1/17. MRI features of intracerebral hemorrhage within 2 hours from symptom onset. BACKGROUND AND PURPOSE: MRI has been increasingly used in the evaluation of acute stroke patients. However, MRI must be able to detect early hemorrhage to be the only imaging screen used before treatment such as thrombolysis. Susceptibility-weighted imaging, an echo-planar T2* sequence, can show intracerebral hemorrhage (ICH) in patients imaged between 2.5 and 5 hours from symptom onset. It is unknown whether MRI can detect ICH earlier than 2.5 hours. We describe 5 patients with ICH who had MRI between 23 and 120 minutes from symptom onset and propose diagnostic patterns of evolution of hyperacute ICH on MRI. methods: As part of our acute imaging protocol, all patients with acute stroke within 24 hours from symptom onset were imaged with a set of sequences that included susceptibility-weighted imaging, diffusion- and perfusion-weighted imaging, T1- and T2-weighted imaging, fluid-attenuated inversion recovery (FLAIR), and MR angiography using echo-planar techniques. Five patients with ICH had MRI between 23 and 120 minutes from the onset of symptoms. RESULTS: ICH was identified in all patients. Distinctive patterns of hyperacute ICH and absence of signs of ischemic stroke were the hallmark features of this diagnosis. The hyperacute hematoma appears to be composed of 3 distinct areas: (1) center: isointense to hyperintense heterogeneous signal on susceptibility-weighted and T2-weighted imaging; (2) periphery: hypointense (susceptibility effect) on susceptibility-weighted and T2-weighted imaging; and (3) rim: hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging, representing vasogenic edema encasing the hematoma. CONCLUSIONS: MRI is able to detect hyperacute ICH and show a pattern of evolution of the hematoma within 2 hours from the onset of symptoms. ( info) |
2/17. Ipsilateral hemiparesis after putaminal hemorrhage due to uncrossed pyramidal tract. OBJECTIVE: Previous case reports supported the presence of the uncrossed pyramidal tract in exceptional patients. However, most of these case reports have not fully discussed involvement of the motor cortex controlling the ipsilateral limbs. DESIGN AND METHOD: The authors investigated a 62-year-old man who developed right hemiparesis after right putaminal hemorrhage by using MRI, transcranial magnetic stimulation, functional MRI (fMRI), and sensory evoked potentials. He had moderate weakness including the face, spasticity with brisk deep tendon reflexes and Babinski sign, and impaired vibration and position sense, all on the right side. RESULT: A MRI study showed hemorrhage in the right putamen and the wedge-shaped medulla. A fMRI study during a sequential finger opposition task showed activation in the motor cortex ipsilateral to the finger movements, but not on the contralateral side. Sensory evoked potentials showed cortical response ipsilateral to the side of stimulation. CONCLUSION: The pyramidal tract and the dorsal column-medial lemniscus pathway did not cross in the medulla in this patient. In view of the presence of the abnormal shape in the medulla and congenital scoliosis, a congenital factor might be responsible for the uncrossed pyramidal tract and dorsal column-medial lemniscus in this patient. ( info) |
3/17. Simultaneous hypertensive intracerebral hematomas: two case reports. We describe two patients (76- and 54-year-old females) with multiple hypertensive intracerebral hematomas occurring simultaneously. One patient had a right thalamic hematoma extending into the internal capsule and basal ganglia together with an other one in the left putamen. The other patient had two hematomas located ipsilaterally in the left putamen and thalamus. Their neurological examinations showed only unilateral deficits. Their magnetic resonance angiograms revealed no vascular malformations. Neuroradiological procedures are essential for the diagnosis of these multiple brain events. ( info) |
4/17. Angiographically verified progression of moyamoya disease in an adult. Case report. The authors present the case of a 37-year-old man with definite moyamoya disease in whom angiographic findings drastically changed. The patient presented with left hemiparesis due to lacunar infarction. Angiography initially disclosed a narrow right carotid artery (CA) siphon and severe stenosis of the horizontal segment of the left middle cerebral artery. Four years later, the patient experienced right-central facial paresis, which developed because of a small putaminal hematoma. Angiography results demonstrated occlusion of the internal CA siphons bilaterally, with moyamoya vessels. It therefore appears that in some adults, moyamoya disease is accompanied by very progressive vascular changes. ( info) |
5/17. August 2000: Two cases with necrosis and hemorrhage in the putamen and white matter. The August COM: Acute methanol poisoning is an uncommon, but well-recognized, cause of central nervous system injury. We present two autopsy cases showing the classic neuropathologic injuries in acute methanol poisoning: putamen and white matter necrosis and hemorrhage. In Case 1, putamen hemorrhages were striking; white matter pathology predominated in Case 2. The precise mechanism of methanol toxicity is unclear. Direct toxicity of metabolites, particularly formic acid, as well as ischemic injury and acidosis likely play a role. methanol is readily available in many commercial products, and may be ingested accidentally or intentionally. ( info) |
6/17. Spontaneous middle cerebral artery occlusion leading to moyamoya phenomenon and aneurysm formation on collateral arteries. BACKGROUND: Spontaneous middle cerebral artery occlusion associated with moyamoya phenomenon is distinct from moyamoya disease. The hemodynamic stress on the collateral channel occasionally leads to aneurysm formation, which may manifest as hemorrhage. The etiology of this disease has not been fully understood. CASE DESCRIPTION: A 63-year-old woman presented with left putaminal hemorrhage. The cerebral angiogram revealed a significant stenosis in the proximal segment of the left middle cerebral artery. Collateral arteries originating from the horizontal segment of the ipsilateral anterior cerebral artery and the ambient segment of the ipsilateral posterior cerebral artery supplied the middle cerebral artery distal to the stenosis. Both of the collateral channels had associated aneurysms that were surgically obliterated. The aneurysm on the collateral artery from the posterior cerebral artery was responsible for the putaminal hemorrhage. CONCLUSIONS: Spontaneous middle cerebral artery occlusion may lead to focal moyamoya phenomenon and aneurysmal intracerebral, intraventricular, or subarachnoid hemorrhage. The presence of a co-existing anomalous collateral artery in the present case suggests a congenital etiology of the focal middle cerebral artery occlusion. ( info) |
7/17. Management of haemorrhagic stroke with hyperbaric oxygen therapy--a case report. Hyperbaric oxygen therapy (HBOT) has been used in the treatment of cerebral ischaemia with positive effects on tissue oxygenation. We present a case of haemorrhagic stroke treated successfully with HBOT and review the literature on its role in cerebrovascular disease. ( info) |
8/17. Simultaneous occurrence of subarachnoid hemorrhage due to ruptured aneurysm and remote hypertensive intracerebral hemorrhage: case report. Simultaneous occurrence of aneurysmal subarachnoid hemorrhage (SAH) and hypertensive intracerebral hemorrhage (ICH) is very rare and only two cases have been previously reported in the literatures. We present a case of 68-yr-old man with a history of untreated hypertension, who suffered from sudden onset of headache followed by right hemiparesis. Computed tomographic (CT) scan revealed SAH in the basal cistern and remote ICH at the left putamen. cerebral angiography showed a saccular aneurysm at the anterior communicating artery. No other vascular anomaly could be found at left putaminal area. Nine days after the ictal attack of SAH, the neck of aneurysm was clipped via the left frontotemporal craniotomy. Because of the ICH at the left frontal lobe and intraventricular hematoma on postoperative CT, we performed hematoma removal and external ventricular drainage 3 hours after the first operation. Postoperative neurological status had been improved to be drowsy and he was discharged in a severely disabled state 4 weeks after surgery. We suggest that the rupture of aneurysm possibly caused a rapid increase in blood pressure and subsequently resulted in hypertensive ICH. ( info) |
| Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of hyperglycemic hyperosmolar syndrome (HHS). A 40-year-old man with a history of diabetes mellitus and chronic alcoholism was admitted with acute impaired mentality. His blood pressure was within the normal range on admission. Laboratory results revealed hyperglycemia and severe metabolic acidosis without ketonuria. After aggressive treatment, plasma sugar fell to 217 mg/dl, but brain CT showed BPH and diffuse CE. Our case demonstrated that HHS should be considered as a cause of BPH with CE. Initial brain imaging study may be recommended for patients with diabetic coma. ( info) |
10/17. Deterioration of pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction. Mechanisms of post-stroke recovery are still poorly understood. Recent evidence suggests that cortical reorganisation in the unaffected hemisphere plays an important role. A 59 year old man developed a small lacunar infarct in the left corona radiata, which then caused marked deterioration in a pre-existing left hemiparesis that had resulted from an earlier right putaminal haemorrhage. Functional magnetic resonance imaging showed that the paretic left hand grip activated the ipsilateral left motor areas, but not the right hemispheric motor areas. This suggests that partial recovery of the left hemiparesis had been brought about by cortical reorganisation of the left hemisphere and intensification of the uncrossed corticospinal tract. The subsequent small infarct may have damaged the uncrossed tract, thereby causing the pre-existing hemiparesis to deteriorate even further. ( info) |