Hyperacute intracranial hemorrhage

Case contributed by Safwat Mohammad Almoghazy
Diagnosis certain

Presentation

Presented with altered mental status and acute left-sided weakness, prompting an evaluation for intracranial bleed. History of hypertension.

Patient Data

Age: 35 years
Gender: Male

Non enhanced CT brain.

ct

Left basal ganglia intra-axial hematoma involving mainly the putamen of the left lentiform nucleus with surrounding hypodense thin zone of edema. No underlying mass is identified. No other parenchymal hemorrhage or mass is seen.

N.B.  evidence of sinusitis with total obliteration of the left maxillary sinus.

Conclusion:

Left basal ganglia acute hematoma most likely hypertensive cause. 

MRI & MRA & MRV

mri

Left intra-axial hematoma involving the left lentiform nucleus with surrounding perifocal edema minimally effacing the left lateral ventricle and left Sylvian fissure. Such hematoma elicits a T1 isointense signal and T2 /FLAIR slightly hyperintense (representing the clot), partially hyperintense (representing a halo of serum outside of the clot). DWI/ADC demonstrates restricted diffusion of the clot, and facilitated diffusion of the halo (serum adjacent to the clot). SWI demonstrating signal loss. A tiny enhanced focus at the posterior aspect of the hematoma. 

The rest of the brain parenchyma shows normal grey-white matter differentiation and signal intensities. No focal mass lesion is seen.

Both lateral and third ventricles are normal in size and position. The septum is in the midline. There is no midline shift.

MR angiography reveals normal course, caliber and outlines of vessels of bilateral CA, ACA, MCA, PCA and their peripheral branches. The vertebrobasilar trunk is also normal in appearance.

The superior sagittal sinus, straight sinus, bilateral transverse sinuses,  their confluence, bilateral hypoplastic left transverse sinus otherwise, sigmoid sinuses and parts of internal jugular vein visualized, show normal course, caliber and outlines. No obvious evidence of any venous sinus thrombosis is seen at present.

Pansinusitis sinusitis and left maxillary an antrochoanal polyp.

Conclusion:

Left basal ganglia acute hematoma with no definite underlying vascular malformation or mass lesion most likely hypertensive cause.

Case Discussion

The patient was admitted to the hospital, where he initially received a non-enhanced CT brain to evaluate his brain. Then subsequently received an MRI and MRA /MRV of the brain (normal MRA/MRV). 

Acute CT (obtained within an hour of symptom onset): Hyperattenuating lesion in the left lentiform nucleus mainly the putamen with surrounding hypodensity consistent with edema. minimal mass effect on the adjacent lateral ventricle and effacement of the nearby sulci is noted.

MRI obtained just after CT (within few hours after symptom onset): left putamen lesion with isointense of T1 and T2/FLAIR / bright signal intensity. Surrounding T2 bright signal consistent with edema. No significant enhancement (compare pre-and post-Gd images) suggestive of a hypertensive basal ganglia hemorrhage.

Hemorrhagic lesions in putamen – differential includes hypertensive hemorrhage, vascular malformation, and neoplasm. Hypertension is the presumed cause in 70-90% of cases.  2/3 hypertensive hemorrhages occur in the putamen. 

CT - hematoma appears as areas of high density with sharply defined borders - the mass effect and the surrounding extruded serum/edema are hypodense - the hematoma changes from high density to isodense and finally to hypodense relative to the brain density over time.

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