Early Stage Of Intracerebral Hemorrhage Research Articles

Advances in Prediction for Perihematomal Edema Growth in Intracerebral Hemorrhage

Perihematomal edema (PHE) has been represented as an important secondary injury after intracerebral hemorrhage (ICH). The evolution of PHE contributed to mass effect, which could induce the increase of intracranial pressure. The volume of PHE increased rapidly in the early stage of ICH and continued to increase for 7 to 11 days after symptom onset, and the edema extension distance (EED) increased rapidly within 24 hours, accounting for 60% of the peak EED [1-2]. For the timepoint of follow-up CT scans was different, the fastest development stage of PHE could also be 48 or 72 hours after symptom onset [3-4]. If patients with ICH could not benefit from early surgical evacuation of the hematoma, anti-edema treatment may bring better therapeutic effect. Thus, the use of anti-edema treatment may need to be considered for reducing PHE volume during the early phase of PHE development. How to appropriately predict PHE growth is important in patients at the early stage of ICH.

Cyclophilin D-induced mitochondrial impairment confers axonal injury after intracerebral hemorrhage in mice.

The mitochondrial permeability transition pore is a nonspecific transmembrane channel. Inhibition of mitochondrial permeability transition pore opening has been shown to alleviate mitochondrial swelling, calcium overload, and axonal degeneration. Cyclophilin D is an important component of the mitochondrial permeability transition pore. Whether cyclophilin D participates in mitochondrial impairment and axonal injury after intracerebral hemorrhage is not clear. In this study, we established mouse models of intracerebral hemorrhage in vivo by injection of autologous blood and oxyhemoglobin into the striatum in Thy1-YFP mice, in which pyramidal neurons and axons express yellow fluorescent protein. We also simulated intracerebral hemorrhage in vitro in PC12 cells using oxyhemoglobin. We found that axonal degeneration in the early stage of intracerebral hemorrhage depended on mitochondrial swelling induced by cyclophilin D activation and mitochondrial permeability transition pore opening. We further investigated the mechanism underlying the role of cyclophilin D in mouse models and PC12 cell models of intracerebral hemorrhage. We found that both cyclosporin A inhibition and short hairpin RNA interference of cyclophilin D reduced mitochondrial permeability transition pore opening and mitochondrial injury. In addition, inhibition of cyclophilin D and mitochondrial permeability transition pore opening protected corticospinal tract integrity and alleviated motor dysfunction caused by intracerebral hemorrhage. Our findings suggest that cyclophilin D is used as a key mediator of axonal degeneration after intracerebral hemorrhage; inhibition of cyclophilin D expression can protect mitochondrial structure and function and further alleviate corticospinal tract injury and motor dysfunction after intracerebral hemorrhage. Our findings provide a therapeutic target for preventing axonal degeneration of white matter injury and subsequent functional impairment in central nervous diseases.

Effects and mechanism of myeloperoxidase on microglia in the early stage of intracerebral hemorrhage.

(1) To clarify the dynamic relationship between the expression of myeloperoxidase (MPO) and microglial activation of intracerebral hemorrhage (ICH), (2) to explore the effect of inhibition of MPO on microglial activation, and (3) to observe the improvement in the neurobehavior of mice with inhibition of MPO. C57 BL/6 mice and CX3CR1 + /GFP mice were used to establish a phosphate-buffered saline (PBS) group, an ICH group, and a 4-aminobenzoic acid hydrazide (ABAH) group. Longa score, open field locomotion, hind-limb clasping test, immunohistochemistry, immunofluorescence, blood routine detection, and flow cytometry were used. The neurobehavior of the mice was significantly impaired following ICH (P < 0.01); the expression of MPO was significantly increased following ICH, and reached a peak value at 6 h post-injury (P < 0.001). Moreover, the microglial activation increased significantly following ICH, and reached a peak level at 24 h post-injury (P < 0.01). Following inhibition of MPO, the activation of microglia in the ICH group decreased significantly (P < 0.001). Moreover, the neurobehavior of the ICH group was significantly improved with MPO inhibition (P < 0.05). MPO may be an upstream molecule activated by microglia and following inhibition of MPO can improve secondary injury resulting from ICH.

Simvastatin Upregulates Lipoxin A4 and Accelerates Neuroinflammation Resolution After Intracerebral Hemorrhage.

Previous studies have demonstrated that statins can relieve inflammatory brain injury after intracerebral hemorrhage (ICH), but the mechanisms remain poorly characterized. This study aims to test whether simvastatin exerts an anti-inflammatory effect by regulating the proresolving mediators. First, male Sprague-Dawley rats had an injection of 200 μL autologous blood. Then, rats were randomly divided into groups treated with simvastatin (i.p. 2 mg/kg) or vehicle. Next, all rats underwent pro-resolving mediator lipoxin A4 (LXA4) level detection, flow cytometric, immunofluorescence, brain edema measurement, neurological scoring and western blot analysis. We found that simvastatin significantly increased the plasma level of LXA4, an endogenous formyl-peptide receptor 2 (FPR2) agonist, in the early stage of ICH. Consistent with the effect of simvastatin, exogenous LXA4 administration also promoted apoptosis of the circulating neutrophils, reduced neutrophils brain infiltration, and ameliorated inflammatory brain injury after ICH. In addition, similar to simvastatin, exogenous LXA4 markedly decreased the level of phosphorylated p38 mitogen-activated protein kinase (MAPK) and the apoptosis-related proteins myeloid cell leukemia 1(Mcl-1)/Bax ratio (a decreased ratio represents the induction of apoptosis) in circulating neutrophils isolated from ICH rats. Notably, all of the aforementioned effects of simvastatin on ICH were significantly abolished by Boc-2, a selective antagonist of FPR2. Moreover, simvastatin led to a similar Mcl-1/Bax ratio reduction as SB203580 (a p38 MAPK inhibitor), but it was abolished by P79350 (a p38 MAPK agonist). Collectively, these results suggest that simvastatin ameliorates ICH-mediated inflammatory brain injury, possibly by upregulating the level of pro-resolving mediator LXA4 and further stimulating the FPR2/p38 MAPK signaling pathway.

Neuroprotection of Heme Oxygenase-2 in Mice AfterIntracerebral Hemorrhage.

There are few effective preventive or therapeutic strategies to mitigate the effects of catastrophic intracerebral hemorrhage (ICH) in humans. Heme oxygenase is the rate-limiting enzyme in heme metabolism; heme oxygenase-2 (HO-2) is a constitutively expressed heme oxygenase. We explored the involvement of HO-2 in a collagenase-induced mouse model of ICH in C57BL/6 wild-type and HO-2 knockout mice. We assessed oxidative stress injury, blood-brain barrier permeability, neuronal damage, late-stage angiogenesis, and hematoma clearance using immunofluorescence, Western blot, MRI, and special staining methods. Our results show that HO-2 reduces brain injury volume and brain edema, alleviates cytotoxic injury, affects vascular function in the early stage of ICH, and improves hematoma absorbance and angiogenesis in the late stage of ICH in this model. Thus, we found that HO-2 has a protective effect on brain injury after ICH.

Brain transforms natural killer cells that exacerbate brain edema after intracerebral hemorrhage

Abstract Perihematomal edema (PHE) occurs within hours after intracerebral hemorrhage (ICH), leading to secondary injury manifested by impaired blood-brain-barrier (BBB) integrity and adjacent tissue destruction. To dissect mechanisms underlying PHE formation, we profiled human and mouse perihematomal tissues and identified natural killer (NK) cells as a predominant immune cell subset that outnumbers other infiltrating immune cell types during early stage of ICH. Unbiased clustering of single cell transcriptional profiles revealed two major NK cell subsets in the brain following ICH that possess either high cytotoxicity or robust chemokine production features, which distinguish them from NK cells in the periphery. NK cells exacerbate BBB disruption and brain edema after ICH via cytotoxicity toward cerebral endothelial cells and recruitment of neutrophils that augment focal inflammation. Thus, brain-bounding NK cells acquire specific features that contribute to PHE formation and neurological deterioration following ICH.

Prognostic Prediction of Dysphagia by Analyzing the Corticobulbar Tract in the Early Stage of Intracerebral Hemorrhage.

We investigated the predictive value of the corticobulbar tract (CBT) for dysphagia using diffusion tensor tractography in the early stage of intracerebral hemorrhage (ICH) for dysphagia. Forty-two patients with spontaneous ICH ± intraventricular hemorrhage (IVH) and 22 control subjects were recruited. The patients were classified into three groups: group A-could remove nasogastric tube (NGT) in the acute stage of ICH, group B-could remove NGT within 6months after onset, and group C-could not remove NGT until 6months after onset. The CBT were reconstructed, and fractional anisotropy (FA) and tract volume (TV) values were determined. The FA of the CBT in the affected hemisphere in group A was lower than in the control group (p < 0.05). The FA and TV of the CBT in the affected hemisphere in group B were lower than those in the control group (p < 0.05). In group C, the FA and TV in the affected hemisphere and unaffected hemispheres were lower than in the control group (p < 0.05). The TV of the CBT in the affected hemisphere in group B showed a moderate negative correlation with the length of time until NGT removal (r = 0.430, p < 0.05). We found that patients with CBT injuries in both hemispheres were not able to remove the NGT until 6months after onset, whereas patients who were injured only in the affected hemisphere were able to remove NGT within 6months of onset. The severity of injury to the CBT in the affected hemisphere appeared to be related to the length of time until NGT removal.

Neurotoxic role of interleukin-17 in neural stem cell differentiation after intracerebral hemorrhage.

Interleukin 17 (IL-17) and its main producer, T cell receptor γδ cells, have neurotoxic effects in the pathogenesis of intracerebral hemorrhage (ICH), aggravating brain injuries. To investigate the correlation between IL-17 and ICH, we dynamically screened serum IL-17 concentrations using enzyme-linked immunosorbent assay and explored the clinical values of IL-17 in ICH patients. There was a significant negative correlation between serum IL-17 level and neurological recovery status in ICH patients (r = -0.498, P < 0.01). To study the neurotoxic role of IL-17, C57BL/6 mice were used to establish an ICH model by injecting autologous blood into the caudate nucleus. Subsequently, the mice were treated with mouse neural stem cells (NSCs) and/or IL-17 neutralizing antibody for 72 hours. Flow cytometry, brain water content detection, Nissl staining, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling results indicated that NSC transplantation significantly reduced IL-17 expression in peri-hematoma tissue, but there was no difference in T cell receptor γδ cells. Compared with the ICH group, there were fewer apoptotic bodies and more Nissl bodies in the ICH + NSC group and the ICH + NSC + IL-17 group. To investigate the potential effect of IL-17 on directional differentiation of NSCs, we cultured mouse NSCs (NE-4C) alone or co-cultured them with T cell receptor γδ cells, which were isolated from mouse peripheral blood mononuclear cells, for 7 days. The results of western blot assays revealed that IL-17 secreted by T cell receptor γδ cells reduced the differentiation of NSCs into astrocytes and neurons, while IL-17 neutralization relieved the inhibition of directional differentiation into astrocytes rather than neurons. In conclusion, serum IL-17 levels were elevated in the early stage of ICH and were negatively correlated with outcome in ICH patients. Animal experiments and cytological investigations therefore demonstrated that IL-17 probably has neurotoxic roles in ICH because of its inhibitory effects on the directional differentiation of NSCs. The application of IL-17 neutralizing antibody may promote the directional differentiation of NSCs into astrocytes. This study was approved by the Clinical Research Ethics Committee of Anhui Medical University of China (For human study: Approval No. 20170135) in December 2016. All animal handling and experimentation were reviewed and approved by the Institutional Animal Care and Use Committee of Anhui Medical University (approval No. 20180248) in December 2017.

MicroRNA-181c provides neuroprotection in an intracerebral hemorrhage model.

Apoptosis is an important factor during the early stage of intracerebral hemorrhage. MiR-181c plays a key regulatory role in apoptosis. However, whether miR-181c is involved in apoptosis of prophase cells after intracerebral hemorrhage remains unclear. Therefore, in vitro and in vivo experiments were conducted to test this hypothesis. In vivo experiments: collagenase type VII was injected into the basal ganglia of adult Sprague-Dawley rats to establish an intracerebral hemorrhage model. MiR-181c mimic or inhibitor was injected in situ 4 hours after intracerebral hemorrhage. Neurological functional defects (neurological severity scores) were assessed 1, 7, and 14 days after model establishment. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling and western blot assay were conducted 14 days after model establishment. In vitro experiments: PC12 cells were cultured under oxygen-glucose deprivation, and hemins were added to simulate intracerebral hemorrhage in vitro. MiR-181c mimic or inhibitor was added to regulate miR-181c expression. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, luciferase reporter system, and western blot assay were performed. Experimental results revealed differences in miR-181c expression in brain tissues of both patients and rats with cerebral hemorrhage. In addition, in vitro experiments found that miR-181c overexpression could upregulate the Bcl-2/Bax ratio to inhibit apoptosis, while inhibition of miR-181c expression could reduce the Bcl-2/Bax ratio and aggravate apoptosis of cells. Regulation of apoptosis occurred through the phosphoinositide 3 kinase (PI3K)/Akt pathway by targeting of phosphatase and tensin homolog deleted on chromosome ten (PTEN). Higher miR-181c overexpression correlated with lower neurological severity scores, indicating better recovery of neurological function. In conclusion, miR-181c affects the prognosis of intracerebral hemorrhage by regulating apoptosis, and these effects might be directly mediated and regulated by targeting of the PTEN\PI3K/Akt pathway and Bcl-2/Bax ratio. Furthermore, these results indicated that miR-181c played a neuroprotective role in intracerebral hemorrhage by regulating apoptosis of nerve cells, thus providing a potential target for the prevention and treatment of intracerebral hemorrhage. Testing of human serum was authorized by the Ethics Committee of China Medical University (No. 2012-38-1) on February 20, 2012. The protocol was registered with the Chinese Clinical Trial Registry (Registration No. ChiCTR-COC-17013559). The animal study was approved by the Institutional Animal Care and Use Committee of China Medical University (approval No. 2017008) on March 8, 2017.

Relationship Between Impaired Consciousness and Injury of Ascending Reticular Activating System in Patients With Intracerebral Hemorrhage.

Background and Purpose- We investigated the relationship between impaired consciousness and ascending reticular activating system (ARAS) characteristics on diffusion tensor tractography during the early stage of spontaneous intracerebral hemorrhage confined to a unilateral supratentorial area. Methods- A total of 29 consecutive patients with impaired consciousness (the patient group A), 31 age- and sex-matched patients without impaired consciousness (the patient group B), and 20 age- and sex-matched healthy control subjects were recruited. The Glasgow Coma Scale was used to evaluate patients' conscious state in the early stage of intracerebral hemorrhage (within 30 days after onset). Three parts of the ARAS (lower dorsal, lower ventral, and upper) were reconstructed, and fractional anisotropy and tract volume values were determined. Results- The tract volume value of the lower dorsal ARAS in the patient group A was significantly lower than those of the patient group B and control group in the affected hemisphere (P<0.05). Among the diffusion tensor tractography parameters, only the tract volume of the lower dorsal ARAS in the affected hemispheres of the patient group A had a moderate positive correlation with Glasgow Coma Scale score (r=0.456; P<0.05). Conclusions- Impaired consciousness during the early stage of intracerebral hemorrhage was closely related to injury of the lower dorsal ARAS in the affected hemisphere. Clinical Trial Registration- URL: http://www.e-irb.com/index.jsp. Unique identifier: 2015-07-064.

Crocin attenuation of neurological deficits in a mouse model of intracerebral hemorrhage

Intracerebral hemorrhage (ICH) is a devastating subtype of stroke that is associated with high morbidity and mortality. However, up to now, there are no effective prevention methods or specific therapies to improve its clinical outcomes. Herein, we explore preliminarily the efficacy of crocin, a carotenoid extracted from the stigma of saffron known for its anti-oxidation and free radical scavenging activities, in a mouse ICH model induced with collagenase infusion. Crocin or saline was administrated 6 h after ICH and then every 12 h for up to 7 days. Neurological scores were examined on days 1, 3, and 7 after ICH. Mice were sacrificed after1, 3, and 7 days of crocin treatment for examination of histology and immunohistochemistry. The results showed that oral administration of crocin attenuated the neurological deficits and reduced the myelin loss, neuron degeneration, iron deposition, reactive oxygen species (ROS) production and heme oxygenase-1 (HO-1) expression in the early stage of ICH, making it potential to be an ideal candidate for medical therapy of ICH in clinic.

TRPA1 Activation-Induced Myelin Degradation Plays a Key Role in Motor Dysfunction After Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is a devastating disease that is characterized by high morbidity and high mortality. ICH has an annual incidence of 10–30/100,000 people and accounts for approximately 10%–30% of all types of stroke. ICH mostly occurs at the basal ganglia, which is rich in nerve fibers; thus, hemiplegia is quite common in ICH patients with partial sensory disturbance and ectopic blindness. In the clinic, those symptoms are considered to originate from the white matter injury in the area, but the exact mechanisms are unknown, and currently, no effective drug treatments are available to improve the prognosis. Clarifying the mechanisms will contribute to the development of new treatment methods for patients. The transient receptor potential ankyrin 1 (TRPA1) channel is a non-selective cation channel that plays a role in inflammatory pain sensation and nociception and may be a potential regulator in emotion, cognition and social behavior. Here, we report that TRPA1 is involved in myelin damage and oxidative stress injury in a mouse ICH model. Intervention with the TRPA1 channel may be a new method to improve the motor function of patients in the early stage of ICH.

Cab45s inhibits neuronal apoptosis following intracerebral hemorrhage in adult rats

Recent studies have shown that Cab45s, belonging to the CREC family, can fight against apoptosis in the cancer cell lines. Here, we report that Cab45s may involve in neuronal apoptosis at the early stage of intracerebral hemorrhage (ICH) in pathophysiology. We found that expression of Cab45s was enhanced in areas contiguous to hematoma following ICH in adult rats, and that so were the expressions of Glucose-regulated protein 78 (GRP78), pro-apoptotic Bcl-2-associated X protein (Bax) and active caspase-3. In vitro, coimmunoprecipitation analysis indicated the interaction between Cab45s and GRP78. Depletion of Cab45s attenuated the expression of GRP78, but increased the expressions of Bax and caspase-3 in PC12 cells treated with hemin, which finally promoted apoptosis. Together, these results reveal that Cab45s might exert its anti-apoptotic function against neuronal apoptosis. Thus, the study may provide evidences for regulating Cab45s as a potentially reliable treatment for the secondary damage following ICH.

Hemostatic Therapy for Intracerebral Hemorrhage

Objective: To reduce the blood pressure and elevate intracranial pressure using nimodipine (Nimotop Intravenous (IV) infusion). Thus, intracerebral hemorrhage was controlled, and the purpose of hemostasis was achieved. Methods: Sixty-eight patients with intracerebral hemorrhage were divided into a treatment group (n = 51), and a control group (n = 35). Nimotop solution (10 mg) was administered as a fast-flowing IV infusion in the treatment group, and 250 ml 20% mannitol infusion was given to patients in the control group twice every day. Patients in both groups received treatment for seven days, and the blood pressure on the treatment day was measured. A brain Computed Tomography (CT) scan was performed as a reexamination within two weeks. Results: The blood pressure in the treatment group was decreased from 179/104 to 151/91 mmHg, averagely, and in the control group was decreased from 181/108 to 180/103 mmHg, averagely. The difference between these two groups was statistically significant (P P Conclusion: Nimodipine can dilate the arteries, reduce blood pressure, and elevate intracranial pressure, lowering pressure gradients across vessel wall which destroy the vessel wall. Also, nimodipine can prevent hemorrhage as well as recurrent hemorrhage, and can used as the first choice of rescue drug. What’s more, dehydration drugs such as mannitol should not be used in the early stage of intracerebral hemorrhage in order to prevent hematoma enlargement.

Distinct role of heme oxygenase-1 in early- and late-stage intracerebral hemorrhage in 12-month-old mice

Intracerebral hemorrhage (ICH) is a devastating form of stroke with high morbidity and mortality. Heme oxygenase-1 (HO-1), the key enzyme in heme degradation, is highly expressed after ICH, but its role is still unclear. In this study, we used an HO-1 inducer and inhibitor to test the role of HO-1 in different stages of ICH in vivo and in vitro. In the early stage of ICH, high HO-1 expression worsened the outcomes of mice subjected to the collagenase-induced ICH model. HO-1 increased brain edema, white matter damage, neuronal death, and neurobehavioral deficits. Furthermore, elevated HO-1 increased inflammation, oxidative stress, matrix metalloproteinase-9/2 activity, and iron deposition. In the later stage of ICH, long-term induction of HO-1 increased hematoma absorption, angiogenesis, and recovery of neurologic function. We conclude that HO-1 activation mediates early brain damage after ICH but promotes neurologic function recovery in the later stage of ICH.

High Serum MiR-130a Levels Are Associated with Severe Perihematomal Edema and Predict Adverse Outcome in Acute ICH

The development and/or progression of perihematomal edema (PHE) in patients with acute spontaneous intracerebral hemorrhage (ICH) vary substantially with different individuals. Although hematoma volume is a useful indicator for predicting PHE, its predictive power was not good at the early stage of ICH. Better predictors are urgently needed. In this study, we found that miR-130a was elevated in the serum of ICH patients and was an independent indicator positively associated with PHE volume within the first 3 days after onset. The R (2) was further evaluated when it is used in combination with hematoma mass. Serum miR-130a levels were associated with clinical outcome (National Institute of Health Stroke Scale (NIHSS) scores at day 14 and modified Rankin Scale (mRS) scores at day 90) only in patients with deep hematoma. Moreover, miR-130a was significantly increased in rat serum and perihematomal tissues and was in line with the change in brain edema. MiR-130a inhibitors reduced brain edema, blood-brain barrier (BBB) permeability, and increased neurological deficit scores, and miR-130a mimics increased monolayer permeability. Thrombin-stimulated brain microvascular endothelial cells (BMECs) were a main source of miR-130a under ICH. In the experimental model, the elevated miR-130a level was accompanied by the decreased caveolin-1 and increased matrix metalloproleinase (MMP)-2/9. Meanwhile, caveolin-1 (cav-1) was reduced by miR-130a mimics, accompanied by an increase in MMP-2/9 expression. The upregulated MMP-2/9 was then downregulated by cavtratin, a cav-1 scaffolding domain peptide. This regulation mechanism was authenticated in a thrombin-induced cellular ICH model. Our results suggest that serum miR-130a may serve as a useful early biomarker for monitoring post-ICH PHE and predicting prognosis and may be helpful in the decision-making of individualized therapy.

Injury of Fornix in Patients With Intracerebral Hemorrhage

ABSTRACTObjectives: Many diffusion tensor tractography (DTT) studies have reported on fornix injury in various diseases. However, there has been no DTT study on fornix injury by intracerebral hemorrhage (ICH). We attempted to investigate fornix body injury in patients with ICH, using DTT. Methods: We identified 58 consecutive stroke patients using the following criteria: (1) first-ever stroke, (2) age: 45–65 years, (3) hemorrhage confined within the corona radiata and basal ganglion level, (4) an available DTT scan performed during the early stage of ICH (1–5 weeks after onset). Among 58 consecutive patients, we identified six patients who showed disruption at the fornix body.Results: Following ICH, 10.7% of patients revealed complete disruption of the fornix body on DTT. Results from DTT of the fornix showed disruption in anterior and posterior portions of the fornix body in three patients, in the anterior portion of the fornix body in two patient, and in the posterior portion of the fornix body in one patient. Conclusions: We report on six patients who showed complete disruption of the fornix body following ICH. It is our belief that the fornix of patients with ICH could be evaluated using DTT.

Corticospinal Tract Change in the Unaffected Hemisphere at the Early Stage of Intracerebral Hemorrhage: A Diffusion Tensor Tractography Study

Objectives: Contribution by the unaffected hemisphere is one of the motor recovery mechanisms following stroke. We attempted to investigate changes in the corticospinal tract (CST) in the unaffected hemisphere at the early stage in patients with intracerebral hemorrhage (ICH), using diffusion tensor tractography (DTT). Subjects and Methods: Fifty-three consecutive hemiparetic patients and 40 age- and sex-matched control subjects were enrolled. DTT was performed using a 1.5-tesla system at the early stage of ICH (7–28 days after onset). We measured the fiber number, fractional anisotropy and apparent diffusion coefficient of CST tractography in the unaffected hemisphere, and assessed the motor function of the affected extremities. Results: The fiber number of the CST in the unaffected hemisphere of the patient group was higher than that of the control group (p = 0.000). In contrast, the fractional anisotropy value was lower than that of the control group (p = 0.018). However, there were no significant differences in the apparent diffusion coefficient values between the 2 groups (p = 0.654). Conclusions: We demonstrated that the CST in the unaffected hemisphere was changed at the early stage in patients with ICH, using DTT.

Comparison of TMS and DTT for predicting motor outcome in intracerebral hemorrhage

Background TMS (transcranial magnetic stimulation) and DTT (diffusion tensor tractography) have different advantages in evaluating stroke patients. TMS has good clinical accessibility and economical benefit. On the contrary, DTT has a unique advantage to visualize neural tracts three-dimensionally although it requires an expensive and large MRI machine. Many studies have demonstrated that TMS and DTT have predictive values for motor outcome in stroke patients. However, there has been no study on the comparison of these two evaluation tools. In the current study, we compared the abilities of TMS and DTT to predict upper motor outcome in patients with ICH (intracerebral hemorrhage). Methods Fifty-three consecutive patients with severe motor weakness were evaluated by TMS and DTT at the early stage (7–28 days) of ICH. Modified Brunnstrom classification (MBC) and the motricity index of upper extremity (UMI) were evaluated at onset and 6 months after onset. Results Patients with the presence of a motor evoked potential (MEP) in TMS or a preserved corticospinal tract (CST) in DTT showed better motor outcomes than those without ( p = 0.000). TMS showed higher positive predictive value than DTT. In contrast, DTT showed higher negative predictive value than TMS. Conclusions TMS and DTT had different advantages in predicting motor outcome, and this result could be a reference to predict final neurological deficit at the early stage of ICH.

Motor outcome according to diffusion tensor tractography findings in the early stage of intracerebral hemorrhage

We tried to investigate the motor outcome according to diffusion tensor tractography (DTT) findings for the corticospinal tract (CST) in the early stage for hemiparetic patients with intracerebral hemorrhage (ICH). Forty patients with severe paralysis of the affected side were enrolled. DTT was obtained in the early stage of the stroke (7-30 days) and was classified into four groups: type A, the CST originating from primary motor cortex was preserved around the hematoma; type B, the CST was similar to type A except the fiber originated from the adjacent areas to the primary motor cortex; type C, the CST was interrupted at or around the hematoma; and type D, the CST did not reach the hematoma due to degeneration (Fig. 1). Six months after onset, motor function was measured and the statistical influence of the DTT type was tested. Initially, none of the motor function scales of the affected side differed among the four DTT types. Six months after the onset of ICH, motor functions of the same side were significantly different according to DTT type (p<0.05). All motor scales were highest in the DTT type A group, and were lowest in the DTT type D group (p<0.0003). The early DTT findings for CST may be used to predict the motor outcome of the affected extremities in hemiparetic patients with ICH.