin administration sooner than 24 hours following thrombolytic therapy did not increase bleeding events. Sooner aspirin administration after ischemic stroke can potentially enhance the prevention of secondary embolization and did not demonstrate worse clinical outcomes; however, further randomized controlled trials are needed.

Objectives: To investigate return to work and workforce detachment in ischemic stroke, including the association with age and level of education.

Methods: Patients in the workforce aged 18 to 60 with first-time ischemic stroke between 1997 and 2017 were identified in Danish registers and followed for 5 years. The cumulative incidence of return to work and subsequent workforce detachment was computed overall and stratified according to age group and education level. Cox regression analysis was used for multivariate analysis.

Results: A total of 28,325 patients were included (median age 52.3 (interquartile range (IQR) 46.1 to 56.6) and 64.3% male). After 1 year, 62.0% were in the workforce, highest in age group 18 to 30 (80.0%) and lowest in patients aged 51 to 60 (58.5%). One-year cumulative incidence of return to work overall was 73.4% (20,475), highest in the young age group (87.0%, 76.7%, 74.5%, and 71.3% for age group 18 to 30, 31 to 40, 41 to 50, and 51 to 60, respectively) and high education (80.3%, 72.1%, and 71.3% for long higher, basic or vocational education, respectively). One-year cumulative incidence of subsequent workforce detachment was 25.6% (5248), lowest in young age (22.4%, 23.1%, 24.1%, and 27.2% for age groups 18 to 30, 31 to 40, 41 to 50, and 51 to 60, respectively) and high level of education (13.0%, 28.4%, and 27.2% for long higher, basic, and vocational education, respectively). During the full follow-up, 10,855 (53.0%) left the workforce again.

Conclusions: A high proportion of patients returned to work within 1 year, but more than half left the workforce again. Young age and long education were associated with a higher incidence of return to work and lower subsequent workforce detachment.