49-year-old woman • headache and neck pain radiating to ears and eyes • severe hypertension • Dx?

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doi:doi: 10.12788/jfp.0659

Case Reports

49-year-old woman • headache and neck pain radiating to ears and eyes • severe hypertension • Dx?

J Fam Pract. 2023 September;72(7):E26-E29 | doi: 10.12788/jfp.0659

By

Christian Saleh, MD

Muhannad Seyam, MD

Kristine A. Blackham, MD

Anna Walter, MD

Philippe Lyrer, MD

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► Headache and neck pain radiating to ears and eyes
► Severe hypertension

References

1. Cloud GC, Markus HS. Diagnosis and management of vertebral artery stenosis. QJM. 2003;96:27-54. doi: 10.1093/qjmed/hcg003

2. Sparaco M, Ciolli L, Zini A. Posterior circulation ischaemic stroke–a review part I: anatomy, aetiology and clinical presentations. Neurol Sci. 2019;40:1995-2006. doi: 10.1007/s10072-019-03977-2

3. Lin DDM, Gailloud P, Beauchamp NJ, et al. Combined stent placement and thrombolysis in acute vertebrobasilar ischemic stroke. AJNR Am J Neuroradiol. 2003;24:1827-1833.

4. Pezzini A, Caso V, Zanferrari C, et al. Arterial hypertension as risk factor for spontaneous cervical artery dissection. A case-control study. J Neurol Neurosurg Psychiatry. 2006;77:95-97. doi:10.1136/jnnp.2005.063107

5. Merwick Á, Werring D. Posterior circulation ischaemic stroke. BMJ. 2014;348:g3175. doi: 10.1136/bmj.g3175

6. Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2018;49:e46-e110. doi: 10.1161/STR.0000000000000158

7. Provenzale JM, Sarikaya B. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. 2009;193:1167-1174. doi: 10.2214/AJR.08.1688

8. Husnoo Q. A case of missed diagnosis of posterior circulation stroke. Clin Med (Lond). 2019;19(suppl 2):63. doi: 10.7861/clinmedicine.19-2-s63

9. Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008;359:1317-1329. doi: 10.1056/NEJMoa0804656

10. Schneider AM, Neuhaus AA, Hadley G, et al. Posterior circulation ischaemic stroke diagnosis and management. Clin Med (Lond). 2023;23:219-227. doi: 10.7861/clinmed.2022-0499

11. Dorňák T, Král M, Šaňák D, et al. Intravenous thrombolysis in posterior circulation stroke. Front Neurol. 2019;10:417. doi: 10.3389/fneur.2019.00417

12. van der Hoeven EJ, Schonewille WJ, Vos JA, et al. The Basilar Artery International Cooperation Study (BASICS): study protocol for a randomised controlled trial. Trials. 2013;14:200. doi: 10.1186/1745-6215-14-200

13. Nouh A, Remke J, Ruland S. Ischemic posterior circulation stroke: a review of anatomy, clinical presentations, diagnosis, and current management. Front Neurol. 2014;5:30. doi: 10.3389/fneur.2014.00030

14. Purrucker JC, Ringleb PA, Seker F, et al. Leaving the day behind: endovascular therapy beyond 24 h in acute stroke of the anterior and posterior circulation. Ther Adv Neurol Disord. 2022;15:17562864221101083. doi: 10.1177/17562864221101083

15. Chimowitz MI, Lynn MJ, Derdeyn CP, et al. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med. 2011;365:993-1003. doi: 10.1056/NEJMoa1105335

16. Markus HS, Michel P. Treatment of posterior circulation stroke: acute management and secondary prevention. Int J Stroke. 2022;17:723-732. doi: 10.1177/17474930221107500

THE CASE

A 49-year-old woman was hospitalized with a headache and neck pain that radiated to her ears and eyes in the context of severe hypertension (270/150 mm Hg). Her medical history was significant for heterozygous factor V Leiden mutation, longstanding untreated hypertension, and multiple severe episodes of HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome during pregnancy.

After receiving antihypertensive treatment at a community hospital, her blood pressure gradually improved to 160/100 mm Hg with the addition of a third medication. However, on Day 3 of her stay, her systolic blood pressure rose to more than 200 mm Hg and was accompanied by somnolence, emesis, and paleness. She was transferred to a tertiary care center.

THE DIAGNOSIS

On admission, the patient had left-side hemiparesis and facial droop with dysarthria, resulting in a National Institutes of Health Stroke Scale (NIHSS) score of 7 (out of 42) and a Glasgow Coma Scale (GCS) score of 13 (out of 15). Noncontrast computed tomography (CT) and CT angiography of the head and neck were ordered and showed occlusion of both intracranial vertebral arteries. There were also signs of multifocal infarction in her occipital lobes, thus systemic recombinant human-tissue plasminogen activator (tPA) could not be administered.

The patient was next taken to the angiography suite, where a digital subtraction angiography confirmed the presence of bilateral vertebral artery occlusions (FIGURE 1A). A thrombectomy was performed to open the left occluded segment, resulting in recanalization; however, a high-grade stenosis remained in the intracranial left vertebral artery (FIGURE 1B). The right vertebral artery had a severe extracranial origin stenosis, and balloon angioplasty was performed in order to reach the intracranial circulation; however, the occlusion of the intracranial right vertebral artery segment could not be catheterized. Subsequent magnetic resonance imaging (MRI) with a time-of-flight magnetic resonance angiography showed that the intracranial left vertebral artery with high-grade stenosis had closed down again; thus, there was occlusion of both intracranial vertebral arteries and absent flow signal in the basilar artery (FIGURE 2). There were scattered small acute strokes within the cerebellum, brainstem, and occipital lobes.

Unfortunately, within 48 hours, the patient’s NIHSS score increased from 7 to 29. She developed tetraplegia, was significantly less responsive (GCS score, 3/15), and required intubation and mechanical ventilation. Reopening the stenosis and keeping it open with a stent would be an aggressive procedure with poor odds for success and would require antithrombotic medications with the associated risk for intracranial hemorrhage in the setting of demarcated strokes. Thus, no further intervention was pursued.

Further standard stroke work-up (echocardiography, extracranial ultrasound of the cerebral circulation, and vasculitis screening) was unremarkable. In the intensive care unit, intravenous therapeutic heparin was initiated because of the potential prothrombotic effect of the factor V Leiden mutation but was subsequently switched to dual anti-aggregation therapy (aspirin 100 mg/d and clopidogrel 75 mg/d) as secondary stroke prevention given the final diagnosis of severe atherosclerosis. Nevertheless, the patient remained tetraplegic with a partial locked-in syndrome when she was discharged, after 2 weeks in the tertiary care center, to a rehabilitation center.

DISCUSSION

Posterior circulation strokes account for 20% to 25% of all ischemic strokes^1,2 and are associated with infarction within the vertebrobasilar arterial system. Common etiologies of these infarctions include atherosclerosis (as seen in our patient), embolism, small-artery penetrating disease, and arterial dissection.² Although the estimated overall mortality of these strokes is low (3.6% to 11%),² basilar occlusion syndrome, in particular, is a life-threatening condition with a high mortality rate of 80% to 90%.³

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