scholarly journals Disseminated inflammation of the central nervous system associated with acute hepatitis E: a case report

BMC Neurology ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jan Rahmig ◽  
Arne Grey ◽  
Marco Berning ◽  
Jochen Schaefer ◽  
Martin Lesser ◽  
...  

Abstract Background Hepatitis E infection affects over 20 million people worldwide. Reports of neurological manifestations are largely limited to the peripheral nervous system. We report a middle-aged genotype 3c male patient with acute hepatitis E virus (HEV) infection and severe neurological deficits with evidence of multiple disseminated inflammatory lesions of the central nervous system. Case presentation A 42-year-old male patient presented to our emergency department with musculoskeletal weakness, bladder and bowel retention, blurred vision and ascending hypoesthesia up to the level of T8. Serology showed elevated liver enzymes and positive IgM-titers of hepatitis E. Analysis of cerebrospinal fluid (CSF) showed mild pleocytosis and normal levels of glucose, lactate and protein. HEV-RNA-copies were detected in the CSF and stool. Within 3 days after admission the patient became paraplegic, had complete visual loss and absent pupillary reflexes. MRI showed inflammatory demyelination of the optic nerve sheaths, multiple subcortical brain regions and the spinal cord. Electrophysiology revealed axonal damage of the peroneal nerve on both sides with absent F-waves. Treatment was performed with methylprednisolone, two cycles of plasma exchange (PLEX), one cycle of intravenous immunoglobulins (IVIG) and ribavirin which was used off-label. Liver enzymes normalized after 1 week and serology was negative for HEV-RNA after 3 weeks. Follow-up MRI showed progressive demyelination and new leptomeningeal enhancement at the thoracic spine and cauda equina 4 weeks after admission. Four months later, after rehabilitation was completed, repeated MRI showed gliotic transformation of the spinal cord without signs of an active inflammation. Treatment with rituximab was initiated. The patient remained paraplegic and hypoesthesia had ascended up to T5. Nevertheless, he regained full vision. Conclusions Our case indicates a possible association of acute HEV infection with widespread disseminated central nervous system inflammation. Up to now, no specific drugs have been approved for the treatment of acute HEV infection. We treated our patient off-label with ribavirin and escalated immunomodulatory therapy considering clinical progression and the possibility of an autoimmune response targeting nerve cell structures. While response to treatment was rather limited in our case, detection of HEV in patients with acute neurological deficits might help optimize individual treatment strategies.

2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.


1963 ◽  
Vol 44 (3) ◽  
pp. 475-480 ◽  
Author(s):  
R. Grinberg

ABSTRACT Radiologically thyroidectomized female Swiss mice were injected intraperitoneally with 131I-labeled thyroxine (T4*), and were studied at time intervals of 30 minutes and 4, 28, 48 and 72 hours after injection, 10 mice for each time interval. The organs of the central nervous system and the pituitary glands were chromatographed, and likewise serum from the same animal. The chromatographic studies revealed a compound with the same mobility as 131I-labeled triiodothyronine in the organs of the CNS and in the pituitary gland, but this compound was not present in the serum. In most of the chromatographic studies, the peaks for I, T4 and T3 coincided with those for the standards. In several instances, however, such an exact coincidence was lacking. A tentative explanation for the presence of T3* in the pituitary gland following the injection of T4* is a deiodinating system in the pituitary gland or else the capacity of the pituitary gland to concentrate T3* formed in other organs. The presence of T3* is apparently a characteristic of most of the CNS (brain, midbrain, medulla and spinal cord); but in the case of the optic nerve, the compound is not present under the conditions of this study.


1985 ◽  
Vol 55 ◽  
Author(s):  
F. Terry Hambrecht

ABSTRACTNeural prostheses which are commercially available include cochlear implants for treating certain forms of deafness and urinary bladder evacuation prostheses for individuals with spinal cord disorders. In the future we can anticipate improvements in bioelectrodes and biomaterials which should permit more sophisticated devices such as visual prostheses for the blind and auditory prostheses for the deaf based on microstimulation of the central nervous system.


2019 ◽  
Vol 19 (8) ◽  
pp. 597-604
Author(s):  
Li Pang ◽  
Shouqin Ji ◽  
Jihong Xing

Background: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine if blocking acid sensing ion channels (ASICs) using amiloride in the Central Nervous System can alleviate neurological deficits after the induction of CA and further examine the participation of PIC signal in the hippocampus for the effects of amiloride. Methods: CA was induced by asphyxia and then cardiopulmonary resuscitation was performed in rats. Western blot analysis and ELISA were used to determine the protein expression of ASIC subunit ASIC1 in the hippocampus, and the levels of PICs. As noted, it is unlikely that this procedure is clinically used although amiloride and other pharmacological agents were given into the brain in this study. Results: CA increased ASIC1 in the hippocampus of rats in comparison with control animals. This was associated with the increase in IL-1β, IL-6 and TNF-α together with Caspase-3 and Caspase-9. The administration of amiloride into the lateral ventricle attenuated the upregulation of Caspase-3/Caspase-9 and this further alleviated neurological severity score and brain edema. Inhibition of central IL-6 and TNF-α also decreased ASIC1 in the hippocampus of CA rats. Conclusion: Transient global ischemia induced by CA amplifies ASIC1a in the hippocampus likely via PIC signal. Amiloride administered into the Central Nervous System plays a neuroprotective role in the process of global ischemia. Thus, targeting ASICs (i.e., ASIC1a) is suggested for the treatment and improvement of CA-evoked global cerebral ischemia.


1908 ◽  
Vol 54 (226) ◽  
pp. 560-561
Author(s):  
David Orr ◽  
R. G. Rows

At a quarterly meeting of this Association held last year at Nottingham, we showed the results of our experiments with toxins upon the spinal cord and brain of rabbits. Our main conclusion was, that the central nervous system could be infected by toxins passing up along the lymph channels of the perineural sheath. The method we employed in our experiments consisted in placing a celloidin capsule filled with a broth culture of an organism under the sciatic nerve or under the skin of the cheek; and we invariably found a resulting degeneration in the spinal cord or brain, according to the situation of the capsule. These lesions we found to be identical in morphological type and anatomical distribution with those found in the cord of early tabes dorsalis and in the brain and cord of general paralysis of the insane. The conclusion suggested by our work was that these two diseases, if toxic, were most probably infections of lymphogenous origin.


1947 ◽  
Vol s3-88 (1) ◽  
pp. 55-63
Author(s):  
R. A. R. GRESSON ◽  
I. ZLOTNIK

1. The Golgi material of the pyramidal cells of the cerebral cortex, the Purkinje cells of the cerebellum, and the multipolar cells of the medulla oblongata and ventral horns of the spinal cord of the sheep is present as filaments and as irregularly shaped bodies. In some of the cells, particularly in the lamb (Sheep V), the Golgi material has the appearance of a network. As it is frequently present as separate bodies it is suggested that it may always consist of discrete Golgi elements which are sometimes situated in close proximity or in contact with one another. Filamentous Golgi elements are present in the basal part of the cell processes. 2. An examination of neurones from the corresponding regions of the central nervous system of sheep infected experimentally with louping-ill showed that the Golgi material undergoes changes consequent upon the invasion of the cells by the virus. The Golgi material undergoes hypertrophy, and at the same time there is a reduction in the number of filamentous Golgi elements and a reduction in the amount of Golgi substance present in the cell processes. These changes are followed by fragmentation. All the neurones of a particular region are not affected equally at the same time. The Golgi material of the Purkinje cells tends to form groups in the cytoplasm prior to fragmentation. In the multipolar cells of the medulla oblongata the hypertrophy of the Golgi material is not as great as in the other regions of the central nervous system. The Golgi material of the motor nerve-cells of the ventral horns of the spinal cord undergoes considerable hypertrophy which is followed by a grouping of the Golgi elements and fragmentation.


2017 ◽  
Vol 37 (8) ◽  
pp. 820-828 ◽  
Author(s):  
Guilherme Konradt ◽  
Daniele M. Bassuino ◽  
Klaus S. Prates ◽  
Matheus V. Bianchi ◽  
Gustavo G.M. Snel ◽  
...  

ABSTRACT: This study describes suppurative infectious diseases of the central nervous system (CNS) in domestic ruminants of southern Brazil. Reports from 3.274 cattle, 596 sheep and 391 goats were reviewed, of which 219 cattle, 21 sheep and 7 goats were diagnosed with central nervous system inflammatory diseases. Suppurative infectious diseases of the CNS corresponded to 54 cases (28 cattle, 19 sheep and 7 goats). The conditions observed consisted of listerial meningoencephalitis (8 sheep, 5 goats and 4 cattle), suppurative leptomeningitis and meningoencephalitis (14 cattle, 2 goats and 1 sheep), cerebral (6 cattle and 2 sheep), and spinal cord (7 sheep) abscesses, and basilar empyema (4 cattle and 1 sheep). Bacterial culture identified Listeria monocytogenes (9/54 cases), Escherichia coli (7/54 cases), Trueperella pyogenes (6/54 cases) and Proteus mirabilis (1/54 cases). All cases diagnosed as listeriosis through histopathology yielded positive immunostaining on immunohistochemistry, while 12/17 of the cases of suppurative leptomeningitis and meningoencephalitis presented positive immunostaining for Escherichia coli. Meningoencephalitis by L. monocytogenes was the main neurological disease in sheep and goats, followed by spinal cord abscesses in sheep. In cattle, leptomeningitis and suppurative meningoencephalitis was the most frequent neurological disease for the species, and E. coli was the main cause of these lesions. Basilar empyema, mainly diagnosed in cattle, is related to traumatic injuries, mainly in the nasal cavity, and the main etiologic agent was T. pyogenes.


2020 ◽  
Vol 19 (4) ◽  
pp. 158-164
Author(s):  
N. A. Strumila ◽  
A. S. Krasnov ◽  
M. M. Andrianov ◽  
G. V. Teresсhenko

Embryonal rhabdomyosarcoma (eRMS) is one of the most common soft tissue sarcomas in children, accounting for 4.5% of all childhood tumors. Half of the eRMS occuring in the head and neck are parameningeal. About 40% of patients with eRMS can develop distant metastases. In patients with intracranial tumors, metastatic spread can occur along the central nervous system (CNS) meninges. The literature describes only 4 clinical cases of eRMS with distant metastases in the spinal cord and along the meninges. Only in two out of these four cases, CSF cytology was positive (meaning that tumor cells were detected in cerebrospinal fluid). Magnetic resonance imaging (MRI) of the central nervous system with contrast enhancement can be used to detect distant metastases in the CNS and meninges. We present a clinical case of a 4-year old girl with parameningeal eRMS. MRI of the CNS performed as part of a diagnostic check-up revealed nodal metastatic foci along the meninges of the spinal cord. In accordance with the treatment protocol, the patient was diagnosed with stage 4 disease and received intensive polychemotherapy resulting in the disappearance of the nodal lesions in the spinal cord and a good prognosis. The parents gave their consent to the use of their child's data, including photographs, for research purposes and in publications.


2021 ◽  
Vol 12 ◽  
Author(s):  
Janaki Manoja Vinnakota ◽  
Robert Zeiser

Allogeneic hematopoietic cell transplantation (allo-HCT) is a curative therapy for patients with hematological malignancies. Acute Graft versus host diseases (GVHD) is a major immune mediated side effect of allo-HCT that can affect the central nervous system (CNS) in addition to post-allo-HCT vascular events, drug toxicity or infections. Here we summarize and discuss recent preclinical data on the CNS as a target of acute GVHD and the known mechanisms contributing to neurotoxicity with a focus on microglia and T cells. We also discuss open questions in the field and place the findings made in mouse models in a clinical context. While in mice the neurological deficits can be assessed in a controlled fashion, in patients the etiology of the CNS damage is difficult to attribute to acute GVHD versus infections, vascular events, and drug-induced toxicity. Ultimately, we discuss novel therapies for GVHD of the CNS. Our understanding of the biological mechanisms that lead to neurotoxicity after allo-HCT increased over the last decade. This review provides insights into CNS manifestations of GVHD versus other etiologies of CNS damage in mice and patients.


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