scholarly journals Iatrogenic Kaposi’s sarcoma following immunosuppressive treatment of the recurrent longitudinally extensive transverse myelitis

2018 ◽  
Vol 146 (5-6) ◽  
pp. 312-315
Author(s):  
Jovan Lalosevic ◽  
Dusan Skiljevic ◽  
Irena Dujmovic ◽  
Jelena Drulovic ◽  
Ljiljana Medenica
Keyword(s):  
Immunosuppressive Treatment ◽  
Transverse Myelitis ◽  
Central Nervous System Disease ◽  
Skin Lesions ◽  
Efficient Treatment ◽  
System Disease ◽  
First Case ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Significant Regression ◽  
Extensive Transverse Myelitis

Introduction. Iatrogenic Kaposi?s sarcoma (KS) represents a multifocal, angioproliferative tumor that develops in patients undergoing immunosuppressive treatment and is considered to be induced by activation of latent human herpes virus type 8 (HHV8) infection. The aim of this report is to present a patient with iatrogenic KS due to immunosuppressive treatment. Case outline. We present a 69-year-old male non-HIV patient, previously treated for anti-aquaporin-4 antibody negative recurrent longitudinal extensive transverse myelitis with prednisolone and azathioprine for one year. The patient developed bluish and violet plaques and nodules on his face, trunk, and extremities. Skin biopsy findings (histopathology and immunohistochemical detection of CD31 expression and anti-HHV8 antibodies in the spindle cells) confirmed the diagnosis of KS. The reduction of immunosuppression and topical treatment with imiquimod resulted in a partial but significant regression of skin lesions, but the patient had another relapse of myelitis following the cessation of azathioprine and a reduction in the dose of prednisolone. Conclusion. To the best of our knowledge, this is the first case of an inflammatory and demyelinating central nervous system disease treated with corticosteroids and azathioprine that was associated with iatrogenic KS. The efficient treatment of both conditions is highly challenging and can be troublesome in specific cases.

scholarly journals Longitudinal extensive transverse myelitis following ChAdOx1 nCOV-19 vaccine: a case report

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wee Yong Tan ◽  
Abdul Hanif Khan Yusof Khan ◽  
Mohd Naim Mohd Yaakob ◽  
Anna Misyail Abdul Rashid ◽  
Wei Chao Loh ◽  
...  
Keyword(s):  
Transverse Myelitis ◽  
Neurological Complications ◽  
High Dose ◽  
Sensory Level ◽  
Limb Weakness ◽  
Efficacy Trials ◽  
First Case ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Magnetic Resonance Imaging Mri ◽  
Extensive Transverse Myelitis

Abstract Background Transverse myelitis (TM) is a relatively uncommon condition, and vaccine-associated myelitis is even rarer. Concern regarding neurological complications following vaccination escalated following the report of TM during the safety and efficacy trials of the COVID-19 vaccine. Case presentation We report the first case of Longitudinal Extensive Transverse Myelitis (LETM) in Malaysia following administration of the chimpanzee adenovirus-vectored (ChAdOx1 nCoV-19) vaccine. A 25-year-old female presented with bilateral lower limb weakness and inability to walk with a sensory level up to T8 with absent visual symptoms. Urgent gadolinium-enhanced magnetic resonance imaging (MRI) of the spine showed long segment TM over the thoracic region. Cerebrospinal fluid autoantibodies for anti-aquaporin-4 and anti-myelin-oligodendrocyte were negative. A diagnosis of LETM following vaccination was made, and the patient was started on a high dose of intravenous methylprednisolone. The patient eventually made a recovery following treatment. Conclusion LETM is a rare but serious adverse reaction following vaccination. Previously reported cases showed an onset of symptoms between 10 to 14 days post-vaccination, suggesting a delayed immunogenic reaction. However, the incidence of myelitis in COVID-19 is much more common, far greater than the risk associated with vaccination.

Longitudinal Extensive Transverse Myelitis following T-ALL

2016 ◽  
Vol 47 (S 01) ◽  
Author(s):  
V. Kraus ◽  
C. Makowski ◽  
H. Jünger ◽  
A. Wawer ◽  
P. Strotmann ◽  
...  
Keyword(s):  
Transverse Myelitis ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Extensive Transverse Myelitis

Neuromyelitis optica spectrum disorder (NMOSD) presenting as acute transverse myelitis with positive aquaporin 4 antibodies

2021 ◽  
Vol 14 (1) ◽  
pp. e238992
Author(s):  
Katherine Thornley ◽  
Carlo Canepa
Keyword(s):  
Spinal Cord ◽  
Transverse Myelitis ◽  
Aquaporin 4 ◽  
Sensory Level ◽  
Mri Scan ◽  
Acute Transverse Myelitis ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Oral Steroids ◽  
Extensive Transverse Myelitis

An 80-year-old, previously healthy patient presents with acute transverse myelitis with sensory level at T8. The MRI scan of the spinal cord showed longitudinal extensive transverse myelitis, and she tested positive for aquaporin 4 antibodies in serum. She received treatment with intravenous and oral steroids, with no improvement and then underwent plasma exchange. She was then started on azathioprine for prevention of relapses, while continuing physiotherapy and occupational therapy. Eventually, she was transferred to a specialised spinal cord centre for long-term rehabilitation.

Evaluation of brain and spinal cord lesion distribution criteria at disease onset in distinguishing NMOSD from MS and MOG antibody-associated disorder

2020 ◽  
pp. 135245852093900 ◽  
Author(s):  
Meng-Ting Cai ◽  
Yang Zheng ◽  
Chun-Hong Shen ◽  
Fan Yang ◽  
Wei Fang ◽  
...  
Keyword(s):  
Chinese Population ◽  
Diagnostic Performance ◽  
Disease Onset ◽  
Transverse Myelitis ◽  
Performance Accuracy ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Periventricular Lesions ◽  
Brain And Spinal Cord ◽  
Aquaporin 4 Antibody ◽  
Extensive Transverse Myelitis

Objective: To validate the recently proposed imaging criteria in distinguishing aquaporin-4 antibody (AQP4-ab)-seropositive neuromyelitis optica spectrum disorder (NMOSD) from multiple sclerosis (MS) and myelin oligodendrocyte glycoprotein antibody-associated disorder (MOG-AD) at disease onset in a Chinese population. Methods: We enrolled 241 patients in this retrospective study, including 143 AQP4-ab-seropositive NMOSD, 73 MS, and 25 MOG-AD. Cacciaguerra’s criteria were described as fulfillment of at least 2/5 conditions including the absence of the combined juxtacortical/cortical lesions, the presence of longitudinal extensive transverse myelitis (LETM) lesions, the presence of periependymal-lateral ventricles lesions, the absence of Dawson’s fingers lesions, and the absence of periventricular lesions. Results: Fulfillment of at least 3/5 conditions was able to differentiate NMOSD from MS with a good diagnostic performance (accuracy = 0.92, sensitivity = 0.91, specificity = 0.93), yet failed to differentiate NMOSD from MOG-AD. LETM lesions showed the highest accuracy (0.78), sensitivity (0.70), and specificity (0.97) for NMSOD. Conclusion: Our research suggested the utility of Cacciaguerra’s criteria in a Chinese population at disease onset. A better diagnostic performance in NMOSD could be attained with at least 3/5 conditions fulfilled. Yet their utility in distinguishing NMOSD from MOG-AD was limited.

Tubercular longitudinally extensive transverse myelitis with lower motor neuron paralysis

2020 ◽  
pp. 004947552095644
Author(s):  
Manjeet Kumar Goyal ◽  
Mahesh Lal
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Spinal Tuberculosis ◽  
Transverse Myelitis ◽  
Lower Motor Neuron ◽  
Neuron Type ◽  
Longitudinally Extensive Transverse Myelitis ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Spinal Segments ◽  
Extensive Transverse Myelitis

Transverse myelitis typically extends two or less spinal segments, whereas longitudinal extensive transverse myelitis (LETM) extends three or more spinal segments in length and may occasionally span all the segments of the spinal cord. We present a case of spinal tuberculosis presenting with LETM with true lower motor neuron-type flaccid paraplegia.

Longitudinal extensive transverse myelitis—it's not all neuromyelitis optica

2011 ◽  
Vol 7 (12) ◽  
pp. 688-698 ◽  
Author(s):  
Corinna Trebst ◽  
Peter Raab ◽  
Elke Verena Voss ◽  
Paulus Rommer ◽  
Mazen Abu-Mugheisib ◽  
...  
Keyword(s):  
Neuromyelitis Optica ◽  
Transverse Myelitis ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Extensive Transverse Myelitis

scholarly journals Case Report: Longitudinal Extensive Transverse Myelitis With Novel Autoantibodies Following Two Rounds of Pembrolizumab

2021 ◽  
Vol 12 ◽  
Author(s):  
Salma Charabi ◽  
Lotte Engell-Noerregaard ◽  
Anna Christine Nilsson ◽  
Christian Stenör
Keyword(s):  
Death Receptor ◽  
Transverse Myelitis ◽  
Immunofluorescence Assay ◽  
Treatment Regimens ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Neuronal Autoantibodies ◽  
Radiological Response ◽  
Magnetic Resonance Imaging Mri ◽  
Underlying Pathophysiology ◽  
Extensive Transverse Myelitis

A 63-year-old male with metastatic non-small cell lung cancer developed longitudinal extensive transverse myelitis (LETM) following two cycles of Pembrolizumab, an immune checkpoint inhibitor (ICI) targeting the programmed cell death receptor 1 (PD-1). Magnetic resonance imaging (MRI) showed centromedullary contrast enhancement at several levels, cerebrospinal fluid (CSF) cytology showed lymphocytic pleocytosis, and indirect immunofluorescence assay (IFA) on the primate cerebellum, pancreas, and intestine revealed strong binding of neuronal autoantibodies to unknown antigens. CSF C–X–C motif ligand 13 (CXCL13) was elevated. The patient was treated with plasma exchange (PEX) and intravenous (i.v.) methylprednisolone (MP) 1 g/day for 5 days followed by oral (p.o.) MP 100 mg/day for 10 days with clinical and radiological response. However, after discontinuation of MP, LETM relapsed and the patient developed paralytic ileus presumably due to autoimmune enteropathy and suffered a fatal gastrointestinal sepsis. Findings of novel neuronal autoantibodies and highly elevated CXCL13 in CSF suggest that the severe neurological immune-related adverse event (nirAE) was B-cell mediated contrary to the commonly assumed ICI-induced T-cell toxicity. An individual evaluation of the underlying pathophysiology behind rare nirAEs is essential for choosing treatment regimens and securing optimal outcome.

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