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469Discussion

Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers All rights reserved. Usage subject to terms and conditions of license.

MRA imaging techniques (Farb et al 2009, Nishimura et al 2010). For diagnosis and post-treatment evaluation, both imaging techniques reach results comparable to DSA (see also Case 32 and Case 40). However, DSA remains the gold standard for diagnosis in uncertain cases,

complex DAVFs, low ﬂ ow ﬁ stulas, and treatment plan- ning as it allows the best visualization of arterial feeders and abnormally draining veins and illustrates possible endovascular access points for embolization (Gandhi et al 2012, Kuwayama 2008).

470

Case 35

Left Distal Vertebral Artery Occlusion and Right Vertebral Artery Hypoplasia with Retrograde Basilar Artery Flow

Clinical Presentation

A 59-year-old man suﬀ ered from a mild isolated transient left brachiofacial sensorimotor hemisyndrome which remitted completely before he was admitted to our hospital for the ﬁ rst time. He had an extensive history of vascular events: 2 years prior to admission, he developed a transient ischemic attack (TIA) and a corresponding right-sided internal carotid artery (ICA) stenosis (70% according to NASCET criteria), which was subsequently treated with carotid endarterectomy (CEA) with patch angioplasty. Five months later, he suﬀ ered a brainstem infarction. Several chronic vascular risk factors were present: arterial hypertension, smoking, and elevated blood lipids.

Initial Neuroradiologic Findings

Cranial CT revealed no acute ischemic lesion. CT angiography (CTA) demonstrated extracranial moderate atherosclerotic caliber alterations in the carotid arteries. The left vertebral artery (VA) was visualized at the mid part of the V2-VA with a minimal caliber. The right VA was hypoplastic and showed severe calciﬁ cations. Normal ﬁ ndings were seen in the intracranial anterior circulation. The basilar artery (BA) showed a reduced diameter and wall irregularities. The left V4-VA diameter corresponded to that of the BA and also a prominent posterior inferior cerebellar artery (PICA) was seen, whereas the right V4-VA had a severely reduced diameter (Fig. B35.1, Fig. B35.2, Fig. B35.3). Cerebral MRI revealed chronic small-vessel basal ganglia lesions and an additional right pontine ischemic lesion, but no acute lesions on diﬀ usion-weighted sequences. MR angiography was not performed.

Suspected Diagnosis

TIA in the left middle cerebral artery (MCA) territory. Assumed left proximal VA occlusion and right VA hypoplasia.

• What was the hemodynamic relevance of the right VA

hypoplasia?

• What was the intracranial ﬂ ow pattern of the posterior

circulation?

Neurosonologic Findings (Day 3)

B-mode imaging revealed extended, mostly hyperechoic, bilateral plaques with predominance in the right carotid bifurcation. The right carotid bulb had a marked dilation with a bidirectional reduced ﬂ ow, assumed to be caused by the patch angioplasty performed during CEA 5 years before. Normal ﬂ ow signals were observed in the left distal ICA and in the right-side carotid arteries. Both V2-VA had small diameters (right 2.4 mm, left 2.2 mm). A stump signal was detected in the left V2-VA indicative of a distal occlusion before the origin of the PICA. The ﬂ ow signal of the right V2-VA cor- responded with an assumed hypoplasia (Fig. B35.4,

Fig. B35.5, Fig. B35.6, Fig. B35.7).

Transcranial Duplex Sonography

Both M1-MCA and A1-ACA had normal ﬂ ow signals. On both sides, a prominent posterior communicating artery (PCoA) was detectable with a ﬂ ow toward the posterior c i r c u l a t i o n . O n t h e l e f t s i d e , a n o b v i o u s r e t r o g r a d e P 1 - p o s t e r i o r c e r e b r a l a r t e r y ( P C A ) ﬂ ow was observed. Both P 2 - P C A s e g m e n t s h a d a l m o s t n o r m a l ﬂ ow signals. On the right side, the P1-PCA was not clearly detectable. Following the left retrograde P1-PCA into the distal BA the retrograde signal remained. Retrograde BA ﬂ ow was conﬁ rmed and appeared more evident during insonation in the posterior coronal plane. Upon transforaminal insonation, the BA ﬂ ow was also retrograde toward the probe with normal ﬂ ow velocities (75/20 cm/s). The left V4-VA yielded a retrograde ﬂ ow signal (53/13 cm/s), whereas the right V4-VA revealed a low antegrade ﬂ ow (20/9 cm/s) (Fig. B35.8–Fig. B35.20; see also Video

B35.1).

Questions to Answer by Ultrasound Techniques

• Was there an explanation for the right-sided clinical symptoms in the anterior circulation?

• Could the left VA occlusion be conﬁ rmed?

Conclusion

Left distal VA occlusion proximal to the PICA oﬀ spring. Right V4-VA hypoplasia. Retrograde BA and retrograde left V4-VA ﬁ lling—at least up to the left PICA—via the left PCoA and left retrograde P1-PCA. Regular anterior c i r c u l a t i o n .

Fig. B35.1 (A,B) MR T2-weighted images, axial plane, revealing lacunar pontine and basal ganglia infarction probably caused by small-vessel disease (arrows).

471Neurosonologic Findings (Day 3)

Fig. B35.2 Extracranial CTA, coronal maximal intensity projection (MIP). Lumen reduction in both VAs with marked calciﬁ cations on the right side (arrowhead) and a markedly reduced diameter on the left side (arrow).

ICA-R

Fig. B35.4 Extracranial duplex, longitudinal plane. Left: B-mode image. Right: Color-mode image. Note the widening of the carotid bulb after CEA with patch angioplasty.

Fig. B35.3 Intracranial CTA, 3D reconstruction. Note the narrow diameters of the vertebrobasilar arteries compared with the vessels of the anterior circulation. Communication of the anterior circulation with the BA head was seen on both sides (arrowheads). The BA revealed wall irregularities (arrows). A marked PICA was seen on the left side (large arrow) and a slim V4-VA was visualized on the right side (short arrow).

472 Case 35 Left Distal Vertebral Artery Occlusion and Right Vertebral Artery Hypoplasia with Retrograde Basilar Artery Flow

ICA-R

Fig. B35.5 Extracranial duplex, longitudinal plane. Bidirectional

ﬂ ow pattern in the right ICA bulb with low ﬂ ow velocities.

V2-VA-R

V2-VA-L

Fig. B35.6 Extracranial duplex, longitudinal plane. Stump signal in the left V2-VA with a diameter of 2.2 mm (ﬂ ow velocity 9/0 cm/s).

PCoA

P2-PCA

ICA

P1-PCA

Fig. B35.7 Extracranial duplex, longitudinal plane. Reduced ﬂ ow velocity in the right V2-VA with a diameter of 2.4 mm (ﬂ ow velocity 30/7 cm/s).

PCoA-L

Fig. B35.9 TCCS (tr anst emporal appro ach) , left -sided insonati on, upper pontine plane. Doppler spectrum analysis in the left PCoA without functional stenosis and normal ﬂ ow velocity (48/12 cm/s).

Fig. B35.8 TCCS (t rans temp oral ap proa ch), le ft-s ided in sona tion , upper pons/midbrain plane. Circle of Willis with prominent left-sided PCoA. Note the retrograde ﬂ ow in the left blue-coded P1-PCA.

P1-PCA-L

Fig. B35.10 TCCS (trans temp oral ap proa ch), left-s ided ins onati on, upper pons/midbrain plane. Doppler spectrum analysis in the left P1-PCA revealing a retrograde ﬂ ow but otherwise normal ﬂ ow ve- locity (59/22 cm/s).

473Neurosonologic Findings (Day 3)

P2-PCA-L

Fig. B35.11 TCC S (t ranstem pora l ap proach) , le ft-s ided ins onation, midbrain plane. Normal ﬂ ow velocity in the left P2-PCA (53/21 cm/s).

PCoA-R

MCA

PCoA

P2-PCA

ICA

PCA

Fig. B35.12 TCCS (transtemporal approach), right-sided insonation, upper pons/midbrain plane. Circle of Willis with prominent right-sided PCoA. No right P1-PCA is seen.

P2-PCA-R

Fig. B35.13 TCCS (transtemporal approach), right-sided insonation, upper pontine plane. Doppler spectrum analysis in the right PCoA revealing a higher pulsatility and mild turbulence compared with the left PCoA (ﬂ ow velocity 63/18 cm/s).

Fig. B35.15 TCCS (transtemporal approach), right-sided insonation, upper/lower pontine plane. Retrograde BA signal in the axial plane with a normal ﬂ ow signal (ﬂ ow velocity 37/13 cm/s).

Fig. B35.14 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normal ﬂ ow velocity in the right P2-PCA (74/30 cm/s). No right P1-PCA is seen.

(TT)

ICA

PCA

Fig. B35.16 TCCS (transtemporal approach), right-sided insonation, posterior coronal plane. The coronal approach facilitates the visualization of vertical orientated vessels if the insonation angle is <90°. Here the BA and the left distal V4-VA can be visualized with a retrograde ﬂ ow.

474 Case 35 Left Distal Vertebral Artery Occlusion and Right Vertebral Artery Hypoplasia with Retrograde Basilar Artery Flow

Fig. B35.17 TCC S (trans fora minal ap proach) . P rominen t r etro grade BA ﬂ ow signal at an insonation depth of 85 mm (ﬂ ow veloc- ity: 75/20 cm/s).

V4-VA-L

Fig. B35.18 TCC S (tr ansforami nal app roach). Tapping of the right extracranial submandibular ICA provokes typical transients in the BA spectrum (arrows) indicating a BA blood supply from the anterior circulation.

V4-VA-R

Fig. B35.19 TCCS (t ransfor amin al ap proa ch). Lef t V4 -VA wit h retrograde ﬂ ow at an insonation depth of 74 mm (ﬂ ow velocity 53/13 cm/s), similar to the BA ﬂ ow.

Clinical Course

The clinical course was uneventful. Clopidogrel was administered instead of aspirin for platelet inhibition and the statin dosage increased. Annual follow-up studies over 4 years showed an unchanged vascular status.

Fig. B35.21 shows a schematic of the patient’s extra-

and intracranial brain-supplying arteries.

Final Diagnosis

Right MCA TIA probably due an artery-to-artery embolism from a wide carotid bulb after CEA. Asymptomatic left distal VA occlusion proximal of the left PICA origin and right VA hypoplasia with assumed additional distal stenosis.

Fig. B35.20 TCC S (tr ansfo ram inal appr oach ). Ri ght V 4-VA se gmen t with an antegrade reduced ﬂ ow velocity and mild poststenotic ﬂ ow pattern (ﬂ ow velocity 20/9 cm/s). The latter indicates a proximal he- modynamically relevant stenosis between the distal V2-VA and V3-VA.

Discussion

Clinical Aspects

Here we describe a 59-year-old man with typical vascular risk factors, who presented with a TIA in the right MCA territory. Two years prior to the TIA, he underwent CEA of the right ICA after a similar event and diagnosis of a symptomatic 70% ICA stenosis (NASCET criteria). The ﬁ rst assumption of a possible right ICA restenosis was not conﬁ rmed by CTA and duplex sonography. Also, no other extra- or intracranial stenosis was detected which could have explained the TIA in the anterior circulation. Because of advanced small-vessel disease signs on MRI, a lacunar TIA was discussed as an alternative cause. F i n a l l y , a n a r t e r y - t o - a r t e r y e m b o l i s m o r i g i n a t i n g f r o m the largely widened ICA bulb after patch angioplasty with

Fig. B35.21 Schematic of the patient’s extra- and intracranial brain-supplying arteries. Right VA hypoplasia with assumed distal stenosis (small circle) and left distal pre- PICA VA occlusion (large circle). Supply of the BA-dependent vessels including the left PICA through the right PCoA and retrograde P1-PCA. Widening of the right ICA bulb following CEA with patch angioplasty (large circle).

subsequently very low ﬂ ow velocities, possibly promot- ing the development of thrombi, was also considered. To date, however, no published literature relates iatrogenic widening of the ICA bulb to stroke risk. A patch angioplasty is often performed to avoid narrowing of the ICA and the distal CCA during conventional CEA and is considered useful to prevent restenosis. Adverse hemodynamic eﬀ ects, however, may be the abnormal width of the proximal ICA with increasing wall shear stress caused by a patch (Harrison et al 2014). Analyzing 13 randomized trials with 1,281 operations, carotid patch angioplasty was shown to decrease the risk of perioperative arterial occlusion, restenosis, and also the long-term risk of stroke (Bond et al 2004). The recent Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) included 1,151 patients of whom 65% received a patch and 29% a primary closure (patients with eversions CEA and missed clinical data were excluded). Again, patch closure was related to lower restenosis rates but not to improved clinical outcome (Malas et al 2015).

Angiologic and Anatomic Aspects

The main ﬁ nding in our patient was a remarkable alter- ation of the vertebrobasilar circulation, which did not cause any brainstem or cerebellar symptoms. Considering the small diameters of the extracranial VAs seen in CTA, a primary hypoplasia may be assumed. In this condition, bilateral fetal-type PCAs or at least prominent PCoAs are often present to supply the PCA territories via the anterior circulation. In our patient, CTA indicated at least a right fetal-type PCA with a residual hypoplastic P1-PCA segment. On the left side, a prominent PCoA was depicted by CTA. However, no information was available with regard to the real ﬂ ow dynamics and ﬂ ow directions.

475Discussion

The real hemodynamic constellation of the case was clariﬁ ed by ultrasound examination. A left-sided distal pre-PICA occlusion of the VA and a right VA hypoplasia were found. Transtemporal and transforaminal insonation unequivocally showed a marked retrograde BA ﬂ ow, including retrograde ﬂ ow into the left V4-VA assuring the blood supply to the left PICA territory.

A prominent retrograde BA ﬂ ow indicates a large blood recipient, i.e., at least ﬂ ow into one PICA territory. In mid-part BA occlusion, less blood is needed as only superior cerebellar arteries (SCAs) and the distal BA perforator arteries have to be supplied, so a clear retrograde BA ﬂ ow signal in color and Doppler mode may be diﬃ cult to obtain, at least at the midpart of the BA (see also Case 21 and Case 41).

In patients with bilateral proximal VA occlusion, a secondary distal ﬁ lling of the VA is often seen by anastomo- ses from external carotid artery (ECA) branches (for further reading, see Chapter 5, “VA Occlusion” under “Extracranial Pathology”). If bilateral distal VA occlusion or—as in our case—unilateral pre-PICA VA occlusion with a contralateral almost PICA-ending hypoplastic VA is present, a retrograde BA ﬂ ow is needed and should be assessed when perform- ing an ultrasound examination. A retrograde BA ﬂ ow may be visualized via the transforaminal or the transtemporal approach. When starting with the transtemporal approach at least one PCoA should reveal a marked ﬂ ow toward the posterior circulation and at least one P1-PCA should have a retrograde ﬂ ow signal. Considering the short length of the P1-PCA (often having only the dimension of the placed ultrasound sample volume) it is sometimes challenging to conﬁ dently visualize the P1-PCA segment. Reducing the size of the color window, lowering the pulse repetition frequency (PRF), and increasing the color gain (in some systems also using the zoom function) will facilitate its recognition as a short blue-coded vessel segment. This signal is then traced caudally and the BA may be detected in cross-sectional planes with a blue-coded signal. However, because of its often elongated course, red-colored signals may also be present, which should not lead to misinterpretations. When in doubt or if there are diﬃ culties with interpretation, the image plane of choice is the posterior coronal plane. Provided that suﬃ cient imaging conditions are present, it is usu- ally possible to clearly identify the ﬂ ow direction of the BA in the coronal plane. As a next step, transforaminal access should be used to analyze the ﬂ ow parameters and ﬂ ow direction of the BA and the V4-VAs. In optimal conditions, the retrograde BA ﬂ ow can be depicted in color mode and Doppler spectrum, in our case as a large, straight red-coded vessel signal at a depth of 80–100 mm. In addition to the above, the presumed BA ﬂ ow signal can be studied during digital tapping of the submandibular ICA. Clearly detectable transients, as in our case, strongly support a retrograde BA ﬂ ow pattern.

Of note, in distal bilateral VA occlusion, prominent anterior and posterior spinal arteries which communicate with branches of the ECA may be of relevance, as has been reported in case of bilateral VA agenesis (Lu et al 2014).

476

Case 36

Postpartum Angiopathy (Reversible Cerebral Vasoconstriction Syndrome)

Clinical Presentation

A 42-year-old woman in her 41st week of pregnancy presented in the delivery ward with a mild holocephalic headache and slightly elevated blood pressure. She was diagnosed with pre-eclampsia and labor was induced without any complications, leading to the birth of a healthy child the following day. During delivery, she suffered from a new, severe bifrontal headache. Her systolic blood pressure was 160 mm Hg. Ten minutes after delivery, she developed dysarthria and left-sided hemiplegia. Her medical history was unremarkable and a pregnancy 2 years prior was uneventful.

Initial Neuroradiologic Findings

Cranial CT showed a right-sided subcortical dorsal striatocapsular hemorrhage of maximal 30 × 25 mm extension with only mild perifocal edema (Fig. B36.1). No other pathology was identiﬁ ed. CT angiography (CTA) revealed no arterial or venous abnormalities. Follow-up cranial CT 24 hours later remained almost identical.

Conventional Angiography (Day 2)

Digital subtraction angiography (DSA) did not oﬀ er any clues regarding the cause of bleeding. Speciﬁ cally, no in- tracranial angiomas, ﬁ stulas, or aneurysms were identi- ﬁ ed. There was also no evidence of cerebral vasospasm (Fig. B36.2).

Suspected Diagnosis

Pre-eclampsia with pregnancy-related intraparenchymal hemorrhage (IPH).

Clinical Course (1)

The patient was transferred to the neurology intensive care unit. Blood pressure control was achieved with urapidil, metoprolol, and dihydralazin. She remained stable from a cardiopulmonary perspective. Mild proteinuria remitted spontaneously and mild thrombocytopenia normalized within 4 days. Plasma coagulation screening was within normal limits. On neurologic examination, she

was transiently disorientated and agitated and required sedation and neuroleptic medication. Clinically, a posterior encephalopathy was assumed. A second follow-up cranial CT showed that the size of the IPH had remained the same but there was a slight increase in focal edema.

Questions to Answer by Ultrasound Techniques

• Was there evidence of an arteriovenous malformation (AVM) hidden by the bleeding during DSA?

• Were there signs of vasospasm suggestive of a reversible cerebral vasoconstriction syndrome (RCVS)?

• Was there evidence of cervical artery dissection?

• If increased intracranial ﬂ ow velocities were present, was there any dynamic change in time?

Initial Neurosonologic Findings (Day 5)

Extracranial Duplex Sonography

B-mode and color-mode imaging revealed no atherosclerosis and no evidence of carotid or vertebral artery dissection. Doppler spectrum analysis showed normal and symmetric ﬂ ow signals in all extracranial brain-supplying arteries.

Transcranial Duplex Sonography

Increased peak systolic ﬂ ow velocities with a turbulent ﬂ ow pattern were detected in all intracranial arteries:

M2-middle cerebral artery (MCA) (left 289 cm/s, right 223 cm/s), M1-MCA (left 198 cm/s, right 182 cm/s), A 1 - A C A ( l e f t 1 8 7 c m / s , r i g h t 1 9 0 c m / s ) , P 2 - p o s t e r i or cerebral artery (PCA) (left 135 cm/s, right 197 cm/s), c a r o t i d s i p h o n ( l e f t 1 5 0 c m / s , r i g h t 2 2 0 c m / s ) , b a s i l a r a r t e r y (BA) (251 cm/s). No poststenotic distal ﬂ ow pattern was observed in any artery (Fig. B36.3, Fig. B36.4, Fig. B36.5, Fig. B36.6). For peak systolic velocities, the Lindegaard Index (LI) was 3.2 on the left side and 1.6 on the right.

Conclusion

Multilocular intracranial stenoses >50% in both M2-MCA and A1-ACA segments, in the right P2-PCA, and in the BA, and to a lesser extent in both carotid siphons, both M1-MCA segments, and the left P2-PCA segment, though

477Initial Neurosonologic Findings (Day 5)

Fig. B36.1 CT scan, axial plane. Right-sided dorsal striatocapsular hemorrhage (30 × 25 mm) with only mild perifocal edema.

M1-MCA-L

Fig. B36.3 TCCS (tr anst emporal appro ach) , left -sided insonati on, axial midbrain plane. Left M1-MCA segment with increased ﬂ ow velocity on day 5 (ﬂ ow velocity 198/104 cm/s).

A1-ACA-L

Fig. B36.2 DSA, left and right common carotid artery (CCA) i n j e c t i o n , p o s t e r o a n t e r i o r v i e w . S u p e r i m p o s e d i m a g e t o f a c i l i t a t e overview of bilateral circulation, showing normal caliber of all intracranial arteries on day 2.

M2-MCA-L

Fig. B36.4 TCCS (tr anst emporal appro ach) , left -sided insonati on, axial midbrain plane. Left M2-MCA segment with increased ﬂ ow velocity on day 5 (ﬂ ow velocity 289/135 cm/s).

P2-PCA-R

Fig. B36.5 TCCS (tr anst emporal appro ach) , left -sided inso nati on, axial midbrain plane. Left A1-ACA segment with increased ﬂ ow velocity on day 5 (ﬂ ow velocity 187/105 cm/s). The Doppler spectrum is inverted.

Fig. B36.6 TCCS (t rans tempo ral approach) , right -sid ed in sona tion, axial thalamic plane. Right distal P2-PCA segment with increased ﬂ ow velocity on day 5 (ﬂ ow velocity 197/96 cm/s). The Doppler spectrum is inverted.

478 Case 36 Postpartum Angiopathy (Reversible Cerebral Vasoconstriction Syndrome)

Fig. B36.7 3D TOF-MRA, coronal maximal intensity projection (MIP). Multiple vessel narrowing suggestive of RCVS. Pronounced narrowing in the left carotid siphon (arrow), left PCA (arrowheads), and left distal M1-MCA near its bifurcation (large arrowhead). Note the long segmental tailored BA and the large artifact caused by the parenchymal hemorrhage.

these were not hemodynamically relevant. Additionally, right hemispheric hyperperfusion with uncertainty regarding a possible generalized hyperperfusion.

Neuroradiologic Findings (Day 6)

Cerebral MRI conﬁ rmed IPH and ruled out secondary hemorrhagic transformation of ischemic stroke. No signs of posterior reversible encephalopathy syndrome (PRES) were seen. Time-of-ﬂ ight MR-angiography (TOF-MRA) was considered to show only mild vessel irregularities. Retrospectively, multiple bilateral vessel narrowing was diagnosed in the anterior and posterior circulation (Fig. B36.7 and Fig. B36.8).

Follow-up Neurosonologic Findings (Day 6)

Transcranial Duplex Sonography

Peak systolic ﬂ ow velocities further increased in both M1-MCAs (left 258 cm/s, right 235 cm/s) and in the right A1-ACA (234 cm/s). Flow remained stable in the left M2MCA, in the left A1-ACA and in both carotid siphons, whereas slightly decreased ﬂ ow velocities were seen in the right M2-MCA (176 cm/s), right P2-PCA (140 cm/s), and left P2-PCA (106 cm/s). Raised systolic peak ﬂ ow ve- locities were seen for the ﬁ rst time in the right A2-ACA (160 cm/s). The LI increased on the left side to 4.4 and on the right side to 2.5 (Fig. B36.9, Fig. B36.10, Fig. B36.11).

Conclusion

Persisting multilocular intracranial stenoses with only mild modiﬁ cations of graduation. Probably less hyper- perfusion on the right side.

Fig. B36.8 3D TOF-MRA, sagittal MIP. Multiple vessel narrowing suggestive of RCVS. Visible are multisegmental PCA narrowing (large and small arrowheads), an A2-ACA narrowing (small arrow), and a narrowing of the carotid siphon (large arrow).

Follow-up Neurosonologic Findings (Days 7–17)

Transcranial Duplex Sonography

Intracranial ﬂ ow velocities declined slowly during the following week. Elevated systolic ﬂ ow velocities were still seen in both M1-MCAs (left 178 cm/s, right 180 cm/s), in the left M2-MCA (120 cm/s), in both A1ACAs (left 128 cm/s, right 157 cm/s), in one of the A2ACAs (159 cm/s), and in the right P2-PCA (100 cm/s). The h i g h e s t L I w a s m e a s u r e d o n d a y 8 a t 4 . 2 o n t h e r i g h t s i d e and 4.5 on the left side (not shown).

Conclusion

Partial remission of intracranial vasoconstriction and complete remission of hyperperfusion.

Clinical Course (2)

Following the initial detection of elevated blood ﬂ ow velocities, calcium channel blockers were administered. The neuropsychologic deﬁ cits disappeared within 1 week and dysarthria and hemiparesis improved substantially. At hospital discharge, only a mild facial asymmetry and a slight disturbance of ﬁ ne motor skills remained. The latter symptoms subsided completely during the f o l l o w i n g m o n t h s . F o l l o w - u p M R I a n d M R A 6 m o n t h s later revealed a residual posthemorrhagic parenchymal lesion on the right side. No vessel abnormalities were seen (not shown).

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