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.

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.

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.

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.

[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.

[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.

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.

[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.

[Expression of urokinase-type plasminogen activator and its receptor in plasma of patients with cerebral infarction].

OBJECTIVE: To measure the urokinase-type plasminogen activator (UPA) and its receptor (UPAR) in the plasma of patients with cerebral infarction and to study the effects of UPA and UPAR on cerebral infarction. METHODS: ELISA sandwich method was used to measure the plasma levels of UPA and UPAR in 89 patients with acute cerebral infarction, subdivided into mild, moderate and severe subgroups according to the modified Edinburgh-Scandinavia stroke scale (mESSS), and 30 patients with other disease and 30 healthy persons as controls. RESULTS: Within 2 days after the onset of cerebral infarction the UPA and UPAR levels were (1663.7 +/- 384.2) ng/L and (1 375.3 +/- 303.0) ng/L respectively, both significantly higher than those of the patients with other diseases [(1 033.0 +/- 122.7) ng/L and (978.3 +/- 120.0) ng/L respectively (P = 0.038 and P = 0.000)] and those of the normal control group [(1 005.0 +/- 128.9) ng/L and (904.7 +/- 158.6) ng/L respectively, both P = 0.000]. Two weeks after the onset of stroke, the plasma UPA level was (1 185.5 +/- 384.6) ng/L, not significantly different from those of the 2 control groups (both P > 0.05); while the plasma UPAR level in the cerebral infarction was (1 159.3 +/- 261.2) ng/L, significantly higher than those in the 2 control groups (P < 0.01). Within 2 days after the onset of infarction the plasma UPA and UPAR levels of the severe subgroup were (1 938.9 +/- 256.5) ng/L and (1 510.8 +/- 378.7) ng/L respectively, both significantly higher than those of the moderate subgroup [(1 593.7 +/- 204.8) ng/L and (1 296.6 +/- 151.2) ng/L respectively, both P < 0.01] and those of the mild subgroup [1 358.5 +/- 175.9] ng/L and (1 226.8 +/- 98.3) ng/L respectively, both P < 0.01], Two weeks after the onset of stroke,the plasma UPA and uPAR levels of the severe subgroup remained significantly higher than those of the mild subgroup [(1 152.6 +/- 170.3) ng/L vs (1 041.9 +/- 187.0) ng/L, (P < 0.05)] and [(1 186.4 +/- 158.3) ng/L vs (1 053.9 +/- 109.4) ng/L, (P < 0.01)]. In addition, the plasma UPA and UPAR levels of the patients who died from cerebral infarction at last were the highest among all the groups. CONCLUSION: The plasma levels pf UPA and UPAR increase in patients with cerebral infarction and may be related with the severity of disease. The UPA and UPAR genes may play an important role via proteolytic degradation of the extracellular matrix and basement membrane during the development of cerebral infarction.

[Serum levels of soluble intercellular adhesion molecule-1 in patients with cerebral infarct].

OBJECTIVE: To observe the changes of the levels of soluble intercellular adhesion molecule-1(sICAM-1) in serum of patients with cerebral infarct and to explore the effect of sICAM-1 on cerebral infarct. METHODS: The serum levels of sICAM-1 in 55 patients with cerebral infarct both in acute stage(within 2 days) and convalescence(2 weeks after attack) were detected by using ELISA. At the same time, we compare the results with those of 32 patients having other neurologic diseases(20 patients with sciatica, 12 with trigeminal neuralgia) and 30 healthy subjects. RESULTS: (1) The serum levels of sICAM-1 of patients with cerebral infarct (acute stage: 766+/-179 microgram/L, convalescence: 602+/-155 microgram/L, respectively) were significantly higher than those of the control groups(530+/-77 microgram/L and 521+/-116 microgram/L, respectively, P<0.01). (2)There was a positive correlation of SICAM levels with the amount of leukocytes in acute stage(r=0.285,P<0.05), but negative correlation to clinical severity of cerebral infarct(r= 0.333,P<0.05). And there was no significant correlation between the level of sICAM-1 and the levels of cholesterol and triglyceride in serum(r= 0.042 and r=0.061, respectively, P>0.05). (3)There was no significant difference between sICAM levels of patients of cerebral cortex infarct and those of patients with basal ganglia infarct(773+/-178 microgram/L and 758+/-183 microgram/L, respectively, P>0.05). (4)The levels of sICAM-1 between patients of cerebral infarct with or without hypertension were no significant difference(774+/-189 microgram/L and 754+/-165 microgram/L, respectively, P>0.05). CONCLUSION: The levels of sICAM-1 increase significantly in patients with cerebral infarct. sICAM-1 may participate in the pathophysiologic process through inflammatory mechanism.

[Study on protective effect of monosialoganglioside (GM1) on injury induced by oxygen glucose deprivation/reperfusion in rat hippocampal slices].

AIM: To investigate the protective effect of monosialoganglioside (GM1) on injury induced by oxygen glucose deprivation/reperfusion (OGD/Rep) in rat hippocampal slices. METHODS: The protective effects of GM1 on hippocampal slices after OGD/Rep were observed by detecting the light transmittance (LT) changes of rat hippocampal slices and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining of rat hippocampal slices. RESULTS: (1) In four groups treated with 0 (control), 0.1, 1.0, 10 micromol/L GM1, the peak of light transmittance (LT) in the slices treated with 1.0 micromol/L GM1 was significantly lower than that of the control and the group treated with 0.10 micromol/L GM1 (P < 0.01, ANOVA), while the peak of LT in the slices treated with 10.0 micromol/L GM1 was significantly lower than that of the other groups (P < 0.01, ANOVA). The time to reach the peak of LT in four groups was significantly different from each other (P < 0.05, Kruskal-Wallis test). The time to reach the peak of LT in the group treated with 1 micromol/L GM1 was the significantly longer than that in the control (P < 0.01, Mann-Whitney U test). (2) There was characteristic dose-response relationship between GM1 and TTC staining of rat hippocampal slices. In the five groups, treated with 0 (control), 0.01, 0.1, 1.0, 10 micromol/L GM1 respectively, TTC staining in the group treated with 1 micromol/L GM1 was the deepest (P < 0.05 vs. control, 0.01 and 0.1 micromol/L GM1 group, ANOVA), and the next was in the group treated with 10 micromol/L GM1 (P < 0.05 vs. control and 0.01 micromol/L GM1 group, ANOVA). CONCLUSION: GM1 could protect injury induced by OGD/Rep in rat hippocampal slices effectively in vitro.