44 Transient Global Amnesia with Left Hippocampal Diffusion-weighted Lesion and Asymptomatic Right Middle Cerebral Artery Infarction in High-grade Right M1 Stenosis

Transient Global Amnesia with Left Hippocampal Diffusion-weighted Lesion and Asymptomatic Right Middle Cerebral Artery Infarction in High-grade Right M1 Stenosis

Clinical Presentation

A 61-year-old man was acutely admitted with suspected stroke. Two hours before his admission, his wife had noticed marked confusion. She reported that they were on vacation and staying in a hotel. Shortly after her husband had defecated in the hotel bathroom, he began repeatedly asking where they were and why. The patient was unable to remember his wife’s answers. Suspecting a stroke, she called the ambulance. His past medical history revealed arterial hypertension. No head trauma was reported. On admission, no focal deficit or headaches were present, but a pronounced anterograde amnestic dysfunction was present. He was unable to build new memories and therefore he was disoriented in time and place but aware of himself. His other cognitive and executive functions appeared normal. As a precautionary measure, he received thiamine 100 mg intravenously in order not to overlook precipitant Wernicke’s encephalopathy. Because of the history and clinical presentation, however, a first episode of a transient global amnesia (TGA) was assumed.

Initial Neuroradiologic Findings

Cranial CT was unremarkable. Diffusion-weighted (DW) brain MRI sequences revealed circumscribed cortical lesions, one in the left hippocampus and two in the right centroparietal region, primarily assumed to be acute ischemia in the left anterior choroidal artery (AChA) and right middle cerebral artery (MCA) territory. Intracranial time-of-flight MR angiography (TOF-MRA) showed an isolated high-grade MCA stenosis of the right M1-MCA with indirect signs of hemodynamic relevance (Fig. B44.1, Fig. B44.2, Fig. B44.3).

Suspected Diagnosis

Amnestic syndrome primarily supposed to be TGA. MRI and MRA showed bilateral ischemia in the territories of the right MCA and the assumed left AChA as well as an M1-MCA stenosis of unknown origin, suggestive of embolic ischemia.

Questions to Answer by Ultrasound Techniques

Were there atherosclerotic vascular changes in the extracranial vessels?
What was the degree of the MCA stenosis?
Was there evidence of further intracranial stenotic processes underrated by MRA?
Was there evidence of internal jugular vein valve insufficiency (IJVVI), reported in the literature in TGA patients?

Initial Neurosonologic Findings (Day 1)

Extracranial Duplex Sonography

B-mode imaging revealed moderate atherosclerotic vascular changes with local lumen reduction of <30% (ECST criteria). Doppler spectrum analysis showed normal and symmetric flow signals. Venous analysis showed a right-dominant internal jugular vein (IJV) defined by a larger area and higher flow velocity. During a Valsalva maneuver (VM), valve competence was seen on the left side. On the right side, a marked reflux of 1.28 seconds affirmed an incompetent IJV valve (Fig. B44.4 and Fig. B44.5).

Transcranial Duplex Sonography

Doppler spectrum analysis revealed an increased flow velocity reaching 313 cm/s peak systolic flow in the right mid-part M1-MCA at a depth of 53 mm. A mild poststenotic flow pattern was detected in the right M2-MCA branches. In comparison with the left side, the right posterior cerebral artery (PCA) P2-P3 segment revealed an increased flow velocity without turbulence (75/32 cm/s versus 54/24 cm/s). Both A1-ACA and the left M1-MCA segment showed normal flow parameters. Venous examination showed normal flow signals in all examined vessels and especially also in the basal vein of Rosenthal (BVR), the deep middle cerebral vein (DMCV), the vein of Galen (VG), and the straight sinus (StS). A mild flow velocity reduction was observed during a forced VM in the examined BVR. The StS initially revealed a sharp short velocity increase but then also decreased mildly his velocity (Fig. B44.6, Fig. B44.7, Fig. B44.8, Fig. B44.9).

Fig. B44.10 shows a schematic of the patient’s extra- and intracranial brain-supplying arteries.

Conclusion

High-grade MCA stenosis of unknown origin in the right M1-MCA segment with hemodynamic relevance. IJV valve incompetence on the right (dominant) side.

Fig. B44.1 DW-MRI, axial plane (A) and coronal plane (B). Hyperintense signals (arrows) in the left hippocampus, typical for TGA.

Fig. B44.2 DW-MRI, axial plane. Hyperintense signals in the right centroparietal cortex (arrows) compatible with a territorial MCA ischemia.

Fig. B44.3 3D TOF-MRA, axial maximal intensity projection (MIP). Short flow gap in the right middle M1-MCA which indicates stenosis >70% (arrow). The hemodynamic relevance is further underlined by the reduced signal in the ipsilateral insular MCA branches (arrows) indicating a poststenotic flow pattern as well as the prominent right PCA signal (arrowheads) indicating leptomeningeal collateral flow activation.

Fig. B44.4 Extracranial duplex, longitudinal plane. Left IJV with undulating flow and low flow velocities at rest and physiologic flow arrest during a Valsalva strain. Note the sharp and short retrograde flow resembling physiologic valve closure (arrow). Note also the marked dilation of the IJV indicating an adequate VM.

Clinical Course

The amnestic episode subsided completely after 4 hours. The patient reported that he had never had a similar episode. Laboratory tests excluded intoxication, infection, and metabolic disturbances (e.g., glucose was normal). Electroencephalography (EEG) was normal. Because of the bilateral DWI-MRI lesions, a profound cardiologic work-up was performed. This showed neither cardioembolic nor aortoembolic causes for the current symptoms. Considering the left-sided hippocampal lesion, the clinical presentation, and evolution, a TGA unrelated to the right-sided ischemic lesions and high-grade M1-MCA stenosis was diagnosed, which were considered incidental findings. Aspirin and statins were added to his antihypertensive medication. At the initial 3-month transcranial color-coded duplex sonography (TCCS) follow-up, he had remained clinically stable. During a subsequent 3-year monitoring, TCCS showed identical findings.

Final Diagnosis

TGA in associated right IJV valve incompetence following a VM. Two incidental asymptomatic right artery-to-artery embolic cortical MCA infarcts caused by an unchanged hemodynamically relevant right M1-MCA stenosis probably of atherosclerotic origin.

Discussion

Clinical Aspects

Here we describe a 61-year-old patient with his first TGA episode lasting for 4 hours after a Valsalva-related maneuver. DW-MRI revealed a typical small signal in the Sommer sector of the left hippocampus seen in axial and coronal planes. Duplex sonography detected jugular valve incompetence in the right IJV. Incidentally, two small acute ischemic lesions were seen in the right MCA territory assumed to be caused by artery-to-artery embolism in high-grade right-sided M1-MCA stenosis.

Fig. B44.5 Extracranial duplex, longitudinal plane. Right IJV with undulating but mostly antegrade flow direction with higher flow velocities compared with the left IJV at rest. An abnormal flow reflux is seen during a Valsalva strain of 1.28 seconds.

Fig. B44.6 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Right M1-MCA with intrastenotic flow velocity of 313/144 cm/s (non-angle-corrected) at a depth of 53 mm. Note the severe turbulent flow pattern.

Fig. B44.7 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Mild poststenotic flow pattern and low flow velocities in a right M2-MCA branch (24/13 cm/s).

Fig. B44.8 TCCS (transtemporal approach), right-sided insonation, thalamic plane. Raised flow velocities in the right P2/P3-PCA (75/32 cm/s) indicating leptomeningeal collateralization of the MCA territory.