MCA infarct and craniectomy

CT Brain

No intracranial hemorrhage. Hyperdense thrombus within the left intracranial ICA and M1 segment. Decreased attenuation of the left caudate and lentiform nucleus and decreased grey-white differentiation in the left insula. Ventricular size is normal. 

CTA COW and perfusion studies (not shown)

Filling defect is demonstrated throughout the entire left intracranial ICA extending into the left M1. The M1 is hyperdense on non contrast images. The cervical ICA opacifies normally from the CCA bifurcation until its distal portion where tapering of contrast opacification is seen before the vessel enters the petrous temporal bone. No dissection flap is identified.

Contrast opacification of the left M2 (inferior branch)-M4 segments is demonstrated presumably via collateral circulation. These vessels are relatively hypoperfused compared with the contralateral vessels.

There is retrograde filling of the left ACA via the circle of willis. The left CCA and ECA opacify normally. 

Perfusion studies demonstrate large area of decreased CBF and CBV, and increased Tmax and MTT in the left MCA territory. This is largely a matched defect with an estimated perfusion mismatch of 124 ml.

Clinical notes: 

12 hour followup CT following left middle cerebral artery stroke. GCS 15, aphasic. Increased edema?

Findings:

Comparison made to CT from 12 hours earlier.

There is loss of grey-white matter differentiation involving the posterior and inferior left frontal lobe, anterior left temporal lobe and the left basal ganglia, in keeping with an establishing infarction of the left middle cerebral artery (MCA) territory. High density thrombus is seen within the M1 segment of the left MCA. There is sulcal effacement of the affected territory, and mild effacement of the left sylvian fissure and left lateral ventricle. No subfalcine, transtentorial or tonsillar herniation. No hemorrhagic transformation. No other new findings.

Compared with CTB 24 hours earlier.

Marked mass effect has developed secondary to the large left MCA territory infarction. There is now 12 mm midline shift to the right and left-sided subfalcine herniation. Progressive sulcal effacement of the left cerebral hemisphere.There is acute hemorrhage in the medial aspect of the infarcted area, extending into the left lateral ventricle, which is compressed. There is prominence of the temporal horn of the right lateral ventricle, likely indicative of early hydrocephalus.

Interval left hemicraniectomy demonstrated with subsequent improvement of the previously demonstrated right sided midline shift. The is currently a region of postsurgical pneumocephalus along the left posterior temporal convexity with tiny locules of air tracking towards the left transverse dural venous sinus. There is a shallow rind of acute cortical hemorrhage adjacent to the region of left posterior temporal pneumocephalus, extending towards the left tentorium cerebelli. 

The established left middle cerebral artery territory infarct is again demonstrated. More extensive hemorrhagic transformation is currently demonstrated within the infarct distribution, particularly along the more peripheral aspect of the vascular territory.

An extensive left-sided cranial decompression has been performed. The left cerebral hemisphere has herniated beyond the margins of the craniectomy site and there is mild (~6mm at level of 3rd ventricle) midline shift to the right, consistent with successful decompression. Diffuse FLAIR signal hyperintensity involves almost the entire left cerebral hemisphere, correlating with extensive ICA territory regional diffusion restriction.

A large amount of blood product within, particularly involving the left parietal lobe and left basal ganglia. Small volume intraventricular blood.

Flattening left lateral ventricle and mild prominence of the right,

Flow is now visible in the left intracranial ICA and the left M1/M2 divisions of the middle cerebral artery.

The remainder of the circle of Willis vessels are unremarkable.

4 weeks post infarct

Left craniectomy again demonstrated. Extensive hypodensity involving the entire left MCA territory is again noted in keeping with infarction. Hemorrhage in the left frontal lobe adjacent the anterior horn of the lateral ventricle is denser and more extensive compared to previous in keeping with intercurrent hemorrhage. There are also traces of hyperdense subarachnoid blood in the left hemisphere. The previously seen posterior frontal, periventricular and temporal hematomas are less conspicuous.

The ventricle have increased in size. As a reference, the 3rd ventricle now measures 12 mm in diameter and there is dilatation of both lateral ventricles, including the temporal horns in keeping with increasing hydrocephalus. A trace of blood persists in the occipital horn of the right lateral ventricle.

CONCLUSION: Increasing hydrocephalus.

Extensive left MCA territory infarct with evidence of interim left frontal hemorrhage since the previous studies.

5 months

Expected evolution of large left MCA territory infarct with evidence of extensive left frontotemporoparietal gliosis and resultant dilation of the left ventricle body and anterior horn. GLiosis extends into left brachium cerebri, midbrain and pons. Craniectomy defect is again noted. No right-sided or other new abnormality identified.

Left-sided surgical clips in interval left cranioplasty is noted. The large left MCA territory infarction with extensive gliosis and exvacuo dilatation of the left lateral ventricle is stable. The small focus of linear hyperdensity within the left frontal lobe superiorly has reduced and may represent cortical petechial hemorrhages.

No other focus of intracranial hemorrhage. No signs of acute ischemia. Mass or mass effect or midline shift.