A large volume of sICH is a devastating disease with high rates of mortality and morbidity.7)
The classic presentation of sICH includes the sudden onset of a focal neurological deficit that progresses over minutes to hours with accompanying headache, nausea, vomiting, decreased consciousness, and elevated blood pressure.5)
The hematoma volume is the most potent predictor of mortality and poor functional outcome in patients with sICH.17)
Furthermore, acute expansion of the hematoma within an hour to a day, has been reported as a cause of severe neurologic deterioration and death.14)
In our patient with a huge sICH exhibited a rapid spontaneous reduction in the volume of the hematoma over a very short period of time. The initial brain CT revealed a large basal ganglia hematoma and signs of impending subfalcial herniation. Fortunately, follow-up brain CT 16 hours after initial insult showed a remarkable decrease of the hematoma volume. However, the patient in our study had a large hematoma that decreased in volume within a short time period without improvement of the symptoms attributed to the hematoma.
The rapid expansion of a sICH has been frequently reported.1)
However, we found limited reports describing the rapid spontaneous decrease in the volume of the hematoma observed in ICH.4)
A patient with a petrous bone fracture after trauma showed a spontaneous cure of ICH by drainage into the middle ear.4)
However, it was a rare case of traumatic ICH unlike our case. In our case, the ICH was not related to head trauma, so it appears to have been a large hematoma which decreased spontaneously.
However, rapid spontaneous resolution and a decrease in the size of the traumatic acute SDH have frequently been reported.2)
The pathophysiology of this phenomenon is not well understood, and many hypotheses have been proposed. Four mechanisms for the rapid resolution of the hematoma have been proposed; dilution and wash out of the hematoma by cerebrospinal flow (CSF) after tearing of the arachnoid membrane; compression and redistribution of the hematoma by acute brain swelling; redistribution of the hematoma through skull fractures; and redistribution of the hematoma to the spinal subdural space.2)
However, the clear mechanism for spontaneous resolution of acute SDH was not identified, especially in that of sICH.
In our case, the patient presented with a basal ganglia hematoma with a margin very close to the subarachnoid and intraventricular spaces. We proposed that pressure from the massive hematoma caused rupture of the adjacent cortical surface and pia mater, resulting in migration of the hematoma into the subarachnoid spaces. In the same way, that resulted in the rupture of the ependymal lining of ventricle and so migration of hematoma into ventricular spaces. On the follow-up brain CT, we found the increased volume of subarachnoid hemorrhages and intraventricular hemorrhages. This finding may support the hypothesis of dilution and wash out of the hematoma by CSF after tearing of the arachnoid membrane. The hematoma mixed with CSF may be a clue in the redistribution process.2)
CSF liquefies the hematoma and the blood clots are redistributed to the subarachnoid and ventricular spaces.11)
In the spontaneous rapid reduction of ICH, we suggest that the hematoma mixed with CSF also may be a same mechanism in the distribution process and CSF liquefies the hematoma and the blood clots are redistributed to the subarachnoid and ventricular spaces like several report on spontaneous resolution of acute SDH.