Working Diagnosis:
Acute Right Lacunar Infarct of unknown etiology

Treatment:
On admission H&P in the Neurology ICU, patient remembered that he had an unprovoked DVT 2 years prior and treated with 3 months of anticoagulation.

He was admitted for 2 days with no further worsening of symptoms and improved numbness and tingling of the left side. He had continued but improved weakness of the left upper and lower extremities. He was discharged to home with Aspirin 325mg QD and no statin due to normal lipid panel.

He returned 6 days after hospital discharge with worsening weakness and new slurred speech. Initial studies were repeated showing no changes on labs or imaging. Hematology/Oncology was consulted and extended hypercoagulability studies including Factor Leiden, B2 glycoprotein, Protein S, Homocysteine, Cardiolipin, Antithrombin III, ANA, and ANCA were all negative. Neurosurgery was consulted with cerebral angiogram performed showing no evidence of vasculitis/dissection/aneurysm. He was hospitalized for 5 more days and required use of a walker to ambulate. He was discharged on Aspirin 325mg QD, Atorvastatin 40mg QHS, and DVT prophylaxis, and went to inpatient rehabilitation for 2 weeks.

Outcome:
7 months later, he returned to the training room during Sports Medicine clinic to ask to return to play after being cleared by Neurology on televisit. He was still on Aspirin on and his statin was discontinued, but Neurology cleared him while deferring the decision to continue or discontinue aspirin for return to play to Sports Medicine. The patient told Neurology he had complete resolution of symptoms, but in the training room clinic, he admitted to residual symptoms.

He had slowed response of the left upper and lower extremity to movement and says "Sometimes my arm or leg doesn't move when I want them to. I have to tell myself to do something several times before it does it." Full discussion with the athlete was completed giving him precautions and possible complications. Aspirin was continued given his prior DVT and stroke. Contact sports were discouraged while on aspirin due to the bleeding risk. The athlete discussed further with his family and decided to not return to football.

Author's Comments:
With regards to ischemic stroke, 15% of people each year who are diagnosed with a stroke are younger than 40 years of age. Strokes in people younger than 40 years of age are frequently missed. 30% of strokes in people younger than 40 have no identifiable cause leading to difficulty in diagnosing, managing, and preventing strokes. With this specific case, although the athlete came from a family of football players and was very disappointed with the final decision, patient safety was of utmost importance.

Editor's Comments:
A patient who presents with focal neurological deficits such as the chief complaint of acute onset left upper extremity weakness in this patient should prompt emergent evaluation with neuro-imaging due to the high likelihood of a vascular ischemic event. The major red herring in this case was the acute onset of symptoms in the setting of a history of migraine headaches. Hemiplegic migraines are a specific type of migraine with aura that can present very similarly with unilateral weakness and can include ataxia as well as upper motor nerve signs such as hyperreflexia and Babinski sign. While this is a key item in the differential diagnoses, it is still important and necessary to rule out the more morbid causes of focal neurological deficit such as stroke and transient ischemic attack.

Lacunar infarcts are the most common type of stroke (20% +/- 5% of all strokes) and occur in subcortical brain regions secondary to the obstruction of blood flow through penetrating arteries arising from major arteries such as the MCA, basilar artery, ACA, or the rest of the Circle of Willis. These vascular insults are most commonly associated with chronic hypertension; however, they may also be caused by atheromatous disease, embolism, or endothelial dysfunction. The presentation of a lacunar stroke is most often a pure motor hemiparesis. Other presentations include ataxic hemiparesis (as seen in this case), pure sensory stroke, dysarthria-clumsy hand syndrome, and sensory-motor stroke. Lacunar infarcts have been tied to future cognitive impairment and are believed to play a role in vascular forms of dementia as well.

This case demonstrates not only the importance of immediate evaluation but also the significance of continued monitoring for return of symptoms. Re-perfusion injury may have led to the representation of his symptoms in a more exaggerated manner. Cerebral re-perfusion syndrome is characterized by the triad of ipsilateral headache, contralateral neurological deficits, and seizures. It can occur at any point from immediately after the insult to one month later with most patients presenting within the first week after initial infarct. When there is ischemia which leads to cell death, once re-perfusion of those tissues occur, the immune system targets the region with leukocyte activity leading to further inflammation and surrounding tissue damage. Patients who have suffered lacunar infarcts may be at greater risk for cell death in the ischemic region due to poor collateral circulation in the penetrating arteries, potentially placing them at greater risk for cerebral re-perfusion syndrome.

References:
Arboix A, et al. Clinical characteristics of acute lacunar stroke in young adults. Expert Review Neurotherapeutics. 2015; 15(7):825-831.

Signal AB, et al. Recognition and management of stroke in young adults and adolescents. Neurology. 2013; 81:1089-1097.

Van Alebeek ME, et al. Risk factors and mechanisms of stroke in young adults: The FUTURE study. Journal of Cerebral Blood Flow and Metabolism. 2017; 38(9):1631-1641.

Zhang B, et al. Admission markers predict lacunar and non-lacunar stroke in young patients. Thrombosis Research. 2011;128(1):14-17.

Wippold FJ. Expert Panel on Neurologic Imaging and Focal neurologic deficit. Am J Neuroradiol. 2008; 29(10):1998-2000.

Kumar A, Samanta D, Emmady PD, et al. Hemiplegic Migraine. StatPearls Publishing; 2022 Jan.

Gore M, Bansal K, Asuncion RMD. Lacunar Stroke. StatPearls Publishing; 2022 Jan.

Ogasawara K, Inoue T, Kobayashi M, Endo H, Fukuda T, Ogawa A. Pretreatment with the free radical scavenger edaravone prevents cerebral hyperperfusion after carotid endarterectomy. Neurosurgery. 2004 Nov; 55(5):1060-7.

Sundt TM Jr, Sharbrough FW, Piepgras DG, Kearns TP, Messick JM Jr, O'Fallon WM. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy: with results of surgery and hemodynamics of cerebral ischemia. Mayo Clin Proc. 1981 Sep; 56(9):533-43.

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