Responsible artery
Case 131
【Progress】Wafarin given following brain infarction was stopped immediately after brain hemorrhage. She was admitted in our hospital and scheduled to have rehabilitation training program for approximately three months.
【Discussion】
Although it is common that the brain infarction lesion is depicted in dark signal on T1WI and bright signal on T2WI, the signal intensity of the hemorrhagic lesion varies on T1WI and T2WI, dependent on the progress of the hemorrhage after the onset. Brain hemorrhage is known to evolve phases to hyperacute(<24hours), acute (1-3 days), early subacute(<7days), late subacute(<14days) and chronic. Hyperacute hematoma with < 24 hours after onset indicates oxyhemoglobin intra-red blood cell, acute hematoma with 1-3 days after onset indicate deoxyhemoglobin intra-red blood cell, early subacute with 4-7 days indicate methemoglobin intra-red blood cell, late subacute with 7-14 days indicate methemoglobin extra-red blood cell and chronic with > 14 days indicate hemosiderin extra-red blood cell (1, 2). It is largely known that the hematoma is depicted in bright signal on T1WI and dark signal on T2WI. Bright signal of hematoma on T1WI is seen during approximately one month after the onset of hemorrhage until entire lysis of hematoma and replacement with cerebral spinal fluid. Dark signal intensity of hematoma on T2WI is seen during approximately one week after the onset until methemoglobin entirely flow out extra-red blood cell.
How about do you imagine what the hematoma is depicted like on Diffusion weighted imaging (DWI) and on T2*WI ? Hyperacute hematoma contains retracted clot and un-clotted blood which are depicted mixed of bright and dark signal intensity on DWI. Because homogeneous high signal intensity is depicted in acute infarction, the mixed signal intensity, especially the presence of low signal intensity is crucial to differentiate hyperacute hematoma from acute infarction. DWI indicates restriction of diffusion plus T2WI. Hematoma from acute phase to subacute one, dark signal intensity of hematoma is shown on DWI because of clot formation and effect of T2WI on DWI, namely called T2 black out (3). In case of subdural hematoma and microbleeds, DWI might not contribute to appear high signal intensity because of clot formation and/or T2 black out. ADC value is not reliable in case of T2 black out because signal intensity of DWIb0 is a denominator (ADC of each interest target equals to the slope of the curve using the acquired signal intensity values of b0 and b1000 or b2000(ADC = Loge Sb/Sb0) except in case of hyperacute phase (2).
Oxyhemoglobin is diamagnetic, while deoxyhemoglobin and methemoglobin are paramagnetic and hemosiderin is super paramagnetic. Then, T2*WI shows the hematoma in acute, subacute and chronic phases as dark signal intensity. Meanwhile, the hematoma in a hyperacute phase is shown as iso-signal intensity in the core and dark signal intensity in the surrounding because of the presences of oxyhemoglobin in the core and deoxyhemoglobin in the surrounding. In the chronic phase, hemosiderin is phagocyted by microglia or macrophages and moved to the surroundings, T2*WI showed low signal intensity in the surroundings, accordingly. Therefore, the lesion with low signal intensity in the surrounding on T2*WI indicate the hematoma, irrespective of hyperacute or chronic. In our hospital, when emergency physicians meet patients with acute stroke, they require to eliminate T1WI and T2WI because of the speedy response for treatment. Then, the above knowledge is crucial for diagnostic radiologists.
There are frequent sites of hypertensive brain hemorrhage: basal ganglion (putamen, globus pallidus), internal capsule and thalamus. Occasionally, the simultaneous hemorrhage of basal ganglion and thalamus occurs. Basal ganglion and internal capsules are blood-supplied by penetrating branches from middle cerebral artery and thalamus is blood-supplied by them from posterior cerebral artery. The mechanism of the simultaneous hemorrhage of thalamus and basal ganglion is that one microaneurysm formed due to hypertension ruptures (lenticulostriate artery commonly involved) and the adjacent perforating artery which has similar process, receives localized pressure caused by hemorrhage, inducing the following rupture. Amount of hemorrhage is dependent on the parenchymal pressure opposed to the intravascular blood pressure. Our patient had the simultaneous hemorrhage of putamen, posterior limb and thalamus with intraventricular hemorrhage.
【Summary】
We present a seventy seven-year-old female who had simultaneous hemorrhage of thalamus, internal capsule and basal ganglion on the left side. It indicates that the arteries responsible to the hemorrhage are penetrating arteries from middle cerebral artery and posterior cerebral artery. We should keep in mind that in hyperacute hemorrhage, DWI shows mixed signal intensity of dark and bright corresponded to blood clot and un-clot blood, respectively. Meanwhile, T2*WI shows iso-signal intensity surrounded by dark signal intensity corresponded to oxyhemoglobin and deoxy hemoglobin, respectively.
Further, bright signal of hematoma on T1WI is seen during approximately one month after the onset of hemorrhage and dark signal intensity of hematoma on T2WI is seen during approximately one week after the onset until methemoglobin entirely flow out extra-red blood cell.
【References】
1.Aoki S et al. Diffusion MRI 3rd edition. Syujunnsha 2013 (Japanese)
2.Kita M. Personal communication in Fuchu Hospital.
3.Silvera, S, et al. Spontaneous Intracerebral Hematoma on Diffusion-weighted Images: Influence of T2-shine-through and T2-blackout Effects. American Journal of Neuroradiology February 2005, 26 (2) 236-241
2018.11.28