Stress-Induced Hyperglycemia and Remote Diffusion-Weighted Imaging Lesions in Primary Intracerebral Hemorrhage.

BACKGROUND AND PURPOSE: Stress-induced hyperglycemia (SIH) is the relative transient increase in glucose during a critical illness such as intracerebral hemorrhage (ICH) and is likely to play an important role in the pathogenesis of remote diffusion-weighted imaging (DWI) lesion (R-DWIL) in primary ICH. We sought to determine the association between SIH and the occurrence of R-DWILs. METHODS: We prospectively enrolled primary ICH patients within 14 days after onset from November 2016 to May 2018. In these patients, cerebral magnetic resonance imaging was performed within 14 days after ICH onset. R-DWIL was defined as a hyperintensity signal in DWI with corresponding hypointensity in apparent diffusion coefficient, and at least 20 mm apart from the hematoma. SIH was measured by stress-induced hyperglycemia ratio (SHR). SHR was calculated by fasting blood glucose (FBG) divided by estimated average glucose derived from glycosylated hemoglobin. The included patients were dichotomized into two groups by the 50th percentile of SHR, and named as SHR (-P50) group and SHR (P50+) group, respectively. We evaluated the association between SHR and R-DWIL occurrence using multivariable logistic regression modeling adjusted for potential confounders. RESULTS: Among the 288 patients enrolled, forty-six (16.0%) of them had one or more R-DWILs. Compared with the patients in the lower 50% of SHR (SHR [-P50]), the odds ratio (OR) [95% confidence interval (CI)] for the higher 50% of SHR (SHR [P50+]) group for R-DWIL occurrence was 3.13 (1.39-7.07) in the total population and 6.33 (2.19-18.30) in population absent of background hyperglycemia after adjusting for potential covariates. Similar results were observed after further adjusted for FBG. CONCLUSIONS: Our study demonstrated that SIH was associated with the occurrence of R-DWILs in patients with primary ICH within 14 days of symptom onset.

Cerebral infarcts associated with adenomyosis: a rare risk factor for stroke in middle-aged women: a case series.

BACKGROUND: Adenomyosis is a benign disease with elevated CA125 level. CASE PRESENTATION: We report 3 cases with adenomyosis who developed ischemic stroke during menstruation. The levels of CA125, CA19-9, and D-dimer were elevated, which dropped markedly after the menstrual phase. The development of nonbacterial thrombotic endocarditis (NBTE) and stenosis of the cerebral arteries associated with hypercoagulable state and the hyperviscosity nature of the mucinous protein may be the underlying mechanisms. CONCLUSION: Our report suggests that adenomyosis might be a risk factor for ischemic stroke in middle-aged patients.

Subarachnoid Hemorrhage due to Spinal Cord Schwannoma Presenting Findings Mimicking Meningitis.

BACKGROUND: Subarachnoid hemorrhage (SAH) of spinal origin is uncommon in clinical practice, and spinal schwannomas associated with SAH are even more rarely reported. We report an unusual case of spinal SAH mimicking meningitis with normal brain computed tomography (CT)/magnetic resonance imaging (MRI) and negative CT angiography. Cerebrospinal fluid examination results were consistent with the manifestation of SAH. Spinal MRI performed subsequently showed an intradural extramedullary mass. The patient received surgery and was finally diagnosed with spinal cord schwannoma. METHOD: A retrospective chart review of the patient was performed. RESULTS: We describe a case of SAH due to spinal cord schwannoma. Our case highlights the importance of careful history taking and complete evaluation. CONCLUSION: We emphasize that spinal causes should always be ruled out in patients with angionegative SAH and that schwannoma should be considered in the differential diagnosis of SAH etiologies even though rare.

Treatment of extracranial internal carotid artery dissecting aneurysm with SUPERA stent implantation: Two case reports.

BACKGROUND: There is no standard endovascular treatment for extracranial internal carotid artery dissecting aneurysms. In the past, stent-graft isolation and stent-assisted coil embolization were commonly used for wide-necked and fusiform aneurysms. Here, we present two cases of extracranial internal carotid artery dissecting aneurysms treated successfully using the SUPERA stent. CASE SUMMARY: Case 1 was a 57-year-old male patient with sudden right limb weakness and vague speech and diagnosed with cerebral infarction in February 2019. Cervical computed tomographic angiography (CTA) revealed left internal carotid artery dissection with stenosis. CTA at 2 mo showed an eccentric wide-necked dissecting aneurysm (5 mm × 5 mm × 12 mm, 10-mm neck) that was enlarged at 4 mo (7 mm × 6 mm × 12 mm, 11-mm neck). The patient underwent SUPERA stent implantation. His condition was stable in July 2020. Case 2 was a 57-year-old man who suddenly felt dizzy and developed unsteady walking in November 2019. Cervical CTA suggested right internal carotid artery dissecting aneurysm (11 mm × 9 mm × 31 mm) complicated with severe lumen stenosis (95%). The patient underwent SUPERA stent implantation. The patient had no residual symptoms and was stable in December 2020. CONCLUSION: SUPERA stent implantation might achieve good results in treating wide-necked or long fusiform internal carotid artery dissecting aneurysms.

Thrombin preconditioning reduces iron-induced brain swelling and brain atrophy.

Cerebral preconditioning with a low dose of thrombin attenuates brain edema induced by intracerebral hemorrhage (ICH), a large dose of thrombin or iron. This study examined whether or not thrombin preconditioning (TPC) reduces neuronal death and brain atrophy caused by iron. The right hippocampus of rats was pretreated with or without thrombin, and iron was then injected into the same location 3 days later. Rats were killed at 1 day or 7 days after iron injection, and the brains were used for histology. We found that TPC reduced neuronal death and brain swelling in the hippocampus 1 day after iron injection, and hippocampal atrophy 7 days later. Western blots showed that thrombin activates p44/42 mitogen-activated protein kinase (p44/42 MAPK) and 70-kDa ribosomal protein S6 kinase (p70 S6K). Our results indicate that TPC reduction of iron-induced neuronal death may be through the p44/42 MAPK /p70 S6K signal transduction pathway.

Red blood cell lysis and brain tissue-type transglutaminase upregulation in a hippocampal model of intracerebral hemorrhage.

Red blood cell (RBC) lysis and iron release contribute to intracerebral hemorrhage (ICH)-induced brain injury. Tissue-type transglutaminase (tTG), which has a role in neurodegeneration, is upregulated after ICH. The current study investigated the effect of RBC lysis and iron release on brain tTG levels and neuronal death in a rat model of ICH. This study had three parts: (1) Male Sprague-Dawley rats received an intrahippocampal injection of 10 µL of either packed RBCs or lysed RBCs; (2) rats had a 10 µL injection of either saline, hemoglobin or FeCl2; (3) rats received a 10 µL injection of hemoglobin and were treated with an iron chelator, deferoxamine or vehicle. All rats were killed 24 h later, and the brains were sectioned for tTG and Fluoro-Jade C staining. Lysed but not packed RBCs caused marked tTG upregulation (p<0.05) and neuronal death (p<0.05) in the ipsilateral hippocampus CA-1 region. Both hemoglobin and iron mimicked the effects of lysed RBCs, resulting in tTG expression and neuronal death (p<0.05). Hemoglobin-induced tTG upreglution and neuronal death were reduced by deferoxamine (p<0.05). These results indicate that RBC lysis and iron toxicity contribute to neurodegeneration after ICH.

Thrombin preconditioning attenuates iron-induced neuronal death.

Pretreatment with a low dose of thrombin attenuated brain injury after intracerebral hemorrhage (ICH) or cerebral ischemia. This phenomenon has been called thrombin preconditioning (TPC). The current study investigated whether or not TPC reduces neuronal death induced by iron in cultured neurons. The roles of protease-activated receptors (PARs) and the p44/42 mitogen-activated protein kinase (p44/42MAPK)/70-kDa ribosomal protein S6 kinase (p70S6K) signal transduction pathway in TPC were also examined. This study had three parts: (1) primary cultured neurons were pretreated with vehicle, thrombin or PAR agonists. Cell death was induced by ferrous iron (500 µM) 24 h later. After 48 h, culture medium was collected for lactate dehydrogenase measurement; (2) neurons were treated with vehicle, thrombin or thrombin plus PPACK (D-Phe-Pro-Arg chloromethylketone) thrombin and were collected for Western blotting; (3) the effect PD098059 on TPC was examined. Cells were treated with 20 µM PD098059 or vehicle 1 h before TPC. Neuron viability was measured 24 h following exposure to ferrous iron. Preconditioning with thrombin or PAR agonists reduced iron-induced neuronal death (p<0.05). Thrombin, but not PPACK thrombin, upregulated the protein levels of activated p44/42 MAPK and p70 S6K (p<0.05) in neurons. PD098059 also abolished the TPC-induced neuronal protection against iron (p<0.05). In conclusion, the protective effect of thrombin preconditioning is partially achieved through activating PARs and the p44/42 MAPK/p70S6K signal transduction pathway.

[Clinical and genetic analysis of a pedigree of Kennedy disease].

OBJECTIVE: To review the clinical and genetic features of a pedigree of Kennedy disease in China. METHODS: The clinical data of patients from a Kennedy disease family were collected. The numbers of trinucleotide CAG repeats in exon 1 of the androgen receptor gene were determined by DNA sequencing and repeat fragment analysis. RESULTS: In the pedigree, 4 patients were identified as Kennedy disease. Clinical manifested with adult-onset, progressive proximal limb muscle weakness and atrophy, gynecomastia, oligospermia were also presented. The number of trinucleotide CAG repeats in exon 1 of the androgen receptor gene was 51 in the proband. The electrophysiological study showed sensory and motor involvement and their serum triglycerides values were elevated significantly. CONCLUSION: Androgen receptors gene testing is the most reliable diagnosing method, the patients suspected as Kennedy disease should have a gene testing of androgen receptors.

The Correlation Between Migraine and Patent Foramen Ovale.

Background: Migraine is a widespread neurological disorder. The patent foramen ovale (PFO) is a remnant of the fetal circulation. Multiple studies suggest that migraine is more prevalent in subjects with PFO and vice versa. It is unclear if there is a causal relationship or simply a co-existence of these two conditions. Furthermore, the treatment of migraine with percutaneous closure PFO remains controversial. Methods: We reviewed studies pertaining to the relationship between PFO and migraine as well as the effects of treatments on migraine attacks. Results: We briefly summarized potential pathophysiological mechanisms of migraine, and elaborated on migraine type, frequency, and clinical symptoms of migraine with PFO and the clinical features of PFO with migraine. We also addressed the effects of PFO closure on migraine attacks. Conclusion: The evidence supports a "dose-response" relationship between migraine and PFO although more work needs to be done in terms of patient selection as well as the inclusion of an antiplatelet control group for PFO closure interventions to uncover possible beneficial results in clinical trials.

[Delayed neuronal degeneration after intracerebral hemorrhage: the role of iron].

OBJECTIVE: To investigate the occurrence of delayed neuronal degeneration, activation of microglia and nuclear factor-kappa B after rat intracerebral hemorrhage (ICH) and the possible role of iron. METHODS: ICH model was induced by infusion of autologous whole blood into the right basal ganglia. To evaluate the possible role of iron on delayed neuron loss, an iron model by injection of FeCl(2) into hippocampus was also set up. Degeneration of neurons and the activation of microglia and NF-kappa B were detected. RESULT: Both whole blood and iron caused neuron degeneration for at least 14 days were revealed by Fluoro-jade C staining. Consistently, activated microglia and NF-kappa B positive cells were also observed in the peri-hematoma area and the ipsilateral hippocampus. CONCLUSION: The iron may participate in the delayed neuron injury followed ICH; the activated microglia and NF-kappa B may be involved in the process of delayed neuronal injury.

[Clinical and cranial MRI analysis on five cases of toxic encephalopathy induced by dichloroethane].

OBJECTIVE: To investigate the clinical features, cranial MRI and treatment of toxic encephalopathy induced by 1, 2-dichloroethane (1, 2-DCE). METHODS: The clinical, MRI features and treatment of 5 patients with toxic encephalopathy induced by 1,2-DCE were observed and analyzed. RESULTS: Five patients all presented with subacute onset with a history of direct exposure to 1,2-DCE. Lumbar cerebrospinal fluid pressures were all increased in 5 patients. All 5 patients had obvious intracranial hypertension. Liver and kidney function had no obvious abnormalities; Cranial MRI showed T1WI low signal and T2WI high signal in bilateral hemispheric white matter, cerebellar dentate nucleus and globus pallidus. After the treatment of dehydrating agent, glucocorticoid and supportive treatment, four patients were clearly improved, and one patient had cerebral hernia formation. CONCLUSION: The main neurological clinical features in patients with 1,2-DEC poisoning is obvious intracranial hypertension. The prognosis is usually good with early and long term use of glucocorticoids and dehydrating agent in poisoning patients.

Effects of thrombin on neurogenesis after intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Neurogenesis in intracerebral hemorrhage (ICH) has not been investigated. Thrombin formation causes acute brain injury after ICH, but thrombin also can stimulate cell proliferation. The present study examined whether neurogenesis takes place in ICH and the role of thrombin in ICH-related neurogenesis. METHODS: This study was divided into four parts. (1) Rats received either an ICH or a needle insertion (sham). The rats were killed for doublecortin (DCX) Western blot analysis and immunohistochemistry. (2) Rats had an ICH or a sham operation, and then received intraperitoneal injections of 5-bromo-2'-deoxyuridine (BrdU) at day-7 and day-9 later. Brains were perfused to identify BrdU-positive cells. (3) Rats had an intracaudate injection of thrombin (1 U) and brains were sampled for Western blots. (4) Rats had an ICH with or without a thrombin inhibitor, hirudin. The brains were sampled for DCX quantitation. RESULTS: DCX levels in the ipsilateral basal ganglia started to increase as early as 7 days after ICH, peaked at 14 days, and then gradually decreased at 1 month. Immunohistochemistry also demonstrated that DCX immunoreactivity was increased in the ipsilateral subventricular zone and basal ganglia at 2 weeks after ICH. Some DCX-positive cells were BrdU-positive. One unit thrombin, which does not cause marked brain injury, was injected into the caudate. Thrombin increased DCX levels in the ipsilateral basal ganglia and hirudin blocked ICH-induced upregulation of DCX. CONCLUSIONS: Our results demonstrated that neurogenesis occurs in the brain after ICH and that thrombin may play a role in ICH-induced neurogenesis.

Factors Associated With Remote Diffusion-Weighted Imaging Lesions in Spontaneous Intracerebral Hemorrhage.

BACKGROUND AND PURPOSE: Remote diffusion-weighted imaging lesions (R-DWILs) have been detected in patients with spontaneous intracerebral hemorrhage (ICH) and may be correlated with clinical outcome. However, the mechanisms and characteristics of R-DWILs have not been fully elucidated. In this study, we sought to demonstrate the clinical characteristics of R-DWILs in spontaneous ICH. METHODS: We prospectively collected data with spontaneous ICH patients from November 2016 to December 2017. In these patients, cerebral magnetic resonance imaging was performed within 28 days after ICH onset. R-DWIL was defined as a hyperintensity signal in diffusion-weighted imaging with corresponding hypointensity in apparent diffusion coefficient, and at least 20 mm apart from the hematoma. We compared two groups of patients with or without R-DWIL with the demographic and clinical characteristics, laboratory parameters, and imaging characteristics, by using univariate and multivariate analysis. RESULTS: Of the 222 patients enrolled, a total of 75 R-DWILs were observed in 41 patients (18.5%). Among these lesions, the cortical and subcortical areas were the predominant locations with a proportion of 77.3%. The median diameter of R-DWILs was 7 mm (range 2-20 mm). Twelve patients were found having more than one lesion, with five among which showed R-DWILs in multiple cerebral arterial territories. In multivariate modeling, higher fasting glucose (OR 1.231; 95% CI 1.035-1.465; p = 0.019) and more severe white matter hyperintensity (WMH) (OR 6.589; 95% CI 2.975-14.592; p < 0.001) were independent factors related to the presence of R-DWILs. CONCLUSION: In our study, approximately one-fifth of ICH patients showed coexistence of R-DWIL. Higher fasting glucose and more severe WMH were associated with R-DWIL occurrence in spontaneous ICH.

A new hippocampal model for examining intracerebral hemorrhage-related neuronal death: effects of deferoxamine on hemoglobin-induced neuronal death.

BACKGROUND AND PURPOSE: There is an urgent need to develop a model in which to study the mechanism of intracerebral hemorrhage-induced neuronal death in vivo. METHODS: This study was divided into 2 parts: (1) Rats received either an infusion of hemoglobin, ferrous iron, or saline into the right hippocampus; (2) Rats had an infusion of hemoglobin and then were treated with either deferoxamine or vehicle. Rats were killed for hippocampus size, DNA damage, and neuronal death measurements. RESULTS: Compared with saline, hemoglobin or iron injection caused hippocampal neuronal death. Systemic use of deferoxamine reduced hemoglobin-induced DNA damage, hippocampal neuronal death, and atrophy. CONCLUSIONS: This article demonstrates a new model and indicates that iron has a key role in hemoglobin-induced neuronal death.

Preconditioning with hyperbaric oxygen attenuates brain edema after experimental intracerebral hemorrhage.

OBJECT: Preconditioning with hyperbaric oxygen (HBO2) reduces ischemic brain damage. Activation of p44/42 mitogen-activated protein kinases (p44/42 MAPK) has been associated with preconditioning-induced brain ischemic tolerance. This study investigated if preconditioning with HBO2 protects against intracerebral hemorrhage (ICH)-induced brain edema formation and examined the role of p44/42 MAPK in such protection. METHODS: The study had three experimental groups. In Group 1, Sprague-Dawley rats received two, three, or five consecutive sessions of preconditioning with HBO2 (3 ata, 100% oxygen, 1 hour daily). Twenty-four hours after preconditioning with HBO2, rats received an infusion of autologous blood into the caudate. They were killed 1 or 3 days later for brain edema measurement. Rats in Group 2 received either five sessions of preconditioning with HBO2 or control pretreatment and were killed 24 hours later for Western blot and immunohistochemical analyses. In Group 3, rats received an intracaudate injection of PD098059 (an inhibitor of p44/42 MAPK activation) before the first of five sessions of preconditioning with HBO2. Twenty-four hours after the final preconditioning with HBO2, rats received an intracaudate blood infusion. Brain water content was measured 24 hours after ICH. RESULTS: Fewer than five sessions of preconditioning with HBO2 did not significantly attenuate brain edema after ICH. Five sessions of preconditioning with HBO2 reduced perihematomal edema 24 and 72 hours after ICH (p < 0.05). Strong p44/42 MAPK immunoreactivity was detected in the basal ganglia 24 hours after preconditioning with HBO2. Intracaudate infusion of PD098059 abolished HBO2 preconditioning-induced protection against ICH-induced brain edema formation. CONCLUSIONS: Preconditioning with HBO2 protects against brain edema formation following ICH. Activation of the p44/42 MAPK pathway contributes to that protection. Preconditioning with HBO2 may be a way of limiting brain injury during invasive neurosurgical procedures that cause bleeding.

Lance-Adams syndrome: a report of two cases.

Chronic post-hypoxic myoclonus, also known as Lance-Adams syndrome (LAS), is a rare complication of successful cardiopulmanry resuscitation often accompanied by action myoclonus and cerebellar ataxia. It is seen in patients who have undergone a cardiorespiratory arrest, regained consciousness afterwards, and then developed myoclonus days or weeks after the event. Worldwide, 122 cases have been reported in the literature so far, including 1 case of Chinese. Here we report 2 Chinese LAS patients with detailed neuroimagings. Cranial single photon emission computed tomography (SPECT) of patient 1, a 52-year-old woman, showed a mild hypoperfusion in her left temporal lobe, whereas patient 2, a 54-year-old woman, manifested a mild bilateral decrease of glucose metabolism in the frontal lobes and a mild to moderate decrease of the N-acetyl aspartate (NAA) peak in the bilateral hippocampi by cranial [(18)F]-fluorodeoxyglucose positron emission tomographic (PET) scan and cranial magnetic resonance spectroscopy (MRS), respectively. We also review the literature on the neuroimaging, pathogenesis, and treatment of LAS.

Intraventricular hemorrhage caused by intracranial venous sinus thrombosis: Case report.

Intraventricular hemorrhage (IVH) may occur as an isolated event from primary ventricular bleeding or as a complication of brain hemorrhage from another etiology. It is associated with high mortality and morbidity. The underlying risk factors include hypertension and aneurysms, among others. However, not all the exact etiologies are known. In this study, a case of a 24-year-old man who suffered from a headache and a decline in memory has been reported. A brain computed tomography scan suggested the diagnosis of spontaneous intraventricular hemorrhage. However, brain magnetic resonance imaging, magnetic resonance venography, and other tests eventually confirmed cerebral venous sinus thrombosis.Cerebral venous sinus thrombosis may be one of the causes of intraventricular hemorrhage and should be considered for unexplained intraventricular hemorrhage.

[Clinical study on Zhuyu Tongfu serial recipe combined with acupuncture and massotherapy in treating hypertensive cerebral hemorrhage].

OBJECTIVE: To observe the clinical efficacy and mechanism of Zhuyu Tongfu (ZYTF) Serial Recipe combined with acupuncture and massotherapy in treating hypertensive cerebral hemorrhage (HCH). METHODS: One hundred and eighteen patients with hypertensive cerebral hemorrhage, on the basis of conventional Western medicine treatment, were randomly divided into ZYTF combined with acupuncture and massotherapy group (treated group) and simple Western medicine group (control group); the clinical efficacy, neurofunction deficit scoring (NDS) alterations and hematoma absorption rate of both groups were observed, and also the plasma superoxide dismutase (SOD) activity, plasma lipid peroxidase (LPO) content, erythrocyte glutathion peroxidase (GSH-Px) activity, hematocrit (Ht) and the whole blood viscosity (Va) change were also observed. RESULTS: In the treated group, the clinical efficacy, NDS improvement and hematoma absorption rate were superior to that of the control group; comparison between the two groups after treatment showed that plasma SOD activity and GSH-Px activity got more elevated and plasma LPO content, Ht and Va more lowered in the the treated group than those in the control group. CONCLUSION: ZYTF combined with acupuncture and massotherapy has better effect, its therapeutic mechanism was possibly correlated to the elevation of plasma SOD activity, GSH-Px activity and lowering of plasma LPO content, Ht and Va.

[Change of serum soluble intercellular adhesion molecule and basic fibroblast growth factor in patients with acute cerebral infarction and its clinical significance].

OBJECTIVE: To explore the changes of the levels of soluble intercellular adhesion molecule-1 (sICAM-1) and basic fibroblast growth factor (bFGF) in serum of patients with acute cerebral infarction, and the effects of sICAM-1 and bFGF on cerebral infarction. METHODS: ELISA was used to detect the serum sICAM-1 and bFGF of 55 patients with acute cerebral infarction (within 2 days) as well as 32 patients diagnosed as with other neurologic diseases (20 patients with sciatica and 12 with trigeminal neuralgia) and 30 healthy persons as controls. RESULTS: (1) Both serum sICAM-1 and bFGF in the infarction group were significantly higher [(766.2 +/- 178.8) micro g/L and (17.4 +/- 8.2) micro g/L respectively] than in other disease control group [(529.6 +/- 76.7) micro g/L and (8.3 +/- 2.8) micro g/L respectively] and normal control group [(520.7 +/- 115.9) micro g/L and (5.8 +/- 2.7) micro g/L respectively] (P = 0.000). (2) Correlation analysis showed that there was a positive correlation between the level of serum sICAM-1 and bFGF (r = 0.471, P = 0.000), the level of sICAM-1 was also positively correlated with the number of leukocytes at acute stage (r = 0.285, P = 0.035), and a negative correlation between sICAM-1 and European stroke scale (r = -0.333, P = 0.013) was found. No significant correlation was observed between the level of sICAM-1 and the levels of serum cholesterol (r = -0.042, P = 0.758) or triglyceride (r = 0.061, P = 0.675). (3) Blood pressure seemed to have no influence on the content of sICAM-1 and bFGF after cerebral infarction, while the level of serum bFGF with large infarct size was obviously higher at acute stage. CONCLUSION: The levels of sICAM-1 and bFGF increase significantly in the patients with acute cerebral infarction. sICAM-1 and bFGF mayin participate in the pathophysiologic process through inflammatory mechanism. The detection of serum sICAM-1 will be helpful in estimating the clinical severity and the determination of bFGF will be helpful in estimating the size of infarct lesion at acute stage of cerebral infarction.