Early-stage differentiation between Alzheimer's disease and frontotemporal lobe degeneration: Clinical, neuropsychology, and neuroimaging features.

Background: Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD) are the two most common forms of neurodegenerative dementia. Although both of them have well-established diagnostic criteria, achieving early diagnosis remains challenging. Here, we aimed to make the differential diagnosis of AD and FTLD from clinical, neuropsychological, and neuroimaging features. Materials and methods: In this retrospective study, we selected 95 patients with PET-CT defined AD and 106 patients with PET-CT/biomarker-defined FTLD. We performed structured chart examination to collect clinical data and ascertain clinical features. A series of neuropsychological scales were used to assess the neuropsychological characteristics of patients. Automatic tissue segmentation of brain by Dr. Brain tool was used to collect multi-parameter volumetric measurements from different brain areas. All patients' structural neuroimage data were analyzed to obtain brain structure and white matter hyperintensities (WMH) quantitative data. Results: The prevalence of vascular disease associated factors was higher in AD patients than that in FTLD group. 56.84% of patients with AD carried at least one APOE ε4 allele, which is much high than that in FTLD patients. The first symptoms of AD patients were mostly cognitive impairment rather than behavioral abnormalities. In contrast, behavioral abnormalities were the prominent early manifestations of FTLD, and few patients may be accompanied by memory impairment and motor symptoms. In direct comparison, patients with AD had slightly more posterior lesions and less frontal atrophy, whereas patients with FTLD had more frontotemporal atrophy and less posterior lesions. The WMH burden of AD was significantly higher, especially in cortical areas, while the WMH burden of FTLD was higher in periventricular areas. Conclusion: These results indicate that dynamic evaluation of cognitive function, behavioral and psychological symptoms, and multimodal neuroimaging are helpful for the early diagnosis and differentiation between AD and FTLD.

Cardiovascular Response of Aged Outpatients With Systemic Diseases During Tooth Extraction: A Single-Center Retrospective Observational Study.

Background: Aged people are maintaining many natural teeth due to improved oral health. However, compromised general health and poor oral hygiene habits at earlier ages resulted in poor status of preserved teeth. Therefore, tooth extraction is required in many aged people. More knowledge is needed because there are many risk factors during the surgery in frail aged adults. The aim of this study was to evaluate the cardiovascular response of such a population during tooth extraction and analyze risk factors to provide clinical guidance. Methods: A retrospective study was performed on aged patients with systemic diseases who underwent tooth extraction. Data regarding demographic profiles and cardiovascular parameters of heart rate and blood pressure were collected preoperative, when local anesthesia was administered, at the beginning of tooth extraction, 5 min after tooth extraction, and postoperative. The effects of risk factors, including age, sex, and systemic diseases on these parameters were analyzed with a multilevel model. Results: Heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) of aged patients increased significantly when performing local anesthesia and tooth extraction. During the operation, the older patients (ß = 2.011, P = 0.005) and the diabetics (ß = 3.902, P < 0.0001) were associated with higher SBP, while those with more tooth extractions exhibited higher HR (ß = 0.893, P = 0.007). Women patients showed both significantly elevated HR (ß = 1.687, P < 0.0001) and SBP (ß = 2.268, P < 0.0001). However, for coronary artery disease patients, HR (ß = -2.747, P < 0.0001) and blood pressure [SBP (ß = -4.094, P < 0.0001) and DBP (ß = -0.87, P = 0.016)] were markedly lower than those of patients without a diagnosis of coronary artery disease. Conclusion: Cardiovascular response of aged outpatients with systemic diseases during tooth extraction is quite significant. Age, sex, systemic diseases, and the number of tooth extraction could be risk factors closely associated with cardiovascular response. The findings might provide safety guidance for dentists on tooth extraction in this population.

Clinical Features of Coexisting Anti-NMDAR and MOG Antibody-Associated Encephalitis: A Systematic Review and Meta-Analysis.

Coexisting anti-NMDAR and MOG antibody (anti-NMDAR-IgG+/MOG-IgG+)-associated encephalitis have garnered great attention. This study aimed to perform a secondary analysis to determine the clinical features of this disease. We searched several databases for related publications published prior to April 2021. A pooled analysis was conducted with the fixed-effects model using the Mante-Haenszel method (I 2 ≤ 50%), or the random-effects model computed by the DerSimonian-Laird method (I 2 > 50%). Stata software (version 15.0 SE) was used for the analyses. Nine observational studies and 16 case reports (58 cases with anti-NMDAR-IgG+/MOG-IgG+, 21.0 [8.5, 29.0] years, male 58.6%) were included. The incidences (95%CI) of anti-NMDAR-IgG+/MOG-IgG+ in the patients with serum MOG-IgG+ and CSF anti-NMDAR-IgG+ were 0.09 (0.02-0.19) and 0.07 (0.01-0.19), respectively. The median [IQR] of CSF anti-NMDAR antibody titer was 32 [10, 100], and the serum anti-MOG antibody titer was 100 [32, 320]. The prominent clinical symptoms were encephalitic manifestations, including seizures (56.9%) and abnormal behavior (51.7%), rather than demyelinating manifestations, such as speech disorder (34.5%) and optic neuritis (27.6%). Relapse occurred in 63.4% of anti-NMDAR-IgG+/MOG-IgG+ patients, in whom 50.0% of cases relapsed with encephalitic manifestations, and 53.8% relapsed with demyelinating manifestations. The common MRI changes were in the cortex or subcortex (70.7%) and brainstem (31.0%). 31.3% of patients presented with unilateral cerebral cortical encephalitis with epilepsy and 12.5% displayed bilateral frontal cerebral cortex encephalitis. Anti-NMDAR-IgG+/MOG-IgG+ patients showed more frequent mental behavior (OR, 95%CI, 68.38, 1.36-3,434.37), involuntary movement (57.86, 2.53-1,325.11), sleep disorders (195.00, 7.07-5,380.15), and leptomeninge lesions (7.32, 1.81-29.58), and less frequent optic neuritis (0.27, 0.09-0.83) compared to anti-NMDAR-IgG-/MOG-IgG+ patients and presented more common relapse (5.63, 1.75-18.09), preceding infection (2.69, 1.03-7.02), subcortical lesions (116.60, 4.89-2,782.09), basal ganglia lesions (68.14, 2.99-1,554.27), brainstem lesions (24.09, 1.01-574.81), and spinal cord lesions (24.09, 1.01-574.81) compared to anti-NMDAR-IgG+/MOG-IgG-. In conclusion, anti-NMDAR-IgG+/MOG-IgG+ was rarely observed, but the incidence rate of relapse was very high. The overall symptoms seemed to be similar to those of NMDAR encephalitis.

[Clavicle fracture after radical neck dissection of mouth floor carcinoma misdiagnosed as cervical metastasis: a case report].

Clavicle fracture, a very rare delayed complication following radical neck dissection of oral carcinoma, is normally ignored by oral and maxillofacial surgeons. We report and analyze a male patient with clavicle fracture after primary extended excision and bilateral radical neck dissection. This case was misdiagnosed as cervical metastasis.

Ginsenoside Ameliorates Cognitive Dysfunction in Type 2 Diabetic Goto-Kakizaki Rats.

BACKGROUND Ginsenoside is the major bioactive component of ginseng, which has been proven to be a neuroprotective drug. The aim of this study was to evaluate the therapeutic effect of ginsenoside in a diabetic Goto-Kakizaki (GK) rat model. MATERIAL AND METHODS Twenty GK rats were randomly divided into a diabetic model (DM) group (n=10) and a ginsenoside + DM group (n=10); Wistar rats with the same age and body weight were used as the control (CON) group (n=10). Food and water intake, body weight, and blood fasting plasma glucose were measured. The Morris water maze test was used to detect learning and memory functions of the rats. Superoxide dismutase (SOD), malondialdehyde (MDA), and inflammatory cytokines (TNF-α, IL-1ß, and IL-6) in the hippocampus were analyzed after ginsenoside treatment. RESULTS The blood glucose, body weight, Morris correlation index, SOD, MDA, and other test results were increased in the diabetic rats. Ginsenoside ameliorated diabetic cognitive decline. CONCLUSIONS The possible mechanism was related to inhibiting brain oxidative/nitrosative damage and affecting the expression of the cytokines IL-1ß, IL-6, and TNF-α.

Effects of butylphthalide on cognitive decline in diabetic rats.

Butylphthalide, a component extracted from seeds of Chinese celery, is an effective neuroprotective agent used for the treatment of ischemic stroke and dementia. Diabetes may cause central nervous system damage, and diabetes is closely associated with dementia. The aim of the present study was to investigate the effects of butylphthalide on cognitive impairment in a streptozotocin­induced diabetic rat model, and the underlying mechanisms of action. A total of 30 healthy male Sprague Dawley rats were randomly divided into the following 2 groups: Normal control (NC; n=10) and diabetes model (DM) groups (n=20). Diabetes was induced in rats in the DM group by intraperitoneal injection of streptozotocin, and these rats were further subdivided into the following 2 groups: Diabetic control (n=10) and butylphthalide­treated groups (n=10). Following 8 consecutive weeks of treatment, a Morris water maze test was performed and the levels of blood fasting plasma glucose (FPG), superoxide dismutase (SOD), malondialdehyde (MDA) and tumor necrosis factor­α (TNF­α), interleukin (IL)­1ß, and IL­6 inflammatory cytokines in the hippocampus were measured. FPG levels were significantly decreased in the butylphthalide­treated group when compared with the DM group. In addition, cognitive deficits in diabetic rats were improved following butylphthalide treatment. Furthermore, butylphthalide significantly increased the level of SOD, reduced MDA levels, and reduced TNF­α, IL­1ß, and IL­6 levels in the hippocampus when compared with the DM group. The results of the present study suggest that butylphthalide may be an effective neuroprotective agent to improve cognitive dysfunction during diabetes.

Resveratrol Improves Cognitive Impairment by Regulating Apoptosis and Synaptic Plasticity in Streptozotocin-Induced Diabetic Rats.

AIMS: To investigate the effects of resveratrol on cognitive impairment in streptozotocin (STZ)-induced diabetic rats and to explore the mechanisms of that phenomenon. METHODS: Sixty healthy male Sprague Dawley rats were randomly divided into four groups: normal control group (Con group, n = 15), Res group (normal Sprague Dawley rats treated with resveratrol, n = 15), diabetes mellitus group (DM group, n = 15) and DM + Res group (diabetic rats treat with resveratrol, n = 15). Streptozotocin (STZ) was injected intraperitoneally to establish the diabetic model. One week after diabetic model induction, the animals in the Res group and the DM + Res group received resveratrol intraperitoneally once a day for consecutive 4 weeks. The Morris water maze test was applied to assess the effect of resveratrol on learning and memory. To explore the mechanisms of resveratrol on cognition, we detected the protein expression levels of Caspase-3, Bcl-2, Bax, NMDAR1 (N-Methyl-d-Aspartate receptor) and BDNF (Brain Derived Neurotrophic Factor) via western blotting analysis. RESULTS: Resveratrol has no obvious effect on normal SD rats. Compared to Con group, cognitive ability was significantly impaired with increased expression of Caspase-3, Bax and down-regulation of Bcl-2, NMDAR1 and BDNF in diabetic rats. By contrast, resveratrol treatment improved the cognitive decline. Evidently, resveratrol treatment reversed diabetes-induced changes of protein expression. CONCLUSIONS: Resveratrol significantly ameliorates cognitive decline in STZ-induced diabetic model rats. The potential mechanism underlying the protective effect could be attributed to the inhibition of hippocampal apoptosis through the Bcl-2, Bax and Caspase-3 signaling pathways and improvement of synaptic dysfunction. BDNF may also play an indispensable role in this mechanism.

Association between serum non-high-density lipoprotein cholesterol and cognitive impairment in patients with acute ischemic stroke.

BACKGROUND: Non-high density lipoprotein cholesterol (HDL-C) could be a good predictor of vascular disease outcomes. To evaluate the association between serum non-HDL-C and cognitive impairment in patients with acute ischemic stroke. METHODS: A total of 725 hospitalized patients with acute ischemic stroke were enrolled. They received conventional treatment. Cognitive function was assessed on the 3rd day after admission using mini-mental state examination (MMSE), Montreal Cognitive Assessment (MoCA), Activity of Daily Living Scale (ADL), and Neuropsychiatric Inventory (NPI, and Hamilton depression rating scale 21-item (HAMD-21). Lipid profile and biochemical markers were measured, and non-HDL-C was calculated. RESULTS: Compared with patients with normal non-HDL-C, those with high non-HDL-C showed lower MMSE (23.1 ± 4.9 vs. 26.0 ± 4.6, P < 0.001) and MoCA (20.4 ± 6.4 vs. 22.2 ± 5.3 P = 0.01) scores, higher NPI (6.2 ± 1.2 vs. 3.3 ± 1.5, P < 0.001) and HADM-21 (6.0 ± 2.2 vs. 4.5 ± 1.9, P < 0.001) scores, and higher homocysteine (16.0 ± 3.8 vs. 14.3 ± 2.0 mmol/L, P = 0.044), fasting blood glucose (6.4 ± 2.7 vs. 6.1 ± 2.1 mmol/L, P = 0.041), and HbA1c (6.80 ± 1.32 % vs. 6.52 ± 1.17 %, P = 0.013) levels. MMSE (r = -0.526, P < 0.001), MoCA (r = -0.216, P < 0.001), and NPI (r = 0.403, P < 0.001) scores were correlated with non-HDL-C levels. High non-HDL-C levels were an independent risk factor for cognitive disorders after acute ischemic stroke (P = 0.034, odds ratio = 3.115, 95 % confidence interval: 1.088-8.917). CONCLUSIONS: High serum non-HDL-C levels, age, education, homocysteine levels, and HAMD score were independent risk factors of cognitive impairment in patients with acute ischemic stroke. The risk of cognitive disorders after acute ischemic stroke increased with increasing non-HDL-C levels. This parameter is easy to assess in the clinical setting.

Systematic review of the prevalence and incidence of Parkinson's disease in the People's Republic of China.

BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative disease, and obtaining accurate epidemiological data for this disease is very important for policy-making in public health. The purpose of this study was to determine the prevalence and incidence of PD in the People's Republic of China and explore possible future research directions. METHODS: We systematically retrieved studies of the prevalence and incidence of PD in the People's Republic of China, Taiwan, and Hong Kong, and standardized the data according to the world's population in 2000. RESULTS: Fifteen eligible studies were retrieved. Most were cross-sectional studies, and two thirds of the research was from the People's Republic of China. The prevalence of PD was reported in all the studies, but only two studies reported incidence data. The prevalence of PD in the People's Republic of China ranged from 16 to 440.3/100,000, and the annual incidence ranged from 1.5 to 8.7/100,000. CONCLUSION: The prevalence of PD in the People's Republic of China has been widely investigated in the studies published to date. However, due to methodological heterogeneity, the data reported by the different studies are not comparable. There is still a lack of information on the incidence of PD in the People's Republic of China. Therefore, future research is required to answer this question.