Hyperacute Transcapillary Stroke IV - Clinical Case Summary
Hyperacute Transcapillary Stroke IV - Clinical Case Summary
Hyperacute Transcapillary Stroke IV - Clinical Case Summary
SummaryHistory
38 yo male w/ Hx hypertension, diffuse rash, chrohn's dz, seizures, brain cysts (biopsied benign), who now presents with stairing spells and acute fatique. Years earlier the patient had surgical drainage of a parenchymal hemorrhage in the left frontal vertex area.
Exams performed
CT Head; CT Perfusion; CTA head; T1-w MR pre and post; MR diffusion; MR T2-w and MR flair; MR susceptibility (SWI)
Prior imaging reports
Noncontrast CT head
1. There are brain changes of chronic nature, which are likely the sequelae of a neonatal TORCH encephalopathy. No apparent hyperacute abnormality is evident
CT Perfusion
1. Possible focal left cortical stroke in the distal left lateral frontal artery territory but whether it is acute ischemia or reduced perfusion on a chronic basis is indeterminate.
2.CT perfusion changes, likely chronic, within both cerebral hemisphere matching the areas of chronic leukomalacia are consistent with the sequelae of a perinatal TORCH infection.
CTA of the head
1. Focal left high convexity anterior frontal cortex with reduced size and beading of the pial arteries plus reduction in extent of venous egress veins. But, whether this is confirmation of angiitis is indeterminate.
Pre and post contrast T1-w sequences
1. This is a complex case, because underlying CNS abnormalities consistent with perinatal TORCH infection with significant brain injuries. However, the patient has had recent neurological changes. There is evidence of coagulative necrosis surrounding dilated Virchow Robin spaces in the deep frontal centrum semiovale on both sides. There is also enhancement in the same sites consistent with active inflammation. These changes in the Virchow-Robins spaces appear unrelated to prior TORCH encephalopathy, nor the prior left frontal hemorrhage drainage sites. They support the idea of a concurrent secondary CNS angiitis.
MR diffusion
1. Chronic changes of completed lacunar defects following the Virchow-Robin spaces bilaterally. Whether these represent sequelae of prior surgery or microhemorrhage versus angiitis with ischemic change is indeterminate. However, there is no positive diffusion to confirm a hyperacute or acute ischemic event.
MR Flair and T2-w sequences
1. There is postive MR flair and T2-w signal change consistent with the diffuse parenchymal tissue injuries and the chronic leukomalacia. What proportion of the parenchymal injuries are related to the perinatal TORCH infection, what part is related to surgery for prior brain hemorrhage, and what proportion to possible secondary CNS angiitis is indeterminate.
MR susceptibility (SWI)
1. Diffuse miconodular SWI changes in both cerebral hemisphere with a differential that includes microhemorrhages, hypertension, secondary CNS angiopathy, or a combination of these. Since there is subtle marginal enhancement along the dilated Virchow-Robin spaces bilaterally on the post contrast T1-w sequence, This would suggest that there is reasonable evidence that a secondaryimmune-based angiitis is present, but without current active ischemia (i.e. negative MR diffusion).
1. There are brain changes of chronic nature, which are likely the sequelae of a neonatal TORCH encephalopathy. No apparent hyperacute abnormality is evident
CT Perfusion
1. Possible focal left cortical stroke in the distal left lateral frontal artery territory but whether it is acute ischemia or reduced perfusion on a chronic basis is indeterminate.
2.CT perfusion changes, likely chronic, within both cerebral hemisphere matching the areas of chronic leukomalacia are consistent with the sequelae of a perinatal TORCH infection.
CTA of the head
1. Focal left high convexity anterior frontal cortex with reduced size and beading of the pial arteries plus reduction in extent of venous egress veins. But, whether this is confirmation of angiitis is indeterminate.
Pre and post contrast T1-w sequences
1. This is a complex case, because underlying CNS abnormalities consistent with perinatal TORCH infection with significant brain injuries. However, the patient has had recent neurological changes. There is evidence of coagulative necrosis surrounding dilated Virchow Robin spaces in the deep frontal centrum semiovale on both sides. There is also enhancement in the same sites consistent with active inflammation. These changes in the Virchow-Robins spaces appear unrelated to prior TORCH encephalopathy, nor the prior left frontal hemorrhage drainage sites. They support the idea of a concurrent secondary CNS angiitis.
MR diffusion
1. Chronic changes of completed lacunar defects following the Virchow-Robin spaces bilaterally. Whether these represent sequelae of prior surgery or microhemorrhage versus angiitis with ischemic change is indeterminate. However, there is no positive diffusion to confirm a hyperacute or acute ischemic event.
MR Flair and T2-w sequences
1. There is postive MR flair and T2-w signal change consistent with the diffuse parenchymal tissue injuries and the chronic leukomalacia. What proportion of the parenchymal injuries are related to the perinatal TORCH infection, what part is related to surgery for prior brain hemorrhage, and what proportion to possible secondary CNS angiitis is indeterminate.
MR susceptibility (SWI)
1. Diffuse miconodular SWI changes in both cerebral hemisphere with a differential that includes microhemorrhages, hypertension, secondary CNS angiopathy, or a combination of these. Since there is subtle marginal enhancement along the dilated Virchow-Robin spaces bilaterally on the post contrast T1-w sequence, This would suggest that there is reasonable evidence that a secondaryimmune-based angiitis is present, but without current active ischemia (i.e. negative MR diffusion).
Overall impression
1. Underlying brain calcifications, likely the chronic sequelae of perinatal TORCH infection (likely toxoplasmosis). There has been a prior left frontal craniotomy, which by report, was performed to drain a parenchymal hemorrhage.
2. There is MRA evidence of diffuse cerebral, likely immune-base inflammatory vasculitis, because of the other comorbid disorders. There is evidence of inflammatory enhancement along the Virchow-Robins spaces consistent inflammation along the long penetrating arteries mainly in the frontal parenchyma. MR diffusion demonstrates no acute water restriction to confirm completed infarction.
3. The SWI demonstrates widespread chronic microhemorrhages also consistent with small vessel vasculopathy; some lesions could represent cavernous angiomata. The noncontrast T1-w sequence demonstrates scattered sites of laminar necrosis, again indicative of end-artery infarctions in active inflammatory vasculitis.
2. There is MRA evidence of diffuse cerebral, likely immune-base inflammatory vasculitis, because of the other comorbid disorders. There is evidence of inflammatory enhancement along the Virchow-Robins spaces consistent inflammation along the long penetrating arteries mainly in the frontal parenchyma. MR diffusion demonstrates no acute water restriction to confirm completed infarction.
3. The SWI demonstrates widespread chronic microhemorrhages also consistent with small vessel vasculopathy; some lesions could represent cavernous angiomata. The noncontrast T1-w sequence demonstrates scattered sites of laminar necrosis, again indicative of end-artery infarctions in active inflammatory vasculitis.
Lessons to be learned
1. The diagnosis of primary and secondary CNS angiitis is often very difficult and the final diagnosis may never be secure. The best evidence of acute CNS angiitis is evidence of enhancement ( mural wall Inflammation) changes along the margins of the terminal penetrating arteries within the Virchow-Robin spaces. Subacute and chronic changes include leukomalacia along the dilated Virchow-Robin spaces due to post ischemic injury of the tissue forming the margins of the same terminal end-arteris supplying the deep central white matter in the centrum semiovale. Similar changes may follow the perforating end-arteries to the centronuclear structures and brainstem, as well.
2. In this case there are background changes related to a likely perinatal TORCH infection, although this is not incorpoated in the current medical record. Nevertheless, the patient has increasing seizure activity and TIA-like symptoms. Most of the imaging reflects the background TORCH destructive changes. However, there is subtle enhancement along penetrating arteries in the cerebral white matter and SWI evidence of widespread microhemorrhages. The changes within the deep frontal Virchow-Robin spaces best fits a secondary, immune-based angiopathy likely superimposed on both the TORCH and cavernous angiomata syndromes.
2. In this case there are background changes related to a likely perinatal TORCH infection, although this is not incorpoated in the current medical record. Nevertheless, the patient has increasing seizure activity and TIA-like symptoms. Most of the imaging reflects the background TORCH destructive changes. However, there is subtle enhancement along penetrating arteries in the cerebral white matter and SWI evidence of widespread microhemorrhages. The changes within the deep frontal Virchow-Robin spaces best fits a secondary, immune-based angiopathy likely superimposed on both the TORCH and cavernous angiomata syndromes.
Recommendations
Watch the included video for this instructional clinical case.