Skip to main content

Two ischemic stroke events within 48 h: a case report of an unusual presentation of thrombotic thrombocytopenic purpura



Thrombotic thrombocytopenic purpura (TTP) considers a rare cause of ischemic stroke (IS). We reported a case of a newly diagnosed patient with acquired immune-mediated TTP (iTTP), in whom two IS events developed during 48 h.

Case presentation

A 59-year-old diabetic male was presented to the hospital 24 h after symptoms onset, including left hemiparesis, dysarthria, and decreased consciousness. A brain CT scan was performed with the suspicion of acute IS, indicating infarct lesions in the right middle cerebral artery (MCA) territory. The patient was not eligible for thrombolytic therapy due to admission delay. Over the next 24 h, the patient’s neurological condition deteriorated, and the second brain CT scan showed new ischemic lesions in the left MCA territory. Initial laboratory evaluation indicated thrombocytopenia without evidence of anemia. However, in the following days, thrombocytopenia progressed, and microangiopathic hemolytic anemia (MAHA) developed. The ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) activity and inhibitors assay confirmed the diagnosis of iTTP. The patient underwent plasma exchange activity and inhibitors assay confirmed the diagnosis of iTTP. The patient underwent and pulse IV methylprednisolone. Rituximab was also added due to the refractory course of the disease. After a prolonged hospital course, he had considerable neurologic recovery and was discharged.


Clinicians should consider two points. First, TTP should be considered in any patient presenting with IS and having thrombocytopenia or anemia without other symptoms of TTP. Second, worsening the patient's condition during hospitalization may indicate a new stroke and should be investigated immediately.

Peer Review reports


Coagulation disorders account for less than 5% of ischemic strokes (IS) [1]. Thrombotic thrombocytopenic purpura (TTP) is a rare, though severe, inherited or acquired disease caused by severe deficiency of the Von Willebrand factor-cleaving serine protease, ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) [2]. The exact incidence and prevalence figures are not available [3]. However, various numbers have been reported, from 2.2 cases per million population per year to 3.7 [4, 5] or even up to 13 cases per million population, according to a French national registry [6]. Patients with TTP might present with severe thrombotic events such as IS, either initially or during the treatment [7,8,9,10]. Stroke develops in 8.16% of patients admitted with TTP, according to the findings from the Nationwide Inpatient Sample (NIS), Healthcare Cost and Utilization Project (HCUP) [11]. Classic clinical manifestations include pentad of fever, microangiopathic hemolytic anemia (MAHA), thrombocytopenic purpura, renal dysfunction, and neurologic symptoms [3, 12]. Laboratory findings include thrombocytopenia and evidence of MAHA, including schistocytes, reticulocytosis, indirect hyperbilirubinemia, undetectable haptoglobin, and high lactate dehydrogenase (LDH) [12]. The diagnosis is suspected based on the clinical and laboratory findings and confirmed by very low ADAMTS-13 levels [12]. Of note, in the absence of other obvious causes, evidence of MAHA or thrombocytopenia without the presence of the classic pentad is strongly suggestive of TTP, hence the importance of immediate total plasma exchange (TPE) [13].

We reported a case of a newly diagnosed patient with acquired immune-mediated TTP (iTTP), in whom two IS events developed during a period of 48 h. This circumstance is unique in several ways. To begin with, iTTP is a rare disorder. Second, stroke is considered to be an unusual inaugural presentation of TTP. Third, there are currently very few reports of new ischemic lesions during hospitalization in individuals with iTTP following the first ischemic stroke event [14, 15]. Notably, some of these patients had the congenital type of the disease, making our patient even more intriguing.

Case presentation

A 59-year-old diabetic male was referred to our emergency room following left-sided weakness, hemifacial paresis, difficulty speaking, and drowsiness from one night before (National Institute of Health Stroke Score (NIHSS) at admission = 10). There was no history of recent head trauma. Family history of premature stroke or thrombotic events was also negative. The patient was a non-smoker, albeit an opiate user. The initial physical exam showed an elderly, confused male who could not answer the questions or follow commands cooperatively. Vitals were as follow: T = 37.4 °C, BP = 150/90 mmHG, HR = 73 bpm (beats per minute), RR = 16/minute, and O2 saturation in the room air = 97%. An electrocardiogram (ECG) showed normal sinus rhythm. On initial physical examination, no signs of pallor, jaundice, petechiae, or organomegaly were evident. Except for left facial paresis, cranial nerves examination was normal. Motor examination revealed left hemiparesis, with a force of 3/5 in the left upper extremity and 4/5 in the left lower extremity. The grimace to pinprick was reduced on the left side. The plantar reflex showed upward movement in the left side (Babinski sign).

Investigations and treatment

The patient underwent a brain CT scan with suspicion of IS. Of note, since the patient's symptoms had been initiated more than 24 h ago, he was not eligible to receive intravenous thrombolysis (IVT) or thrombectomy [16]. The first brain CT scan showed an acute stroke in the right middle cerebral artery (MCA) territory, including the right parietotemporal lobe infarct (Fig. 1). The patient's level of consciousness deteriorated over the next 24 h, necessitating further evaluation; the second brain CT scan revealed evidence of new ischemic lesions in the left MCA territory, including the left frontal lobe (Fig. 2). Progressive thrombocytopenia was found in the patient (initial platelet count: 77*\({10}^{3/}\mathrm{\mu L}\) reduced to 21*\({10}^{3/}\mathrm{\mu L}\)). Although the patient was not anemic at first (initial Hgb: 15 g/dL), evidence of hemolytic anemia gradually emerged, including a reticulocyte percentage of 2.6%, reduced Hgb (from 15 g/dL to 11.8 g/dL on day 6), indirect hyperbilirubinemia (total bilirubin 1.9 mg/dL increased up to 4.4 mg/dL, and indirect bilirubin 1.1 mg/dL increased up to 3.1 mg/dL), and elevated LDH (1148 U/L). Additionally, acute phase reactants, including ESR, CRP, ferritin, fibrinogen, and D-dimer, were also elevated. Troponin, coagulation tests, liver function tests, lipid profile, and electrolytes were normal. Peripheral blood smear (PBS) showed occasional schistocytes. Direct and indirect Coombs tests were negative. TTP diagnosis was highly suspected based on the patient’s clinical manifestations and progressive thrombocytopenia. Therefore further evaluation was performed, indicating an ADAMTS-13 activity level of 0.3 IU/mL (our laboratory cut-off for a positive value was < 0.4 IU/mL) and ADAMTS-13 inhibition screen of 18 U/mL (our laboratory cut-off for a positive value was > 15 U/mL), confirming the diagnosis of iTTP. Other Serologic evaluations (antinuclear antibody (ANA), anti-double strands DNA antibody (anti-dsDNA Ab), perinuclear anti-neutrophil cytoplasmic antibodies (P-ANCA), cytoplasmic anti-neutrophil cytoplasmic autoantibody (C-ANCA), rheumatoid factor (RF), complement 3 (C3), complement 4 (C4), anticardiolipin IgM and IgG antibodies, antiphospholipid IgM and IgG antibodies, and anti–Sjögren's-syndrome-related antigen A and B autoantibodies (SSA and SSB) were within normal limits. HIV, hepatitis B virus, and hepatitis C virus serology were also nonreactive (Table 1).

Fig. 1
figure 1

Brain CT scan on admission showed the right parietotemporal lobe infarct

Fig. 2
figure 2

Brain CT scan 24 h after admission showed a new infarct in the left frontal lobe

Table 1 The results of patients' laboratory evaluation at presentation, day 7 hospitalization, and discharge

Although the cardioembolic source of stroke was suspected due to the bihemispheric infarcts, ECG Holter monitoring, trans-thoracic, and trans-esophageal echocardiography revealed no signs of arrhythmia, clot, or vegetation, and the ejection fraction (EF) was 50–55%. Brain MRI on day 8 demonstrated evidence in favor of subacute infarctions with restriction and mild hemorrhagic transformation in the right parietotemporal, left frontal lobe, and left centrum semiovale (Fig. 3). There was no evidence of venous thrombosis or vascular lesions on magnetic resonance angiography (MRA) and magnetic resonance venography (MRV). Since malignant bone marrow infiltration is one of the main differential diagnoses in a patient with MAHA and thrombocytopenia [14], hematology was consulted. They asked for a bone marrow aspiration and biopsy (day 8), which showed normocellular marrow with increased erythroid series. Informed consent was obtained, and the patient underwent therapeutic plasma exchange (TPE) on day 8 with iTTP diagnosis. Consequently, the patient’s level of consciousness improved so that he was completely alert and responsive 9 days after TPE (day 17 hospitalization). The platelet count also gradually increased from 21*\({10}^{3/}\mathrm{\mu L}\) up to 91*\({10}^{3/}\mathrm{\mu L}\) a week after TPE initiation, although it again started to decrease. Hence, pulse IV methylprednisolone therapy was added on day 17 of hospitalization for 3 days, followed by oral prednisolone (1 mg/kg). Rituximab (750 mg/m2) was also initiated on day 30 of hospitalization. The patient's clinical condition, as well as the MAHA, gradually improved (NIHSS at discharge = 3), and the PLT count reached 189*\({10}^{3/}\mathrm{\mu L}\) at discharge (48 days of hospitalization, including 17 days at the stroke care unit (SCU), 5 days at the neurology ward, and 26 days at the hematology ward). During the follow-up, the neurological symptoms progressively improved, and he did not experience further relapses or report adverse effects. (modified Rankin Scale = 1, 75 days after discharge). The patient’s timeline is shown in Table 2.

Fig. 3
figure 3

Brain MRI on day 8 showed subacute infarctions with restriction and mild hemorrhagic transformation in the right parietotemporal, left frontal lobe, and left centrum semiovale; A: Diffusion-weighted imaging (DWI); B: Fluid attenuated inversion recovery (FLAIR); C: T1-weighted

Table 2 An overview of the patient’s timeline during hospitalization


In this study, we reported a 59-year-old male presented with hemiparesis, dysarthria, and decreased consciousness who developed two ischemic stroke events during 48 h, which is extremely rare. The results of neuroimaging revealed evidence of infarction in the right (at admission) and left (24 h after admission) MCA territories, respectively. Initial laboratory findings indicated progressive thrombocytopenia. However, MAHA was not found at presentation. Further evaluations, including measurement of ADAMTS-13 activity level and ADAMTS-13 inhibitor, confirmed the diagnosis of iTTP. The patient underwent therapeutic plasma exchange and pulse IV methylprednisolone therapy. Rituximab was also given since it could reduce relapses, and is increasingly recommended for use in refractory cases [17, 18]. Notably, studies showed that although iTTP considers an autoimmune disease, ADAMTS-13 inhibitors are not easily detectable in many patients [19], which was not the case in our patient. Similar to the prolonged course of treatment in our patient, studies showed that high titers of inhibitors of ADAMTS-13 are associated with delayed response to therapy, high risk of complications, and higher rates of refractory disease and relapses [19, 20]. Of note, while there are reports of patients with TTP who presented with IS as an atypical presentation [15, 21], there are very few reports of new ischemic lesions during hospitalization following the first ischemic stroke event [14, 15]. One was a 70-year-old female who presented with confusion, fever, and gastrointestinal symptoms who deteriorated neurologically during hospitalization, and the brain MRI revealed multiple acute and subacute infarcts in both cerebral hemispheres, midbrain, and right cerebellum. The patient had a history of hypertension, diabetes, rheumatoid arthritis, two miscarriages complicated by disseminated intravascular coagulation, two transient ischemic attacks, and a left occipital infarct and she was diagnosed with congenital TTP [14]. Another one was a 43-year-old female who was admitted with left hemiparesis, homonymous hemianopia, and dysarthria. The first brain CT showed an acute stroke in the right MCA territory, and follow-up MRIs during the first week of her hospitalization demonstrated new ischemic lesions in various territories [15].

TTP is a relapsing and life-threatening condition characterized by clot formation in small blood vessels [22]. Clinical manifestations vary from mild nonspecific symptoms to severe organ damages, including kidney and brain, and death [3]. Neurologic involvements, such as headaches, confusion, focal neurologic deficit, etc., are common as the initial presentation of TTP usually as a result of diffuse microthrombi formation in the microvasculature of the central nervous system (CNS), resulting in transient or permanent ischemic brain damage [3, 7,8,9, 23]. However, TTP considers a rare cause of ischemic stroke [15], although there are similar cases in the literature of patients being diagnosed with TTP after a cerebrovascular accident [9, 21, 24,25,26]. A recent study on patients with TTP who presented with neurological symptoms suggested that old age, hypertension, smoking, and high plasma concentrations of anti-ADAMTS-13 IgG may be the risk factors for developing cerebral infarction in these patients [27]. Furthermore, they reported no association between iTTP stroke and diabetes, however, our patient was diabetic [27]. Additionally, it is suggested that decreased level of ADAMTS-13 is associated with stroke recurrence after remission [28], hence the importance of patients’ follow-up.

A literature review conducted in 2018 reported 17 cases of IS due to iTTP [15]. Interestingly, none of the patients showed the classical TTP pentad, and wide non-specific heterogeneity in clinical manifestations was observed [15]. The combination of thrombocytopenia and hemolysis was found in less than half of the patients (41%). In 41% of cases, the stroke was multifocal and included major artery strokes, with proximal occlusion in 3 cases. Considerably, refractory and relapsing forms were observed in nearly half of the patients (47%). They reported small and large artery strokes in these patients, with the majority being multifocal and without a specific pattern [15]. These findings confirm the claim that although TTP is classified as a thrombotic microangiopathic condition, which results in small vessels obstruction, it should also be considered in patients with proximal intracranial artery occlusion [9, 15, 24, 29].


In alignment with previous studies, this study showed that although TTP is considered an uncommon cause of ischemic stroke, it should be considered in every IS patient with isolated anemia or thrombocytopenia even in the absence of other classic symptoms or laboratory findings. This study also suggests that clinicians should consider the possibility that worsening of the patient’s clinical condition could be attributed to emerging of new infarcts, emphasizing the importance of early diagnosis and treatment of iTTP to prevent multiple infarcts and a poor prognosis.

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.



A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13


Antinuclear antibody


Anti-double strands DNA


Beats per minute


Cytoplasmic antineutrophil cytoplasmic autoantibody


Central nervous system


Complement 3


Complement 4




Ejection fraction


Healthcare cost and utilization project




Ischemic stroke


Immune-mediated thrombotic thrombocytopenic purpura


Intravenous thrombolysis


Lactate dehydrogenase


Microangiopathic hemolytic anemia


Middle cerebral artery


Magnetic resonance angiography


Magnetic resonance venography


National institute of health stroke score


Nationwide inpatient sample


Perinuclear anti-neutrophil cytoplasmic antibodies


Peripheral blood smear


Rheumatoid factor


Sjögren's-syndrome-related antigen A


Sjögren's-syndrome-related antigen B


Therapeutic plasma exchange


Thrombotic thrombocytopenic purpura


  1. Fields MC, Levine SR. Thrombophilias and stroke: diagnosis, treatment, and prognosis. J Thromb Thrombolysis. 2005;20(2):113–26.

    Article  Google Scholar 

  2. Ferro JM, Infante J. Cerebrovascular manifestations in hematological diseases: an update. J Neurol. 2021;268(9):3480–92.

    Article  Google Scholar 

  3. Wun T. Thrombotic Thrombocytopenic Purpura (TTP). Medscape J Med. 2021.

  4. Miller DP, Kaye JA, Shea K, Ziyadeh N, Cali C, Black C, et al. Incidence of thrombotic thrombocytopenic purpura/hemolytic uremic syndrome. Epidemiology. 2004;15(2):208–15.

    Article  Google Scholar 

  5. Török TJ, Holman RC, Chorba TL. Increasing mortality from thrombotic thrombocytopenic purpura in the United States—analysis of national mortality data, 1968–1991. Am J Hematol. 1995;50(2):84–90.

    Article  Google Scholar 

  6. Mariotte E, Azoulay E, Galicier L, Rondeau E, Zouiti F, Boisseau P, et al. Epidemiology and pathophysiology of adulthood-onset thrombotic microangiopathy with severe ADAMTS13 deficiency (thrombotic thrombocytopenic purpura): a cross-sectional analysis of the French national registry for thrombotic microangiopathy. The Lancet Haematology. 2016;3(5):e237–45.

    Article  Google Scholar 

  7. Rinkel GJ, Wijdicks EF, Hené RJ. Stroke in relapsing thrombotic thrombocytopenic purpura. Stroke. 1991;22(8):1087–9.

    Article  CAS  Google Scholar 

  8. Downes KA, Yomtovian R, Tsai HM, Silver B, Rutherford C, Sarode R. Relapsed thrombotic thrombocytopenic purpura presenting as an acute cerebrovascular accident. J Clin Apher. 2004;19(2):86–9.

    Article  Google Scholar 

  9. Boattini M, Procaccianti G. Stroke due to typical thrombotic thrombocytopenic purpura treated successfully with intravenous thrombolysis and therapeutic plasma exchange. BMJ Case Rep. 2013;2013:bcr2012008426.

    Article  Google Scholar 

  10. Arboix A, Besses C. Cerebrovascular disease as the initial clinical presentation of haematological disorders. Eur Neurol. 1997;37(4):207–11.

    Article  CAS  Google Scholar 

  11. Subramanian KS, Kolte D, Syed RZ, Balasubramaniyam N, Palaniswamy C, Aronow WS, et al. Predictors of Stroke in Hospitalized Patients with Thrombotic Thrombocytopenic Purpura. Am Heart Assoc. 2013;6(Issue suppl_1):Abstract 201.

  12. Blennerhassett R, Curnow J, Pasalic L, editors. Immune-mediated thrombotic thrombocytopenic purpura: a narrative review of diagnosis and treatment in adults. Seminars in thrombosis and hemostasis; Thieme Medical Publishers. 2020;41(3):289-301.

  13. Coppo P, Veyradier A. Current management and therapeutical perspectives in thrombotic thrombocytopenic purpura. La Presse Medicale. 2012;41(3):e163–76.

    Article  Google Scholar 

  14. Tenison E, Asif A, Sheridan M. Congenital thrombotic thrombocytopenic purpura presenting in adulthood with recurrent cerebrovascular events. BMJ Case Rep. 2019;12(10):e229481.

    Article  Google Scholar 

  15. Tomich C, Debruxelles S, Delmas Y, Sagnier S, Poli M, Olindo S, et al. Immune-thrombotic thrombocytopenic purpura is a rare cause of ischemic stroke in young adults: case reports and literature review. J Stroke Cerebrovasc Dis. 2018;27(11):3163–71.

    Article  Google Scholar 

  16. Ghabaee M, Farahmand G, Balali P, Magrouni H, Alizadeh-Broujeni F, Amani K, et al. Modified 8Ds algorithm improves door-to-needle time in patients with acute ischemic stroke eligible for alteplase or thrombectomy: A prospective Cohort study. Journal of the Neurological Sciences. 2021;429:119710.

  17. Coppo P. Microangiopathies FRCfT. Treatment of autoimmune thrombotic thrombocytopenic purpura in the more severe forms. Transfus Apher Sci. 2017;56(1):52–6.

    Google Scholar 

  18. Jestin M, Benhamou Y, Schelpe A-S, Roose E, Provôt F, Galicier L, et al. Preemptive rituximab prevents long-term relapses in immune-mediated thrombotic thrombocytopenic purpura. Blood J Am Soc Hematol. 2018;132(20):2143–53.

    CAS  Google Scholar 

  19. Zheng XL, Kaufman RM, Goodnough LT, Sadler JE. Effect of plasma exchange on plasma ADAMTS13 metalloprotease activity, inhibitor level, and clinical outcome in patients with idiopathic and nonidiopathic thrombotic thrombocytopenic purpura. Blood. 2004;103(11):4043–9.

    Article  CAS  Google Scholar 

  20. Vesely SK, George JN, Lämmle B, Studt J-D, Alberio L, El-Harake MA, et al. ADAMTS13 activity in thrombotic thrombocytopenic purpura–hemolytic uremic syndrome: relation to presenting features and clinical outcomes in a prospective cohort of 142 patients. Blood. 2003;102(1):60–8.

    Article  CAS  Google Scholar 

  21. Badugu P, Idowu M. Atypical thrombotic thrombocytopenic purpura presenting as stroke. Case Rep Hematol. 2019;2019:7425320.

    Google Scholar 

  22. Joly BS, Coppo P, Veyradier A. Thrombotic thrombocytopenic purpura. Blood J Am Soc Hematol. 2017;129(21):2836–46.

    CAS  Google Scholar 

  23. Silverstein A. Thrombotic thrombocytopenic purpura: the initial neurologic manifestations. Arch Neurol. 1968;18(4):358–62.

    Article  CAS  Google Scholar 

  24. Sevy A, Doche E, Squarcioni C, Poullin P, Serratrice J, Nicoli F, et al. Stroke in a young patient treated by alteplase heralding an acquired thrombotic thrombocytopenic purpura. J Clin Apheresis. 2011;26(3):152–5.

    Article  Google Scholar 

  25. Vicente-Pascual M, Zamora-Martinez C, Amaro-Delgado S. Ischaemic stroke as the predecessor event of an episode of thrombotic thrombocytopenic purpura. Neurologia (Engl Ed). 2019;34(9):609–11.

    Article  CAS  Google Scholar 

  26. Acır İ, Erdoğan HA, Yayla V, Taşdemir N, Çabalar M. Incidental thrombotic thrombocytopenic purpura during acute ischemic stroke and thrombolytic treatment. J Stroke Cerebrovasc Dis. 2018;27(5):1417–9.

    Article  Google Scholar 

  27. Memon R, Sui J, Lin C, Zheng XL. Cerebral infarction in immune thrombotic thrombocytopenic purpura is associated with old age, hypertension, smoking, and anti-ADAMTS13 Ig, but not with mortality. TH Open. 2021;5(1):e1–7.

    Article  Google Scholar 

  28. Upreti H, Kasmani J, Dane K, Braunstein EM, Streiff MB, Shanbhag S, et al. Reduced ADAMTS13 activity during TTP remission is associated with stroke in TTP survivors. Blood. 2019;134(13):1037–45.

    Article  CAS  Google Scholar 

  29. Sugarman R, Tufano AM, Liu JM. Large vessel stroke as initial presentation of thrombotic thrombocytopenic purpura. BMJ Case Rep. 2018;2018:bcr2017221857.

    Article  Google Scholar 

  30. Association WM. World medical association declaration of helsinki: ethical principles for medical research involving human subjects. JAMA. 2013;310(20):2191–4.

    Article  Google Scholar 

Download references


We would like to thank the patient and his brother for their participation and consent for publication.


The authors received no financial support for the research, authorship, and publication of this manuscript.

Author information

Authors and Affiliations



HA and MG provided the patient with appropriate treatment according to the guidelines. SH collected the data and had a major role in the patient’s treatment. MJ assisted with the patient’s follow-up and was a major contributor in writing the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Hamed Amirifard.

Ethics declarations

Ethics approval and consent to participate

This study was conducted at an academic hospital complex affiliated with Tehran University of Medical Sciences (TUMS), Tehran, Iran, and approved by the ethics committee of the university. Written informed consent was obtained from the patient. This study was conducted according to the Declaration of Helsinki [30].

Consent for publication

The patient provided written informed consent for the submission and possible publication of this manuscript. During the patient's hospitalization, consent for treatment was also obtained in the usual manner.

Competing interest

There are no conflicts of interest.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Jameie, M., Heydari, S., Ghabaee, M. et al. Two ischemic stroke events within 48 h: a case report of an unusual presentation of thrombotic thrombocytopenic purpura. BMC Neurol 23, 47 (2023).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: