Resumo
Purpose: Various postoperative protocols have been proposed to improve outcomes and accelerate nerve regeneration. Recently, the use of physical exercise in a post-surgical neurorraphy procedure has shown good results when started early. We experimentally investigated the hypothesis that post-operative exercise speeds up results and improves clinical and morphologic parameters. Methods: Isogenic rats were randomly divided into four groups: 1 SHAM; 2 SHAM submitted to the exercise protocol (EP); 3 Grafting of the sciatic nerve; and 4 Grafting of the sciatic nerve associated with the EP. The EP was based on aerobic activities with a treadmill, with a progressive increase in time and intensity during 6 weeks. The results were evaluated by the sciatic functional index (SFI), morphometric and morphologic analysis of nerve distal to the lesion, and the number of spinal cord motor neurons, positive to the marker Fluoro-Gold (FG), captured retrogradely through neurorraphy. Results: Functional analysis (SFI) did not show a statistical difference between the group grafted with (50.94) and without exercise (-65.79) after 90 days. The motoneurons count (Spinal cord histology) also showed no diference between these groups (834.5 × 833 respectively). Although functionally there is no difference between these groups, morphometric study showed a greater density (53.62) and larger fibers (7.762) in GRAFT group. When comparing both operated groups with both SHAM groups, all values were much lower. Conclusions: The experimental model that this aerobic treadmill exercises protocol did not modify nerve regeneration after sciatic nerve injury and repair with nerve graft.
Assuntos
Animais , Ratos , Nervo Fibular , Neuropatias Fibulares/terapia , Teste de Esforço , Regeneração Nervosa , Hipertensão/veterinária , Neurônios Motores/fisiologiaResumo
ABSTRACT: Forty 1-2-y-old water buffaloes were simultaneously treated with trichlorfon and chlorpyrifos products in the recommended dose for cattle. After a week, 19 animals started presenting clinical signs characterized by apathy, diarrhea, aggressiveness, dehydration, and motor incoordination, followed by flaccid paralysis and permanent lateral recumbency. All affected buffaloes died after a clinical course of 1-4 days. Reduction of serum cholinesterase activity in three cases was indicative of significant exposure to organophosphorus compounds (OPs). Pathological examination of three buffaloes revealed no gross and histological lesions. By thin layer chromatography, chlorpyrifos residues and trace of trichlorfon residues were detected in fresh tissue samples. The epidemiological, clinical, pathological, and toxicological findings were highly compatible with OPs-induced delayed neurotoxicity, a neurological manifestation rarely described in domestic animals.
RESUMO: Quarenta búfalos foram simultaneamente tratados com clorpirifós e triclorfom na dose recomendada para bovinos. Após uma semana, 19 animais apresentaram sinais clínicos caracterizados por apatia, diarreia, agressividade, desidratação e incoordenação motora, seguidos por paralisia flácida e decúbito lateral permanente. Todos os búfalos afetados morreram após um curso clínico de 1-4 dias. Redução da atividade da colinesterase sérica em três casos foi indicativa de exposição significativa a organofosforados (OPs). O exame patológico de três búfalos não revelou lesões macroscópicas e histológicas. Por cromatografia em camada delgada, resíduos de clorpirifós e traços de resíduos de triclorfon foram detectados em amostras de tecidos frescos. Os achados epidemiológicos, clínicos, patológicos e toxicológicos foram compatíveis com neuropatia tardia induzida por OPs, uma manifestação neurológica raramente descrita em animais domésticos.
Resumo
Background: Peripheral neuropathies result in sensory, motor or autonomic dysfunctions due to impairment of peripheral spinal or cranial nerves. Neoplasms such as lymphoma are cited as one of the many aetiological causes and it mayaffect the nerve directly, by compression, or indirectly (paraneoplastic) by remote action of the neoplasm located in anextra-neural site. This study aimed to report two cases of cranial nerve neuropathy (trigeminal and facial) associated withcanine lymphoma, contributing to a better understanding of its paraneoplastic effects on the nervous system, as well asthe diagnosis and treatment of these conditions.Cases: Two cases of canine lymphoma associated with possible signs of paraneoplastic peripheral neuropathy were attendedat the Veterinary Hospital from the Universidade Federal de Minas Gerais (HV UFMG). Case 1. A spayed mixed breedbitch, with lethargy and unilateral exophthalmos. Brain computed tomography revealed a retrobulbar mass and cytology wasdiagnostic for extranodal lymphoma. Subsequent to computed tomography, the dog was presented with hypotrophy of thefacial musculature and difficulty in grasping food, consistent with trigeminal nerve palsy, which resolved after institutionof the 19-week chemotherapy protocol from the University of Wisconsin. Nevertheless, disease reccurred and a rescueprotocol was initiated. Case 2. A female Dalmatian, spayed, was diagnosed with multicentric lymphoma, after cytologyof the left mandibular lymph node. Chemotherapy was initiated with the same protocol of the previous case. However,the disease progressed and it was observed facial asymmetry with ptosis of the left eyelid, pina and lips, in addition todifficulty in grasping food, suggesting facial and trigeminal cranial nerve palsy. Clinical signs resolved after institutionof a rescue chemotherapy protocol. However, in both cases, disease progression and poor clinical condition resulted in...
Assuntos
Feminino , Animais , Cães , Doenças do Nervo Facial/veterinária , Doenças do Nervo Trigêmeo/veterinária , Linfoma/veterinária , Biópsia/veterinária , Tomografia/veterináriaResumo
Background: Peripheral neuropathies result in sensory, motor or autonomic dysfunctions due to impairment of peripheral spinal or cranial nerves. Neoplasms such as lymphoma are cited as one of the many aetiological causes and it mayaffect the nerve directly, by compression, or indirectly (paraneoplastic) by remote action of the neoplasm located in anextra-neural site. This study aimed to report two cases of cranial nerve neuropathy (trigeminal and facial) associated withcanine lymphoma, contributing to a better understanding of its paraneoplastic effects on the nervous system, as well asthe diagnosis and treatment of these conditions.Cases: Two cases of canine lymphoma associated with possible signs of paraneoplastic peripheral neuropathy were attendedat the Veterinary Hospital from the Universidade Federal de Minas Gerais (HV UFMG). Case 1. A spayed mixed breedbitch, with lethargy and unilateral exophthalmos. Brain computed tomography revealed a retrobulbar mass and cytology wasdiagnostic for extranodal lymphoma. Subsequent to computed tomography, the dog was presented with hypotrophy of thefacial musculature and difficulty in grasping food, consistent with trigeminal nerve palsy, which resolved after institutionof the 19-week chemotherapy protocol from the University of Wisconsin. Nevertheless, disease reccurred and a rescueprotocol was initiated. Case 2. A female Dalmatian, spayed, was diagnosed with multicentric lymphoma, after cytologyof the left mandibular lymph node. Chemotherapy was initiated with the same protocol of the previous case. However,the disease progressed and it was observed facial asymmetry with ptosis of the left eyelid, pina and lips, in addition todifficulty in grasping food, suggesting facial and trigeminal cranial nerve palsy. Clinical signs resolved after institutionof a rescue chemotherapy protocol. However, in both cases, disease progression and poor clinical condition resulted in...(AU)
Assuntos
Animais , Feminino , Cães , Linfoma/veterinária , Doenças do Nervo Trigêmeo/veterinária , Doenças do Nervo Facial/veterinária , Tomografia/veterinária , Biópsia/veterináriaResumo
Forty 1-2-y-old water buffaloes were simultaneously treated with trichlorfon and chlorpyrifos products in the recommended dose for cattle. After a week, 19 animals started presenting clinical signs characterized by apathy, diarrhea, aggressiveness, dehydration, and motor incoordination, followed by flaccid paralysis and permanent lateral recumbency. All affected buffaloes died after a clinical course of 1-4 days. Reduction of serum cholinesterase activity in three cases was indicative of significant exposure to organophosphorus compounds (OPs). Pathological examination of three buffaloes revealed no gross and histological lesions. By thin layer chromatography, chlorpyrifos residues and trace of trichlorfon residues were detected in fresh tissue samples. The epidemiological, clinical, pathological, and toxicological findings were highly compatible with OPs-induced delayed neurotoxicity, a neurological manifestation rarely described in domestic animals.
Quarenta búfalos foram simultaneamente tratados com clorpirifós e triclorfom na dose recomendada para bovinos. Após uma semana, 19 animais apresentaram sinais clínicos caracterizados por apatia, diarreia, agressividade, desidratação e incoordenação motora, seguidos por paralisia flácida e decúbito lateral permanente. Todos os búfalos afetados morreram após um curso clínico de 1-4 dias. Redução da atividade da colinesterase sérica em três casos foi indicativa de exposição significativa a organofosforados (OPs). O exame patológico de três búfalos não revelou lesões macroscópicas e histológicas. Por cromatografia em camada delgada, resíduos de clorpirifós e traços de resíduos de triclorfon foram detectados em amostras de tecidos frescos. Os achados epidemiológicos, clínicos, patológicos e toxicológicos foram compatíveis com neuropatia tardia induzida por OPs, uma manifestação neurológica raramente descrita em animais domésticos.
Assuntos
Animais , Bovinos , Compostos Organofosforados/toxicidade , Doenças dos Bovinos/patologia , Síndromes Neurotóxicas/complicações , Síndromes Neurotóxicas/diagnóstico , Síndromes Neurotóxicas/patologia , Síndromes Neurotóxicas/veterináriaResumo
Forty 1-2-y-old water buffaloes were simultaneously treated with trichlorfon and chlorpyrifos products in the recommended dose for cattle. After a week, 19 animals started presenting clinical signs characterized by apathy, diarrhea, aggressiveness, dehydration, and motor incoordination, followed by flaccid paralysis and permanent lateral recumbency. All affected buffaloes died after a clinical course of 1-4 days. Reduction of serum cholinesterase activity in three cases was indicative of significant exposure to organophosphorus compounds (OPs). Pathological examination of three buffaloes revealed no gross and histological lesions. By thin layer chromatography, chlorpyrifos residues and trace of trichlorfon residues were detected in fresh tissue samples. The epidemiological, clinical, pathological, and toxicological findings were highly compatible with OPs-induced delayed neurotoxicity, a neurological manifestation rarely described in domestic animals.(AU)
Quarenta búfalos foram simultaneamente tratados com clorpirifós e triclorfom na dose recomendada para bovinos. Após uma semana, 19 animais apresentaram sinais clínicos caracterizados por apatia, diarreia, agressividade, desidratação e incoordenação motora, seguidos por paralisia flácida e decúbito lateral permanente. Todos os búfalos afetados morreram após um curso clínico de 1-4 dias. Redução da atividade da colinesterase sérica em três casos foi indicativa de exposição significativa a organofosforados (OPs). O exame patológico de três búfalos não revelou lesões macroscópicas e histológicas. Por cromatografia em camada delgada, resíduos de clorpirifós e traços de resíduos de triclorfon foram detectados em amostras de tecidos frescos. Os achados epidemiológicos, clínicos, patológicos e toxicológicos foram compatíveis com neuropatia tardia induzida por OPs, uma manifestação neurológica raramente descrita em animais domésticos.(AU)
Assuntos
Animais , Bovinos , Doenças dos Bovinos/patologia , Síndromes Neurotóxicas/complicações , Síndromes Neurotóxicas/diagnóstico , Síndromes Neurotóxicas/patologia , Síndromes Neurotóxicas/veterinária , Compostos Organofosforados/toxicidadeResumo
Background: Intrathecal injection of voltage-sensitive calcium channel blocker peptide toxins exerts analgesic effect in several animal models of pain. Upon intrathecal administration, recombinant Phα1β exerts the same analgesic effects as the those of the native toxin. However, from a clinical perspective, the intrathecal administration limits the use of anesthetic drugs in patients. Therefore, this study aimed to investigate the possible antinociceptive effect of intravenous recombinant Phα1β in rat models of neuropathic pain, as well as its side effects on motor, cardiac (heart rate and blood pressure), and biochemical parameters. Methods: Male Wistar rats and male Balb-C mice were used in this study. Giotto Biotech® synthesized the recombinant version of Phα1β using Escherichia coli expression. In rats, neuropathic pain was induced by chronic constriction of the sciatic nerve and paclitaxel-induced acute and chronic pain. Mechanical sensitivity was evaluated using von Frey filaments. A radiotelemeter transmitter (TA11PA-C10; Data Sciences, St. Paul, MN, USA) was placed on the left carotid of mice for investigation of cardiovascular side effects. Locomotor activity data were evaluated using the open-field paradigm, and serum CKMB, TGO, TGP, LDH, lactate, creatinine, and urea levels were examined. Results: Intravenous administration of recombinant Phα1β toxin induced analgesia for up to 4 h, with ED50 of 0.02 (0.01-0.03) mg/kg, and reached the maximal effect (Emax = 100% antinociception) at a dose of 0.2 mg/kg. No significant changes were observed in any of the evaluated motor, cardiac or biochemical parameters. Conclusion: Our data suggest that intravenous administration of recombinant Phα1β may be feasible for drug-induced analgesia, without causing any severe side effects.(AU)
Assuntos
Animais , Masculino , Ratos , Venenos de Aranha/química , Toxinas Biológicas/administração & dosagem , Toxinas Biológicas/efeitos adversos , Analgésicos , Neuropatia Ciática/terapia , Paclitaxel , Ratos Wistar , Camundongos Endogâmicos BALB C , Administração IntravenosaResumo
Background: Intrathecal injection of voltage-sensitive calcium channel blocker peptide toxins exerts analgesic effect in several animal models of pain. Upon intrathecal administration, recombinant Phα1β exerts the same analgesic effects as the those of the native toxin. However, from a clinical perspective, the intrathecal administration limits the use of anesthetic drugs in patients. Therefore, this study aimed to investigate the possible antinociceptive effect of intravenous recombinant Phα1β in rat models of neuropathic pain, as well as its side effects on motor, cardiac (heart rate and blood pressure), and biochemical parameters. Methods: Male Wistar rats and male Balb-C mice were used in this study. Giotto Biotech® synthesized the recombinant version of Phα1β using Escherichia coli expression. In rats, neuropathic pain was induced by chronic constriction of the sciatic nerve and paclitaxel-induced acute and chronic pain. Mechanical sensitivity was evaluated using von Frey filaments. A radiotelemeter transmitter (TA11PA-C10; Data Sciences, St. Paul, MN, USA) was placed on the left carotid of mice for investigation of cardiovascular side effects. Locomotor activity data were evaluated using the open-field paradigm, and serum CKMB, TGO, TGP, LDH, lactate, creatinine, and urea levels were examined. Results: Intravenous administration of recombinant Phα1β toxin induced analgesia for up to 4 h, with ED50 of 0.02 (0.01-0.03) mg/kg, and reached the maximal effect (Emax = 100% antinociception) at a dose of 0.2 mg/kg. No significant changes were observed in any of the evaluated motor, cardiac or biochemical parameters. Conclusion: Our data suggest that intravenous administration of recombinant Phα1β may be feasible for drug-induced analgesia, without causing any severe side effects.
Assuntos
Masculino , Animais , Ratos , Analgésicos , Neuropatia Ciática/terapia , Paclitaxel , Toxinas Biológicas/administração & dosagem , Toxinas Biológicas/efeitos adversos , Venenos de Aranha/química , Administração Intravenosa , Camundongos Endogâmicos BALB C , Ratos WistarResumo
Background: Idiopathic trigeminal neuropathy is a peripheral neuropathy whose clinical signs include inability to close themouth. A neurological examination reveals mainly flaccid paralysis of the masticatory muscles, which may be accompaniedby atony/hypotonia of the masseter and temporalis muscles. Altered sensitivity may also be present in very rare cases.This article reports a case of idiopathic trigeminal neuropathy with involvement of the motor and sensory nerve fibers in adog, describing the clinical symptoms, neurological findings, exclusion of other diseases, and evolution of the condition.Case: A 5-year-old bitch showing signs of difficulty in picking up food, swallowing water, and hypersalivation was takento a veterinary clinic. According to her owner, these signs had started spontaneously 2 days earlier. A physical examinationof the animal revealed only a persistently open mouth, although the mouth opening and closing movements could be performed manually by manipulating the jaw. The patient showed swallowing ability, and her tongue movements were intact.The neurological examination revealed that the animal also presented bilateral absence of nasal sensitivity and absenceof palpebral reflex. The animals blood test results showed changes only in the CK and AST levels, which were 1,182.60U/L (reference: 1.5 to 28.4 U/L) and 87.1 IU/L (reference: 6.2 to 13 IU/L), respectively. The animal tested negative fordistemper, leishmaniasis, toxoplasmosis and neosporosis. Abdominal ultrasound and thoracic radiography were performedto investigate neoplasia, as well as radiography of the temporomandibular joints, and none of these imaging tests revealedany alterations. A cerebrospinal fluid (CSF) analysis was also within the normal range of reference parameters. In view ofthe possibility of idiopathic trigeminal neuropathy, prednisolone...
Assuntos
Feminino , Animais , Cães , Nervo Trigêmeo , Neurite (Inflamação)/patologia , Neurite (Inflamação)/veterinária , Doenças Mandibulares/veterináriaResumo
Background: Idiopathic trigeminal neuropathy is a peripheral neuropathy whose clinical signs include inability to close themouth. A neurological examination reveals mainly flaccid paralysis of the masticatory muscles, which may be accompaniedby atony/hypotonia of the masseter and temporalis muscles. Altered sensitivity may also be present in very rare cases.This article reports a case of idiopathic trigeminal neuropathy with involvement of the motor and sensory nerve fibers in adog, describing the clinical symptoms, neurological findings, exclusion of other diseases, and evolution of the condition.Case: A 5-year-old bitch showing signs of difficulty in picking up food, swallowing water, and hypersalivation was takento a veterinary clinic. According to her owner, these signs had started spontaneously 2 days earlier. A physical examinationof the animal revealed only a persistently open mouth, although the mouth opening and closing movements could be performed manually by manipulating the jaw. The patient showed swallowing ability, and her tongue movements were intact.The neurological examination revealed that the animal also presented bilateral absence of nasal sensitivity and absenceof palpebral reflex. The animals blood test results showed changes only in the CK and AST levels, which were 1,182.60U/L (reference: 1.5 to 28.4 U/L) and 87.1 IU/L (reference: 6.2 to 13 IU/L), respectively. The animal tested negative fordistemper, leishmaniasis, toxoplasmosis and neosporosis. Abdominal ultrasound and thoracic radiography were performedto investigate neoplasia, as well as radiography of the temporomandibular joints, and none of these imaging tests revealedany alterations. A cerebrospinal fluid (CSF) analysis was also within the normal range of reference parameters. In view ofthe possibility of idiopathic trigeminal neuropathy, prednisolone...(AU)
Assuntos
Animais , Feminino , Cães , Neurite (Inflamação)/patologia , Neurite (Inflamação)/veterinária , Nervo Trigêmeo , Doenças Mandibulares/veterináriaResumo
Background: The glaucoma is a progressive optical neuropathy generally associated to the increase of the intraocular pressure (IOP). It is a disease of difficult therapeutic conduct and potential cause of blindness. The dorzolamide at 2% and the latanoprost at 0.005% are topical antiglaucoma drugs that cause significant reduction of the IOP. We decided to evaluate the local adverse effects of the dorzolamide at 2% and of the latanoprost at 0.005% in rabbits treated during 120 days. Materials, Methods & Results: Eighteen adult male rabbits were used in this study. They were randomly distributed into 3 groups (G) [n = 6]. Each animal received topical treatment in both eyes: GI (latanoprost at 0.005%, SID); GII (dorzolamide at 2%, TID) and GIII (ultra-pure water, TID) during 120 days. Ophthalmological evaluation was carried out through daily clinical examination, and at the end of the 120 days of treatment, it was verified clinical-ophthalmological alterations in the eyelids. The measurement of ECC was performed in triplicate, obtaining the lowest value among them as a result. They were carried out at the same time, in the morning between 9 and 10 am in order to avoid the effects of daytime ECC variation related to corneal hydration. In animals from group I, changes were observed in two eyes. Conjunctival hyperemia and ocular secretion, both in mild degree, were evidenced, respectively, in 13.75% and 9.1% of the observations. Conjunctival hyperemia was characterized from the 16th day and lasted until the final time (120 days). The animals from GII, treated with dorzolamide at 2%, presented the highest number of ophthalmological alterations. At the end of the experiment, conjunctival and eyelid changes and presence of ocular secretion, both ranging from mild to moderate, were observed in 60% and 16.32% of eyes, respectively. The animals from control group, GIII, did not present ophthalmological alterations. Discussion: Clinical signs observed in eyes...
Assuntos
Animais , Coelhos , Latanoprosta/administração & dosagem , Latanoprosta/análise , Olho , Pressão Intraocular/efeitos dos fármacos , Soluções Oftálmicas/administração & dosagem , Soluções Oftálmicas/análise , Cegueira/veterinária , Glaucoma/tratamento farmacológico , Glaucoma/veterináriaResumo
Neuropathies of pharyngeal branches of glossopharyngeal and vagus are often associated with guttural pouches diseases; however, these branches of injury due to stylopharyngeus muscle compression are not reported. A case was reported of a quarter horse mare, 8 years old, 450 kg, presenting dyspnea and respiratory noise associated with weight loss. Clinical examination observed mixed dyspnea, tachycardia, dysphagia, sialorrhea, lung crackles and submandibular and parotid lymphadenopathy. Endoscopic exam showed right arytenoid chondritis, nasopharyngeal collapse, generalized larynx edema and dorsal displacement of the soft palate. Right guttural pouch evaluation showed swelling in the origin of stylopharyngeus muscle with consequent compression of the XII, X and IX cranial nerves. Tracheotomy, systemic treatment with corticosteroids, beta lactams and aminoglycosides antibiotics were performed. No resolution was observed and, after 16 days, the animal showed clinical worsening, developed pleuropneumonia, uveitis, severe sepsis, acute renal failure and was euthanized. The mixed neuropathy resulted in rapid clinical deterioration of the animal, due to the difficulty in swallowing and consequent associated respiratory processes. This report emphasizes the importance of evaluating stylopharyngeus muscle origin in cases of nasopharyngeal collapse associated with dysphagia in horses, given the possibility that structural changes in this muscle can result in laryngeal neuropathy.(AU)
As neuropatias do glossofaríngeo e vago são frequentemente associadas com enfermidade das bolsas guturais. A ocorrência desta lesão secundária a compressão pelo músculo estilofaríngeo não é reportada. Relata-se o caso de uma égua quarto de milha, 8 anos de idade, 450 kg, apresentando dispneia, ruído respiratório e perda de peso. No exame clínico observou-se dispnéia mista, taquicardia, disfagia, sialorréia, crepitação pulmonar e linfadenopatia submandibular e parotídea. Ao exame endoscópico identificou-se condrite aritenóide direita, colapso nasofaríngeo, edema generalizado da laringe e deslocamento dorsal do palato mole. Na avaliação da bolsa gutural direita identificou-se aumento de volume na origem do músculo estilofaríngeo com consequente compressão dos nervos cranianos XII, X e IX. Foi realizada traqueotomia, tratamento sistêmico com corticosteróides e antibióticos. Nenhuma resolução foi observada, após 16 dias o animal apresentou piora clínica, pleuropneumonia, uveíte, sepse grave, insuficiência renal aguda e foi submetido à eutanásia. A neuropatia mista resultou em rápida deterioração clínica do animal, devido à dificuldade de deglutição e processos respiratórios associados. Salienta-se a importância de se avaliar a origem do músculo estilofaríngeo em casos de colapso nasofaríngeo associado a disfagia em cavalos, dada a possibilidade de que alterações estruturais nesse músculo possam resultar em neuropatia laríngea.(AU)
Assuntos
Animais , Transtornos de Deglutição/diagnóstico , Doenças Nasofaríngeas/veterinária , Cavalos/anormalidades , DispneiaResumo
Neuropathies of pharyngeal branches of glossopharyngeal and vagus are often associated with guttural pouches diseases; however, these branches of injury due to stylopharyngeus muscle compression are not reported. A case was reported of a quarter horse mare, 8 years old, 450 kg, presenting dyspnea and respiratory noise associated with weight loss. Clinical examination observed mixed dyspnea, tachycardia, dysphagia, sialorrhea, lung crackles and submandibular and parotid lymphadenopathy. Endoscopic exam showed right arytenoid chondritis, nasopharyngeal collapse, generalized larynx edema and dorsal displacement of the soft palate. Right guttural pouch evaluation showed swelling in the origin of stylopharyngeus muscle with consequent compression of the XII, X and IX cranial nerves. Tracheotomy, systemic treatment with corticosteroids, beta lactams and aminoglycosides antibiotics were performed. No resolution was observed and, after 16 days, the animal showed clinical worsening, developed pleuropneumonia, uveitis, severe sepsis, acute renal failure and was euthanized. The mixed neuropathy resulted in rapid clinical deterioration of the animal, due to the difficulty in swallowing and consequent associated respiratory processes. This report emphasizes the importance of evaluating stylopharyngeus muscle origin in cases of nasopharyngeal collapse associated with dysphagia in horses, given the possibility that structural changes in this muscle can result in laryngeal neuropathy.(AU)
As neuropatias do glossofaríngeo e vago são frequentemente associadas com enfermidade das bolsas guturais. A ocorrência desta lesão secundária a compressão pelo músculo estilofaríngeo não é reportada. Relata-se o caso de uma égua quarto de milha, 8 anos de idade, 450 kg, apresentando dispneia, ruído respiratório e perda de peso. No exame clínico observou-se dispnéia mista, taquicardia, disfagia, sialorréia, crepitação pulmonar e linfadenopatia submandibular e parotídea. Ao exame endoscópico identificou-se condrite aritenóide direita, colapso nasofaríngeo, edema generalizado da laringe e deslocamento dorsal do palato mole. Na avaliação da bolsa gutural direita identificou-se aumento de volume na origem do músculo estilofaríngeo com consequente compressão dos nervos cranianos XII, X e IX. Foi realizada traqueotomia, tratamento sistêmico com corticosteróides e antibióticos. Nenhuma resolução foi observada, após 16 dias o animal apresentou piora clínica, pleuropneumonia, uveíte, sepse grave, insuficiência renal aguda e foi submetido à eutanásia. A neuropatia mista resultou em rápida deterioração clínica do animal, devido à dificuldade de deglutição e processos respiratórios associados. Salienta-se a importância de se avaliar a origem do músculo estilofaríngeo em casos de colapso nasofaríngeo associado a disfagia em cavalos, dada a possibilidade de que alterações estruturais nesse músculo possam resultar em neuropatia laríngea.(AU)
Assuntos
Animais , Transtornos de Deglutição/diagnóstico , Doenças Nasofaríngeas/veterinária , Cavalos/anormalidades , DispneiaResumo
Recurrent laryngeal neuropathy (RLN) etiology can be acquired, iatrogenic or idiopathic. There are no previous reports of RLN caused by recurrent laryngeal nerve compression by melanomas. This report describes a horse presenting severe dyspnea and progressive weight loss. Physical exam demonstrated tachycardia, tachypnea, inspiratory dyspnea at rest, neck extension and mydriasis. Temporary tracheotomy was performed and videoendoscopic examination diagnosed grade IV laryngeal paralysis. The animal came suddenly to death by suppurative bacterial pneumonia. At necropsy, it was possible to observe multiple melanotic epithelioid melanoma nodules compressing the recurrent laryngeal nerve, alongside with lung and parotid metastasis. This finding emphasizes the importance of establishing a differential diagnosis for tumor mass compression in the etiology of RLN, especially melanomas in gray horses, with or without cutaneous manifestations of masses.(AU)
A neuropatia laríngea recorrente (NLR) pode apresentar etiologia adquirida, iatrogênica ou idiopática. Não há relatos prévios da ocorrência da NLR causada pela compressão do nervo laríngeo recorrente por melanomas. Este relato descreve um equino apresentando dispneia grave e perda de peso progressiva. O exame físico demonstrou taquicardia, taquipneia, dispneia inspiratória em repouso, extensão do pescoço e midríase. Foi realizada traqueotomia temporária e exame videoendoscópico, mediante o qual se diagnosticou paralisia laríngea grau IV. O animal veio a óbito por pneumonia bacteriana supurativa. Na necropsia, foi possível observar múltiplos nódulos de melanoma epitelioide amelanótico comprimindo o nervo laríngeo recorrente, juntamente com metástases pulmonares e parotídeas. Este achado enfatiza a importância de estabelecer um diagnóstico diferencial nos casos de NLR, pensando-se na compressão nervosa por massas tumorais, especialmente melanomas em cavalos tordilhos, com ou sem manifestações cutâneas de massas.(AU)
Assuntos
Animais , Masculino , Cavalos , Laringe/fisiopatologia , Melanócitos/patologia , Melanoma/fisiopatologia , Melanoma/veterináriaResumo
Recurrent laryngeal neuropathy (RLN) etiology can be acquired, iatrogenic or idiopathic. There are no previous reports of RLN caused by recurrent laryngeal nerve compression by melanomas. This report describes a horse presenting severe dyspnea and progressive weight loss. Physical exam demonstrated tachycardia, tachypnea, inspiratory dyspnea at rest, neck extension and mydriasis. Temporary tracheotomy was performed and videoendoscopic examination diagnosed grade IV laryngeal paralysis. The animal came suddenly to death by suppurative bacterial pneumonia. At necropsy, it was possible to observe multiple melanotic epithelioid melanoma nodules compressing the recurrent laryngeal nerve, alongside with lung and parotid metastasis. This finding emphasizes the importance of establishing a differential diagnosis for tumor mass compression in the etiology of RLN, especially melanomas in gray horses, with or without cutaneous manifestations of masses.(AU)
A neuropatia laríngea recorrente (NLR) pode apresentar etiologia adquirida, iatrogênica ou idiopática. Não há relatos prévios da ocorrência da NLR causada pela compressão do nervo laríngeo recorrente por melanomas. Este relato descreve um equino apresentando dispneia grave e perda de peso progressiva. O exame físico demonstrou taquicardia, taquipneia, dispneia inspiratória em repouso, extensão do pescoço e midríase. Foi realizada traqueotomia temporária e exame videoendoscópico, mediante o qual se diagnosticou paralisia laríngea grau IV. O animal veio a óbito por pneumonia bacteriana supurativa. Na necropsia, foi possível observar múltiplos nódulos de melanoma epitelioide amelanótico comprimindo o nervo laríngeo recorrente, juntamente com metástases pulmonares e parotídeas. Este achado enfatiza a importância de estabelecer um diagnóstico diferencial nos casos de NLR, pensando-se na compressão nervosa por massas tumorais, especialmente melanomas em cavalos tordilhos, com ou sem manifestações cutâneas de massas.(AU)
Assuntos
Animais , Masculino , Cavalos , Laringe/fisiopatologia , Melanócitos/patologia , Melanoma/fisiopatologia , Melanoma/veterináriaResumo
Purpose: To evaluate the effects of Dexmedetomidine (Dex) on spinal pathology and inflammatory factor in a rat model of Diabetic neuropathic pain (DNP). Methods: The rats were divided into 3 groups (eight in each group): normal group (N group), diabetic neuropathic pain model group (DNP group), and DNP model with dexmedetomidine (Dex group). The rat model of diabetes was established with intraperitoneal streptozotocin (STZ) injections. Nerve cell ultrastructure was evaluated with transmission electron microscopy (TEM). The mechanical withdrawal threshold (MWT) and motor nerve conduction velocity (MNCV) tests documented that DNP rat model was characterized by a decreased pain threshold and nerve conduction velocity. Results: Dex restored the phenotype of neurocytes, reduced the extent of demyelination and improved MWT and MNCV of DNP-treated rats (P=0.01, P=0.038, respectively). The expression of three pain-and inflammation-associated factors (P2X4, NLRP3, and IL-IP) was significantly upregulated at the protein level in DNP rats, and this change was reversed by Dex administration (P=0.0022, P=0.0092, P=0.0028, respectively). Conclusion: The P2X4/NLRP3 signaling pathway is implicated in the development and presence of DNP in vivo, and Dex protects from this disorder.(AU)
Assuntos
Animais , Dexmedetomidina/análise , Dexmedetomidina/farmacocinética , Ratos/lesões , Neuropatias Diabéticas/veterinária , DorResumo
Descreve-se o caso de uma égua, da raça Campeiro, utilizada como doadora de embriões, que apresentava quadros de cistite recorrente e incontinência urinária. Os sinais clínicos evoluíram para emagrecimento progressivo, anorexia, apatia e isolamento do plantel. Ao exame físico, foi identificada hipotonia da cauda, hipoalgesia da região perineal, flacidez retal e vesical, compatíveis com sinais relacionados à síndrome da cauda equina. Exames complementares laboratoriais, exame ultrassonográfico e necropsia confirmaram o diagnóstico de insuficiência renal crônica (IRC), a qual foi atribuida à pielonefrite ascendente. O exame de urocultura demonstrou crescimento de bactérias do gêneroStreptococcus sp. Este é um caso raro em equinos em que a disfunção de neurônio motor inferior propiciou o desenvolvimento de processo infeccioso no trato urinário, progredindo para um quadro crônico renal incompatível com a vida.(AU)
Descreve-se o caso de uma égua, da raça Campeiro, utilizada como doadora de embriões, que apresentava quadros de cistite recorrente e incontinência urinária. Os sinais clínicos evoluíram para emagrecimento progressivo, anorexia, apatia e isolamento do plantel. Ao exame físico, foi identificada hipotonia da cauda, hipoalgesia da região perineal, flacidez retal e vesical, compatíveis com sinais relacionados à síndrome da cauda equina. Exames complementares laboratoriais, exame ultrassonográfico e necropsia confirmaram o diagnóstico de insuficiência renal crônica (IRC), a qual foi atribuida à pielonefrite ascendente. O exame de urocultura demonstrou crescimento de bactérias do gênero Streptococcus sp. Este é um caso raro em equinos em que a disfunção de neurônio motor inferior propiciou o desenvolvimento de processo infeccioso no trato urinário, progredindo para um quadro crônico renal incompatível com a vida.(AU)
Assuntos
Animais , Cavalos/anormalidades , Pielonefrite/veterinária , Insuficiência Renal/classificaçãoResumo
Descreve-se o caso de uma égua, da raça Campeiro, utilizada como doadora de embriões, que apresentava quadros de cistite recorrente e incontinência urinária. Os sinais clínicos evoluíram para emagrecimento progressivo, anorexia, apatia e isolamento do plantel. Ao exame físico, foi identificada hipotonia da cauda, hipoalgesia da região perineal, flacidez retal e vesical, compatíveis com sinais relacionados à síndrome da cauda equina. Exames complementares laboratoriais, exame ultrassonográfico e necropsia confirmaram o diagnóstico de insuficiência renal crônica (IRC), a qual foi atribuida à pielonefrite ascendente. O exame de urocultura demonstrou crescimento de bactérias do gêneroStreptococcus sp. Este é um caso raro em equinos em que a disfunção de neurônio motor inferior propiciou o desenvolvimento de processo infeccioso no trato urinário, progredindo para um quadro crônico renal incompatível com a vida.(AU)
This report describes the case of a mare, of the Campeiro breed, used as an embryo donor, which had recurrent cystitis and urinary incontinence crisis. Clinical signs evolved to progressive weight loss, anorexia, apathy, and isolation from the group. Physical examination showed tail hypotonia, perineal hypalgesia, rectal and bladder sagging compatible with signs related to cauda equina syndrome. Complementary laboratory and sonographic assessment, and necropsy confirmed the diagnosis of chronic renal failure (CRF), which was attributed to the ascending pyelonephritis. The examination of urine culture showed growth of bacteria of the genus Streptococcus sp. This is a rare case in the equine species where the lower motor neuron dysfunction led the development of infectious process in the urinary tract, progressing to renal chronic condition incompatible with life.(AU)
Assuntos
Animais , Cavalos/anormalidades , Insuficiência Renal/classificação , Pielonefrite/veterináriaResumo
Diabetes mellitus is one of the most common endocrine disorders characterized by relative or absolute lack of insulin; this can lead to several ocular manifestations, among them diabetic retinopathy and cataracts. Diabetic retinopathy (DR) is a microangiopathy that involves retinal precapillary arterioles, postcapillary venules, and large vessels, causing them to be functionally and anatomically incompetent. Hyperglycemia seems to be the most probable cause of damage to the retina due to interference in cellular metabolism and transduction processes. The aim of this study was to evaluate retinal thickness in eight diabetic dogs, four females and four males of different breeds and ages ranging from 6 to 15 years, by optical coherence tomography (OCT) and to compare them with non-diabetic dogs. Assessment provided by OCT in diabetic dogs showed retinal layers thinning and loss of stratification when compared to non-diabetic dogs (198μm versus 219μm respectively), with statistical significance (p=0.008). OCT images may suggest that diabetes mellitus causes retinal neuropathy in dogs, as also seen in diabetic humans.(AU)
Diabete melito é umas das principais endocrinopatias, caracterizada pela deficiência relativa ou absoluta de insulina, que pode resultar em diversas manifestações oculares, sendo as mais frequentes a retinopatia diabética e a catarata. Retinopatia diabética (RD) é uma microangiopatia que afeta primeiramente as arteríolas pré-capilares, capilares, vênulas pós-capilares e vasos de maior calibre, causando incompetência funcional e anatômica dos vasos retinianos. A hiperglicemia parece ser a causa mais provável da lesão retiniana, interferindo nas vias de metabolismo celular e no processo de transdução. Objetivou-se neste estudo avaliar e comparar a espessura retiniana total em oito cães diabéticos, quatro fêmeas e quatro machos, de diversas raças, com idade variando de seis a 15 anos, com auxílio de tomografia de coerência óptica (OCT) e comparar com a de cães não diabéticos. A espessura e arquitetura retiniana realizada pela OCT nos cães diabéticos, demonstrou afinamento das camadas da retina e perda da estratificação em comparação com os cães não diabéticos (198μm versus 219μm, respectivamente), sendo esta redução estatisticamente significante (p=0,008). Baseado nas imagens da OCT pode-se sugerir que a diabete melito, no cão, cause neuropatia retiniana como descrito em humanos diabéticos.(AU)
Assuntos
Animais , Cães , Retina/diagnóstico por imagem , Diabetes Mellitus/veterinária , Retinopatia Diabética/veterinária , Cães , Tomografia de Coerência Óptica/veterinária , Complicações do DiabetesResumo
Diabetes mellitus is one of the most common endocrine disorders characterized by relative or absolute lack of insulin; this can lead to several ocular manifestations, among them diabetic retinopathy and cataracts. Diabetic retinopathy (DR) is a microangiopathy that involves retinal precapillary arterioles, postcapillary venules, and large vessels, causing them to be functionally and anatomically incompetent. Hyperglycemia seems to be the most probable cause of damage to the retina due to interference in cellular metabolism and transduction processes. The aim of this study was to evaluate retinal thickness in eight diabetic dogs, four females and four males of different breeds and ages ranging from 6 to 15 years, by optical coherence tomography (OCT) and to compare them with non-diabetic dogs. Assessment provided by OCT in diabetic dogs showed retinal layers thinning and loss of stratification when compared to non-diabetic dogs (198μm versus 219μm respectively), with statistical significance (p=0.008). OCT images may suggest that diabetes mellitus causes retinal neuropathy in dogs, as also seen in diabetic humans.(AU)
Diabete melito é umas das principais endocrinopatias, caracterizada pela deficiência relativa ou absoluta de insulina, que pode resultar em diversas manifestações oculares, sendo as mais frequentes a retinopatia diabética e a catarata. Retinopatia diabética (RD) é uma microangiopatia que afeta primeiramente as arteríolas pré-capilares, capilares, vênulas pós-capilares e vasos de maior calibre, causando incompetência funcional e anatômica dos vasos retinianos. A hiperglicemia parece ser a causa mais provável da lesão retiniana, interferindo nas vias de metabolismo celular e no processo de transdução. Objetivou-se neste estudo avaliar e comparar a espessura retiniana total em oito cães diabéticos, quatro fêmeas e quatro machos, de diversas raças, com idade variando de seis a 15 anos, com auxílio de tomografia de coerência óptica (OCT) e comparar com a de cães não diabéticos. A espessura e arquitetura retiniana realizada pela OCT nos cães diabéticos, demonstrou afinamento das camadas da retina e perda da estratificação em comparação com os cães não diabéticos (198μm versus 219μm, respectivamente), sendo esta redução estatisticamente significante (p=0,008). Baseado nas imagens da OCT pode-se sugerir que a diabete melito, no cão, cause neuropatia retiniana como descrito em humanos diabéticos.(AU)