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“Spectacular shrinking
deficit”- rapid recovery from a major hemispheric syndrome. Clinical and
neuroradiologial pecularities |
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In patients with various heart diseases transient internal
carotid artery (ICA) - middle cerebral artery (MCA) occlusion caused by
cardiogenic embolism can lead to spectacular shrinking deficit (SSD)
[1]. SSD refers to sudden major hemispheric stroke syndrome followed by
rapid improvement within a few hours after stroke, leaving mild or no
deficit compared with stroke patient with the same major initial
manifestation, but without rapid recovery. Cardioembolic stroke due to atrial fibrillation share definite neuroradiologic features, common for brain infarction. Experimental brief MCA occlusion causes selective neuronal necrosis and apoptosis with intact glial cells and microvessels [2, 3]. This ischemic lesion has been termed “incomplete infarction” and some researchers reported that incomplete damage slowly progressed in the dorsolateral striatum during 4 weeks after 15 minutes MCA occlusion [4, 5]. Only few reports are available on serial changes in human brain after transient hemispheric ischemia leading to SSD, which represent the clinical equivalent of the experimental conditions described above. In the present study, we focused on the sequential neuroradiological changes in the basal ganglia and cerebral cortex of the brains in patients after brief cerebral hemispheric ischemia, leading to SSD Subject and Methods: We repeatedly studied CT and MRI scans obtained at 0,2 T in two patients after SSD. The patients included in the study satisfy the following criteria: 1. No apparent history of neurological disease diagnosed clinically and/or neurororadiologically; 2. Patients suffering from SSD were observed by medical staff from the onset of the neurological symptoms to the beginning of the rapid improvement; 3. Cardiogenic source of cerebral embolism was evident, type of heart disease was determined as atrial fibrillation; 4. No apparent stenosis or occlusion of ipsilateral ICA_MCA was detected by Doppler ultrasonography. SSD was defined as transient cerebral hemispheric ischemic syndrome with sudden onset that began to disappear within 60 minutes after the onset without remaining deficit. Transient cerebral hemispheric ischemic syndrome included moderate to severe disturbance of consciousness, hemiparesis, aphasia, apraxia, and amnesia. These ischemic symptoms were resulted from occlusion of the ICA or the main trunk of the MCA.. Two such patients were encountered at the Tbilisi Medical University Hospital during the period from October 2000 to December 2003. In these patients the ischemic symptoms began to disappear after 25 - 50 minutes from the onset of the stroke. Both patients recovered completely to a normal neurological state within a few days. All patients underwent CT scanning on the first day of the event. MRI was performed after 2 days and repeated after 7 days from the onset of the neuological symptoms. In one patient MRI images repeatedly were performed 3 month after onset. Results and Discussion: CT scan demonstrated no abnormal findings in the brain of the 2 patients. The first MRI obtained on 2nd day did not reveal any changes either. MRI image obtained 7 days later revealed lesions in basal ganglia and cerebral cortex. These lesions were determined as hyperintensity on T-1 weighted and relatively hypointensity on T-2 weighted images in contrast to ischemic stroke (non-SSD) patients, where ischemic lesions were hypointense on T-1 and hyperintense on T-2 weighted images. The present neuroragiological data obtained in patients with SSD significantly differed from those of ischemic stroke. These data can be interpreted as follows: (1) Specific ischemic lesions developed in the basal ganglia and cerebral cortex in the ischemic hemisphere of patients after brief MCA occlusion leading to SSD; (2) These lesions appeared on MRI but not on CT scans; (3) The lesions appeared after 7 days, but they aren’t visible on second day; (4) The localized ischemic lesions exhibited persistent hyperintensity/hypointensity on T1W/ T2W MRI This specific ischemic change of delayed onset and hyperintensity/hypointensity on T1W/T2W MRI and isodensity on CT scans differ from known ischemic changes. The latest include the following 3 neuroradiological entities: · Ischemic edema and infarct appear hypointense and hyperintense on T1W and T2W MRI ,respectively , to normal parenchyma; · The signal intensity of hemorrhagic brain tissue changes according to the process of hemoglobin degradation. Intracellular deoxyhemoglobin leads to hypointensity on T2W but little change on T1W imaging. In parallel with the oxidation of deooxyhemoglobin to methemoglobin in red blood cells (RBC) the signal intensivity increases on T1W images. After RBC lysis, extracellular methemoglobin appears hyperintense on both T1W and T2W images.with advancing hemoglobin degradation, hemosiderin in macrofages causes selective shortenings of the T2 relaxation time.These signal changes progress from the periphery to the center of a hemorrage. · Ectopic calcifications can appear hyperintense and hypointense on T1W and T2W MRI . First description of SSD with pecular MRI data appeared in 1992 [1]. In 1999 this novel form of ischemic change on MRI, different from typical ischemic brain damage was designated as “delayed ischemic hyperintensityon T1W MRI (DIH) [6]. It is difficult to elucidate precisely what this DIH represented histologically. However, several clinical and experimental data [7-10] can lead to suggestion that when reperfusion is instituted within a short period of time, transient MCA occlusion leads to selective neuronal death and various glial responses without pannecrosis of the brain tissue in the ischemic region. SSD causes selective neuronal necrosis and apoptosis with intarct glial cells and microvessels in the caudoputamen and cerebral cortex. In these ischemic lesions the brain tissue framework is preserved and no cavitation develops. This ischemic lesion with selective neuronal death and gliosis has been termed incomplete infarction [13-16]. These specific MRI lesions of hyperintensity on T1W observed in SSD, differ from infarction and hemorrhage. It is supposed that these lesions represent incomplete ischemic injury, including selective neuronal death, proliferation of glial cells, paramagnetic substance deposition, and/or lipid accumulation. Our present study demonstrates very slowly progressive neuroradiological changes that can occcur in human brain after focal ischemia, leading to SSD. |
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