BACKGROUND Comorbid non-insulin-dependent diabetes mellitus (NIDDM) and stroke significantly contribute to mortality among older adults. This study examines age-adjusted mortality rates (AAMRs) and disparities by demographics, region, and age groups to identify trends and guide public health efforts. AIM To analyze trends in AAMRs due to comorbid NIDDM and stroke among older adults. The study aims to identify demographic, geographic, and age-related disparities to inform targeted public health strategies. METHODS Mortality data from the Centers for Disease Control records were analyzed. AAMRs per 100000 and annual percentage changes (APCs) with 95%CI were calculated using Joinpoint Regression RESULTS Between 1999 and 2022, 209001 deaths among adults aged 55+ were attributed to comorbid NIDDM and stroke, with women accounting for 111481 and men 97520 deaths. Urban-rural disparities revealed distinct patterns, with a sharper rise in metropolitan areas post-2014 (APC: 8.6) as compared to non-metropolitan areas. Racial disparities were pronounced, particularly among the Asian/Pacific Islander population, with a steep increase post-2018 (APC: 17.6). Age-stratified analysis showed a marked rise in mortality for ages 55- 64 and 85+ from 2015 onwards (APC: 14.3 and 13.5, respectively). Regional trends highlighted the West as having the highest AAMR (14.4), while the Northeast exhibited the lowest (7.0). State-level analysis showed West Virginia with the highest AAMR (18.7) and Nevada the lowest (3.8). CONCLUSION Rising mortality from comorbid NIDDM and stroke underscores increasing disparities across gender, race, age, and regions. Urgent, tailored interventions are required to mitigate these inequities.
BACKGROUND A stroke is a significant brain event that impinges on individual motor or cognitive functions. In the lacunar stroke subtype of ischemic stroke, which results from blocked blood flow in certain brain areas, cases of dysarthria due to impaired blood flow are not uncommon. However, limited literature and research on the relevant pathophysiology and neural pathways exist. CASE SUMMARY We focus on a 60-year-old female with subacute stroke presenting symptoms including tongue deviation to the right, speech difficulty, choking on water, and biting the oral mucosa. She did not exhibit abnormalities in limb movement or sensation except for numbness in the tongue. We use single-photon emission computed tomography to reveal reduced blood flow in the left parietal lobe and bilateral temporal lobes. This report presents an atypical case of dysarthria, who exhibits abnormal articulation along with abnormal sensation and numbness in the tongue, prompting further investigation into the association between lacunar stroke subtypes, altered blood perfusion in affected brain regions, and neurological clinical status. CONCLUSION Dysarthria-plus syndrome in lacunar stroke isn’t solely related to motor function but also affects sensory function such as oral numbness.
BACKGROUND The sympathetic nervous system makes medium and large peripheral arteries smaller to slow the blood flowing through them.AIM To observe brachial artery sympathetic innervation.METHODS We developed a neurophysiological autonomous test that measured the effects of peripheral sympathetic fibres on peripheral arteries. Our specific objective was to find the sympathetic innervation of the brachial artery. To accomplish this purpose, the brachial artery baseline diameter and flow rate were measured in the right arm of the patients. Afterwards, electrical stimulus was applied to the medial nerve for 5 s. Through electrical sympathetic activation, the vessel diameter and overall flow rate will decrease. After 7 d, a similar experiment was repeated using the ulnar nerve.RESULTS The differences in diameter and flow rate of the brachial artery in response to median and ulnar nerve activation were compared. In the total group, no significant difference in diameter was seen between medial and ulnar nerve stimulation（P = 0.648）. The difference in absolute slowdown of flow rate between median nerve stimulation and ulnar nerve stimulation was not statistically significant for the entire group（P = 0.733）.CONCLUSION As a target organ, the brachial artery receives an equal amount of sympathetic innervation from the median and the ulnar nerves.
BACKGROUND The case report supports the recent findings regarding the correlation of posttraumatic stress disorder（PTSD） and schizophrenia. The report accomplished the following objectives:（1） To present a case of an adult female manifesting with somatic type of delusion（foul body odor） and history of PTSD;（2） To discuss the biopsychosocial factors, psychodynamics and management of the patient; and（3） To differentiate delusional disorder from schizophrenia according to recent studies. Schizophrenia and delusional disorder have certain defining features that separate the two. However, at times it may be difficult to actually classify one from the other. A psychiatrist must be able to carefully examine and assess the history of the patient, helping them share early life experiences of past traumatic events. The early past traumatic experiences and life events greatly influence the predisposition of a patient to develop schizophrenia. However, people with schizophrenia were known to underreport their trauma experience.CASE SUMMARY This is a case of a young adult female diagnosed with delusional disorder with a history of PTSD and associated depression. The patient manifested with somatic type of delusion with a fixed false belief that a foul body odor was coming from her underarms.CONCLUSION Developing a therapeutic alliance is vital in achieving therapy goals through empathy, support and warmth between the patient and physician. History of PTSD predisposes patients with schizophrenia to develop depressive disorders as a comorbidity.
BACKGROUND Clarithromycin is a macrolide antibiotic commonly prescribed to patients with upper respiratory and otolaryngological infections. Neuropsychiatric adverse effects of clarithromycin include agitation, insomnia, delirium, psychosis, and seizure.CASE SUMMARY A 52-year-old man was admitted to our hospital with a convulsion. He had ＞ 10-year history of clarithromycin intake for chronic sinusitis. One week before admission, he started to take diltiazem for angina pectoris. On admission, his convulsion subsided. His electroencephalography showed frontal intermittent rhythmic delta activity. One week after he ceased clarithromycin, his electroencephalographic abnormalities disappeared. We suggested that the patient developed convulsions due to increased blood levels of clarithromycin caused by oral administration of diltiazem, which is involved in CYP3A metabolism.CONCLUSION Clarithromycin has a relatively high safety profile and is a frequently prescribed drug. However, there are a few previous reports of clarithromycin-related convulsive disorders. Clinicians should be aware of the drug interaction and rare side effects of seizures.
Early diagnosis and prognosis of ischemic stroke remains a critical challenge in clinical settings. A blood biomarker can be a promising quantitative tool to represent the clinical manifestations in ischemic stroke. Cell-free DNA (cfDNA) has recently turned out to be a popular circulating biomarker due to its potential relevance for diagnostic applications in a variety of disorders. Despite bright outlook of cfDNA in clinical applications, very less is known about its origin, composition, or function. Several recent studies have identified cell-derived mitochondrial components including mitochondrial DNA (mtDNA) in the extracellular spaces including blood and cerebrospinal fluid. However, the time course of alterations in plasma mtDNA concentrations in patients after an ischemic stroke is poorly understood. DNA is thought to be freed into the plasma shortly after the commencement of an ischemic stroke and then gradually decreased. However, the importance of cell-free mtDNA (cf-mtDNA) in ischemic stroke is still unknown. This review summarizes about the utility of biomarkers which has been standardized in clinical settings and role of cfDNA including cf-mtDNA as a non-invasive potential biomarker of ischemic stroke. Core Tip: Early and accurate diagnosis of ischemic stroke is critical to achieve favorable clinical outcome. Cell-free DNA can be used as a useful biomarker for early diagnosis and prognosis of ischemic stroke for saving time and increasing the likelihood of successful intervention. Discriminative quantification of cell free mitochondrial DNA instead of overall circulating DNA may provide more significant value for identifying real-time host response. The future practical adoption of this strategy may be aided by reliable and standardized quantification of cell-free mitochondrial DNAs in ischemic stroke patients to design more effective diagnosis, prognosis and therapeutic strategies.
Periodontal surgery in a stage II Parkinson’s disease patient: Report of a case with special considerations
Sleep is essential for maintaining normal physiological processes. It has been broadly divided into rapid eye movement sleep（REMS） and non-REMS（NREMS）; one spends the least amount of time in REMS. Sleep（both NREMS and REMS） disturbance is associated with most altered states, disorders and pathological conditions. It is affected by factors within the body as well as the environment, which ultimately modulate lifestyle.Noradrenaline（NA） is one of the key molecules whose level increases upon sleep-loss, REMS-loss in particular and it induces several REMS-loss associated effects and symptoms. The locus coeruleus（LC）-NAergic neurons are primarily responsible for providing NA throughout the brain. As those neurons project to and receive inputs from across the brain, they are modulated by lifestyle changes, which include changes within the body as well as in the environment. We have reviewed the literature showing how various inputs from outside and within the body integrate at the LC neuronal level to modulate sleep（NREMS and REMS） and vice versa. We propose that these changes modulate NA levels in the brain, which in turn is responsible for acute as well as chronic psychosomatic disorders and pathological conditions.
Alcohol is a well-recognized teratogen that can causevariable physical and behavioral effects on the fetus.Alcohol use and abuse during pregnancy is one of the major health and societal problems and has been linked to a wide range of birth defects in the offspring collectively termed as fetal alcohol spectrum disorder（FASD）. The severity of abnormalities may depend on a number of factors that include the amount, the frequency, the period during gestation and the route of alcohol administration. The current knowledge about the neurobiological basis of FASD is limited. However, recent studies have suggested that the membrane-derived lipids especially bioactive endogenous cannabinoids（eCB）such as arachidonyl ethanolamide and 2-arachidonyl glycerol resulting from alcohol exposure, may play a significant role in modulating neurophysiological and neurobehavioral effects in chronic alcohol exposed adult animals. Based on these findings and on reported studies on the role of eCB signaling in neurodevelopment and behavior, it is speculated that the eC B signaling may play a critical role in fetal alcohol syndrome and FASD-related behavioral effects. The current discussion will touch upon some of the mechanistic explanations about the role of eCB signaling system in FASD and provide further guidance for future direction.
AIM:To investigate predictors of incident stroke in a large epidemiological sample of cognitively healthy individuals in their early 60’s.METHODS:Cardiovascular（systolic and diastolic blood pressure, hypertension status and medication, body mass index, lung forced vital capacity）, lifestyle（alcohol intake, smoking, physical activity）, mental health（anxiety and depression status, medication and symptomatology）, cognition（executive function, processing speed, working memory, sensorimotor skills）, and personality measures（behavioural inhibition and activation, positive and negative affect, neuroticism, psychoticism, extraversion） were investigated as predictors of incident stroke in 1774 participants from the Personality and Total Health Through Life Project over an 8-year follow-up.Logistic regression analyses controlled for age, gender, and education were conducted in the whole cohort as well as in case-control subanalyses including precisely matched controls to identify factors associated with stroke incidence.RESULTS:The cohort selected had a mean age of 62.5 years（SD = 1.5） and was 48.6% female with an average of 14.1 years of education（SD = 2.6）.When 28 individuals with incident stroke were compared to 1746 cognitively healthy individuals in multivariate logistic regression analyses the only significant predictors of stroke across the five domains considered（cardiovascular, lifestyle, mental health, cognition, personality） and after controlling for gender, age, and education were systolic blood pressure（per unit above 140 mm Hg:OR = 1.04, 95%CI:1.01-1.07, P = 0.002）, smoking（trend OR = 2.28, 95%CI:0.99-5.24, P = 0.052）, and sensorimotor skills（purdue pegboard:OR = 0.80, 95%CI:0.62-0.96, P = 0.037）.Similarly, in matched-control analyses significant group differences were found for systolic blood pressure（P = 0.001）, smoking（P = 0.036）, and sensorimotor skills（P = 0.028）.CONCLUSION:Identified predictors of incident stroke in community-living individuals included high systolic blood pressure and smoking- but also, sensorimotor performance, a measure which has not yet been reported in the literature.
Edema formation is a major problem following traumatic spinal cord injury (SCI) that acts to exacerbate secondary damage. Severity of edema correlates with reduced neurological outcome in human patients. To date, there are no effective treatments to directly resolve edema within the spinal cord. The aquaporin-4 (AQP4) water channel is found on membranes of astrocytic endfeet in direct contact with blood vessels, the glia limitans in contact with the cerebrospinal fluid and ependyma around the central canal. Being so locally expressed at the interface between fluid and tissue allow AQP4 channels to play an important role in the bidirectional regulation of water homeostasis under normal conditions and following trauma. With the need to better understand the pathophysiology underlying the devastating cellular events in SCI, animal models have become an integral part of exploration. Inevitably, several injury models have been developed (contusion, compression, transection) resulting in difficult interpretation between studies with conflicting results. This is true in the case of understanding the role of AQP4 in the progression and resolution of edema following SCI, whose role is still not completely understood and is highly dependent on the type of edema present (vasogenic vs cytotoxic). Here, we discuss regulation of AQP4 in varying injury models and the effects of potential therapeutic interventions on expression, edema formation and functional recovery. Better understanding of the precise role of AQP4 following a wide range of injuries will help to understand optimal treatment timing following human SCI for prime therapeutic benefit and enhanced neurological outcome.
The primary purpose of this article was to review the current literature regarding the clinical consequences of centipede envenomation in humans,in order to determine whether the bite of these arthropods is neurotoxic to humans or not. A thorough search of the literature regarding the clinical consequences of centipede bites in humans was applied,with great respect to neurological symptoms potentially caused by such bites. Centipede bite commonly causes only local reactions,which usually resolve within a few days without sequelae. The patients in the majority of centipede envenomations describe a painful but benign syndrome. However,mild constitutional symptoms are relatively frequent. Remarkably,centipedes can rarely cause severe systematic reactions such as anaphylaxis or even hypotension and myocardial ischemia. Factors such as patient age,comorbidity,anatomic site of envenomation,and size/species of centipede should be considered when evaluating a centipede envenomation victim. According to the current literature,the centipede bite does not seem to be neurotoxic to humans. However,it commonly causes symptoms mediated by the nervous system. These include local and generalized symptoms,with the first dominated by sensory disturbances and the second by non-specific symptoms such as headache,anxiety and presyncope. Based on our results,the answer to our study’s question is negative. The centipede bite is not neurotoxic to humans. However,it commonly causes symptoms mediated by the nervous system,which include primarily local pain and sensory disturbances,as well as generalized non-specific symptoms such as headache,anxiety and vagotonia.
Human T-cell lymphotropic virus type 1（HTLV-1）-associated myelopathy/tropical spastic paraparesis（HAM/TSP） is a slowly progressive neurodegenerative disorder in which lesions of the central nervous system cause progressive weakness, stiffness, and a lower limb spastic paraparesis. In some cases, polymyositis, inclusion bodymyositis, or amyotrophic lateral sclerosis-like syndromes are associated with HTLV-1. TSP was first described in Jamaica in 1888 and known as Jamaican peripheral neuritis before TSP was related to HTLV-1 virus, the first retrovirus being identified, and the disease is since named HAM/TSP. There is no established treatment program for HAM/TSP. Prevention is difficult in lowincome patients（i.e., HTLV-1 infected breast feeding mothers in rural areas, sex workers）. Thus, there is a need for new therapeutic avenues. Therapeutic approaches must be based on a better understanding, not only of clinical and clinicopathological data, but also of the pathophysiology of the affection. Consequently, a better understanding of existing or newly developed animal models of HAM/TSP is a prerequisite step in the development of new treatments.
Time windows for postnatal changes in morphology and membrane excitability of genioglossal and oculomotor motoneurons
TWIK-related acid-sensitive K+（TASK） channels give rise to leak K+ currents which influence the resting membrane potential and input resistance. The wide expression of TASK1 and TASK3 channels in the central nervous system suggests that these channels are critically involved in neurological disorders. It has become apparent in the past decade that TASK channels play critical roles for the development of various neurological disorders. In this review, I describe evidence for their roles in ischemia, epilepsy, learning/memory/cognition and apoptosis.
