Introduction
: A 51‐year‐old lady with a past medical history of Essential Hypertension, Hypothyroidism, prior Herpes Zoster infection 8 weeks ago was admitted with complaints of abdominal pain, bilateral flank pain, and restlessness. Her initial workup was significant for hyponatremia and hypokalemia. On the 3rd day of admission, she developed acute hypoxemic respiratory failure which led to intubation. At that time, CTA Chest was not done but CT Chest revealed prominent mucous plugging with left side glass ground opacities, Ultrasound of lower extremities revealed right common femoral vein DVT which led to concerns that she may have suffered from Pulmonary Embolism and led to starting Heparin drip. On the 6th day of admission, she developed Acute Encephalopathy, MRI Brain revealed acute infarcts in bilateral cerebral cortices and cerebella, CT Angiogram Head showed acute subarachnoid hemorrhage in the high posterior right parietal lobe, stenosis of the right high cervical internal carotid artery, and irregular, the appearance of the arterial vasculature throughout and CT Angiogram Neck abrupt change in caliber of the right ICA, 1.5 cm distal to the bifurcation with markedly severe narrowing of the majority of the extracranial right ICA throughout its course. A cerebral Angiogram was done which showed diffuse tandem segments of tandem cervical and intracranial portions of the right internal carotid artery and she was given nitroglycerin was administered as a therapeutic intervention. Lumbar Puncture showed WBC 2, RBC 7, Protein 162, Glucose 64, VZV PCR was negative, CSF VZV IgG Antibody positive at 303 IV (>165 IV indicative of current or past infection). Serum VZV IgG Antibody was positive at >4000 IV. Infectious Diseases were consulted after Lumbar Puncture, they initially started Acyclovir but once the Serum VZV IgG Antibody came back much higher than Serum VZV IgG Antibody levels, their assessment was that VZV vasculitis is unlikely and Acyclovir was discontinued. Eventually, the case was discussed at Neuroradiology which led to us getting a repeat MRA Neck without contrast which showed a concentric T1 and T2 hyperintensity along with a small and irregular caliber right cervical ICA consistent with dissection. She eventually completed a 21‐day course of Nimodipine due to underlying Subarachnoid Hemorrhage.
Methods
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Results
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Conclusions
: Our case demonstrates how it can become difficult to ascertain the etiology of stroke in certain patients. Our patient presented with multiple non‐specific symptoms initially and it was later on due to her Acute Encephalopathy that her Strokes and Subarachnoid Hemorrhage were discovered. It is still difficult to pinpoint whether the cause of strokes was dissection or VZV infection. Lumbar Puncture remains an essential tool to complete work up on uncommon etiologies of stroke.
Reply to Dravet, C. Different Outcomes of Acute Encephalopathy after Status Epilepticus in Patients with Dravet Syndrome. How to Avoid Them? Comment on “De Liso et al. Fatal Status Epilepticus in Dravet Syndrome. Brain Sci. 2020, 10, 889”
