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Lacunar Stroke as the Sole Manifestation of COVID-19

2020; Lippincott Williams & Wilkins; Volume: 28; Issue: 6 Linguagem: Inglês

10.1097/ipc.0000000000000935

1536-9943

Jacobo Lester, Luis Gerardo López-Segovia, Armando Rojo, Carlos Behmaras, Carla García-Moreno,

Infectious Encephalopathies and Encephalitis

To the Editor: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters cells via angiotensin-converting enzyme 2 receptors, which are expressed on pulmonary epithelial cells and arterial and venous endothelial cells.1 In January 2020, angiotensin-converting enzyme 2 was identified as the functional receptor for SARS-CoV-2,2 the virus responsible for the pandemic that the world faces today. COVID-19 has been reported as causing thrombotic and neurological manifestations, including both ischemic and hemorrhagic strokes.3 This is the case of a 74-year-old right-handed patient with a personal history of systemic hypertension treated with angiotensin receptor blocker, successfully controlled. His condition initiated during sleep, suddenly waking up to a feeling of numbness and loss of strength of the right upper extremity of distal predominance, inability to emit language, and a feeling of instability when walking. After 20 minutes, the patient recovered his strength in the right arm and the numbness disappeared; speech was recovered after 2 hours. Exploration at the emergency room highlighted dysarthria, right central facial palsy, normal strength, generalized normal reflexes, and bilateral extensor plantar response. Incidentally, rest, postural and action tremor, rigidity, and bradykinesia predominantly on the left side were identified. Magnetic resonance imaging (MRI) showed an acute lacunar stroke (AIS) in the left precentral gyrus with mismatch (Fig. 1). Electroencephalogram findings showed left frontal and temporal slow and epileptic activity with electrical focus on F7.FIGURE 1: MRI was done at 3.0 T. A lacunar hyperacute stroke is depicted at the precentral left gyrus. It shows high signal in the diffusion-weighted images (DWIs) (b = 1000 s/mm2) and low signal in the apparent diffusion coefficient images (ADCs) (yellow arrows). There are no changes in the fluid attenuated inversion recovery images (FLAIRs). There is mismatch with the cerebral perfusion maps in which there is prolonged mean transit time (rMTT) in the precentral and postcentral left gyri, shown in the 3 contiguous slices (white arrows).As part of the patient approach, a transesophageal echocardiogram was requested, which showed left ventricle hypertrophy, along with an ejection fraction of 53% and small atheromatous plaques in the descending aorta without other relevant findings. Carotid Doppler ultrasound was performed, which found small stable atheroma plaques, with no hemodynamic repercussion. Antiphospholipid tests were negative. The patient was on continuous cardiac monitoring during 4 days of hospitalization, showing sinus rhythm, with no episodes of atrial fibrillation or other types of arrhythmia. Polymerase chain reaction (PCR) for SARS-CoV-2 was positive. Because of this result, a thorax computed tomography (CT) scan was performed; there were no signs of lung parenchyma affection. Treatment was based on anticoagulation, statin, and specific treatment with hydroxychloroquine; he was discharged after 5 days of hospitalization. At 2 months follow-up, the patient remains without added symptoms, with negative SARS-CoV-2 PCR controls. There are reports of COVID-19 cases with transient ischemic attack and AIS as clinical debuts. These patients presented pulmonary abnormalities on thorax CT scan, which were accompanied or not by respiratory symptoms.4 Our patient debuted with symptoms that suggested transient ischemic attack, with complete resolution after 2 hours; however, brain MRI showed an AIS responsible for the patient's clinical condition. Since the COVID-19 pandemic started, there have been reports of patients who debut4 with thromboembolic complications caused by SAR-CoV-2. These data suggest that 2.5% of infected patients experience AIS.5 For this reason, we requested a PCR for SARS-CoV-2, which was positive. Thorax CT scan results with no signs of pulmonary affection were reported. We excluded all cardiovascular causes, and thus, we considered that COVID-19 was the etiology of the lacunar stroke in the patient, who, after a 2-months follow-up, continued without systemic affection. We propose the hypothesis that lacunar stroke could be the sole presentation and manifestation of COVID-19 without necessarily requiring condition outside the central nervous system, causing a specific focal condition and not only being a thrombotic coexistence or coincidence as established by other reports.5 We consider this COVID-19 proposal to be very important as there are many patients without respiratory affection who may actually show other thrombotic or embolic symptoms in any part of the body without the infection being previously diagnosed. Jacobo Lester, MD Neurology Instituto Mexicano de Neurociencias Hospital Angeles Lomas Huixquilucan, Estado de México, México [email protected]Luis Gerardo López-Segovia, MD Internal Medicine Department Hospital Angeles Lomas Huixquilucan, Estado de México, MéxicoArmando Rojo, MD Infectology Hospital Angeles Lomas Huixquilucan, Estado de México, MéxicoCarlos Behmaras, MD Cardiology Hospital Angeles Lomas Huixquilucan, Estado de México, MéxicoCarla García-Moreno, MD Radiology/Magnetic Resonance Department Hospital Angeles Lomas Huixquilucan, Estado de México, México