BACKGROUND: The effect of arteriosclerotic intracranial arterial vessel wall enhancement (IAVWE) on downstream collateral flow found in vessel wall imaging (VWI) is not clear. Regardless of the mechanism underlying IAVWE on VWI, damage to the patient's nervous system caused by IAVWE is likely achieved by affecting downstream cerebral blood flow. The present study aimed to investigate the effect of arteriosclerotic IAVWE on downstream collateral flow. METHODS: The present study recruited 63 consecutive patients at the Second Hospital of Hebei Medical University from January 2021 to November 2021 with underlying atherosclerotic diseases and unilateral middle cerebral artery (MCA) M1-segment stenosis who underwent an magnetic resonance scan within 3 days of symptom onset. The patients were divided into 4 groups according to IAVWE and the stenosis ratio (Group 1, n = 17; Group 2, n = 19; Group 3, n = 13; Group 4, n = 14), and downstream collateral flow was analyzed using three-dimensional pseudocontinuous arterial spin labeling (3D-pCASL) and RAPID software. The National Institutes of Health Stroke Scale (NIHSS) scores of the patients were also recorded. Two-factor multivariate analysis of variance using Pillai's trace was used as the main statistical method. RESULTS: No statistically significant difference was found in baseline demographic characteristics among the groups. IAVWE, but not the stenosis ratio, had a statistically significant significance on the late-arriving retrograde flow proportion (LARFP), hypoperfusion intensity ratio (HIR), and NIHSS scores ( F = 20.941, P <0.001, Pillai's trace statistic = 0.567). The between-subject effects test showed that IAVWE had a significant effect on the three dependent variables: LARFP ( R2 = 0.088, F = 10.899, P = 0.002), HIR ( R2 = 0.234, F = 29.354, P <0.001), and NIHSS ( R2 = 114.339, F = 33.338, P <0.001). CONCLUSIONS: Arteriosclerotic IAVWE significantly reduced downstream collateral flow and affected relevant neurological deficits. It was an independent factor affecting downstream collateral flow and NIHSS scores, which should be a focus of future studies. TRIAL REGISTRATION ChiCTR.org.cn, ChiCTR2100053661.
Humans ; Constriction, Pathologic/pathology* ; Magnetic Resonance Imaging/methods* ; Middle Cerebral Artery/pathology* ; Tomography, X-Ray Computed

We present the case of a 23-year-old man who suddenly collapsed during a physical altercation with his friends while in a drunken state. The post-mortem computed tomography (CT) with angiography revealed acute basal subarachnoid hemorrhage with rupture of the left middle cerebral artery. On autopsy, the head, face, mandible and neck showed multifocal hemorrhages with fracture of the hyoid bone, and the pathologic findings of the brain was consistent with CT findings. However, the vascular rupture site was not observed macroscopically. On histologic examination, a microscopic focal rupture was identified at the proximal portion of the middle cerebral artery, and possibility of arteriopathy was considered. This case illustrates that other parts of intracerebral arteries (other than the vertebral arteries) can be the culprit of rupture in the case of traumatic basal subarachnoid hemorrhage, and the post-mortem angiographic findings can be helpful in targeting the site of vascular injury. Furthermore, meticulous sampling of intracranial vessels could help find the vascular rupture site and identify any histologic findings suspicious of arteriopathy. Therefore, we suggest that post-mortem angiography can be an effective and adjunctive tool for a tailored approach in finding the vascular injury, and that histologic examination of both the intracranial and extracranial arteries be important to medicolegally ensure the death of traumatic basal subarachnoid hemorrhage and to examine presence of arteriopathy as a predisposing factor.
Angiography ; Arteries ; Autopsy ; Brain ; Causality ; Forensic Pathology ; Friends ; Head ; Hemorrhage ; Humans ; Hyoid Bone ; Mandible ; Middle Cerebral Artery ; Neck ; Rupture ; Subarachnoid Hemorrhage ; Subarachnoid Hemorrhage, Traumatic ; Vascular System Injuries ; Young Adult

Brain ; pathology ; Brain Infarction ; diagnosis ; Cerebral Angiography ; Cerebral Arterial Diseases ; diagnosis ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Posterior Cerebral Artery ; pathology

PURPOSE: Patients with superficial middle cerebral artery (MCA) territory infarction may have concomitant lenticulostriate artery (LSA) territory infarction. We investigated the mechanisms thereof and the outcomes of patients with superficial MCA territory infarction according to the presence or absence of LSA involvement. MATERIALS AND METHODS: Consecutive patients with first-ever infarction in the unilateral superficial MCA territory were included in this study. They were divided into the superficial MCA only (SM) group and the superficial MCA plus LSA (SM+L) group. RESULTS: Of the 398 patients, 84 patients (21.1%) had LSA involvement (SM+L group). The SM+L group more frequently had significant stenosis of the proximal MCA or carotid artery and high-risk cardioembolic sources. Stroke severity and outcomes were remarkably different between the groups. The SM+L group showed more severe neurologic deficits (National Institute of Health Stroke Scale score 10.8±7.1 vs. 4.0±5.0, p<0.001) and larger infarct in the superficial MCA territory (40.8±62.6 cm³ vs. 10.8±21.8 cm³, p<0.001) than the SM group. A poor functional outcome (mRS >2) at 3 months was more common in the SM+L group (64.3% vs. 15.9%, p<0.001). During a mean follow-up of 26 months, 67 patients died. All-cause (hazard ratio, 2.246) and stroke (hazard ratio, 9.193) mortalities were higher in the SM+L group than the SM group. In multivariate analyses, LSA involvement was an independent predictor of poor functional outcomes and stroke mortality. CONCLUSION: LSA territory involvement is predictive of poor long-term outcomes in patients with superficial MCA territory infarction.
Carotid Stenosis/mortality/pathology ; Constriction, Pathologic/pathology ; Female ; Humans ; Infarction, Middle Cerebral Artery/mortality/*pathology ; Male ; Middle Cerebral Artery/*pathology ; Multivariate Analysis ; Severity of Illness Index ; Stroke/mortality/pathology

OBJECTIVETo explore the neuroprotective effect and mechanism of picroside II on extracellular regulated protein kinases1/2 (ERK1/2) signal transduction pathway in cerebral ischemia injuryrats. METHODS The middle cerebral artery occlusion (MCAO) model was established by inserting a monofilament into middle cerebral artery. Totally 96 successfully modeled Wistar rats were divided into the modelgroup, the treatment (picroside II) group, the Lipopolysachcaride (LPS) group, and the U0126 group according to random digit table. Each group was further divided into 3 subgroups, i.e. 6, 12, and 24 h sub-groups. Picroside II (20 mg/kg) was peritoneally injected to rats in the treatment group 2 h after ischemia.LPS (20 mg/kg) and Picroside II (20 mg/kg) were peritoneally injected to rats in the LPS group 2 h after ischemia. U0126-EtOH (20 mg/kg)and Picroside II (20 mg/kg) were peritoneally injected to rats in the U0126group 2 h after ischemia. Equal volume of normal saline was peritoneally injected to rats in the control groupand the model group. The neurobehavioral function was evaluated by modified neurological severity score(mNSS) test. The structure of neurons was observed using hematoxylin-eosinstaining (HE) staining. Theapoptotic cells were detected using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression of phosphorylated extracellular signal-regulated protein kinase1,2 (pERK1,2) in cortex was detected using immunohistochemistry (IHC) and Western blot.

RESULTSAfter cerebral ischemia injury neurological impairment score increased, the damage of neuron in the cortical area was aggravated, apoptotic cells increased in the model group as time went by. The expression of pERK1/2 increased more significantly in the model group than in the control group (P <0.05). The damage of neuron in the cortical area was milder, while apoptotic cells decreased, the expression of pERK1f2 obviously decreased more in the treatment group and the U0126 group (P < 0.05). The early damage of neuron in the cortical area was more severe, apoptotic cells and the expression of pERK12 were comparatively higher in early stage of the LPS group, but the expression of pERK1/2 was somewhat decreased in late stage.

CONCLUSIONSActivating ERK12 pathway could mediate apoptosis and inflammatory reactions of neurons after cerebral ischemia injury. Picroside II could protect the nerve system possibly through reducing activation of ERKI2 pathway, inhibiting apoptosis of neurons and inflammation reaction.

Animals ; Apoptosis ; Brain Ischemia ; drug therapy ; Cinnamates ; pharmacology ; Infarction, Middle Cerebral Artery ; drug therapy ; Iridoid Glucosides ; pharmacology ; MAP Kinase Signaling System ; drug effects ; Neurons ; pathology ; Neuroprotective Agents ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar

The histopathological features of the middle cerebral artery (MCA) and superficial temporal artery (STA) from moyamoya disease (MMD) and their relationships with gender, age, angiography stage were explored. The causes and the clinical significance of vasculopathy of STA were also discussed. The clinical data and specimens of MCA and STA from 30 MMD patients were collected. Twelve samples of MCA and STA from non-MMD patients served as control group. Histopathological examination was then performed by measuring the thickness of intima and media, and statistical analysis was conducted. The MCA and STA specimens from MMD group had apparently thicker intima and thinner media than those from the control group. There was no significant pathological difference between the hemorrhage group and non-hemorrhage group, and between the males and females in MMD patients. Neither the age nor the digital subtraction angiography (DSA) stage was correlated with the thickness of intima in MCA and STA. MMD is a systemic vascular disease involving both intracranial and extracranial vessels. Preoperative external carotid arteriography, especially super-selective arteriography of the STA, benefits the selection of donor vessel.
Adult ; Angiography ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; Middle Cerebral Artery ; diagnostic imaging ; pathology ; Moyamoya Disease ; diagnostic imaging ; pathology ; surgery ; Temporal Arteries ; diagnostic imaging ; pathology ; Tunica Intima ; diagnostic imaging ; pathology

A 61-year-old female presented with 4 years history of left-sided hemifacial spasm. Head MRI and angiography indicated left vertebral artery dissecting aneurysm which compressed ipsilateral cranial nerves Ⅶ and Ⅷ. Microvascular decompression was performed. The dissecting aneurysm was pushed apart and the distal part of the parent artery was adhered to the dura on the petrosum. The compressed nerves were totally decompressed. The symptom of facial spasm was completely resolved immediately after surgery and did not recur during 6 months of follow up.
Cerebral Angiography ; Facial Nerve ; pathology ; Female ; Hemifacial Spasm ; surgery ; Humans ; Magnetic Resonance Imaging ; Microvascular Decompression Surgery ; Middle Aged ; Nerve Compression Syndromes ; diagnosis ; etiology ; surgery ; Vertebral Artery Dissection ; diagnostic imaging ; surgery ; Vestibulocochlear Nerve ; pathology

OBJECTIVETo explore a method for combining Fluoro-Jade B (FJB) staining with immunofluorescent staining in rats with focal cortical infarction.

METHODPermanent distal middle cerebral artery occlusion (dMCAO) was induced in rats by electrocoagulation. The rat models were randomized into two groups, and frozen sections of the brain tissues from each group were stained with FJB followed by immunofluorescent staining or in the reverse order.

RESULTSFJB staining followed by immunofluorescence staining clearly visualized both FJB-positive and immunofluorescence-positive cells in the frozen sections, but the staining protocol in the reverse sequence failed to clearly show the immunofluorescence-positive cells.

CONCLUSIONFJB staining prior to immunofluorescence staining does not affect the staining effect of protein immunofluorescent staining and better visualizes the positive cells.

Animals ; Brain ; pathology ; Fluoresceins ; chemistry ; Fluorescent Antibody Technique ; methods ; Fluorescent Dyes ; chemistry ; Infarction, Middle Cerebral Artery ; Rats ; Staining and Labeling ; methods

OBJECTIVETo introduce the imaging characteristics of moyamoya disease (MMD) using high-resolution magnetic resonance imaging (HR-MRI) and to discuss the role of HR-MRI in differentiating MMD from other intracranial artery diseases, especially intracranial atherosclerotic disease (ICAD).

DATA SOURCESThis review was based on the data in articles published between 2005 and 2015, which were obtained from PubMed. The keywords included HR-MRI, MMD, ICAD, and intracranial artery diseases.

STUDY SELECTIONArticles related to HR-MRI for MMD or other intracranial artery diseases were selected for review.

RESULTSThere are differences between the characteristic patterns of HR-MRI in MMD and ICAD. MMD is associated with inward remodeling, smaller outer diameters, concentric occlusive lesions and homogeneous signal intensity, while ICAD is more likely to be associated with outward remodeling, normal outer diameters, eccentric occlusive lesions, and heterogeneous signal intensity. Other intracranial artery diseases, such as dissection and vasculitis, also have distinctive characteristics in HR-MRI. HR-MRI may become a useful tool for the differential diagnosis of MMD in the future.

CONCLUSIONSHR-MRI of MMD provides a more in-depth understanding of MMD, and it is helpful in evaluating pathological changes in the vessel wall and in differentiating MMD from other intracranial artery steno-occlusive diseases, particularly ICAD.

Animals ; Diagnosis, Differential ; Humans ; Magnetic Resonance Imaging ; methods ; Middle Cerebral Artery ; pathology ; Moyamoya Disease ; diagnosis

BACKGROUNDMotor dysfunction is common in stroke patients. Clinical electrophysiological studies suggest that transsynaptic degeneration occurred in the lower motor neurons, while pathological evidence is lacked. This study aimed to combine the electrophysiological and pathological results to prove the existence of transsynaptic degeneration in the motor system after stroke.

METHODSModified neurologic severity score, electrophysiological, and pathological assessments were evaluated in rats before middle cerebral artery occlusion (MCAO), and at 24 hours, 7 days, and 14 days after MCAO. Paired and independent-sample t-tests were applied to assess the changes of electrophysiological and pathological data.

RESULTSCompound motor action potential amplitude in the paretic side was significantly lower than the nonparetic side at both 24 hours (61.9 ± 10.4 vs. 66.6 ± 8.9, P < 0.05) and 7 days (60.9 ± 8.4 vs. 67.3 ± 9.6, P < 0.05) after MCAO. Motor unit number estimation of the paretic side was significantly less than the nonparetic side (379.0 ± 84.6 vs. 445.0 ± 89.5, P < 0.05) at 7 days after MCAO. Until 14 days after stroke, the pathological loss of motor neurons was detected. Motor neurons in 14-day MCAO group were significantly decreased, compared with control group (5.3 ± 0.7 vs. 7.3 ± 1.8, P < 0.05).

CONCLUSIONSBoth electrophysiological and pathological studies showed transsynaptic degeneration after stroke. This study identified the asynchronization in changes of electrophysiology and pathology. The abnormal physiological changes and function impairment can be detected in the early stage and recovered quickly, while the pathological loss of motor neuron can be detected only in a later stage.

Animals ; Electrophysiology ; Infarction, Middle Cerebral Artery ; pathology ; physiopathology ; Male ; Motor Neurons ; pathology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; pathology ; physiopathology