Kuniyasu Wada

Transoral Carotid Ultrasonography

BACKGROUND AND PURPOSE We attempted ultrasonographic evaluation of the distal extracranial internal carotid artery (ICA) using the transoral method (transoral carotid ultrasonography [TOCU]). METHODS The subjects consisted of five healthy volunteers and seven stroke patients. Examinations were performed with a color Doppler flow imaging system equipped with convex array transducers (7 or 9.5 MHz), originally designed for transrectal use. After local anesthesia of the pharynx, we inserted a probe covered with thin gum transorally, touching the tip to the pharyngeal posterolateral wall. We then attempted to detect the ICA and measure flow velocity of the distal extracranial ICA using principal images obtained by TOCU. RESULTS TOCU was successfully performed in all subjects without any difficulty. In the healthy volunteers, the ICA was identified at a depth of 2.2+/-0.6 cm and visualized as a vertical linear vessel 2.9+/-0.3 cm in length and bent slightly backward. The diameter and mean flow velocity of the distal extracranial ICA were 4.7+/-0.2 mm and 50+/-7 cm/s, respectively. In the stroke patients, some remarkable findings were obtained, including a narrow ICA with low flow velocity in a patient with possible ICA dissection, a lucent echo without flow signal in a patient with acute cardioembolic ICA occlusion, and decreased ICA flow velocity in a patient with ipsilateral MCA stenosis. CONCLUSIONS These preliminary data demonstrate the potential applicability of TOCU to the evaluation of flow in the far distal extracranial ICA. TOCU definitely warrants further investigation in patients with carotid artery disease.

Oscillating thromboemboli within the extracranial internal carotid artery demonstrated by ultrasonography in patients with acute cardioembolic stroke

We detected oscillating thromboemboli at the extracranial internal carotid artery (ICA) by duplex carotid ultrasonography in patients with acute cardioembolic stroke. Using B-mode ultrasonography, we evaluated the extracranial ICA in 11 patients with acute cardioembolic ICA occlusion. A homogeneous, elastic, oscillating intraluminal mass echo originating in the extracranial ICA extended distally in 5 (46%) of these patients. The echoes moved quickly and distally during the systolic phase of the cardiac cycle and returned slowly to the original position during the diastolic phase. We performed a postmortem study 24 days after stroke onset in 1 patient with an oscillating intraluminal mass echo that had been demonstrated by duplex ultrasonography. The ICA lumen was obstructed with a fresh string-like thrombus. The findings of oscillating intraluminal mass echo may help establish a diagnosis of acute embolic ICA occlusion.

Lesions visualized by contrast-enhanced magnetic resonance imaging in transient ischemic attacks.

In patients with transient ischemic attacks (TIAs), contrast-enhanced magnetic resonance imaging (MRI) is more sensitive to visualize the recent ischemic lesions than conventional MRI. We examined the clinical characteristics of TIA patients presenting with enhanced lesions visualized by contrast-enhanced MRI. We retrospectively evaluated 64 patients with carotid TIAs. We evaluated the frequency and topography of TIA associated infarcts on contrast-enhanced MRI and compared the clinical background of patients with and without such lesions. Twenty-three patients underwent plain MRI only, while the remaining 41 patients underwent contrast-enhanced MRI. Of the latter 41 patients, 16 had abnormal enhanced lesions (39%: group L), while 25 had no lesions (61%: group NL). In group L, all lesions were spotty, and they were located in the cerebral cortex in 13 patients (81%), the subcortex in two (12%), and the perforator territory in one (6%). Aphasia or confusional state, hypertension, and emboligenic cardiac or arterial disease (stenosis > or =50%) were more frequently observed in group L than in group NL (38 vs. 8%, 81 vs. 48%, and 93 vs. 60%, respectively, P<0. 05). The TIA patients with enhanced lesions on MRI may be associated with an emboligenic cardiac or arterial disease, severe neurologic symptom compared to those without them.

Early neurological deterioration represents recurrent attack in acute small non-lacunar stroke.

The aim of this study was to identify the frequency and possible pathogenic mechanisms of early neurological deterioration in patients with acute small non-lacunar infarction. We studied 46 patients (35 men, 11 women; age, 70.3+/-10.4 years) with acute small non-lacunar infarction. Small non-lacunar infarction was diagnosed using diffusion-weighted magnetic resonance imaging (DWI) as being <15 mm in diameter and located in the cortex and centrum ovale in the middle cerebral artery territory. The patients were divided into two groups; Group D (n=6) had neurological deterioration within 7 days after symptom onset, while Group N (n=40) did not have any neurological deterioration. In Group D, the interval from symptom onset to clinical deterioration was 3.3+/-1.5 days (range 2-6 days). Blood pressure on admission was higher in Group D than in Group N (p<0.05). In Group D, four of these five patients with follow-up DWI had new acute small ischemic lesions in addition to the initial lesions, indicating recurrent attacks of brain infarction. Neurological deterioration occurred within 7 days after symptom onset in 13% of patients. Neurological deterioration was frequently caused by recurrent infarction detected by DWI.

Combined carotid and transcranial color-coded sonography in acute ischemic stroke

The objective of this study is to clarify whether the combination of carotid duplex sonography (CD) and transcranial color-coded sonography (TCCS) can accurately detect occlusive lesions in extra and intracranial brain arteries in acute stroke patients, using angiography as the standard. Just before angiography, we performed CD and TCCS in 40 consecutive patients within 24 h after stroke onset. We assessed 320 vessels in total, bilateral internal carotid arteries, vertebral arteries, M1 segments of middle cerebral arteries (MCAs), and P2 segments of posterior cerebral arteries (PCAs). Out of all vessels, 250 (78.1%) could be evaluated by neurosonography because 32 MCAs and 38 PCAs were excluded due to inadequate acoustic windows for TCCS. Significant occlusive lesions (>50%) were observed in 21 out of 250 vessels by neurosonography. Angiography confirmed 20 occlusive lesions as revealed by neurosonography. In the remaining 229 neurosonographically normal vessels, angiography showed no significant lesions except M2 occlusions. The accuracy, sensitivity, and specificity of neurosonography for the detection of occlusive vessels were 99.6, 100 and 99.6%, respectively. Occlusive lesions were observed in 20 of all patients by neurosonography. Nineteen of them were confirmed by angiography. The combination of CD and TCCS can make an accurate diagnosis for significant occlusive lesions in brain arteries in acute stroke patients.

Evaluation of posterior cerebral artery flow velocity by transcranial color-coded real-time sonography

Using transcranial color-coded real-time sonography (TCCS), we measured peak-systolic flow velocities (PSVs) in segment P2 of 102 posterior cerebral arteries (PCAs) in 61 patients, with angiography. We divided 102 PCAs into four groups: control group (n = 70) with no significant stenotic lesions; PCS group (n = 7) with stenosis >/= 50% of P2 segment; Col (+) group (n = 13) and Col (-) group (n = 12) had occlusive lesions in the carotid system with or without collateral flow from PCA to the middle cerebral artery through the leptomeningeal anastomosis. In the PCS group, PSV (255.7 +/- 67.2 cm/s) was higher than in the other three groups (p < 0.0001). PSV was higher in the Col (+) group (127.6 +/- 31.2) than in the Col (-) (86.6 +/- 20.1) and control (83.8 +/- 24.8) groups (p < 0.001). The measurement of PSV in the P2 segment of PCA using TCCS may help to identify a significant stenosis in PCA.

Incongruous homonymous hemianopic scotoma

We report a patient presenting with incongruous homonymous hemianopic scotoma due to infarction in the territory of the lateral posterior choroidal artery. Imaging studies showed that the patient had a fresh infarct in the lateral geniculate body causing this unusual visual field defect.

Spuriously Large Subcortex Infarct due to Confluent Smaller Lesions: A Diffusion-Weighted MRI/CT Study

Introduction A lacunar infarction is defi ned as a small, deep infarction that involves a perforating artery that branches from a large cerebral artery [1] . Most autopsy studies have documented that lacunar infarctions are small, ranging from 0.2 to 15 mm in size [2] . Thus, the term lacunar infarction is commonly used as a clinical category for small lesions ( ! 15 mm in the largest diameter on CT or MRI) in the territory of the deep and single perforating arteries. However, occasionally, deep infarcts larger than 15 mm in diameter without arterial disease are found. Fisher and Curry [3] termed such lesions ‘giant lacunes’. However, the pathogenesis of these lesions has been poorly understood. We report a case with two small lacunes seen on diffusion-weighted MRI that merged to form a giant lacunar infarct seen on CT. We believe that this new fi nding provides CT documentation of the pathogenesis of giant lacunar infarcts.

Cerebral infarction related to varicella zoster virus vasculopathy

A 14-year-old girl developed transient disturbance of consciousness, dysarthria, and clumsiness of the right upper limb 4 months after herpes zoster ophthalmicus. Brain MRI showed acute cerebral infarction in the left middle cerebral artery (MCA) territory. CT angiography demonstrated mild stenosis in the top of the left internal carotid artery and the proximal side of the MCA. Cerebrospinal fluid (CSF) examination showed slightly mononuclear pleocytosis (6/μl). Titer of the anti-varicella zoster virus (VZV) IgG antibodies in CSF was increased, and gadolinium-enhanced brain MRI (T1-weighted imaging) revealed enhancement of the vessel walls at the stenotic lesions. Based on the diagnosis of VZV vasculopathy, methylprednisolone and valacicrovir were administered, followed by acyclovir, in addition to antithrombotic therapy using aspirin and warfarin. After these treatment, her right upper clumsiness was resolved and gadolinium-enhancement of the vessel walls was disappeared on MRI. VZV vasculopathy may cause ischemic stroke in young patients, especially in children. A careful history-taking about herpes is necessary to detect the disease as a potential cause in young stroke patients.

Calcified Cerebral Embolism Due to a Calcified Amorphous Tumor

A 59-year-old man developed brain embolism in the frontal and parietal cortex. Brain CT showed a high-density spot in the upper branch of the left middle cerebral artery, indicating calcified cerebral embolism. Calcified amorphous tumor attached to the mitral valve was identified as the cause of embolism. After surgical resection, anticoagulation was started and recurrent stroke did not occur.