RESUMEN
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.
Asunto(s)
Hemorragia Cerebral/diagnóstico , Imagen por Resonancia Magnética/métodos , Enfermedad Aguda , Adulto , Anciano , Anciano de 80 o más Años , Edema Encefálico/diagnóstico , Isquemia Encefálica/diagnóstico , Imagen Eco-Planar/métodos , Femenino , Hematoma/diagnóstico , Humanos , Procesamiento de Imagen Asistido por Computador/métodos , Cápsula Interna/patología , Angiografía por Resonancia Magnética , Masculino , Tamizaje Masivo , Bulbo Raquídeo/patología , Persona de Mediana Edad , Puente/patología , Hemorragia Putaminal/diagnóstico , Accidente Cerebrovascular/diagnóstico , Tálamo/patología , Terapia Trombolítica , Factores de TiempoAsunto(s)
Fármacos Cardiovasculares , Accesibilidad a los Servicios de Salud , Indigencia Médica , Cardiología , Enfermedades Cardiovasculares/economía , Enfermedades Cardiovasculares/epidemiología , Demografía , Industria Farmacéutica , Humanos , Programas Nacionales de Salud , Sociedades Médicas , Estados UnidosRESUMEN
A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.