Hyperacute Transcapillary Stroke V - Clinical Case Summary
CA0000-Hyperacute Transcapillary Stroke V - Clinical Case Summary
CA0000-Hyperacute Transcapillary Stroke V - Clinical Case Summary
SummaryHistory
47 yo female who presents with right sided acute weakness. Hx: cocaine abuse and an unruptured right MCA aneurysm.
Exams performed
CT Head; MRA of the neck; MRA of the head; Noncontrast T1-w MR; MR diffusion; MR T2-w and MR flair
Prior imaging reports
Noncontrast CT head
1. Given the history of cocaine abuse and hypertension, there is substantial global brain atrophy for chronological age, plus end-artery type of completed lacunar infarctions.
MRA of the neck
1. Normal MRA of the neck without vascular stenoses nor dissection.
MRA of the head
1. Right MCA bifurcation saccular aneurysm, as above.
2. Suspicious evidence of distal left MCA and PCA vasospasm plus minimal delay in filling rate, which are consistent with cocaine related distal arterial vasospasm. Otherwise, negative head MRA for arterial occlusion or dissection
Noncontrast T1-w MR
1. There are a myriad of the lacunar-type strokes affecting terminal arteries in the centrum semiovale and the corona radiata bilaterally. There are multicentric lacunar-type strokes in the lenticulostriate perforators, the thalamic perforators, and the brainstem perforators bilaterally. The lacunes follow the Virchow-Robin spaces; they are tubular in shape characteristic of end-artery types of ischemia. This is evident in this case of chronic vasospasm and ithe CNS angiits cases, as well. All the changes appear chronic and there is global brain injury, as well. With the history of drug abuse these findings are consistent with terminal artery ischemic effects of vasoactive drugs (i.e. cocaine and metamphetamines, etc.) or occasionally with microembolization of the foreign body material from IV drug use.
2. There is some T1-w signal increase deep to the left insula, which represents chronic lower grade oligemic effects likely with microhemorrhage; this does not represent laminar necrosis.
MR diffusion
1. Multicentric completed end-artery strokes, as described previously. MR diffusion is negative are any recent infarctions.
MR T2-w and MR flair sequences
1. Multicentric completed end-artery type of strokes with marginal leukomalacia. There is no acute cytogenic edema.
1. Given the history of cocaine abuse and hypertension, there is substantial global brain atrophy for chronological age, plus end-artery type of completed lacunar infarctions.
MRA of the neck
1. Normal MRA of the neck without vascular stenoses nor dissection.
MRA of the head
1. Right MCA bifurcation saccular aneurysm, as above.
2. Suspicious evidence of distal left MCA and PCA vasospasm plus minimal delay in filling rate, which are consistent with cocaine related distal arterial vasospasm. Otherwise, negative head MRA for arterial occlusion or dissection
Noncontrast T1-w MR
1. There are a myriad of the lacunar-type strokes affecting terminal arteries in the centrum semiovale and the corona radiata bilaterally. There are multicentric lacunar-type strokes in the lenticulostriate perforators, the thalamic perforators, and the brainstem perforators bilaterally. The lacunes follow the Virchow-Robin spaces; they are tubular in shape characteristic of end-artery types of ischemia. This is evident in this case of chronic vasospasm and ithe CNS angiits cases, as well. All the changes appear chronic and there is global brain injury, as well. With the history of drug abuse these findings are consistent with terminal artery ischemic effects of vasoactive drugs (i.e. cocaine and metamphetamines, etc.) or occasionally with microembolization of the foreign body material from IV drug use.
2. There is some T1-w signal increase deep to the left insula, which represents chronic lower grade oligemic effects likely with microhemorrhage; this does not represent laminar necrosis.
MR diffusion
1. Multicentric completed end-artery strokes, as described previously. MR diffusion is negative are any recent infarctions.
MR T2-w and MR flair sequences
1. Multicentric completed end-artery type of strokes with marginal leukomalacia. There is no acute cytogenic edema.
Overall impression
1. There is evidence of substantial brain atrophy, which is consistent with the sequelae of chronic cocaine abuse. Additionally, there are linear lacunar strokes that follow the entire course of the A1, M1, P1 perforating arteries , plus the penetrating branches off the basilar artery; the defects are not just terminal lacunar strokes, as usually occurs with embolic disease. These findings of widespread lacunar infarctions in the cerebrum, centronuclear structures and brain stem, are consistent with chronic, repetitive arterial vasospastic process, likely the result of vasoactive drug use.
2. The MR diffusion demonstrates T2 shine-through in all the completed lacunes, but also demonstrates other sites of positive diffusion consistent with recent completed acute ischemia. These are mainly evident in the left centrum semiovale, which would account for the acute ischemic symptoms. There is hemosiderin deposition along the margins of several of the lacunes.
3. There is an incidental 2 x 4 mm, MCA bifurcation saccular aneurysm.
2. The MR diffusion demonstrates T2 shine-through in all the completed lacunes, but also demonstrates other sites of positive diffusion consistent with recent completed acute ischemia. These are mainly evident in the left centrum semiovale, which would account for the acute ischemic symptoms. There is hemosiderin deposition along the margins of several of the lacunes.
3. There is an incidental 2 x 4 mm, MCA bifurcation saccular aneurysm.
Lessons to be learned
1. Transcapillary strokes can occur as a result of very distal artery or arteriole vasospasm with or without progression to thrombosis. Occlusion at the level of arteriole-venocapillary bed precludes any functional pial collateral. As a group, the transcapillary strokes are caused by disorders affecting end-arteries, both penetrating and perforating types. These disorders include small arterial angiitis, small vessel vasospasm (as seen in vasoactive drug use in this case), microembolization (like fat,air, and foreign body embolization), and blood sludging disorders (like sickle cell disease); instructional sickle cell cases are presented in the Pediatric Stroke Module).
2. The pattern produced by end-artery strokes include tissue loss, or enhancement if inflammatory arteritis, that follows the Virchow-Robin spaces. Transcapillary strokes, by precluding piall collateralizatin, can also cause sequestered infarctions within the cortex capillary bed (i.e. laminar necrosis) or parenchymal sequestered infarctions that often do not exhibit a recognizable arterial or venous perfusion zone.
2. The pattern produced by end-artery strokes include tissue loss, or enhancement if inflammatory arteritis, that follows the Virchow-Robin spaces. Transcapillary strokes, by precluding piall collateralizatin, can also cause sequestered infarctions within the cortex capillary bed (i.e. laminar necrosis) or parenchymal sequestered infarctions that often do not exhibit a recognizable arterial or venous perfusion zone.
Recommendations
Watch the included video for this instructional clinical case.