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The Neurologist Sep 2022Neurological manifestations of acute lymphoblastic leukemia (ALL) have been reported as cranial neuropathies or meningeal symptoms most common in children. However, ALL...
INTRODUCTION
Neurological manifestations of acute lymphoblastic leukemia (ALL) have been reported as cranial neuropathies or meningeal symptoms most common in children. However, ALL can rarely involve the nerve roots causing symmetrical polyradiculopathy which can present with rapid onset paralysis, mimicking Guillain-Barré Syndrome (GBS). The symmetrical polyradiculopathy can be the earliest manifestation of ALL occurring even before the hematological and systemic manifestations.
CASE REPORT
We report a case of a healthy 29-year-old man who presented with subacute bilateral lower extremity weakness and numbness preceded by a respiratory infection. He was initially treated as a suspected (GBS) but cerebrospinal fluid (CSF) findings suggested an alternative diagnosis. His prior TB exposure created a diagnostic confusion. Lumbar spine magnetic resonance imaging revealed nerve root enhancements at L4-L5 and L5-S1 that are seen in GBS and TB arachnoidids. Brain magnetic resonance imaging demonstrated bilateral distention of the optic nerve sheath complexes with CSF suggestive of intracranial hypertension. CSF revealed elevated protein, nucleated cells 2145 leukocytes/mm 3 , numerous atypical lymphoid cells. He was later diagnosed with ALL associated symmetrical polyradiculopathy presenting with GBS-like symptoms.
CONCLUSION
Symmetrical polyradiculopathy is a rare complication of ALL and can be confused with acute inflammatory demyelinating polyneuropathy. ALL associated polyradiculopathy in young individuals can be clinically indistinguishable from GBS. Our case highlights that when CSF findings are atypical for GBS, ALL should be considered on the differential diagnosis in patients presenting with GBS like symptoms.
Topics: Adult; Child; Cranial Nerve Diseases; Guillain-Barre Syndrome; Humans; Male; Muscle Weakness; Polyradiculopathy; Precursor Cell Lymphoblastic Leukemia-Lymphoma
PubMed: 34855661
DOI: 10.1097/NRL.0000000000000397 -
Veterinary Pathology May 2023Ocular involvement in systemic diseases is frequent in cats; however, without concurrent clinical and ophthalmic examinations with gross and/or histologic analysis of...
Ocular involvement in systemic diseases is frequent in cats; however, without concurrent clinical and ophthalmic examinations with gross and/or histologic analysis of the eye, these findings can be underdiagnosed. This article aims to provide gross, histologic, and immunohistochemical characteristics of ocular lesions from cats submitted to necropsy, focusing on those caused by systemic infectious agents. Cats that died due to a systemic infectious disease were selected based on necropsy diagnosis and presence of ocular lesions. Gross, histologic, and immunohistochemical findings were recorded. From April 2018 to September 2019, 849 eyes of 428 cats were evaluated. Histologic abnormalities were seen in 29% of cases, which were classified as inflammatory (41%), neoplastic (32%), degenerative (19%), and metabolic/vascular (8%). Macroscopic changes were present in one-third of eyes with histologic lesions. Of these, 40% were attributed to inflammatory or neoplastic diseases associated with infectious agents. The most important infectious agents causing ocular disease in this study were feline leukemia virus, feline infectious peritonitis virus, and sp. The most common ocular abnormalities associated with infectious agents were uveitis (anterior, posterior, or panuveitis), optic neuritis, and meningitis of the optic nerve. Ocular lesions secondary to systemic infections in cats are frequent; however, these are not always diagnosed because gross lesions are less common than histologic lesions. Therefore, both gross and histologic evaluation of the eyes of cats is recommended, mainly for cases in which the clinical suspicion or necropsy diagnosis suggests that an infectious agent might be related to the cause of death.
Topics: Cats; Animals; Eye; Uveitis; Neoplasms; Sepsis; Communicable Diseases; Cat Diseases; Feline Infectious Peritonitis
PubMed: 36869834
DOI: 10.1177/03009858231158075 -
The Lancet. Child & Adolescent Health Mar 2020Leptomeningeal malignancy complicates childhood cancers, including leukaemias, brain tumours, and solid tumours. In leukaemia, such malignancy is thought to invade... (Review)
Review
Leptomeningeal malignancy complicates childhood cancers, including leukaemias, brain tumours, and solid tumours. In leukaemia, such malignancy is thought to invade leptomeninges via the vascular route. In brain tumours, dissemination from the primary tumour, before or after surgery, via CSF pathways is assumed; however, evidence exists to support the vascular route of dissemination. Success in treating leptomeningeal malignancy represents a rate-limiting step to cure, which has been successfully overcome in leukaemia with intensified systemic therapy combined with intra-CSF therapy, which replaced cranial radiotherapy for many patients. This de-escalated CNS-directed therapy is still associated with some neurotoxicity. The balanced benefit justifies exploration of ways to further de-escalate CNS-directed therapy. For primary brain tumours, standard therapy is craniospinal radiotherapy, but attendant risk of acute and delayed brain injury and endocrine deficiencies compounds post-radiation impairment of spinal growth. Alternative ways of treating leptomeninges by intensifying drug therapy delivered to CSF are being investigated-preliminary evidence suggests improved outcomes. This Review seeks to describe methods of intra-CSF drug delivery and drugs in use, and consider how the technique could be modified and additional drugs might be selected for this route of administration.
Topics: Brain; Brain Neoplasms; Clinical Trials as Topic; Craniospinal Irradiation; Drug Delivery Systems; Drug Therapy, Combination; Endocrine System; Humans; Leukemia; Meningeal Neoplasms; Neurotoxicity Syndromes; Spine
PubMed: 31958415
DOI: 10.1016/S2352-4642(19)30333-5 -
Chinese Medical Journal Sep 2019
Topics: Brain; Female; Humans; Leukemia, Myeloid, Acute; Male; Meningeal Neoplasms; Meningioma; Neoplasm Proteins; Prognosis
PubMed: 31478925
DOI: 10.1097/CM9.0000000000000398 -
BMJ Case Reports Mar 2020Herein we report a case of a 67-year-old man with chronic lymphocytic leukaemia who developed acute onset of fever and altered mental status while receiving ibrutinib...
Herein we report a case of a 67-year-old man with chronic lymphocytic leukaemia who developed acute onset of fever and altered mental status while receiving ibrutinib therapy. He was eventually found to have meningitis. Timely diagnosis and appropriate antimicrobial therapy was associated with a favourable outcome. We describe challenges associated with appropriate identification of, and briefly review infections caused by sp. To our knowledge, this is the first case of invasive infection in the setting of ibrutinib therapy, and adds to the growing list of serious infections that have been associated with this agent.
Topics: Adenine; Aged; Anti-Infective Agents; Capnocytophaga; Diagnosis, Differential; Gram-Negative Bacterial Infections; Humans; Leukemia, Lymphoid; Male; Meningitis, Bacterial; Piperidines; Pyrazoles; Pyrimidines
PubMed: 32193175
DOI: 10.1136/bcr-2019-231825 -
Experimental Cell Research Apr 2024A major obstacle in improving survival in pediatric T-cell acute lymphoblastic leukemia is understanding how to predict and treat leukemia relapse in the CNS. Leukemia...
A major obstacle in improving survival in pediatric T-cell acute lymphoblastic leukemia is understanding how to predict and treat leukemia relapse in the CNS. Leukemia cells are capable of infiltrating and residing within the CNS, primarily the leptomeninges, where they interact with the microenvironment and remain sheltered from systemic treatment. These cells can survive in the CNS, by hijacking the microenvironment and disrupting normal functions, thus promoting malignant transformation. While the protective effects of the bone marrow niche have been widely studied, the mechanisms behind leukemia infiltration into the CNS and the role of the CNS niche in leukemia cell survival remain unknown. We identified a dysregulated gene expression profile in CNS infiltrated T-ALL and CNS relapse, promoting cell survival, chemoresistance, and disease progression. Furthermore, we discovered that interactions between leukemia cells and human meningeal cells induced epigenetic alterations, such as changes in histone modifications, including H3K36me3 levels. These findings are a step towards understanding the molecular mechanisms promoting leukemia cell survival in the CNS microenvironment. Our results highlight genetic and epigenetic alterations induced by interactions between leukemia cells and the CNS niche, which could potentially be utilized as biomarkers to predict CNS infiltration and CNS relapse.
Topics: Child; Humans; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma; Cell Survival; Precursor Cell Lymphoblastic Leukemia-Lymphoma; T-Lymphocytes; Recurrence; Cell Cycle; Tumor Microenvironment
PubMed: 38561062
DOI: 10.1016/j.yexcr.2024.114015 -
Journal of Neurosurgery. Case Lessons Jun 2021Acute promyelocytic leukemia (APL) has long been associated with coagulation disorders. The proposed mechanism is a combination of fibrinolysis, proteolysis, platelet...
Concomitant central venous sinus thrombosis and subdural hematoma in acute promyelocytic leukemia: middle meningeal artery embolization enables safe anticoagulation. Illustrative case.
BACKGROUND
Acute promyelocytic leukemia (APL) has long been associated with coagulation disorders. The proposed mechanism is a combination of fibrinolysis, proteolysis, platelet dysfunction, thrombocytopenia, and possibly disseminated intravascular coagulation. Hemorrhagic complications are prominent.
OBSERVATIONS
In this case, a 25-year-old female with newly diagnosed APL developed extensive cerebral venous thrombosis (CVT) and was initiated on a protocol with idarubicin and all- retinoic acid. The general recommendation for treating CVT is anticoagulation to stabilize the existing thrombus and prevent propagation. The patient was initiated on a heparin drip, but her clinical course was complicated by subdural hemorrhage (SDH) and epidural hemorrhage in the setting of thrombocytopenia. Anticoagulation was held, and her CVT propagated on follow-up imaging. To restart anticoagulation for CVT with a limited risk of SDH, the authors pursued middle meningeal artery (MMA) embolization. The patient was transitioned to apixaban and discharged to home.
LESSONS
MMA embolization enables safe anticoagulation in patients with concomitant CVT and SDH. The authors report the complex clinical course and effective management of this rare clinical scenario.
PubMed: 36046512
DOI: 10.3171/CASE2080 -
Annals of Palliative Medicine Sep 2020This study was conducted to summarize the clinical, magnetic resonance imaging (MRI) and pathological features of IgG4-realated hypertrophic pachymeningitis (IgG4-RHP)...
BACKGROUND
This study was conducted to summarize the clinical, magnetic resonance imaging (MRI) and pathological features of IgG4-realated hypertrophic pachymeningitis (IgG4-RHP) and its differential diagnosis from similar diseases.
METHODS
Data of IgG4-RHP patients admitted to Department of Neurology, Neurosurgery and Infection, the First Affiliated Hospital of Medical School of Zhejiang University from January 1, 2015 to July 31, 2019 were collected and their clinical symptoms, laboratory examinations, imaging and pathological features were investigated. At the same time, the clinicopathological and imaging findings of other dura thickening diseases diagnosed in our hospital were compared and analyzed.
RESULTS
The clinical symptoms of 4 IgG4-RHP patients include chronic headache and cranial nerves injury, etc. Levels of serum IgG4 and cerebrospinal fluid (CSF) IgG4 increased in all patients. Focal enhancement of dura mater could be seen on plain and enhanced cranial MRI. Pathological results were consistent with IgG4-RHP symptoms. Among other diseases that cause dural thickening, the content of serum C-reactive protein in patients with Rosai-Dorfman disease declined. Patients with intracranial hypotension syndrome often have postural headache. Patients with tuberculous meningitis can have previous pulmonary tuberculosis. The diagnosis of patients with atypical meningioma depends on the results of operation and pathology. Patients with central nervous system leukemia can be diagnosed with reference to the results of laboratory results.
CONCLUSIONS
The clinicopathological and imaging manifestations of IgG4-RHP are summarized in this study. Meanwhile, the clinical data of several other diseases with similar imaging characteristics are analyzed in order to clarify the diagnostic strategy of IgG4-RHP and provide help for the next treatment.
Topics: Humans; Hypertrophy; Immunoglobulin G; Magnetic Resonance Imaging; Meningitis; Skull
PubMed: 32819129
DOI: 10.21037/apm-19-452 -
Cureus Jun 2020is a multidrug-resistant gram-positive bacterium of the human skin flora and one of the most clinically important nondiphtherial corynebacteria in the acute care...
is a multidrug-resistant gram-positive bacterium of the human skin flora and one of the most clinically important nondiphtherial corynebacteria in the acute care setting. can cause different forms of infections, especially in immunocompromised patients with underlying risk factors and comorbidities. was initially described in 1976 as a highly resistant coryneform bacteria causing severe sepsis in patients with hematologic malignancies and profound neutropenia. infection has also been reported in the setting of endocarditis, septicemia, meningitis, pneumonia, and soft tissue infections. Management of disseminated infection in immunocompromised cancer patients can be challenging due to its high virulence and rapid skin colonization. We present two cases of disseminated infection in patients with acute myelogenous leukemia (AML) and underlying comorbidities. Both patients presented with neutropenic fever resistant to initial standard empiric antibiotic therapy.
PubMed: 32714702
DOI: 10.7759/cureus.8764 -
British Journal of Haematology May 2020Central nervous system (CNS) relapse is a common cause of treatment failure in patients with acute lymphoblastic leukaemia (ALL) despite current CNS-directed therapies...
Central nervous system (CNS) relapse is a common cause of treatment failure in patients with acute lymphoblastic leukaemia (ALL) despite current CNS-directed therapies that are also associated with significant short- and long-term toxicities. Herein, we showed that leukaemia cells exhibit decreased proliferation, elevated reactive oxygen species (ROS) and increased cell death in cerebral spinal fluid (CSF) both in vitro and in vivo. However, interactions between leukaemia and meningeal cells mitigated these adverse effects. This work expands our understanding of the pathophysiology of CNS leukaemia and suggests novel therapeutic approaches for more effectively targeting leukaemia cells in the CNS.
Topics: Humans; Meninges; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Survival Analysis
PubMed: 31930492
DOI: 10.1111/bjh.16270