Parkinson's disease patients with absence of normal dipping status were more vulnerable to cognitive impairment from the early stages.

INTRODUCTION: The objective of this study was to determine the characteristics of cognitive function in Parkinson's disease (PD) patients with different dipping statuses. METHODS: Consecutive PD patients were recruited for this study. All participants underwent 24-h ambulatory blood pressure monitor (ABPM). Corresponding scales were employed to evaluate both motor and non-motor symptoms. The subjects were categorized into reverse, reduced, normal, and extreme dipping groups based on dipping patterns. Additionally, they were divided into early and non-early stage groups according to the disease duration being more than 5 years. RESULTS: The proportions of the four dipping groups in the early and non-early stage groups exhibited no significant differences. The Montreal Cognitive Assessment (MoCA) scores in the reverse group were significantly lower than those in the normal dipping group (16.2 ± 5.8 vs 21.1 ± 6.1,P = 0.003). The attention as well as delayed recall scores in the reverse dipping group were significant lower than those in the normal dipping group (P = 0.042; P < 0.001). The multivariate linear regression analysis revealed that absence of normal dipping was an independent risk factor (OR = -2.252; P = 0.027) for MoCA scores for PD patients. CONCLUSIONS: PD patients with absence of normal dipping status were more vulnerable to cognitive impairment from the early stages of the disease. The 24-h ABPM is recommended for early detection of abnormal dipping status and identification of individuals at risk for cognitive decline.

Co-infection with Mycobacterium tuberculosis and Nocardia farcinica in a COPD patient: a case report.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a common respiratory disease characterized by persistent airflow limitation. Infection with either Mycobacterium tuberculosis or Nocardia in COPD patients has been reported. However, co-infection with Mycobacterium tuberculosis and Nocardia is rare. Herein, we described such a patient with COPD in a primary hospital, and the diagnosis process. CASE PRESENTATION: A 79-year-old female farmer with COPD was consecutively admitted to two hospitals with chief complaints of worsening cough, sputum and gasping since January10, 2022. Microbiological examination was not performed at the first hospital due to unknown reasons, and empirical antibiotic treatment was not effective. The patient was subsequently referred to our hospital. After screening the source of infection and the pathogen, she was diagnosed with tuberculosis. However, the patient did not benefit from antituberculosis treatment, with no remission of respiratory tract symptoms. Cerebrospinal fluid and bronchoalveolar lavage fluid specimens were subsequently sent for microbiological examination. The results indicated Mycobacterium tuberculosis and Nocardia.spp. After four days of bacterial culture, Nocardia.spp grew on medium, and Nocardia.farcinica was identified by the MALDI-TOF MS system and 16 s RNA. The patient was prescribed trimethoprim sulfamethoxazole (TMP/SMX) in combination with anti-tuberculosis drugs to treat the co-infection. She showed gradual improvement and was discharged from the hospital on February 19, 2022. However, the follow-up results were unclear. CONCLUSIONS: Co-infection with Nocardia and Mycobacterium tuberculosis should be considered in COPD patients. Repeated microbiological and microscopy examinations are essential in primary hospitals.

SIM imaging resolves endocytosis of SARS-CoV-2 spike RBD in living cells.

It is urgent to understand the infection mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) for the prevention and treatment of COVID-19. The infection of SARS-CoV-2 starts when the receptor-binding domain (RBD) of viral spike protein binds to angiotensin-converting enzyme 2 (ACE2) of the host cell, but the endocytosis details after this binding are not clear. Here, RBD and ACE2 were genetically coded and labeled with organic dyes to track RBD endocytosis in living cells. The photostable dyes enable long-term structured illumination microscopy (SIM) imaging and to quantify RBD-ACE2 binding (RAB) by the intensity ratio of RBD/ACE2 fluorescence. We resolved RAB endocytosis in living cells, including RBD-ACE2 recognition, cofactor-regulated membrane internalization, RAB-bearing vesicle formation and transport, RAB degradation, and downregulation of ACE2. The RAB was found to activate the RBD internalization. After vesicles were transported and matured within cells, RAB was finally degraded after being taken up by lysosomes. This strategy is a promising tool to understand the infection mechanism of SARS-CoV-2.

The clinical value of serum xanthine oxidase levels in patients with acute ischemic stroke.

Xanthine oxidase (XO), a form of xanthine oxidoreductase, is widely distributed in various human tissues. As a major source for the generation of superoxide radicals, XO is involved in the induction of oxidative stress and inflammation during ischemic and hypoxic tissue injury. Therefore, we designed this study to identify the role of serum XO levels in acute ischemic stroke (AIS) pathogenesis. In this single-center prospective study, 328 consecutive patients with AIS for the first time were included, and 107 age- and sex-matched healthy controls from a community-based stroke screening population were also included. The serum levels of XO and several conventional stroke risk factors were assessed. Multivariate analysis was applied to evaluate the relationship between serum levels of XO and clinical outcomes, and nomogram models were developed to predict the onset, progression and prognosis of AIS. Compared with the healthy control group, the serum level of XO was significantly higher in the AIS group (P < 0.05) and was an independent risk factor for AIS (OR 8.68, 95% CI 4.62-14.33, P < 0.05). Patients with progressive stroke or a poor prognosis had a much higher serum level of XO than patients with stable stroke or a good prognosis (all P < 0.05). In addition, the serum level of XO was an independent risk factor for stroke progression (OR 1.98, 95% CI 1.12-3.50, P = 0.018) and a poor prognosis (OR 2.51, 95% CI 1.47-3.31, P = 0.001). The nomogram models including XO to predict the onset, progression and prognosis of AIS had good prediction and differentiation abilities. The findings of this study show that the serum level of XO on admission was an independent risk factor for AIS and had certain clinical predictive value for stroke progression and prognosis in patients with AIS.

The effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on ischemic stroke and the possible underlying mechanisms.

Purpose: As of November 28, 2020, COVID-19 has been reported in 220 countries with 61,036,793 confirmed cases and 1,433,316 confirmed deaths; countries became vigilant around the world. In addition to SARS-CoV-2 causing pneumonia, many studies have reported ischemic stroke in patients with COVID-19. This article describes the effects and possible underlying mechanisms of SARS-CoV-2 on ischemic stroke.Materials and methods: A literature search was performed using PubMed, Web of Science, and other COVID-dedicated databases and the combination of the keywords 'SARS-CoV-2', 'COVID-19' and 'ischemic stroke' up to November 28, 2020.Results: SARS-CoV-2 invades the host through angiotensin converting enzyme 2 (ACE2). ACE2 is expressed not only in the lungs, but also in the brain and vascular endothelial cells. SARS-CoV-2 infection might cause direct vascular disease or enhance the immunogenic thrombosis environment through several mechanisms. SARS-CoV-2 infection can modulate the host immune response and can cause inflammation, coagulation disorders, renin angiotensin system disorders, hypoxia, and stress disorders, which may lead to the occurrence of ischemic stroke.Conclusions: Some patients with COVID-19 can develop ischemic stroke. Ischemic stroke has a high risk of causing disability and is associated with a high mortality rate. It is hoped that when medical staff treat patients with COVID-19, they would pay attention to the occurrence of ischemic stroke to improve the prognosis of patients with COVID-19.

Mental health and fatigue status of the medical workforce during the COVID-19 outbreak in the Yangzhou city, China.

Background: When the coronavirus disease 2019 (COVID-19) erupted in Yangzhou, China, at the end of July 2021, medical workers in Yangzhou immediately joined the frontline for the fight against the pandemic. This study aimed to identify the mental health and fatigue experienced by the medical workers in Yangzhou during the COVID-19 outbreak. Methods: We included 233 medical workers who participated in the front-line work for more than 1 month through the questionnaire, including doctors, nurses, medical technicians and medical students. The generalized anxiety disorder-7 (GAD-7), patient health questionnaire-9 (PHQ-9), and Fatigue self-assessment scale (FSAS) were administered to the participants and their responses were evaluated. Results: A total of 233 eligible questionnaires were received. Among them, 130 people (57.08%) were probably anxious and 141 (60.52%) people were clinically depressed. Poor sleep was considered an independent risk factor for anxiety (OR = 7.164, 95% CI: 3.365 15.251, p = 0.000) and depression (OR = 6.899, 95% CI: 3.392 14.030, p = 0.000). A high PHQ-9 score was considered an independent risk factor for general fatigue (OR = 1.697, 95% CI: 1.481 1.944, p = 0.000). Mental fatigue (OR = 1.092, 95% CI: 1.027 1.161, p = 0.005) and fatigue response to sleep/rest (OR = 1.043, 95% CI: 1.011 1.076 p = 0.008) were considered independent risk factors for general fatigue. Conclusion: Poor quality of sleep led to probable anxiety, depression, and general fatigue. Mental fatigue and fatigue response to sleep/rest were independent risk factors for depression, which merits attention for battling COVID-19.

Case Report: Paroxysmal hyperhidrosis as an initial symptom in a patient with anti-LGI1 encephalitis.

Anti-leucine-rich glioma-inactivated 1 (LGI1) encephalitis is the second most common cause of autoimmune encephalitis and is characterized by cognitive impairment, psychiatric disorders, and faciobrachial dystonic seizures. In recent decades, literature reports have expanded the phenotypic spectrum associated with the LGI1 autoantibody. The present report describes the case of a 58-year-old man who presented with repetitive unilateral hyperhidrosis of the body and arm as an initial symptom and gradually developed psychiatric symptoms, involuntary movements of the face and arms, and progressive cognitive decline. Anti-LGI1 antibodies were positive in both the serum and cerebrospinal fluid at approximately 2 months after symptom onset, and the patient was, therefore, diagnosed with anti-LGI1 encephalitis. His symptoms, namely hyperhidrosis and involuntary movements, were not relieved by antiepileptic drug treatment, but responded favorably to high-dose steroid therapy and intravenous immunoglobulin. We interpreted the repetitive unilateral hyperhidrosis as possible epilepsy. Based on this case, unilateral hyperhidrosis of the body and arm as a rare neurological presentation can be added to the phenotypic spectrum of anti-LGI1 encephalitis, and early recognition of this manifestation might support timely diagnosis and treatment.

[Design and application of a multi-assisted function incision and orifice closure buckle].

Incision infection is one of the common complications in surgery. Infected incisions usually need to perform procedures including suture removal, debridement, drainage, sterilization and anti-inflammatory. Until, the wound edge was sutured again after the wound infection was controlled. This contributes to considerable physical and psychological suffering for patients. To this end, with Dalian Medical University as the main inventor and other several experts, a multi-assistance function incision and orifice closure buckle have been designed and obtained the national utility model patent (patent number: ZL 2019 2 1803918.4). The closure buckle with was composed of two blocks with an adhesive layer and one tensioning mechanism. The device is easy to operate, and could effectively play an analgesic, antibacterial and promote healing on the basis of perfecting its wound margins and orifice. It has certain clinical application value.

Immune biomarkers are associated with poststroke fatigue at six months in patients with ischemic stroke.

Poststroke fatigue (PSF) is detrimental to rehabilitation and the pathogenesis is still indefinite. The neutrophil-to-lymphocyte ratio (NLR) and prognostic nutritional index (PNI) are immune indicators reflecting the status of inflammation and nutrition and have been widely applied as prognostic biomarkers. We pointed to examine the connections between PSF and NLR, PNI in acute ischemic stroke patients. Between October 2020 and September 2021, 333 participants radiologically confirmed with first-ever ischemic stroke were enrolled from patients consecutively admitted to the Department of Neurology. Fatigue severity was evaluated by Fatigue Severity Scale (FSS) at 6 months after stroke. A total of 130 (39.0%) stroke survivors had PSF at 6 months after stroke. Patients in the PSF group had higher NLR and lower PNI on admission. The correlations between PSF and NLR (r = 0.750), and PNI (r = -0.685) were significant. In multivariate analyses, NLR (odds ratio [OR] = 11.132, 95% confidence internal [CI]:4.640-26.704, P < 0.001), PNI (OR = 0.420, 95%CI:0.292-0.603, P < 0.001), and self-rating depression scale score (OR = 1.125, 95%CI:1.028-1.232, P < 0.001) stayed as independent predictors for PSF at 6 months after adjusting potential confounders. With the Receiver Operating Characteristic curve, the areas under the curve were 0.898 (95%CI:0.862-0.934, P < 0.001), and 0.862 (95%CI:0.819-0.904, P < 0.001), respectively; and the optimal cut-off values of NLR and PNI that best identified PSF were 4.05 (sensitivity:70.8%, specificity:96.1%), and 48.4 (sensitivity:71.5%, specificity:90.1%), respectively. In conclusion, NLR and PNI on admission were independently associated with PSF at 6 months in ischemic stroke persons. NLR and PNI can be used to early screen individuals at high risk for PSF.

Hashimoto's encephalopathy presenting as Wernekinck commissure syndrome: A case report.

The Wernekinck commissure syndrome is extremely rare in a clinical setting. This condition has been previously reported in association with midbrain infarction, midbrain hemorrhage, demyelinating pseudotumor, and optic neuromyelitis spectrum disease, but not with Hashimoto's encephalopathy. Herein, we report the case of a 44-year-old hypertensive man who developed cerebellar ataxia, internuclear ophthalmoplegia, and cognitive decline. Magnetic resonance imaging (MRI) of the brain revealed brain stem damage involving Wernekinck commissure. Initially, this patient was diagnosed with acute midbrain infarction in another hospital. However, his symptoms did not improve after the administration of anti-platelet aggregation drugs, statin, and free radicals scavenging treatment. Re-examination of cranial MRI revealed abnormal signals in the left parietal lobe. After a series of investigations that excluded cerebral infarction and neurodegenerative diseases, Hashimoto's encephalopathy was finally diagnosed. The patient's symptoms improved remarkably after treatment with methylprednisolone and γ-globulin. To the best of our knowledge, there are no other reports on the onset of Wernekinck commissure syndrome in the clinical manifestations of Hashimoto's encephalopathy.

Bioactive lipids and their metabolism: New therapeutic opportunities for Parkinson's disease.

Parkinson's disease (PD) is a neurological disorder characterized by motor dysfunction, which can also be associated with non-motor symptoms. Its pathogenesis is thought to stem from a loss of dopaminergic neurons in the substantia nigra pars compacta and the formation of Lewy bodies containing aggregated α-synuclein. Recent works suggested that lipids might play a pivotal role in the pathophysiology of PD. In particular, the so-called 'bioactive' lipids whose changes in the concentration may lead to functional consequences and affect many pathophysiological processes, including neuroinflammation, are closely related to PD in terms of symptoms, disease progression and incidence. This study aimed to explore the molecular metabolism and physiological functions of bioactive lipids, such as fatty acids (mainly unsaturated fatty acids), eicosanoids, endocannabinoids, oxysterols, representative sphingolipids, diacylglycerols and lysophosphatidic acid, in the development of PD. The knowledge of bioactive lipids in PD gained through preclinical and clinical studies is expected to improve the understanding of disease pathogenesis and provide novel therapeutic avenues.

Alzheimer's disease in elderly COVID-19 patients: potential mechanisms and preventive measures.

Advanced age correlates with higher morbidity and mortality among patients affected with the novel coronavirus disease 2019 (COVID-19). Because systemic inflammation and neurological symptoms are also common in severe COVID-19 cases, there is concern that COVID-19 may lead to neurodegenerative conditions such as Alzheimer's disease (AD). In this review, we summarize possible mechanisms by which infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, may cause AD in elderly COVID-19 patients and describe preventive measures to mitigate risk. Potential mechanisms include NLRP3 inflammasome activation and IL-1ß release, renin-angiotensin system hyperactivation, innate immune activation, oxidative stress, direct viral infection, and direct cytolytic ß-cell damage. Anti-inflammatory therapies, including TNF-α inhibitors and nonsteroidal anti-inflammatory drugs, antioxidants such as the vitamin E family, nutritional intervention, physical activity, blood glucose control, and vaccination are proposed as preventive measures to minimize AD risk in COVID-19 patients. Since several risk factors for AD may converge during severe SARS-CoV-2 infection, neurologists should be alert for potential symptoms of AD and actively implement preventive measures in patients presenting with neuropsychiatric symptoms and in high-risk patients such as the elderly.

High red blood cell distribution width levels could increase the risk of hemorrhagic transformation after intravenous thrombolysis in acute ischemic stroke patients.

The association between the red blood cell distribution width (RDW) and hemorrhagic transformation (HT) after thrombolysis in acute ischemic stroke patients remains inconclusive. Our study aimed to assess whether high RDW levels are associated with the occurrence of HT after thrombolysis. Data were consecutively collected and retrospectively analyzed for stroke patients treated with thrombolysis between 1 January 2017 and 31 December 2019. The primary outcomes were the occurrence of HT and symptomatic HT. Among the 286 patients enrolled, 36 (12.6%) developed HT and15 (5.2%) were classified as symptomatic HT. Patients with high RDW levels were associated with a higher percentage of HT and symptomatic HT (P<0.05). The RDW levels in the HT and symptomatic HT groups were also greater compared with the no-HT group (P<0.001). Multivariable logistic regression analysis revealed that high RDW levels were independently associated with an increased risk of HT (adjusted odds ratio 2.5, 95 % CI, 1.74-3.83 P < 0.001). In conclusion, we found that high RDW levels may be an independent predictor of HT in stroke patients after thrombolysis.

Possible inflammatory mechanisms and predictors of Parkinson's disease patients with fatigue (Brief Review).

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopamine-producing neurons in the substantia nigra and the abnormal cytoplasmic accumulation of proteinaceous aggregates called Lewy bodies (LBs), mainly composed of α-synuclein (α-syn). In recent years, it has been gradually recognized that fatigue is one of the most common and disabling symptoms in PD patients, with a prevalence of approximately 50%. Although neuroinflammation, a pathological hallmark of PD, is closely associated with fatigue, present mechanisms of fatigue in PD patients have not yet been systematically summarized, with their inflammatory predictors remaining controversial. Therefore, the aim of this brief review is to fill in the gaps in our understanding on the inflammatory factors involved in the pathophysiological mechanisms of fatigue and predicting its occurrence in PD patients. The determination of fatigue is mainly assessed using the Parkinson Fatigue Scale 16 (PFS-16) and Fatigue Severity Scale 9 (FSS-9). Several studies have reported that inflammatory marker levels, such as interleukin-6 (IL-6), and other inflammatory predictors closely associated with fatigue, such as soluble IL-2 receptor (sIL-2R), tumor necrosis factor alpha (TNF-α), high-sensitivity C-reactive protein (hs-CRP), neutrophil-to-lymphocyte ratio (NLR), and red blood cell distribution width (RDW), may help detect fatigue. Moreover, the following inflammatory mechanisms may be involved. (1) Abnormal aggregation of α-syn undergoes a conformational change, which then activates toll-like receptor 4 (TLR4) to release a large number of proinflammatory cytokines, causing fatigue symptoms. (2) Chronic peripheral inflammation and immune activation responses induce elevated levels of proinflammatory cytokines in PD patients, which enter the brain mainly through the traditional endocrine route or via direct vagus nerve transmission. The rising levels of proinflammatory cytokines cause the destruction of the blood-brain barrier (BBB) by combining with BBB endothelial cells, allowing many proinflammatory cytokines to cross the destroyed BBB and enter the brain, preventing astrocytes from reuptaking glutamate and laying foundations for the occurrence of fatigue. Furthermore, studies have suggested that fatigue symptoms in PD patients often represent a poor prognosis. Nevertheless, if the aforementioned inflammatory markers can effectively predict the occurrence of fatigue and allow early intervention, the prognosis of PD patients could be significantly improved. At present, its management mainly includes medical treatment (levodopa, dopamine receptor agonists, rasagiline, and antidepressants) and non-medical treatment (acupuncture and yoga). Thus, it is of great significance to be able to practice early detection and intervention in fatigue and improve the prognosis of patients with PD.

The neuroprotective effect of phillyrin in intracerebral hemorrhagic mice is produced by activation of the Nrf2 signaling pathway.

Phillyrin, a natural plant extract, has significant antioxidant and anti-apoptotic effects. However, its effect on intracerebral hemorrhage (ICH) remains unclear. In this study, we investigated a potential role for phillyrin in the regulation of the oxidative stress and apoptosis induced by ICH. A model of ICH was induced by collagenase IV (0.2 U in 1 µl sterile normal saline) in male C57BL/6J (B6) mice and different doses of phillyrin (5, 15, or 30 mg/kg) were intraperitoneally (i.p.) injected at 30 min, 6 h, and 22 h after modeling. We found that phillyrin significantly reduced neural function and lesion volume, improved injury of white and grey matter around the lesion, decreased apoptosis and oxidative stress, increased the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase 1(HO-1), NADPH quinone oxidoreductase 1 (NQO1) and Superoxide Dismutase-1(SOD-1) in vitro and in vivo, and protected neurons from the stimulation of hemin by promoting Nrf2 nuclear translocation. Treatment with ML385 (Nrf2 inhibitor) completely reversed the protective effects of phillyrin in vivo after ICH injury. Based on our findings, we conclude that phillyrin treatment alleviates ICH injury-induced apoptosis and oxidative stress via activation of the Nrf2 signaling pathway, highlighting a potential role for phillyrin as an ICH therapeutic.

ASPECT scores of patients with focal intracerebral hemorrhage were correlated with their short- and medium-term functional outcomes.

PURPOSE: The Alberta Stroke Program Early CT Score (ASPECTS) is widely used to guide thrombolytic therapy and predict the functional outcome of patients with acute ischemic stroke (AIS). Whether ASPECTS can predict the functional outcome of patients with intracerebral hemorrhage (ASPECTS-H) remains unclear. METHODS: Patients with primary intracerebral hemorrhage (ICH) were collected and retrospectively analyzed. ASPECTS-H was assessed at admission. Patients were followed up at 30 days and 90 days after the onset of ICH. Occurrence of death within 90 days after ICH was the primary endpoint. Modified Rankin Scale (mRS) ≥ 3 was considered a poor functional outcome. RESULTS: A total of 149 patients met eligibility criteria; 61 (40.9%) had poor functional outcome at 30 days, and 37 (24.8%) had poor functional outcome at 90 days. Using binary logistic regression modeling, we found that a low ASPECTS-H was associated with a poor functional outcome. The risk ratio of a low ASPECTS-H was 2.31 at 30 days (P = 0.000; 95% CI, 1.560-3.421) and 2.711 at 90 days (P = 0.000; 95% CI, 1.677-4.381). The optimal cutoff value of ASPECTS-H to discriminate good and poor 30-day and 90-day outcomes was 7.5 (Sensitivity30-day = 0.636, 1-Specificity30 - day = 0.311; Sensitivity90-day = 0.580, 1-Specificity90-day = 0.270). CONCLUSIONS: A low ASPECTS-H was an indicator of poor short-term and long-term functional outcomes of ICH.

Leukoaraiosis and acute ischemic stroke.

Ischaemic stroke is characterized by high morbidity, high disability rate, high mortality and high recurrence rate, which can have a grave impact on the quality of life of the patients and consequently becomes an economic burden on their families and society. With the developments in imaging technology in recent years, patients with acute cerebral infarction are predominantly more likely to be diagnosed with leukoaraiosis (LA). LA is a common degenerative disease of the nervous system, which is related to cognitive decline, depression, abnormal gait, ischaemic stroke and atherosclerosis. The aetiology of LA is not clear and there is no gold standard for imaging assessment. Related studies have shown that LA has an adverse effect on the prognosis of cerebral infarction, but some experts have contrary beliefs. Hence, we undertook the present review of the literature on the mechanism and the effect of LA on the prognosis of patients with acute ischaemic stroke.

Spontaneous extracranial arterial dissections in a case of patient with osteogenesis imperfecta.

Background: Osteogenesis imperfecta (OI), also known as brittle bone disease, is an inherited disease characterized by increased bone brittleness and decreased bone mass. OI patients may also be associated with exoskeleton manifestations such as hearing loss, articular ligament laxity, and heart valve lesions. Reports of internal carotid and cerebral artery dissection related to OI patients are very rare. We present the first case of acute cerebral infarction caused by the progressive stripping of the carotid artery dissection Chinese patient with Osteogenesis imperfecta.Case: A 48-year-old Chinese male who had no prior medical history or bad habits was to admitted the hospital due to leftside temporal headache, paroxysmal right limb weakness, and prolonged blurred vision experienced for a week. After a series of tests were performed to exclude superficial temporal arteritis, the patient was diagnosed with transient ischemic attack and was given aspirin, clopidogrel and atorvastatin without further headache and blurred vision. However, he was again admitted to the emergency department the following day due to right limb weakness for 7 h that was considered acute cerebral infarction caused by left carotid artery dissection.Conclusion: The findings in this case support that internal carotid and cerebral artery dissection may be one of the complications of Osteogenesis imperfecta.