scholarly journals Primary leptomeningeal gliomatosis in a domestic shorthaired cat

2019 ◽  
Vol 31 (1) ◽  
pp. 94-97
Author(s):  
Whitney M. Zoll ◽  
Andrew D. Miller ◽  
Carston Bandt ◽  
Jeffrey R. Abbott

A 15-y-old neutered male domestic shorthaired cat was presented with a 16-d history of hindlimb paralysis in conjunction with 1-wk duration of inappetence and lethargy. Given intractable clinical signs, development of seizures, and poor prognosis, euthanasia was elected. Gross examination revealed mild, chronic, multifocal intervertebral disk disease; however, no gross abnormalities were noted in the spinal cord. Histologic examination of the cervical, thoracic, and lumbar spinal cord and the myelencephalon revealed diffuse and variable expansion of the meninges by sheets of neoplastic round-to-polygonal cells. The cells formed sheets and clusters, supported by a variably eosinophilic, fibrillar-to-basophilic, homogeneous matrix, and contained a small amount of eosinophilic cytoplasm. The nuclei were round with finely stippled to hyperchromatic chromatin and 1–2 small nucleoli. Mild white matter degeneration was present in the dorsal and ventral funiculi multifocally throughout the spinal cord, but was most severe in the ventral lumbar sections. Immunohistochemistry revealed strong intranuclear immunoreactivity for Olig2, and intracytoplasmic immunoreactivity for glial fibrillary acidic protein, MAP2, and vimentin in the neoplastic glial cells. To our knowledge, primary leptomeningeal gliomatosis has not been reported previously in a cat.

2008 ◽  
Vol 45 (6) ◽  
pp. 934-938 ◽  
Author(s):  
C. J. Gibson ◽  
N. M. A. Parry ◽  
R. M. Jakowski ◽  
D. Eshar

A 2–year-old, female hedgehog presented with an 8–month history of progressive, ascending paresis/paralysis and was tentatively diagnosed with wobbly hedgehog syndrome. She died awaiting further diagnostic tests, and the owners consented to postmortem examination. Grossly, the bladder was large and flaccid and the cervical and lumbar spinal cord were regionally enlarged, light grey, and friable with multifocal hemorrhages. The thoracic spinal cord was grossly normal. Microscopically all regions of the spinal cord had similar changes, although the cervical and lumbar sections were most severely affected. These regions were completely effaced by a moderately cellular infiltration of highly pleomorphic polygonal to spindle shaped cells, mineralization, and necrosis, which were most consistent with anaplastic astrocytoma. The thoracic spinal cord white matter was similarly infiltrated by the neoplastic cells, with perivascular extension into the otherwise normal grey matter. A diagnosis of anaplastic astrocytoma was confirmed using immunohistochemical stains that were positive for glial fibrillary acidic protein and S100.


Neurosurgery ◽  
1979 ◽  
Vol 4 (2) ◽  
pp. 152-156 ◽  
Author(s):  
J. E. Smith ◽  
P. V. Hall ◽  
M. R. Galvin ◽  
A. R. Jones ◽  
R. L. Campbell

Abstract Twelve female mongrel dogs were made paraplegic by midthoracic spinal cord transection. Beginning at 9 weeks posttransection, either glycine (50 mg/kg) or saline was injected intramuscularly each day and the signs of spinal spasticity were assessed clinically. After treating the dogs for 3 weeks, we removed the lumbar enlargement of each dog and microdissected it into gray and white areas which we assayed for glycine, glutamate, and aspartate content. Some of the clinical signs of spasticity improved in the animals injected with glycine compared to the saline-injected controls. The content of glycine was significantly elevated in the central gray matter and ventral medial white matter of the glycinetreated dogs. The levels of glutamate were also significantly elevated in the central, lateral ventral, and medial ventral gray matter and in the dorsal lateral and ventral medial white matter of the glycine-treated dogs. The possible role of these segmental putative neurotransmitters in spinal spasticity is discussed.


2018 ◽  
Vol 46 (05) ◽  
pp. 323-329 ◽  
Author(s):  
Nele Ondreka ◽  
Sara Malberg ◽  
Emma Laws ◽  
Martin Schmidt ◽  
Sabine Schulze

SummaryA 2-year-old male neutered mixed breed dog with a body weight of 30 kg was presented for evaluation of a soft subcutaneous mass on the dorsal midline at the level of the caudal thoracic spine. A further clinical sign was intermittent pain on palpation of the area of the subcutaneous mass. The owner also described a prolonged phase of urination with repeated interruption and re-initiation of voiding. The findings of the neurological examination were consistent with a lesion localization between the 3rd thoracic and 3rd lumbar spinal cord segments. Magnetic resonance imaging revealed a spina bifida with a lipomeningocele and diplomyelia (split cord malformation type I) at the level of thoracic vertebra 11 and 12 and secondary syringomyelia above the aforementioned defects in the caudal thoracic spinal cord. Surgical resection of the lipomeningocele via a hemilaminectomy was performed. After initial deterioration of the neurological status postsurgery with paraplegia and absent deep pain sensation the dog improved within 2 weeks to non-ambulatory paraparesis with voluntary urination. Six weeks postoperatively the dog was ambulatory, according to the owner. Two years after surgery the owner recorded that the dog showed a normal gait, a normal urination and no pain. Histopathological diagnosis of the biopsied material revealed a lipomeningocele which confirmed the radiological diagnosis.


1996 ◽  
Vol 16 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Ming Zhou ◽  
Noboru Goto ◽  
Chen Zhang ◽  
Wei Tang

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Marco Bonizzato ◽  
Nicholas D. James ◽  
Galyna Pidpruzhnykova ◽  
Natalia Pavlova ◽  
Polina Shkorbatova ◽  
...  

AbstractA spinal cord injury usually spares some components of the locomotor circuitry. Deep brain stimulation (DBS) of the midbrain locomotor region and epidural electrical stimulation of the lumbar spinal cord (EES) are being used to tap into this spared circuitry to enable locomotion in humans with spinal cord injury. While appealing, the potential synergy between DBS and EES remains unknown. Here, we report the synergistic facilitation of locomotion when DBS is combined with EES in a rat model of severe contusion spinal cord injury leading to leg paralysis. However, this synergy requires high amplitudes of DBS, which triggers forced locomotion associated with stress responses. To suppress these undesired responses, we link DBS to the intention to walk, decoded from cortical activity using a robust, rapidly calibrated unsupervised learning algorithm. This contingency amplifies the supraspinal descending command while empowering the rats into volitional walking. However, the resulting improvements may not outweigh the complex technological framework necessary to establish viable therapeutic conditions.


Pain ◽  
1990 ◽  
Vol 41 ◽  
pp. S113
Author(s):  
J.A. Beal ◽  
K.N. Nandi ◽  
D.S. Knight

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