Hind Limb Paresis Research Articles

RETROPERITONEAL ABSCESSES IN TWO WESTERN LOWLAND GORILLAS (GORILLA GORILLA GORILLA)

This report describes two cases of retroperitoneal abscesses in female western lowland gorillas (Gorilla gorilla gorilla). Clinical symptoms included perivulvar discharge, lameness, hindlimb paresis, and general malaise. Retroperitoneal abscesses should be considered as part of a complete differential list in female gorillas with similar clinical signs.

Spinal cord degeneration compatible with a central distal axonopathy in periparturient Holstein-Friesian dairy cows

Several diseases characterized by dysfunction of the central nervous system with significant involvement of the spinal cord have been documented in the bovine species. This report describes a spontaneously occurring degenerative spinal cord condition in two 4-year-old Holstein-Friesian dairy cows derived from different farms. The animals presented with anteparturient or postparturient onset of clinical signs encompassing hind limb ataxia, paresis, and recumbency. Both cows were euthanatized 2 days after the onset of clinical signs. Histopathology of the spinal cord in the two cows revealed bilaterally symmetrical degeneration of the white matter that was characterized primarily by Wallerian-type changes of myelinated axons with associated myelin sheath degradation and hypertrophy of astrocytes. These lesions were most marked in the ventral and lateral corticospinal tracts of the middle to caudal thoracic cord segments. Neurons in the dorsal and ventral gray horns were unremarkable. Although its etiology remains unknown, this degenerative myelopathy is possibly a new variant of neurodegenerative disorder compatible with a central distal axonopathy.

The Role of Copper and Vitamin A Deficiencies Leading to Neurological Signs in Captive Cheetahs (<i>Acinonyx jubatus</i>) and Lions (<i>Panthera leo</i>) in the United Arab Emirates

Neurological signs like ataxia and hind limb paresis have often been reported in cheetahs (Acinonyx jubatus), lions (Panthera leo) and snow leopards (Panthera unica). As a cause, copper and Vitamin A deficiencies have been discussed. Many cases were seen in cheetahs and lions in the United Arab Emirates (UAE) within the last years. The aim of this study was to find correlations between nutrition, serum, and tissue levels, focusing on copper and Vitamin A. Blood and tissue samples of affected and unaffected animals were analyzed at the Central Veterinary Research Laboratory in Dubai, UAE. Animals were split into three different groups (A, B and C) according to their diets. Minerals were determined in serum, tissue, food and water samples, and serum was additionally analyzed for Vitamin A and E. Liver, kidney and spinal cord samples were taken for histopathological investigations. Mean serum copper and liver copper levels of animals fed pure chicken muscle meat without supplements were significantly lower (0.41 ± 0.71 μM/L; 2.16 ± 0.95 ppm wet weight) than in animals fed a whole carcass prey diet (12.16 ± 3.42 μM/L; 16.01 ± 17.51 ppm wet weight) (p < 0.05). Serum Vitamin A and E levels were highest in animals fed whole carcass prey diets (1.85 ± 0.68; 27.31 ± 5.69 μM/L). Liver zinc concentrations were highest in animals fed pure chicken meat only (43.75 ± 16.48 ppm wet weight). In histopathology, demyelination of the spinal cord was found in all of the affected animals and most commonly when fed a diet based on poultry without supplements.

Cerebellar Ataxia Suspected to Be Caused by &lt;i&gt;Oxytropis glabra&lt;/i&gt; Poisoning in Western Mongolian Goats

ABSTRACTIn the last five years in western Mongolia, a neurological disorder and resultant economic loss have developed in goats, sheep, cattle and horses: association of the disease with ingestion of Oxytropis glabra, a toxic plant, was suggested. Affected goats showed neurological signs, including ataxia, incoordination, hind limb paresis, fine head tremor and nystagmus. Three goats, one with moderate clinical signs and the other two with severe clinical signs, were necropsied and examined to describe and characterize the histologic, immunohistochemical and ultrastructural lesions. Although no gross pathological changes were observed in a variety of organs including the central nervous system of these goats, microscopic examination of the cerebellum demonstrated degenerative changes in all these goats, such as vacuolar changes and loss of Purkinje cells, torpedo formation in the granular layer, increased number of spheroids in the cerebellar medulla, and loss of axons and myelin sheaths of Purkinje cells. The chemical analysis of the dried plant detected 0.02–0.05% (dry weight basis) of swainsonine. This is the first report describing the clinical and pathological findings in Mongolian goats suspected to be affected by O. glabra poisoning.

PERK Activation Preserves the Viability and Function of Remyelinating Oligodendrocytes in Immune-Mediated Demyelinating Diseases

Remyelination occurs in multiple sclerosis (MS) lesions but is generally considered to be insufficient. One of the major challenges in MS research is to understand the causes of remyelination failure and to identify therapeutic targets that promote remyelination. Activation of pancreatic endoplasmic reticulum kinase (PERK) signaling in response to endoplasmic reticulum stress modulates cell viability and function under stressful conditions. There is evidence that PERK is activated in remyelinating oligodendrocytes in demyelinated lesions in both MS and its animal model, experimental autoimmune encephalomyelitis (EAE). In this study, we sought to determine the role of PERK signaling in remyelinating oligodendrocytes in MS and EAE using transgenic mice that allow temporally controlled activation of PERK signaling specifically in oligodendrocytes. We demonstrated that persistent PERK activation was not deleterious to myelinating oligodendrocytes in young, developing mice or to remyelinating oligodendrocytes in cuprizone-induced demyelinated lesions. We found that enhancing PERK activation, specifically in (re)myelinating oligodendrocytes, protected the cells and myelin against the detrimental effects of interferon-γ, a key proinflammatory cytokine in MS and EAE. More important, we showed that enhancing PERK activation in remyelinating oligodendrocytes at the recovery stage of EAE promoted cell survival and remyelination in EAE demyelinated lesions. Thus, our data provide direct evidence that PERK activation cell-autonomously enhances the survival and preserves function of remyelinating oligodendrocytes in immune-mediated demyelinating diseases.

Forma nervosa da artrite-encefalite caprina

São descritos dois casos de caprinos, fêmeas, mestiços da raça Saanen de dois meses de idade com sinais clínicos de paresia de membros posteriores, incoordenação, dificuldade respiratória e caquexia, que foram submetidos à eutanásia, devido ao prognóstico desfavorável. Na necropsia, observou-se congestão do sistema nervoso central (SNC) e consolidação pulmonar nos dois caprinos. Microscopicamente, as alterações foram caracterizadas por leucoencefalomielite linfoplasmocítica multifocal, com vacuolização do neurópilo e esferoides axonais, leptomeningite, pneumonia intersticial não supurativa no caprino A e broncopneumonia bacteriana no caprino B. O exame de imuno-histoquímica (IHQ) foi positivo para o vírus da artrite-encefalite caprina em fragmento de tálamo. A prova de imunodifusão em gel de ágar (IDGA) foi realizada em vinte animais do rebanho de origem e dezesseis animais foram positivos. O diagnóstico da forma nervosa da infecção pelo vírus da artrite-encefalite caprina (CAEV) foi baseado no quadro clínico-patológico, IHQ e IDGA. Esta apresentação clínica da CAE pode ser pouco comum no Brasil, mas deve ser considerada em caso de doenças neurológicas em pequenos ruminantes.

Intervertebral Disc Protrusion in a Ferret with Triple Thoracic Block Vertebrae

Hind limb paresis or plegia in ferrets is a common sign of illness, which can be produced by intervertebral disc (IVD) extrusion or protrusion along with many other systemic diseases. This case report describes a ferret (Mustela putorius furo) with chronic onset paraplegia in which T7-T8, T8-T9, and T10-T11 IVD herniations and T9-T10 block vertebrae were diagnosed with the assistance of myelography. It is believed that the excessive stress on the adjacent annulus fibrosus and vertebral endplates resulting from block vertebrae could have been the cause of IVD disease in the atypical location described in this case.

Resveratrol Exacerbates Both Autoimmune and Viral Models of Multiple Sclerosis

The polyphenol compound resveratrol is reported to have multiple functions, including neuroprotection, and no major adverse effects have been reported. Although the neuroprotective effects have been associated with sirtuin 1 activation by resveratrol, the mechanisms by which resveratrol exerts such functions are a matter of controversy. We examined whether resveratrol can be neuroprotective in two models of multiple sclerosis: experimental autoimmune encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD). EAE was induced in C57BL/6 mice, which were fed a control diet or a diet containing resveratrol during either the induction or effector phase or through the whole course of EAE. SJL/J mice were infected with TMEV and fed a control diet or a diet containing resveratrol during the chronic phase of TMEV-IDD. In EAE, all groups of mice treated with resveratrol had more severe clinical signs than the control group. In particular, resveratrol treatment during the induction phase resulted in the most severe EAE, both clinically and histologically. Similarly, in the viral model, the mice treated with resveratrol developed significantly more severe TMEV-IDD than the control group. Thus, surprisingly, the resveratrol treatment significantly exacerbated demyelination and inflammation without neuroprotection in the central nervous system in both models. Our findings indicate that caution should be exercised in potential therapeutic applications of resveratrol in human inflammatory demyelinating diseases, including multiple sclerosis.

Chronic exposure to rotenone, a dopaminergic toxin, results in peripheral neuropathy associated with dopaminergic damage

Rotenone, a widely used pesticide, causes a syndrome in rats that replicates, both pathologically and behaviorally, the symptoms of Parkinson's disease (PD). In the present study, we sought to determine if a chronic exposure to rotenone, resulting in dopaminergic loss, could also lead to peripheral neuronal damage related to motor dysfunction. Adult male Sprague-Dawley rats (n=14) were treated with rotenone (1 or 2mg/kg, s.c., once daily) on days 1, 3, 6, 8, 10, 13, 15, 17, 21, 22, and 27 to minimize mortality. Control rats received vehicle (DMSO) injections. Animals were weighed on the days of injection and monitored daily. A mortality of 21% was observed in rotenone treated rats. The motor nerve conduction velocity (MCV) was assessed using action potentials detected from the tail muscle through surface receiver electrodes installed around the distal portion of the tail. Rats exposed to rotenone often developed hind limb paresis with a significant decrease in MCV as detected in tail nerves (p<0.05). Animals were then sacrificed, either 24h after rotenone exposure on day 6 or 24h after the last dose of rotenone on day 27. The striatum and sciatic nerves were dissected on dry ice and flash-frozen and kept at −80°C until further analysis. Striatal dopamine (DA) was analyzed using HPLC-ECD and sciatic nerve pathology was analyzed for neurodegeneration. A time-dependent rotenone-induced striatal depletion of DA (60% after 7 days and 80% after 27 days) was observed. Furthermore, Neurofilament-neurofilament B, Flouro-Jade C and myelin basic protein analyses suggested a time-dependent rotenone-induced neurodegeneration in sciatic nerves. These data, for the first time, indicate an association between dopaminergic damage and peripheral motor nerve degeneration in an animal model of dopaminergic toxicity. Peripheral motor nerve dysfunction in rats following a chronic exposure to rotenone may serve not only as a relevant experimental model of motor neuropathy but also as a peripheral marker of dopaminergic neuronal damage to the central nervous system.

Spinal fracture in a dog with diffuse idiopathic skeletal hyperostosis

A six-year-old, spayed female Weimaraner dog was first presented with the complaint of hindlimb paresis and then hindlimb paralysis two years later after colliding with a tree. Radiographs and computed tomography revealed spinal fractures at lumbar vertebrae (L)2-3 and at L4-5. In addition, the spinal column was affected by new bone formation along the vertebral bodies, bridging the disc spaces, as seen in diffuse idiopathic skeletal hyperostosis (DISH). Open reduction and internal fixation was achieved with standard vertebral body plating. This is the first report of DISH-associated spinal fractures after minor trauma in a dog. Surgery resulted in return of the full function after the first, and in improvement of neurologic function after the second incident.

PULMONARY ADENOCARCINOMA WITH OSSEOUS METASTASIS AND SECONDARY PARESIS IN A BLUE AND GOLD MACAW (ARA ARARAUNA)

A 16-yr-old female blue and gold macaw (Ara ararauna) was presented with an acute history of lethargy, inappetance, ataxia, and paralysis. The bird had rapidly progressed from a normal state to complete inability to perch or ambulate within a 48-hr period. Neurologic examination revealed bilateral hind limb paresis with upper motor neuron signs present in both legs and the vent. Radiographs identified multiple nodular soft-tissue opacities within the cranial coelomic cavity and a single nodule superimposed with the thoracic spine. The bird was euthanized and submitted for necropsy, which revealed a primary pulmonary adenocarcinoma with multiple sites of osseous metastasis, including the vertebrae, and subsequent spinal cord compression. This is the first report of pulmonary adenocarcinoma in this species, although reports of similar tumors in other psittacines have been published. This report, along with others previously published, suggests that vertebral metastasis of primary pulmonary tumors may be more common in psittacine species than previously recognized and, as such, should be considered as a differential diagnosis in psittacine birds exhibiting signs of neurologic dysfunction attributed to a spinal cord lesion.

Naturally Occurring Parelaphostrongylus tenuis–Associated Choriomeningitis in a Guinea Pig With Neurologic Signs

An adult male guinea pig (Cavia porcellus) with a 1-month history of hind limb paresis, torticollis, and seizures was euthanized and submitted for necropsy. Gross examination was unremarkable, but histologic examination revealed multifocal eosinophilic and lymphoplasmacytic choriomeningitis and cross sections of nematode parasites within the leptomeninges of the midbrain and diencephalon. Morphologic features of the nematode were consistent with a metastrongyle, and the parasite was identified as Parelaphostrongylus tenuis by polymerase chain reaction testing and nucleotide sequencing. Further questioning of the owner revealed that the guinea pig was fed grass from a yard often grazed by white-tailed deer (Odocoileus virginianus). To the authors' knowledge, this is the first report of a naturally occurring P. tenuis infection in a guinea pig.

Use of Magnetic Resonance Imaging in the diagnosis of spinal empyema caused by a migrating grass awn in a dog

CASE HISTORY: A 13 kg 3.5-year-old male neutered Cocker Spaniel presented with a 6-day history of deteriorating hindlimb paresis. Approximately 10 weeks previously the owner reported removing a large number of barley grass seeds from the dog's coat and ears. Eight weeks later the dog was treated for pneumonia, based on clinical findings and thoracic radiographs. In the 4 days prior to referral the dog had a decreased appetite, was lethargic and appeared unable to urinate voluntarily. CLINICAL FINDINGS: The dog was bright and alert but unable to walk. Upper motor neuron signs were indicative of T3–L3 spinal lesion. Using magnetic resonance imaging (MRI), an abnormal low signal linear structure within the left T12–T13 neural foramen extending to the left lateral aspects of the thoracic spinal cord was detected, consistent with a foreign body. A left T12–T13 lateral hemilaminectomy was performed and a grass seed removed from a tract extending caudally from the T12–13 space, dorsal to the lumbar transverse processes and the rib head. The dog made a rapid recovery after surgery with full resolution of clinical signs. DIAGNOSIS: Spinal empyema caused by a migrating barley grass awn (Hordeum spp.). CLINICAL RELEVANCE: Advanced imaging using MRI can bea valuable method for localising foreign bodies prior to exploratory surgery. Animals presenting with neurological signs should have foreign body reactions included as a differential diagnosis.

Permanent monoparesis in a dog after intramedullary injection of iohexol into the lumbar spinal cord

CASE HISTORY: An 8-year-old, spayed, Doberman Pinscher bitch presented for assessment of acute hindlimb paresis. CLINICAL FINDINGS: During a lumbar myelographic contrast study a small volume of iohexol contrast agent was inadvertently injected into the cord parenchyma. After surgical hemilaminectomy for an intervertebral disc extrusion at L1–2 the dog recovered use of one hindlimb, but had ongoing extensor weakness of the left hindlimb. Left femoral nerve function had not returned after 14 months. DIAGNOSIS: EMG findings 14 months after the incident indicated persistent femoral neuropathy consistent with the intramedullary contrast injection at L3–4. CLINICAL RELEVANCE: Inadvertent deposition of iohexol into spinal cord parenchyma may be rare, but if it occurs it can have long-lasting consequences.

Clinical conundrum

An 11-year-old Domestic Shorthair presented with acute-onset right hindlimb paresis and respiratory distress. The diagnosis and subsequent management of an arterial thromboembolism are described.

Air Gun Impactor—A Novel Model of Graded White Matter Spinal Cord Injury in Rodents

Understanding mechanisms of spinal cord injury and repair requires a reliable experimental model. We have developed a new device that produces a partial damage of spinal cord white matter by means of a precisely adjusted stream of air applied under high pressure. This procedure is less invasive than standard contusion or compression models and does not require surgical removal of vertebral bones. We investigated the effects of spinal cord injury made with our device in 29 adult rats, applying different experimental parameters. The rats were divided into three groups in respect to the applied force of the blast wave. Functional outcome and histopathological effects of the injury were analyzed during 12-week follow-up. The lesions were also examined by means of magnetic resonance imaging (MRI) scans. The weakest stimulus produced transient hindlimb paresis with no cyst visible in spinal cord MRI scans, whereas the strongest was associated with permanent neurological deficit accompanied by pathological changes resembling posttraumatic syringomyelia. Obtained data revealed that our apparatus provided a spinal cord injury animal model with structural changes very similar to that present in patients after moderate spinal cord trauma.

Intramedullary lumbosacral teratoma in a domestic ferret (Mustela putorius furo)

An 18-month-old, female, spayed domestic ferret (Mustela putorius furo) was presented for progressive hind limb paresis of 1 week duration. The ferret was mentally appropriate but cachexic and ataxic with neurological deficits, which localized the lesion to the lumbosacral region. A depression in the lumbosacral spine was associated with discomfort on palpation. Results of whole body radiographs were consistent with an abnormal angle between vertebrae L6 and S1, which resulted in hyperflexion of the spine. The ferret was euthanized, and histopathological examination revealed an intramedullary lumbosacral teratoma effacing much of the spine in the region of the mass.

Intrathecal recombinant human 4-sulfatase reduces accumulation of glycosaminoglycans in dura of mucopolysaccharidosis VI cats

Mucopolysaccharidosis VI (MPS-VI) is caused by a deficiency in N-acetylgalactosamine-4-sulfatase activity, resulting in lysosomal accumulation of partially degraded glycosaminoglycans (GAGs). Compressive myelopathy in early-onset MPS-VI patients has been partly attributed to thickening of the dura mater following engorgement with GAG. In this study, we therefore tested whether the dural abnormalities could be prevented in a feline model of the disorder. All intrathecal injections (IT-INJs) were well tolerated. MPS-VI cats treated with IT-INJ of recombinant human N-acetylgalactosamine-4-sulfatase (rhASB) exhibited reduced vacuolation in the dural fibroblasts, diminished levels of sulfated-N-acetylhexosamine (HNAc(+S)) in the cerebrospinal fluid (CSF) and no hind-limb paresis. Serum anti-rhASB antibodies remained low in MPS-VI cats treated with intravenous enzyme replacement therapy (IV-ERT) and increased slightly in normal cats treated with IT-INJ of rhASB alone. Anti-rhASB antibodies in CSF remained undetectable. These data indicate that repeated IT-INJ of rhASB can safely prevent GAG storage in MPS-VI dura. Cats were assigned to three groups: (i) receiving weekly IV-ERT of rhASB from birth plus six monthly IT-INJs of rhASB from age 2 months; (ii) receiving six monthly IT-INJs of vehicle; or (iii) untreated. Additional normal cats received five fortnightly IT-INJs of rhASB or vehicle alone.

Parasite meningomyelitis in cats in Uruguay

Two outbreaks of progressive hind limb paresis in cats (Felis catus) caused by parasitic meningomyelitis in Uruguay are reported. The case studies occurred in 2008 and 2009 respectively, in the rural areas of Fray Bentos (33° 07' 40.39'' S) and were characterized by hindquarter paralysis. This paralysis was progressive and had a chronic progression of approximately 12 months until the death or euthanasia of the animals. Clinical symptoms started with ataxia of the hindquarters with lateral side-to-side swaying and culminated in total paralysis. Two animals were sent for necropsy in 2009. The main histopathological findings were severe myelitis in the lumbar spinal cord with perivascular cuffing and white matter necrosis, severe nonsuppurative meningitis with thrombi in subarachnoid blood vessels, and intravascular presence of multiple adult parasites. From the morphological characteristics of the parasites and location in the leptomeninges, the parasite was identified as the nematode Gurltia paralysans.

Naturally occurring and experimental Stachys arvensis (staggerweed) toxicity in lambs in New Zealand

Stachys arvensis (staggerweed) is a common, widely distributed weed of cultivated and waste land with the potential to intoxicate sheep. Two naturally occurring outbreaks of suspected staggerweed toxicity in the lower North Island were investigated. Affected lambs had been recently moved onto staggerweed-contaminated Brassica spp. crops. In total, 150/1,200 (13%) lambs developed hindlimb paresis, a fine generalised muscular tremor, and hunched posture. When forced to move, many became recumbent. Most lambs recovered within 48 h of removal from staggerweed, although a few developed clinical signs again when transported 2–3 weeks later. Grossly, affected lambs had large amounts of staggerweed plant material and seeds within the rumen. Histopathology showed mild, multifocal degeneration of the white matter tracts of the central nervous system (CNS), most commonly in the ventral funiculi of the spinal cord, and acute, mild to moderate, multifocal degeneration of skeletal muscles. Creatine kinase (CK) activity in serum was mildly to markedly elevated in affected lambs. In a feeding trial, ten 10-month-old Romney lambs were randomly assigned to equal treatment and control groups. Treated lambs were drenched with a liquid extract of staggerweed once daily for 7 days. Three of five treated lambs developed mild exercise intolerance, and 1/5 displayed mild paresis of the hindlimbs, slightly crouched hindlimb stance, and shortened gait, on days 6 and 7. Histologically, 4/5 treated lambs had degeneration in white matter tracts of the CNS, indistinguishable from those seen in the lambs in the outbreak, and in 1/5 lambs there was scattered regeneration of skeletal muscle. CK activity in serum in treated lambs was not significantly higher than that in control lambs. None of the control lambs developed significant clinical signs, histological changes or increases in CK activity in serum. The clinical signs and lesions observed in both the outbreaks and feeding trial were similar to those previously described in studies in Australia, with the exception that myodegeneration was more prominent in the outbreaks in New Zealand. Further characterisation of the pathogenesis of staggerweed toxicity and its potential role as a food safety hazard will be facilitated through identification of the toxic principle(s).