Cerebral venous thrombosis and submandibular lithotripsy: A case report.

We present the case of a 38-year-old woman with a diagnosis of cerebral venous thrombosis that developed after lithotripsy of the submandibular gland. Few cases of vessel thrombosis after lithotripsy have been reported in other organs, this is the unique cerebral case reported.

Opalski syndrome detected on DWI MRI: A rare lateral medullary infarction. Case report and review.

INTRODUCTION: Wallenberg's syndrome and ipsilateral paresis due to combined infarction of the lateral medullary and cervical spinal infarction is known as Opalski syndrome. This rarely described syndrome was reported, to our knowledge, with DWI MRI, only once. CASE REPORT: We report the case of a 43-year-old man with autosomal dominant polycystic kidney disease who, after a brief episode of coma, developed Wallenberg syndrome and ipsilateral hemiparesis. Initial diffusion weighted-imaging MRI showed a high-intensity signal involving the lateral medulla oblongata and the spinal cord; but FLAIR MRI sequences showed bilateral high-intensity signals in the lateral medulla oblongata and spinal cord and high-intensity signals in the right and left cerebellar hemisphere in the PICA territories. MRI performed one year later showed an infarction involving the left medullary area and adjacent spinal segments alone. CONCLUSION: This observation illustrates a rare syndrome of lateral medullary infarction, associated with spinal cord infarction related to a possible transient basilar occlusion.

[Bithalamic infarct: is there an evocative aspect? Radioclinical study]. / Accident vasculaire ischémique bithalamique: existe-t-il un tableau évocateur ? Etude radioclinique.

INTRODUCTION: Bithalamic paramedian infarcts are uncommon. This stroke results in a complex clinical syndrome. CASE REPORT: We report four cases of bithalamic paramedian infarcts with a presumed mechanism of occlusion of a single thalamic paramedian artery. DISCUSSION: This normal anatomic variant corresponds to an asymmetrical common trunk for the two thalamosubthalamic paramedian arteries arising from a P1 segment (type IIb in the G. Percheron classification dating from 1977). A literature analysis (from 1985 to 2006) allowed us to identify the most widely reported clinical signs. Four main clinical findings are described: vertical gaze palsy (65%), memory impairment (58%), confusion (53%) and coma (42%). We also found these symptoms in our patients but rarely associated; however, all four patients had exhibited episodes of drowsiness. In this article, we discuss the anatomy-function correlation responsible for such clinical variability. CONCLUSION: Clinicians should be aware of this diagnosis to better understand the imaging results which provide confirmation. Although the literature describes frequently severe consciousness disorders such as coma, this diagnosis must also be considered in patients presenting a simple fluctuation of consciousness, e.g. hypersomnia.

[Stroke due to spontaneous calcified cerebral embolus as presenting feature of calcified aortic stenosis]. / Infarctus cérébral par embolie calcaire spontanée révélant un rétrécissement aortique calcifié.

We report a case of calcified aortic stenosis revealed by an ischemic stroke. An 81-year-old man with hyperlipidemia, hypertension and renal function impairment presented with acute onset of right-sided hemiparesis and aphasia. Head CT scan revealed a rounded calcified high-density mass within the distal segment of the left anterior cerebral artery, consistent with a calcified cerebral embolus, and an infarct in the left paracentral lobule. Transesophageal echocardiography demonstrated a sclerotic aortic valve. The patient was discharged from hospital on aspirin and atorvastatin, and the outcome was favorable. Calcified embolus remains a rare event and it has been not yet reported in the territory of anterior cerebral artery. It may be observed in aortic and mitral valve diseases, calcified plaques of the internal carotid artery and aortic arch. Renal failure promotes their development and is the cause of cardiovascular diseases. To date, aortic valve calcification is not considered as a marker of stroke risk, except when associated with severe stenosis or left ventricular hypertrophy.