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Dispersion and ‘salted pretzel sign’ from thrombolysis of a spontaneous calcified embolus in an acute stroke
  1. Markus Gschwind1,
  2. Stefano Binaghi2,
  3. Anastasia Zekeridou1,
  4. Patrik Michel1
  1. 1Department of Clinical Neuroscience, Neurology Service, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Lausanne, Switzerland
  2. 2Interventional Neuroradiology, Radiology Department, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland
  1. Correspondence to Dr Markus Gschwind, Neurology Service BH13, Department of Clinical Neuroscience, Center Hospitalier Universitaire Vaudois (CHUV), University of Lausanne, Rue du Bugnon 46, Lausanne CH-1011, Switzerland; markus.gschwind{at}

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Emboli are one of the main causes of cerebral ischaemia and acute stroke. Calcified emboli are much less frequent, and most of the few reported cases occurred secondary to manipulation (aortic valve disease and cardiac catheterisation).1 Cases of spontaneous calcified emboli from the carotid artery, without previous manipulation, are very rare.2 While intravenous thrombolysis is the standard therapy of acute stroke, there are, to our knowledge, only two reported cases of a thrombolytic treatment after a calcified embolus, but with contradictory outcomes.1 ,3 Here we present a case of a massive right hemispheric stroke due to a spontaneous calcified embolus, which recanalised after thrombolysis and dispersed into a shower of multiple cortical emboli (‘salted pretzel sign’4).

A 79-year-old hypertensive smoker presented with a complete left-sided hemiplegia, dysarthria, hemineglect and anosognosia (National Institute of Health Stroke Scale (NIHSS) 19, modified Rankin scale before stroke was 0). The CT scan showed a complete right middle cerebral artery (MCA) stroke (figure 1) with a large calcification in the M1 segment, confirmed by the CT angiography showing also a T-occlusion of the terminal carotid artery. Thrombolysis with rtPA was initiated 2 h 45 m after stroke onset achieving recanalisation of the carotid T and proximal MCA, contrasting with one of the two other cases reporting no recanalisation.3 We also observed a dispersion of multiple calcified particles into cortical MCA branches (figure 2). Doppler ultrasound showed moderate atheromatosis with strongly calcified plaques in both carotid arteries, and a stenosis of 60% in the right carotid artery. Given the negative work-up for cardiac and aortic sources, the calcified carotid stenosis was incriminated for the spontaneous embolus.4 Clinical outcome was rather favourable with, at 3 months, the patient being at home partially independent with an NIHSS of 4 and a modified Rankin scale of 3.

Figure 1

Initial presentation: (A) CT shows a calcified thrombus in the right middle cerebral artery (MCA). (B) 3D reconstruction from CT angiography. (C) Perfusion CT with infarct core (red) and potentially salvageable tissue (green) in right MCA territory. (D) Carotid CT angiography with multiples calcified plaques.

Figure 2

After thrombolysis: (A) Control CT showing a complete disappearance of the initial thrombus. (B) Middle cerebral artery (MCA) repermeabilisation at CT angiography. (C) Multiple calcified emboli in the cortical MCA territory (‘salted pretzel sign’4). (D) MRI at 12 days showing multiple minor cortical infarctions.

This case with a positive outcome adds to the two other reported cases. It seems that thrombolytic treatment might be efficient in cases of calcified emboli.



  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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