scholarly journals Benefit of dorsal laminectomy without lumbosacral stabilization in lumbosacral traumatic cat

2019 ◽  
Vol 2 (1) ◽  
pp. 24-26
Author(s):  
Piyabongkarn Damrongdej
Keyword(s):  
Spinal Cord ◽  
Clinical Signs ◽  
Orthopedic Implants ◽  
Spinal Nerve ◽  
Spinal Injuries ◽  
Fixation Methods ◽  
Dorsal Laminectomy ◽  
Vertebral Trauma ◽  
External Stabilization ◽  
Spinal Cord Edema

Two cats were diagnosed with depression of caudal equina spinal nerve and lumbosacral spinal trauma that revealed rapid improving clinical signs after 1 month of dorsal laminectomy at the region of lumbar and sacral vertebrae without internal and external stabilization devices. This report showed that dorsal laminectomy was a powerful procedure for decompression caudal equina spinal injuries in stable lumbosacral vertebral trauma in cats without ancillary fixation methods. Dorsal laminectomy is valuable technique for correction of fracture/luxation of vertebrae that this procedure can reduce spinal cord edema, and axonal disruption. Stabilization of vertebrae by the orthopedic implants may be not necessary in small cat that has enough vertebral stability as the same in two these cases.

scholarly journals An Inherited Lower Motor Neuron Disease of Pigs: Clinical Signs in Two Litters and Pathology of an Affected Pig

1994 ◽  
Vol 6 (1) ◽  
pp. 62-71 ◽  
Author(s):  
Donal O'Toole ◽  
James Ingram ◽  
Val Welch ◽  
Katie Bardsley ◽  
Tom Haven ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Clinical Signs ◽  
Spinal Nerve ◽  
Neuronal System ◽  
Motor Neuron Diseases ◽  
System Degeneration ◽  
Progressive Neurodegeneration ◽  
Gross Lesions

A chronic progressive neurodegeneration, called hereditary porcine neuronal system degeneration (HPNSD), was recognized in a swine herd in Devon, England. Adult pigs that were presumed carriers of the dominantly inherited trait for HPNSD were transferred from England, where a breeding colony was maintained for 9 years, to the Wyoming State Veterinary Laboratory (WSVL) for study. Two litters of affected piglets were born to 2 carrier sows at the WSVL. Clinical signs of muscular tremors, paresis, or ataxia developed at 12–59 days of age in 4 of 6 liveborn pigs. Three other pigs were stillborn. In the 4 affected livebom pigs, clinical signs progressed and included symmetrical (3 pigs) or asymmetrical (1 pig) posterior paresis, bilateral knuckling of metatarsal-phalangeal or carpal joints, poor exercise tolerance, and in 1 pig, marked hind limb hypermetria. A 34-kg gilt exhibiting clinical signs of muscular tremors and posterior paresis and clinical signs for 22 days was euthanized and examined postmortem at 83 days of age. Apart from decubitus ulcers, gross lesions were absent. Microscopically, perikaryal vacuolation and osmiophilic lipid droplets were observed in atrophic alpha motor neurons in the spinal cord. There was axonal (Wallerian) degeneration in sulcomarginal and dorsal spinocerebellar tracts. Axonal degeneration also involved ventral but not dorsal spinal nerve roots, and was present in eight peripheral nerves sampled for histopathology. Changes in skeletal muscles were consistent with denervation atrophy and were most pronounced in M. tibialis cranialis of the 6 muscles sampled. Immunohistochemical staining of spinal cord for phosphorylated and nonphosphorylated neurofilaments did not reveal abnormal patterns, unlike some well-characterized inherited motor neuron diseases in other species.

scholarly journals Ultrastrutitural Pathology of an Inherited Lower Motor Neuron Disease of Pigs

1994 ◽  
Vol 6 (2) ◽  
pp. 230-237
Author(s):  
Donal O'Toole ◽  
Gerald Wells ◽  
James Ingram ◽  
William Cooley ◽  
Stephan Hawkins
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Peripheral Nerves ◽  
Axonal Degeneration ◽  
Clinical Signs ◽  
Spinal Nerve ◽  
Spinal Nerve Roots ◽  
Nerve Roots ◽  
Lumbar Spinal

The ultrastructural features of a recently described inherited lower motor neuron disease were studied in 5 affected pigs. Clinical signs comprised progressive ataxia and paresis of variable severity. Affected pigs, 6, 7, 15, 15, and 19 weeks of age, and 2 unrelated healthy pigs, 9 and 15 weeks of age, were anesthetized and their tissues were fixed by whole body perfusion with mixed aldehydes. From 1 or more affected pigs, samples of cervical and lumbar spinal ventral horn, lateral and ventral spinal columns, dorsal and ventral lumbar spinal nerve roots, 2 peripheral nerves (Nn. phrenicus and fibularis communis), and 2 skeletal muscles (Mm. diaphragma and tibialis cranialis) were examined ultrastructurally. There was widespread degeneration of myelinated axons in peripheral nerves and in lateral and ventral columns of lumbar and cervical segments of spinal cord. Axonal degeneration was present in ventral spinal nerve roots and was absent in dorsal spinal nerve roots sampled at the same lumbar levels. Unmyelinated axons in peripheral nerves and spinal nerve roots were unaffected. In 4 of 5 affected pigs, there were atrophic alpha motor neurons in cervical spinal cord that contained dense, round osmiophilic perikaryal inclusions up to 4 μm in diameter and round swollen mitochondria. Axonal regeneration was present in N. phrenicus of the 19-week-old affected pig that had clinical signs of longest duration (10 weeks). There was no morphologic evidence of axonal degeneration or spinal neuronal atrophy in either control pig. The ultrastructural features of this motor neuron disease distinguish it from other reported progressive spinal neuropathies of pigs.

scholarly journals Efficacy of Intravenous Liposomal Amphotericin B (AmBisome) against Coccidioidal Meningitis in Rabbits

2002 ◽  
Vol 46 (8) ◽  
pp. 2420-2426 ◽  
Author(s):  
Karl V. Clemons ◽  
Raymond A. Sobel ◽  
Paul L. Williams ◽  
Demosthenes Pappagianis ◽  
David A. Stevens
Keyword(s):  
Spinal Cord ◽  
Amphotericin B ◽  
Liposomal Amphotericin ◽  
White Blood Cells ◽  
Clinical Signs ◽  
Liposomal Amphotericin B ◽  
Coccidioides Immitis ◽  
Lower Protein ◽  
Motor Abnormalities ◽  
The Brain

ABSTRACT The efficacy of intravenously administered liposomal amphotericin B (AmBisome [AmBi]) for the treatment of experimental coccidioidal meningitis was compared with those of oral fluconazole (FLC) and intravenously administered conventional amphotericin B (AMB). Male New Zealand White rabbits were infected by intracisternal inoculation of arthroconidia of Coccidioides immitis. Starting 5 days postinfection, animals received one of the following: 5% dextrose water diluent; AMB given at 1 mg/kg of body weight; AmBi given at 7.5, 15, or 22.5 mg/kg intravenously three times per week for 3 weeks; or oral FLC given at 80 mg/kg for 19 days. One week after the cessation of therapy, all survivors were euthanatized, the numbers of CFU remaining in the spinal cord and brain were determined, and histological analyses were performed. All AmBi-, FLC-, or AMB-treated animals survived and had prolonged lengths of survival compared with those for the controls (P < 0.0001). Treated groups had significantly lower numbers of white blood cells and significantly lower protein concentrations in the cerebrospinal fluid compared with those for the controls (P < 0.01 to 0.0005) and had fewer clinical signs of infection (e.g., weight loss, elevated temperature, and neurological abnormalities including motor abnormalities). The mean histological scores for AmBi-treated rabbits were lower than those for FLC-treated and control rabbits (P < 0.016 and 0.0005, respectively); the scores for AMB-treated animals were lower than those for the controls (P < 0.0005) but were similar to those for FLC-treated rabbits. All regimens reduced the numbers of CFU in the brain and spinal cord compared with those for the controls (P ≤0.0005). AmBi-treated animals had 3- to 11-fold lower numbers of CFU than FLC-treated rabbits and 6- to 35-fold lower numbers of CFU than AmB-treated rabbits. Three of eight animals given 15 mg of AmBi per kg had no detectable infection in either tissue, whereas other doses of AmBi or FLC cleared either the brain or the spinal cord of infection in fewer rabbits. In addition, clearance of the infection from both tissues was achieved in none of the rabbits, and neither tissue was cleared of infection in AMB-treated animals. Overall, these data indicate that intravenously administered AmBi is superior to oral FLC or intravenous AMB and that FLC is better than AMB against experimental coccidioidal meningitis. These data indicate that AmBi may offer an improvement in the treatment of coccidioidal meningitis. Additional studies are warranted.

scholarly journals Changes of Dorsal Root Ganglion Volume in Dogs with Clinical Signs of Degenerative Myelopathy Detected by Water-Excitation Magnetic Resonance Imaging

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1702
Author(s):  
Eiji Naito ◽  
Kohei Nakata ◽  
Yukiko Nakano ◽  
Yuta Nozue ◽  
Shintaro Kimura ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Spinal Cord ◽  
Magnetic Resonance ◽  
Clinical Signs ◽  
Intervertebral Disc Herniation ◽  
Resonance Imaging ◽  
Diagnostic Potential ◽  
Water Excitation ◽  
Spinal Cord Segment ◽  
Degenerative Myelopathy

Canine degenerative myelopathy (DM) is a progressive and fatal neurodegenerative disease. However, a definitive diagnosis of DM can only be achieved by postmortem histopathological examination of the spinal cord. The purpose of this study was to investigate whether the volumetry of DRG using the ability of water-excitation magnetic resonance imaging (MRI) to visualize the DRG in dogs has premortem diagnostic value for DM. Eight dogs with DM, twenty-four dogs with intervertebral disc herniation (IVDH), and eight control dogs were scanned using a 3.0-tesla MRI system, and water-excitation images were obtained to visualize and measure the volume of DRG, normalized by body surface area. The normalized mean DRG volume between each spinal cord segment and mean volume of all DRG between T8 and L2 in the DM group was significantly lower than that in the control and the IVDH groups (P = 0.011, P = 0.002, respectively). There were no correlations within the normalized mean DRG volume between DM stage 1 and stage 4 (rs = 0.312, P = 0.128, respectively). In conclusion, DRG volumetry by the water-excitation MRI provides a non-invasive and quantitative assessment of neurodegeneration in DRG and may have diagnostic potential for DM.

Spinal Cord Edema, 5-Hydroxytryptamine, Lipid Peroxidation, and Lysosomal Enzyme Release After Acute Contusion and Compression Injury in Primates

1985 ◽  
Vol 2 (1) ◽  
pp. 45-58 ◽  
Author(s):  
JACOB ABRAHAM ◽  
AIYLAM S. BALASUBRAMANIAN ◽  
D.R. THEODORE ◽  
SHANMUGAM NAGARAJAN ◽  
C.A. APTE ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Lipid Peroxidation ◽  
Lysosomal Enzyme ◽  
Enzyme Release ◽  
Compression Injury ◽  
Spinal Cord Edema

scholarly journals Croonian lecture.— The mammalian spinal cord as an organ of reflex action

1897 ◽  
Vol 61 (369-377) ◽  
pp. 220-221 ◽  
Keyword(s):  
Spinal Cord ◽  
Spinal Nerve ◽  
Spinal Reflex ◽  
Reflex Action

The channels of connection between spinal nerve-centres. Long spinal reflex paths and short spinal reflex paths. The First Law of Pflüger: examples of it and exceptions to it; relation between it and microscopical features of the cord.

Clinical signs and histopathology of brain, spinal cord and muscle of the pelvic limb of rats experimentally infected with Trypanosoma evansi

2012 ◽  
Vol 208 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Aleksandro S. Da Silva ◽  
Camila B. Oliveira ◽  
Claudia M. Bertoncheli ◽  
Rosmarine P. Santos ◽  
Diego V. Beckmann ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Clinical Signs ◽  
Trypanosoma Evansi ◽  
Pelvic Limb

scholarly journals Inhibition of the phosphoinositide 3-kinase-AKT-cyclic GMP-c-Jun N-terminal kinase signaling pathway attenuates the development of morphine tolerance in a mouse model of neuropathic pain

2021 ◽  
Vol 17 ◽  
pp. 174480692110033
Author(s):  
Travis Okerman ◽  
Taylor Jurgenson ◽  
Madelyn Moore ◽  
Amanda H Klein
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Signaling Pathway ◽  
Intracellular Signaling ◽  
Morphine Tolerance ◽  
Spinal Nerve ◽  
Intracellular Signaling Pathway ◽  
Spinal Cord Dorsal ◽  
Phosphoinositide 3 Kinase ◽  
Induced Tolerance

Research presented here sought to determine if opioid induced tolerance is linked to activity changes within the PI3Kγ-AKT-cGMP-JNK intracellular signaling pathway in spinal cord or peripheral nervous systems. Morphine or saline injections were given subcutaneously twice a day for five days (15 mg/kg) to male C57Bl/6 mice. A separate cohort of mice received spinal nerve ligation (SNL) one week prior to the start of morphine tolerance. Afterwards, spinal cord, dorsal root ganglia, and sciatic nerves were isolated for quantifying total and phosphorylated- JNK levels, cGMP, and gene expression analysis of Pik3cg, Akt1, Pten, and nNos1. This pathway was downregulated in the spinal cord with increased expression in the sciatic nerve of morphine tolerant and morphine tolerant mice after SNL. We also observed a significant increase in phosphorylated- JNK levels in the sciatic nerve of morphine tolerant mice with SNL. Pharmacological inhibition of PI3K or JNK, using thalidomide, quercetin, or SP600125, attenuated the development of morphine tolerance in mice with SNL as measured by thermal paw withdrawal. Overall, the PI3K/AKT intracellular signaling pathway is a potential target for reducing the development of morphine tolerance in the peripheral nervous system. Continued research into this pathway will contribute to the development of new analgesic drug therapies.

scholarly journals Experimental and iatrogenic poisoning by sodium selenite in pigs

2017 ◽  
Vol 37 (6) ◽  
pp. 561-569
Author(s):  
Paulo V. Peixoto ◽  
Krishna D. Oliveira ◽  
Ticiana N. França ◽  
David Driemeier ◽  
Marcos D. Duarte ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Sodium Selenite ◽  
Clinical Signs ◽  
Lung Edema ◽  
Distilled Water ◽  
Histological Changes ◽  
Chronic Stage ◽  
Hind Limbs ◽  
Proprioceptive Deficit ◽  
Histiocytic Infiltration

ABSTRACT: Following a case of iatrogenic selenium poisoning in a young pig, an experimental study was carry out. Sodium selenite was orally and parenterally administered to 13 pigs that were subdivided into three groups (G1, G2 and G3). The animals in groups G1 and G3 received sodium selenite intramuscularly (IM), G1 received a comercial formula, and G3 received sodium selenite mixed with distilled water at different dosages, and those in group G2 were fed commercial sodium selenite. Acute and subacute poisoning was observed in both groups, although the onset of clinical signs was slower in group G2. Only one pig (in group G1) that had received the highest dose showed a peracute course. Apathy, anorexia, dyspnea, vomiting, muscular tremors, proprioceptive deficit, ataxia and paresis of the hind limbs progressing to the front limbs evolving to tetraplegia were observed. Postmortem findings differed whether the animals received the injected (G1 and G3) or oral (G2) sodium selenite. The liver was moderately atrophic in some animals of G2. Some of the animals in groups G1 and G3 presented with lung edema. One pig in G3 had yellowish-brown areas in the ventral horns of the cervical intumescences of the spinal cord. The most important histological changes were present in the ventral horns of the cervical and lumbar intumescences of the spinal cord. In one animal, changes were present in the brainstem and mesencephalon. The initial lesion was a perivascular and astrocyte edema that progressing to lysis and death of astrocytes and neurons. In the chronic stage of the lesions, there were extensive areas of liquefaction necrosis with perivascular lymphocytic and histiocytic infiltration and occasional eosinophils. It seems that disruption of the blood-brain barrier due to astrocyte edema is the most likely mechanism of CNS lesion.

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