Jun Niwa

Detection of Hemosiderin Deposition by T2*-Weighted MRI After Subarachnoid Hemorrhage

Background and Purpose— Subarachnoid hemorrhage (SAH) is very difficult to diagnose several months after its onset. We thus investigated subarachnoid hemosiderin deposition well after SAH by T2*-weighted MRI, a sensitive method for hemosiderin detection. Methods— To investigate how hemosiderin deposition as confirmed by T2*-weighted MRI contributes to the determination of prior SAH and how the extent of hemosiderin deposition is associated with a number of clinical factors, we retrospectively analyzed 58 patients >3 months after SAH associated with ruptured aneurysms. We also investigated 209 healthy volunteers as controls. Results— T2*-weighted MRI demonstrated subarachnoid hemosiderin deposition in 72.4% of the SAH patients, whereas no deposition was seen in the healthy volunteer group. The hemosiderin was preferentially deposited in the subarachnoid space near a ruptured aneurysm. Odds ratios (ORs) were estimated from logistic regression analyses correlating hemosiderin deposition with other factors. Age (≥54 years) (OR, 5.1; 95% CI, 1.03 to 25.0; P =0.046), Fisher grade 3 on initial CT (OR, 8.0; 95% CI, 1.26 to 50.4; P =0.027), and Karnofsky Scale score ≤80% 6 months after onset of SAH (OR, 12.8; 95% CI, 1.97 to 83.3; P =0.0077) were all found to be independently associated with hemosiderin deposition levels. Conclusions— T2*-weighted MRI is an effective means of diagnosing prior SAH and may also reveal the location of a ruptured aneurysm. The extent of hemosiderin deposition was significantly associated with several factors, including age, CT findings, and poor prognosis.

Dot-like hemosiderin spots on gradient echo T2^*-weighted magnetic resonance imaging are associated with past history of small vessel disease in patients with intracerebral hemorrhage

Background and Purpose. Lipohyalinosis is considered an important cause of cerebral small vessel disease (SVD), including hypertensive intracerebral hematoma (ICH) and lacunar infarction. Dot‐like low‐intensity spots (dot‐like hemosiderin spots [dotHSs]) on gradient‐echo T2*‐weighted (T2*‐w) magnetic resonance imaging (MRI) have been histologically diagnosed as old microbleeds associated with microangiopathies (lipohyalinosis, amyloid angiopathy) and located in territories of perforating arteries (deep dotHSs) and subcortical regions (subcortical dotHSs). If dotHSs indicate the severity of lipohyalinosis, larger numbers of deep dotHSs may be associated with past history of SVD.Methods. The number of dotHSs was investigated in 213 patients with deep ICH (106 men, 107 women, 37 to 94 years old, mean age = 65.8 ± 11.2 years). Patients were divided into 2 subgroups according to past history of SVD. Odds ratio (OR) for the history was estimated from logistic regression analyses of the number of deep or subcortical dotHSs, as well as other factors.Results. Of 213 patients, 36 had a past history of SVD (symptomatic deep ICH in 18, symptomatic lacunar infarction in 17, and both in 1). An increased rate of history of SVD was found for patients with subcortical dotHSs. The OR per 1 subcortical dotHS was 1.09 (95% confidence internal (CI), 1.03–1.17;P= .005), and per deep dotHS, the OR was 1.07 (95% CI, 1.00–1.13;P= .039). Conclusions. The findings suggest that deep and subcortical dotHSs on T2*‐w MRI may indicate the severity of microangiopathy and may predict recurrence of SVD in patients with deep ICH.

Dynamics of Dotlike Hemosiderin Spots Associated With Intracerebral Hemorrhage

The authors observed dotlike, low‐intensity spots in T2*‐weighted magnetic resonance imaging (MRI), subsequently diagnosed histologically as previous microbleeds associated with lipofibrohyalinosis, amyloid angiopathy, and small vessel disease. The nature of dotlike hemosiderin spots (dotHSs), however, is still unknown. This case report seeks to demonstrate the dynamics of dotHSs associated with an intracerebral hematoma (ICH). T2*‐weighted MRI of a 72‐year‐old man with a history of hypertension demonstrated 4 dotHSs 24 months after a left putaminal hemorrhage. Follow‐up T2*‐weighted MRI 40 months after the acute event demonstrated the asymptomatic formation of 3 more dotHSs, even with good control of blood pressure. Fifty months after the stroke, T2*‐weighted MRI showed that 2 of the new dotHSs had become fainter, whereas the hemosiderin associated with the ICH scar remained detectable. To the authors knowledge, this is the first description of dotHS dynamics associated with ICH.

Dotlike Hemosiderin Spots Are Associated With Past Hemorrhagic Strokes in Patients With Lacunar Infarcts

Background and Purpose. Dotlike hemosiderin spots ongradient‐echo T2*‐weighted magnetic resonance imaging of the brain have been histologically diagnosed as old microbleeds associated with small vessel disease (SVD). The authors hypothesize that the presence of many dotHSs may be correlated with the fragility of small vessels and the recurrence of SVD, including lacunar infarction and deep intracerebral hemorrhage (ICH). Methods. To investigate how dotHSs are related to past history of SVD, the number of subcortical or deep dotHSs was investigated in 146 patients with lacunar infarctions (95men, 51 women, age 38 to 90 [66.6 ± 9.4] years). They were divided into 2 subgroups according to history of deep ICHs or lacunar infarctions. The odds ratio (OR) for past history was estimated from logistic regression analyses with the number of subcortical or deep dotHSs as well as other factors. Results. Of 146 patients with lacunar infarctions, 11 had past symptomatic ICHs and 19 had past symptomatic lacunar infarctions. An elevated rate of history of ICH was found for lacunar infarction patients with many deep dotHSs (≥3; OR, 9.1; 95% confidence interval, 1.6–51, P= .015). However, history of lacunar infarction was not significantly associated with the number of subcortical or deep dotHSs. Conclusions. Our findings suggest that many deep dotHSs on T2*‐weighted magnetic resonance imaging may be correlated with deep ICH—lacunar infarction type of SVD recurrence but not lacunar infarction—lacunar infarction type.

Dynamics of Dot‐Like Hemosiderin Spots on T2*‐Weighted MRIs Associated with Stroke Recurrence

Background and Purpose. Dot‐like low‐intensity spots (dot‐like hemosiderin spots: dotHSs) on gradient echo T2*‐weighted (‐w) brain magnetic resonance imaging (MRIs) are frequently associated with cerebral small vessel disease (SVD), including deep intracerebral hemorrhages and lacunar infarctions. This study investigated how numbers of newly appeared dotHSs contribute to recurrent SVD. Methods. We prospectively analyzed numbers of newly appeared dotHSs in 12 patients with prior SVD (8 males, 4 females; mean 67.6 ± 10.7 years old) readmitted with recurring SVD between October 2001 and March 2003. Numbers of appeared dotHSs per year were counted on T2*‐w MRI scans after SVD recurrence and compared to previous MRIs. Seventy‐one outpatients (35 males, 36 females; mean 64.3 ± 9.6 years old) with histories of intracerebral hemorrhages (ICH) that came to the hospital during the study period served as controls. The hazard ratio (HR) for recurrence was estimated from a multivariate logistic regression model, using the number of appeared dotHSs (per year) and other risk factors. Results. Multivariate analyses revealed that an elevated rate of recurrence was found in patients with substantial numbers of appeared dotHSs (≥5/year) (HR, 7.34; P= 0.0008). We also analyzed factors associated with the numbers of appeared dotHSs. A number of appeared dotHSs (≥5/year) was significantly and independently associated with the initial number of dotHSs (≥10) on T2*‐w MRIs following the first SVD (HR, 18.6; P= 0.0001). Conclusions. Though a small sample size limited the power of our analyses, our findings suggest that a number of newly appeared dotHSs may be associated with SVD recurrence.

Hematoma Size in Deep Intracerebral Hemorrhage and its Correlation with Dot-Like Hemosiderin Spots on Gradient Echo T2*-Weighted MRI

Background and Purpose. Dot‐like low intensity spots (dot‐like hemosiderin spots: dotHSs) on gradient echo T2*‐weighted MRI have been histologically diagnosed to represent old cerebral microbleeds associated with microangiopathies. They have also been correlated to the fragility of small vessels and the tendency to bleed. Therefore, a substantial number of dotHSs might be associated with a large‐sized, deep intracerebral hematoma (ICH). On the other hand, dotHSs may reflect old microbleeds that did not enlarge to symptomatic size.

Dot‐Like Hemosiderin Deposition on T2*‐Weighted MR Imaging Associated with Nonhypertensive Intracerebral Hemorrhage

Background and Purpose. Microangiopathy, a disorder often related to hypertension, is an important cause of deep intracerebral hematoma (ICH). The microangiopathy is associated with dot‐like low‐intensity spots (a dot‐like hemosiderin spot: dotHS) on gradient‐echo T2*‐weighted MR images that have been histologically diagnosed as old microbleeds. The locations of dotHS are consistent with deep ICH. Methods. To investigate how dotHS or other risk factors contribute to nonhypertensive deep ICH, the number and location of dotHSs, as well as other risk factors were examined in 213 deep ICH patients (106 males, 107 females, age: 37‐94 (65.8 ± 11.2) years) consecutively admitted to Hakodate Municipal Hospital. Patients were divided into two subgroups according to the presence or absence of hypertension. DotHSs were also divided into deep and subcortical dotHS and investigated independently. Odds ratios (ORs) were estimated from logistic regression analyses. Furthermore, nonhypertensive ICH patients were compared with nonhypertensive healthy volunteers matched for age and sex. Results. No risk factors were identified in the 31 nonhypertensive deep ICH patients that differed from those found in the 182 hypertensive deep ICH patients. Deep dotHS ≥ 1 (OR: 25.5; 95% CI: 4.76‐137; P= .0002), subcortical dotHS ≥ 1 (OR: 9.0; 95% CI: 1.79‐44.9; P= .046), diabetes mellitus (OR: 9.0; 95% CI: 1.53‐52.3; P= .015), and smoking (OR, 9.6; 95% CI; 1.8‐49.8, P= .007) significantly elevated the risk of nonhypertensive ICH, compared to the healthy volunteers. Conclusions. Our findings suggest that deep and subcortical dotHSs may be risk factors for the development of non‐hypertensive deep ICH.

Acquired factor VIII inhibitors in a patient associated with neurosurgery: case report and review of the literature.

OBJECTIVE AND IMPORTANCE: Acquired factor VIII inhibitors in patients without hemophilia is rare event characterized by severe bleeding as a result of antibody against factor VIII. We describe a patient who developed subcutaneous and epidural bleeding after the clipping of an unruptured aneurysm. CLINICAL PRESENTATION: A 57-year-old man suddenly developed coagulopathy after undergoing a neurosurgical operation. Coagulation tests showed a prolongation of activated partial thromboplastin time and a marked reduction in factor VIII activity. Measurement of the factor VIII inhibitor level revealed 2 Bethesda units/ml. INTERVENTION: The hematoma was removed surgically, and bleeding was controlled with recombinant factor VIII. The patients then received prednisolone (80 mg/d) and cyclosporine. The laboratory tests normalized within 8 weeks. In the 5 years since cessation of corticosteroids, the clinical and laboratory courses of the patient have been uneventful. CONCLUSION: Autoimmune factor VIII inhibitors associated with a neurosurgical procedure are rare. Our case supports an association between surgery and the triggering of factor VIII inhibitors. This complication was probably the result of the surgical procedure or anesthetic agents or other drugs administrated during the perioperative period.

Cerebral Blood Flow before and after Treatment with Amlodipine in Elderly Patients with Lacunar Infarction

ment of hypertension reduces the risk of ischaemic Patients were eligible for inclusion if they were stroke.[4-10] Moreover, a BP reduction in subacute admitted to Hakodate Municipal Hospital with and chronic stroke may also prevent lipohyalinosis symptomatic lacunar infarction from October 2000 and other vascular lesions associated with stroke. to September 2001. Infarctions were 90mm Hg or a systolic BP of >150mm Hg 3 weeks the lower limit of CBF autoregulation downwards in after the onset of lacunar infarction. Patients with spontaneously hypertensive rats.[16] Amlodipine lacunar infarction associated with embolism (exdoes not significantly affect relative indices of CBF cluding atrial fibrillation or ulcerations of the cerviin elderly hypertensive patients after BP lowering[17] cal internal carotid arteries) or lacunar infarction and it reduces the rate of carotid artery atherosclerorelated to the stenosis of a main trunk of a cerebral sis.[18] BP lowering with amlodipine has been shown artery, as determined by magnetic resonance angioto reduce stroke occurrence.[9] Such findings suggest graphy and/or digital subtraction angiography, were that amlodipine may be a suitable antihypertensive excluded. medication for elderly patients with acute stroke. Written informed consent was obtained from In our experience, reduction of systolic/diastolic either the patient or their closest relative. The study BP to normal (<140/85mm Hg) for lacunar infarcprotocol was approved by the Ethics Committee of tion is not harmful 2 weeks after the onset of stroke. Hakodate Municipal Hospital, Hokkaido, Japan. BP is reduced 2 weeks after stroke; the reduction Patients were treated medically with ozagrel for may be associated with normalisation of the sympa14 days after the onset of the infarction.[19] Rehabilithetic tone. At that time, further rehabilitation retation, including speech therapy, was started 2–3 quires stabilisation of BP. days after admission if the neurological deficit could