8 de out de 2014

Total vertebrectomy for stabilisation of chronic spinal lumbar luxation in a paraplegic dog without nociception


Journal of Small Animal Practice,Volume 55, Issue 10, Pages 485–541, October 2014

P. V. Tertuliano Marinho,C. C. Zani, F. De Biasi and M. V. Bahr Arias


         An adult male crossbred dog was referred with a history of a road traffic accident that took place 1 month earlier. Neurological examination revealed paraplegia with absent nociception in the pelvic limbs. On epaxial palpation, significant curvature of the anatomical axis of the spine between the third and fourth lumbar vertebrae was observed, with the presence of a bone end almost piercing the dog's skin. Survey radiographs of the lumbar spine revealed severe dislocation between L3 and L4 vertebrae. During surgery, the spinal cord was not visible between the dislocated segments. Because of difficulties in reducing the lumbar luxation during surgery, vertebrectomy and vertebral shortening were performed. After alignment between vertebrae L3 and L5, eight cortical orthopaedic screws and bone cement were used for fixation. After 30 days, the dog started to use a wheelchair and was considered by its owner to have a good quality of life with no evidence of pain. To the authors’ knowledge, this is the first case of severe luxation treated by total vertebrectomy and spine shortening in a dog. This surgery can be considered as an option in the management of severe spine luxation when the spinal cord is physically transected.

3 de out de 2014

Abiotrofia cerebelar em um canino American Staffordshire Terrier adulto no Brasil

 Cerebellar Abiotrophy in an American Staffordshire Terrier Adult Dog in Brazil


Acta Scientiae Veterinariae, 2014. 42(Suppl 1): 52.

Cristine Mari, Daniele Mariath Bassuino, Angelica Terezinha Barth Wouters, Marcele Bettim Bandinelli, David Driemeier & Saulo Petinatti Pavarini

Cerebellar abiotrophy is a spontaneous, progressive degenerative disease of the cerebellum in which Purkinje cell loss and functional disorders occur secondary to an intrinsic metabolic defect. Clinically, all animals with cerebellar  abiotrophy are normal at birth, and neurological signs become evident during development. This work aimed to report  and describe a case of cerebellar cortical abiotrophy in an adult American Staffordshire Terrier in Brazil, highlighting the  pathologic findings of the cerebellar lesions. A 10-year-old female American Staffordshire Terrier presented with a 3-year history of progressive neurological  changes.  These changes began with mild ataxia of the hind limbs that involved the forelimbs after 2 years. In the recent  months prior to presentation, the patient spent most of her time lying down with a head tilt. When she stood with her head  raised, she exhibited abasia and required a broad base of support. When she attempted to walk, she quickly fell and rolled  over if not supported. She could not eat on her own because of intense intention tremors. Because of the severity of her  condition, the decision was made to euthanize the animal. Necropsy examination revealed no signifi cant findings. Various organ specimens were collected, fi xed in 10% formalin, and processed for routine histology. The tissue sections were  stained with hematoxylin and eosin. Cerebellar specimens were subjected to immunohistochemistry (IHC). Two cerebellar specimens from two normal 8- to 9-year-old American Staffordshire Terriers were used as positive controls for IHC andand  comparative evaluation of the lesions. Histologically, the main changes were observed in the cerebellum and were characterized by necrosis, degeneration, and marked segmental loss of Purkinje cells; moderate reduction in the granular cells of  the cerebellar cortex; and thinning of the molecular layer. Cerebellar IHC in the affected canine showed a slight reduction
in immunoreactivity for neurofi laments in both the molecular layer and white matter as well as a marked increase in immunostaining for glial fi brillary acidic protein, indicating astrogliosis, in the molecular layer, granular layer, and white matter.  The diagnosis of cerebellar abiotrophy in this canine patient was based on clinical, pathologic, and immunohistochemical fi ndings. The framework cerebellar syndrome in an adult dog, slowly progressive, as in this case (10 years old with a 3-year clinical progression) is compatible with abiotrophy in the American Staffordshire Terrier. The main gross  lesions observed in the cerebellum of canines with abiotrophy are projected to decline; however, these changes can be subtle,  as in this case. Histopathology revealed a primary loss of Purkinje cells and depletion of the molecular and granular layers.  These characteristics have been identifi ed as hereditary in American Staffordshire Terriers and other breeds. The clinical  signs observed in this patient, namely ataxia, intention tremors, and abasia, refl ect the loss of function of the inhibitory  neurons of the cerebellar cortex. The fact that cerebellar abiotrophy is relatively common in purebred dogs and the great  variety in the early clinical signs and progression suggests different genetic etiologies in different breeds. An association  with breed is evidenced by the fact that the clinical manifestations of cerebellar abiotrophy in American Staffordshire Terriers start late and have been shown to be hereditary. This paper reports the occurrence of cerebellar cortex  abiotrophy as  a cause of neurological disease in an American Staffordshire Terrier in Brazil.