The experimental transmission of Pneumostrongylus tenuis to caribou (Rangifer tarandus terraenovae)

1968 ◽  
Vol 46 (3) ◽  
pp. 503-510 ◽  
Author(s):  
Roy C. Anderson ◽  
Uta R. Strelive
Keyword(s):  
Spinal Cord ◽  
North America ◽  
Grey Matter ◽  
Rangifer Tarandus ◽  
Histological Study ◽  
Eastern North America ◽  
Experimental Transmission ◽  
Dorsal Horns ◽  
Traumatic Lesions ◽  
The Brain

Two caribou calves (Rangifer tarandus terraenovae) were infected experimentally with Pneumostrongylus tenuis Dougherty from white-tailed deer (Odocoileus virginianus borealis). The female calf showed slight neurologic signs from the 5th to the 14th day when she died from a mycotic infection. The male calf first showed neurologic signs on the seventh day. These signs became progressively more extreme and by the 29th day, when the animal was necropsied, it showed severe locomotory ataxia with knuckling and posterior weakness. Histological study of the spinal cord of the male revealed numerous worms in all regions of the spinal cord and in the brain stem and medulla oblongata. Traumatic lesions and worms were unusually numerous in lateral and dorsal funiculi. It is suggested that the more severe neurologic signs were caused by migration of worms into funiculi from dorsal horns of grey matter. The results are discussed in relation to the management of woodland caribou in eastern North America.

Spinal cord grey matter lesions in multiple sclerosis detected by post-mortem high field MR imaging

2008 ◽  
Vol 15 (2) ◽  
pp. 180-188 ◽  
Author(s):  
CP Gilmore ◽  
JJG Geurts ◽  
N Evangelou ◽  
JCJ Bot ◽  
RA van Schijndel ◽  
...  
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Mr Imaging ◽  
High Field ◽  
Grey Matter ◽  
Great Majority ◽  
Proton Density ◽  
Post Mortem ◽  
Mr Images ◽  
The Brain

Background Post-mortem studies demonstrate extensive grey matter demyelination in MS, both in the brain and in the spinal cord. However the clinical significance of these plaques is unclear, largely because they are grossly underestimated by MR imaging at conventional field strengths. Indeed post-mortem MR studies suggest the great majority of lesions in the cerebral cortex go undetected, even when performed at high field. Similar studies have not been performed using post-mortem spinal cord material. Aim To assess the sensitivity of high field post-mortem MRI for detecting grey matter lesions in the spinal cord in MS. Methods Autopsy material was obtained from 11 MS cases and 2 controls. Proton Density-weighted images of this formalin-fixed material were acquired at 4.7Tesla before the tissue was sectioned and stained for Myelin Basic Protein. Both the tissue sections and the MR images were scored for grey matter and white matter plaques, with the readers of the MR images being blinded to the histopathology results. Results Our results indicate that post-mortem imaging at 4.7Tesla is highly sensitive for cord lesions, detecting 87% of white matter lesions and 73% of grey matter lesions. The MR changes were highly specific for demyelination, with all lesions scored on MRI corresponding to areas of demyelination. Conclusion Our work suggests that spinal cord grey matter lesions may be detected on MRI more readily than GM lesions in the brain, making the cord a promising site to study the functional consequences of grey matter demyelination in MS.

scholarly journals P.059 Brachial plexus enhancement in acute flaccid myelitis: A novel radiographic finding

2019 ◽  
Vol 46 (s1) ◽  
pp. S30
Author(s):  
SC Hammond ◽  
M Almomen ◽  
A Mineyko ◽  
A Pauranik
Keyword(s):  
Spinal Cord ◽  
Peripheral Nerves ◽  
Grey Matter ◽  
Pediatric Patients ◽  
Radiographic Finding ◽  
Mri Imaging ◽  
Full Spectrum ◽  
Acute Flaccid Myelitis ◽  
History Of ◽  
The Brain

Background: Acute flaccid myelitis (AFM) is a condition which causes acute paralysis in pediatric patients. Although awareness of AFM is increasing, the pathophysiology and full spectrum of clinical, biochemical, and radiographic features remain to be fully elucidated. Methods: We report a 5 year-old, previously healthy, male patient who presented with acute right upper extremity weakness following a two day history of fever, cough, and fatigue. The patient underwent extensive inflammatory and infectious workup in addition to MRI imaging of the brain, spinal cord, and bilateral brachial plexuses. Results: Infectious and inflammatory workup did not identify a causative agent. The patient was seen to have bilateral asymmetric (R>L) thickening and enhancement of the anterior horn cells of his cervical (C3-C7) spine, consistent with the spinal grey matter lesions previously described in patients with AFM. Enhancement of the corresponding anterior nerve rootlets and bilateral brachial plexuses was also seen. Conclusions: Patients with acute flaccid myelitis may demonstrate grey matter enhancement extending beyond the spinal cord to the peripheral nerves and plexuses, a radiographic finding which has not previously been published.

FURTHER EXPERIMENTAL STUDIES OF PNEUMOSTRONGYLUS TENUIS IN CERVIDS

1966 ◽  
Vol 44 (5) ◽  
pp. 851-861 ◽  
Author(s):  
Roy C. Anderson ◽  
Murray W. Lankester ◽  
Uta R. Strelive
Keyword(s):  
Grey Matter ◽  
Mule Deer ◽  
Experimental Studies ◽  
Clinical Signs ◽  
Odocoileus Hemionus ◽  
Eastern North America ◽  
Dorsal Horns ◽  
The Central Nervous System ◽  
Histopathologic Findings ◽  
Traumatic Damage

Two young wapiti (Cervus canadensis nelsoni) and a female mule deer fawn (Odocoileus hemionus hemionus) were infected experimentally with Pneumostrongylus tenuis from white-tailed deer (Odocoileus virginianus borealis). The male wapiti showed only slight clinical signs after infection, and first-stage larvae appeared in its faeces 92 days later. The female wapiti showed severe neurological signs that terminated in general paralysis on the 54th day. The mule deer showed severe neurologic signs and died of paralysis on the 62nd day. Numerous worms were found in the subdural space and neural parenchyma, especially in the dorsal horns of grey matter, of the female wapiti and the mule deer. Traumatic damage in the dorsal horns was extensive, especially in the wapiti. Histopathologic findings were similar to those reported earlier in moose calves (Alces americana americana) infected with P. tenuis. Study of worms recovered from experimentally infected cervids indicates that P. tenuis develops similarity in white-tailed deer, moose, wapiti, and mule deer although in the first species it causes little damage to the central nervous system. The possibility that P. tenuis could become established in wapiti introduced into eastern North America is noted.

Toxoplasma-like Encephalomyelitis in the Horse

1974 ◽  
Vol 11 (1) ◽  
pp. 87-96 ◽  
Author(s):  
Jill Beech ◽  
D. C. Dodd
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Mononuclear Cell ◽  
Hemagglutination Inhibition ◽  
Grey Matter ◽  
Cell Infiltration ◽  
Mononuclear Cell Infiltration ◽  
Hemagglutination Inhibition Test ◽  
Brain And Spinal Cord ◽  
The Brain

Eight horses with progressive neurologic signs had encephalomyelitis associated with toxoplasma-like protozoan bodies. There were scattered hemorrhagic, malacic lesions in white and grey matter in the brain and spinal cord. Microscopically there was malacia, mononuclear cell infiltration, especially perivascularly, gliosis, and various degrees of necrosis and hemorrhage. Other tissues were normal, except for the lung of one horse that had focal bronchopneumonia. The cerebrospinal fluid did not contain measurable amounts of IgM, IgG, or IgA. Serum from one horse was negative at 1:64 by the hemagglutination-inhibition test for toxoplasma antibodies.

scholarly journals Bovine congenital babesiosis

2021 ◽  
Vol 14 (1) ◽  
pp. 70-74
Author(s):  
Luan Henker ◽  
Marina Lorenzett ◽  
Saulo Pavarini
Keyword(s):  
Spinal Cord ◽  
Urinary Bladder ◽  
Grey Matter ◽  
Clinical Signs ◽  
Clinical History ◽  
Postmortem Examination ◽  
Comparative Pathology ◽  
Calving Season ◽  
The Brain

Diagnostic Exercise from The Latin Comparative Pathology Group. Clinical History: A crossbred, stillborn bovine fetus, with nine months of gestation, was submitted for postmortem examination. The dam that aborted was a 2-year-old heifer that did not have any additional clinical signs. The owner observed several late-term abortions and stillbirths in this farm during the referred calving season. Necropsy Findings: Necropsy findings included moderate accumulation of light red fluid in the abdominal and thoracic cavities, mild hemoglobin imbibition, as well as collapsed lungs. The liver was markedly enlarged, had rounded edges, and moderate, diffuse yellow discoloration. The gallbladder was filled with thick, grumous bile, and the spleen was moderately enlarged. The kidneys had moderate diffuse dark red discoloration, and the urinary bladder was distended with dark-red urine. The grey matter of the brain and the spinal cord was markedly pink-red discolored. Squashes of the spleenand brain were prepared and routinely stained with PanóticoRápido® (Laborclin, Brazil).

Inhibition of Hsp90 in the spinal cord enhances the antinociceptive effects of morphine by activating an ERK-RSK pathway

2020 ◽  
Vol 13 (630) ◽  
pp. eaaz1854
Author(s):  
David I. Duron ◽  
Wei Lei ◽  
Natalie K. Barker ◽  
Carrie Stine ◽  
Sanket Mishra ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Side Effects ◽  
Opioid Therapy ◽  
Mechanical Stimuli ◽  
Hsp90 Inhibition ◽  
Chaperone Protein ◽  
Dorsal Horns ◽  
Antinociceptive Effects ◽  
Μ Opioid Receptor ◽  
The Brain

Morphine and other opioids are commonly used to treat pain despite their numerous adverse side effects. Modulating μ-opioid receptor (MOR) signaling is one way to potentially improve opioid therapy. In mice, the chaperone protein Hsp90 mediates MOR signaling within the brain. Here, we found that inhibiting Hsp90 specifically in the spinal cord enhanced the antinociceptive effects of morphine in mice. Intrathecal, but not systemic, administration of the Hsp90 inhibitors 17-AAG or KU-32 amplified the effects of morphine in suppressing sensitivity to both thermal and mechanical stimuli in mice. Hsp90 inhibition enabled opioid-induced phosphorylation of the kinase ERK and increased abundance of the kinase RSK in the dorsal horns of the spinal cord, which are heavily populated with primary afferent sensory neurons. The additive effects of Hsp90 inhibition were abolished upon intrathecal inhibition of ERK, RSK, or protein synthesis. This mechanism downstream of MOR, localized to the spinal cord and repressed by Hsp90, may potentially be used to enhance the efficacy and presumably decrease the side effects of opioid therapy.

THE INCIDENCE, DEVELOPMENT, AND EXPERIMENTAL TRANSMISSION OF PNEUMOSTRONGYLUS TENUIS DOUGHERTY (METASTRONGYLOIDEA: PROTOSTRONGYLIDAE) OF THE MENINGES OF THE WHITE-TAILED DEER (ODOCOILEUS VIRGINIANUS BOREALIS) IN ONTARIO

1963 ◽  
Vol 41 (5) ◽  
pp. 775-792 ◽  
Author(s):  
Roy C. Anderson
Keyword(s):  
Spinal Cord ◽  
Odocoileus Virginianus ◽  
Dura Mater ◽  
Interstitial Tissue ◽  
Experimental Transmission ◽  
Brain And Spinal Cord ◽  
Eggs And Larvae ◽  
The Brain

Pneumostrongylus tenuis was found throughout the year in the cranium of 41% of 172 adult deer examined in Algonquin Park. Incidence was higher in summer (46%) than winter (24%). Two fawns were infected (October and March). Worms also occurred on the spinal dura mater and in veins of the dura. Thus, incidence of infection was higher than indicated by examinations of craniums. Larvae developed in species of Discus, Zonitoides, Deroceras, Triodopsis, Stenotrema, and Lymnea sp. Four fawns were infected experimentally. Fourth- and fifth-stage larvae were found in the brain and spinal cord of one fawn examined at 25 days. Fifth stages were found in the tissue and between the meninges of the spinal cord of a fawn examined at 40 days. Subadults were found on the spinal and cerebral dura mater of a fawn autopsied at 50 days. The final fawn passed larvae 91 days after exposure. At 115 days after exposure, mature worms were found on or in the cerebral dura; two were found in the intercavernous sinus. The inflamed dura was covered by haemorrhagic, fibrous exudate containing larvae and developing eggs. Eggs and larvae were found in vessels in the pia-arachnoid and near veins in the dura. Lungs contained minute nodules with one to three eggs. Undeveloped eggs, reaching the lungs via the blood, formed embolisms that fibrosed. In regions of the lungs with numerous developing eggs and larvae there was congestion, inflammation, haemorrhage, and fibrosis of interstitial tissue.

scholarly journals Reversible Tau Phosphorylation Induced by Synthetic Torpor in the Spinal Cord of the Rat

2021 ◽  
Vol 15 ◽  
Author(s):  
Timna Hitrec ◽  
Fabio Squarcio ◽  
Matteo Cerri ◽  
Davide Martelli ◽  
Alessandra Occhinegro ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Glycogen Synthase ◽  
Physiological Mechanism ◽  
Cellular Level ◽  
Microglia Activation ◽  
Morphometric Analyses ◽  
Dorsal Horns ◽  
The Brain ◽  
Related Process

Tau is a key protein in neurons, where it affects the dynamics of the microtubule system. The hyperphosphorylation of Tau (PP-Tau) commonly leads to the formation of neurofibrillary tangles, as it occurs in tauopathies, a group of neurodegenerative diseases, including Alzheimer's. Hypothermia-related accumulation of PP-Tau has been described in hibernators and during synthetic torpor (ST), a torpor-like condition that has been induced in rats, a non-hibernating species. Remarkably, in ST PP-Tau is reversible and Tau de-phosphorylates within a few hours following the torpor bout, apparently not evolving into pathology. These observations have been limited to the brain, but in animal models of tauopathies, PP-Tau accumulation also appears to occur in the spinal cord (SpCo). The aim of the present work was to assess whether ST leads to PP-Tau accumulation in the SpCo and whether this process is reversible. Immunofluorescence (IF) for AT8 (to assess PP-Tau) and Tau-1 (non-phosphorylated Tau) was carried out on SpCo coronal sections. AT8-IF was clearly expressed in the dorsal horns (DH) during ST, while in the ventral horns (VH) no staining was observed. The AT8-IF completely disappeared after 6 h from the return to euthermia. Tau-1-IF disappeared in both DH and VH during ST, returning to normal levels during recovery. To shed light on the cellular process underlying the PP-Tau pattern observed, the inhibited form of the glycogen-synthase kinase 3β (the main kinase acting on Tau) was assessed using IF: VH (i.e., in motor neurons) were highly stained mainly during ST, while in DH there was no staining. Since tauopathies are also related to neuroinflammation, microglia activation was also assessed through morphometric analyses, but no ST-induced microglia activation was found in the SpCo. Taken together, the present results show that, in the DH of SpCo, ST induces a reversible accumulation of PP-Tau. Since during ST there is no motor activity, the lack of AT8-IF in VH may result from an activity-related process at a cellular level. Thus, ST demonstrates a newly-described physiological mechanism that is able to resolve the accumulation of PP-Tau and apparently avoid the neurodegenerative outcome.

Central Nerve System Impairment, AMA Guides, Sixth Edition: An Overview

2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurological Impairment ◽  
Sixth Edition ◽  
Central Nerve System ◽  
The Central Nervous System ◽  
The One ◽  
Nerve System ◽  
The Brain

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.

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