Importance: Reported cerebrovascular events in patients with COVID-19 are mainly ischemic, but hemorrhagic strokes and cerebral venous sinus thrombosis (CSVT), especially in critically ill patients, have also been described. To date, it is still not clear whether cerebrovascular manifestations are caused by direct viral action or indirect action mediated by inflammatory hyperactivation, and in some cases, the association may be casual rather than causal. Objective: To conduct a systematic review on the cerebrovascular events in COVID-19 infection. Evidence review: A comprehensive literature search on PubMed was performed including articles published from January 1, 2020, to July 23, 2020, using a suitable keyword strategy. Additional sources were added by the authors by reviewing related references. The systematic review was conducted in accordance with the PRISMA guidelines. Only articles reporting individual data on stroke mechanism and etiology, sex, age, past cardiovascular risk factors, COVID symptoms, admission NIHSS, D-dimer levels, and acute stroke treatment were selected for the review. Articles that did not report the clinical description of the cases were excluded. A descriptive statistical analysis of the data collected was performed. Finding: From a total of 1,210 articles published from January 1, 2020, to July 23, 2020, 80 articles (275 patients), which satisfied the abovementioned criteria, were included in this review. A total of 226 cases of ischemic stroke (IS), 35 cases of intracranial bleeding, and 14 cases of CVST were found. Among patients with IS, the mean age was 64.16 ±14.73 years (range 27-92 years) and 53.5% were male. The mean NIHSS score reported at the onset of stroke was 15.23 ±9.72 (range 0-40). Primary endovascular thrombectomy (EVT) was performed in 24/168 patients (14.29%), intravenous thrombolysis (IVT) was performed in 17/168 patients (10.12%), and combined IVT+EVT was performed in 11/168 patients (6.55%). According to the reported presence of large vessel occlusion (LVO) (105 patients), 31 patients (29.52%) underwent primary EVT or bridging. Acute intracranial bleeding was reported in 35 patients: 24 patients (68.57%) had intracerebral hemorrhage (ICH), 4 patients (11.43%) Fraiman et al. COVID-19 and Cerebrovascular Diseases had non-traumatic subarachnoid hemorrhage (SAH), and the remaining 7 patients (20%) had the simultaneous presence of SAH and ICH. Fourteen cases of CVST were reported in the literature (50% males), mean age 42.8 years ±15.47 (range 23-72). Treatment was reported only in nine patients; seven were treated with anticoagulant therapy; one with acetazolamide, and one underwent venous mechanical thrombectomy. Conclusion: Cerebrovascular events are relatively common findings in COVID-19 infection, and they could have a multifactorial etiology. More accurate and prospective data are needed to better understand the impact of cerebrovascular events in COVID-19 infection.
Amyloid Protein Precursor gene duplication is a rare cause of early-onset Alzheimer's disease that can be associated with Cerebral Amyloid Angiopathy. This condition predisposes cerebrovascular events, specifically, intracerebral hemorrhagic stroke. This report describes a case of first-time intracerebral hemorrhage in a patient with APP gene duplication during SARS-CoV-2 infection, a typically pro-thrombotic and pro-inflammatory condition, as a possible trigger for this condition.
A 56-year-old woman developed progressive subacute lower limb weakness with sensory and autonomic abnormalities. She had received a living-donor kidney transplantation 21 years before for end-stage chronic kidney disease and took mycophenolate mofetil and prednisolone. MR scan of the spinal cord showed bilateral cauda equina gadolinium enhancement and MR scan of the brain showed enhancing nodular hyperintensities in the internal capsule and globus pallidus. Cerebrospinal fluid (CSF) showed a pleocytosis with extremely low glucose, and positive DNA-PCR for Epstein-Barr virus. Her condition worsened despite empirically guided antimicrobial treatment. CSF immunophenotyping later identified mature, clonal B lymphocytes of large size, expressing CD19, CD20, CD200 antigens, and kappa light chain immunoglobulin, with absent CD5 and CD10 expression. We diagnosed a myeloradiculopathy from a monomorphic post-transplant lymphoproliferative disorder. This condition occurs after kidney transplantation and falls on the lymphoma spectrum. We review its clinical features, diagnosis and management.
Introduction: Aceruloplasminemia is a rare autosomal recessive disorder, characterized by transmembrane cerulopasmin deficiency. Impaired iron metabolism occurs, leading to its systemic accumulation, including brain. This is a case report based on retrospective analysis of a single patient’s medical record. Case report: This case reports a 57-year-old female, previously functional, with metabolic syndrome, admitted due to dystonia and ataxia with compound heterozygosis for ACP gene. Over the course of two years and six months, she manifested: depression, anedhonia, some instrumental activities limitations, plus walking and speech disturbances. Her physical examination presented disorientation in time/space, dysarthrophonia, saccadic intrusions, dysdiadocokinesia, enlarged base gait, oral dyskinesia and cervical dystonia. Brian magnetic resonance image (MRI) demonstrated GRE/SWI signal attenuation diffusely in cortex and bilaterally in lentiform and caudate nucleus. Laboratory tests: ferritin 2.540 ng/ml; serum iron 27 ug/dL; serum ceruloplasmine below 8 mg/dL; negative infectious and rheumatological serologies; normal levels of cobalamin, hemoglobin and thyroid hormones. Genetic testing confirmed compound heterozygosis for ACP gene (variant C1149 G>A |p.trp 383*), compatible with the aceruloplasminemia hypothesis. Conclusion: Attention should be drawn to this patient’s MRI showing SWI hyposignal on basal ganglia and cortex, because it’s a highly suggestive finding. Individual case reports indicate the effectiveness of Deferiprone as a treatment in individuals with aceruloplasminemia, however there is no universally accepted treatment regimen.
Introduction: Quetiapine, an atypical antipsychotic, works through the agonism of multiple brain receptors, including dopaminergic, serotonergic, and adrenergic receptors. Compared to typical antipsychotics, quetiapine has a more favorable profile of adverse reactions. Myoclonus is infrequent. However, there have been reports of quetiapine overdose associated with generalized myoclonus. Electroencephalogram (EEG) modifications linked to the use of quetiapine are unusual. Aldicarb, commonly known as ‘chumbinho’ in Brazil, is a carbamate used as a rodenticide. Its toxicity is caused by the inhibition of acetylcholinesterase. A few reported cases of myoclonus related to its use may be due to the anticholinesterase effect causing hyperactivity. This is a case report based on retrospective analysis of the patient’s records. Case report: A 23-year-old woman was admitted after a suicide attempt by ingesting carbamate and quetiapine 36 hours after the attempt. Her initial symptoms were vomiting and sialorrhea, followed by generalized tonic-clonic seizures and coma. At admission, she was already sedated with midazolam, with her last tonic-clonic generalized seizure two hours earlier. Her pupils were myotic, with persistent tachycardia and diffuse muscular hyperexcitability – clonic movements were evoked with minimal stimuli. Brain imaging and cerebrospinal fluid analysis showed no alterations. A loading dose of 20 mg/kg of phenytoin was administered. Upon admission, an EEG showed status myoclonus. Midazolam was then titrated to 0.8 mg/kg/h, and clobazam (30 mg/day) and levetiracetam (1.500 mg/day) were added, with resolution of the status epilepticus after three days. Conclusion: Status epilepticus should be considered a possible presentation of quetiapine and carbamate intoxication.
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