Monitoração da pressão intracraniana em cães e gatos: o que sabemos? / Intracranial pressure monitoring: what do we know? / Monitoreo de la presión intracraneal en perros y gatos: ¿qué sabemos?

Monitorar a pressão intracraniana (PIC) permite otimizar o tratamento de pacientes com diversas afecções, já que a hipertensão intracraniana (HIC) pode causar isquemia. A aferição da PIC pode ser realizada de maneira invasiva, que é o método mais acurado, mas requer a introdução de um sensor no ventrículo ou parênquima, o que pode causar hemorragia e infecção. Existem ainda diversos métodos não invasivos, que aliados aos parâmetros clínicos, podem ser utilizados como alternativa para avaliar a PIC. O uso de cateter ventricular, epidural e microtransdutores são descritos na veterinária como métodos invasivos, porém, nenhum deles é considerado padrão ouro em pequenos animais, mas presume-se que o uso de microtransdutores intraparenquimatosos seja o mais preciso. Dentre os métodos não invasivos, a mensuração do diâmetro da bainha do nervo óptico (DBNO), ressonância magnética, ultrassonografia (US) com doppler transcraniano e elasticidade óssea intracraniana foram relatados. Em gatos, o DBNO foi mensurado por US transpalpebral em animais saudáveis e com HIC presumida e mostrou ser um método viável. A monitoração da PIC não é rotineiramente usada na medicina veterinária, mas poderia guiar e otimizar o tratamento em diversas afecções, portanto, o objetivo desta revisão narrativa é descrever os métodos de monitoração da PIC em cães e gatos.

Monitoring intracranial pressure (ICP) allows for the optimization of treatment in patients with various conditions, as intracranial hypertension (ICH) can lead to ischemia. ICP measurement can be conducted invasively, which is the most accurate method, but it requires the introduction of a sensor into the ventricle or parenchyma, posing risks of hemorrhage and infection. Additionally, there are various non-invasive methods that, when combined with clinical parameters, can serve as alternatives for assessing ICP. The use of ventricular catheters, epidural catheters, and microtransducers is described in veterinary medicine as invasive methods; however, none are considered the gold standard in small animals, although the use of intraparenchymal microtransducers is presumed to be the most precise. Among non-invasive methods, measurement of the optic nerve sheath diameter (ONSD), magnetic resonance imaging, transcranial Doppler ultrasound, and intracranial bone elasticity have been reported. In cats, ONSD has been measured via transpalpebral ultrasound in healthy animals and those with presumed ICH, proving to be a viable method. While ICP monitoring is not routinely employed in veterinary medicine, it could guide and optimize treatment for various conditions. Therefore, the aim of this narrative review is to describe the methods of ICP monitoring in dogs and cats.

Monitorear la presión intracraneal (PIC) permite optimizar el tratamiento de pacientes con diversas afecciones, ya que la hipertensión intracraneal (HIC) puede causar isquemia. La medición de la PIC puede realizarse de manera invasiva, que es el método más preciso, pero requiere la introducción de un sensor en el ventrículo o parénquima, lo que puede causar hemorragia e infección. Existen también diversos métodos no invasivos que, combinados con parámetros clínicos, pueden utilizarse como alternativa para evaluar la PIC. El uso de catéteres ventriculares, epidurales y microtransductores se describe en la medicina veterinaria como métodos invasivos; sin embargo, ninguno de ellos se considera el estándar de oro en pequeños animales, aunque se presume que el uso de microtransductores intraparenquimatosos sea el más preciso. Entre los métodos no invasivos, se han reportado la medición del diámetro de la vaina del nervio óptico (DVNO), la resonancia magnética, la ecografía (US) con doppler transcraneal y la elasticidad ósea intracraneal. En gatos, se ha medido el DVNO por ecografía transpalpebral en animales sanos y con HIC presumida, demostrando ser un método viable. La monitorización de la PIC no se utiliza de manera rutinaria en la medicina veterinaria, pero podría guiar y optimizar el tratamiento en diversas afecciones. Por lo tanto, el objetivo de esta revisión narrativa es describir los métodos de monitorización de la PIC en perros y gatos.

Polineuropatia motora em cão adulto / Motor polyneuropathy in an adult dog

Background: Nonambulatory flaccid tetraparesis can be the result of diseases of the peripheral nervous system and it is characterized by generalized lower motor neuron (LMN) signs, as weakness, tetraparesis/tetraplegia, decreased muscle tone and reflexes. The term polyneuropathy is used for dysfunction of multiple peripheral nerves. In Brazil, there are several etiologies for polyneuropathy in dogs, such as acute idiopathic polyradiculoneuritis, botulism and myasthenia gravis. Toxoplasma gondii is an uncommon cause of LMN diseases in dogs. The aim of this report was to describe a case of flaccid tetraplegia toxoplasmosis in an adult dog with a Toxoplasma gondii serology with a markedly elevated IgG titer of 1:4096. Case: A 4-year-old intact mongrel male dog, weighing 19.6 kg, was referred to the Veterinary Medical Teaching Hospital of the Universidade Estadual de Londrina (UEL) with a 5-day history of weakness that progressed to tetraparesis. Physical examination revealed no significant changes other than the dull and unkempt coat. Neurologic examination revealed severe tetraparesis that was worse in the pelvic limbs, with decreased muscle tone in all four limbs. Postural reactions and the interdigital reflex were absent in all four limbs, as was the patellar reflex, but pain perception was present. There were no clinical signs of dysfunction on examination of the cranial nerves. Laboratory tests were performed, and creatine kinase was elevated (819 U/L). Blood was drawn to look for antibodies to Toxoplasma gondii and Neospora caninum class IgG using the indirect immunofluorescence technique. The antibody titer for Toxoplasma gondii (IgG) was 1:4096. A chest radiograph was performed to look for megaesophagus, and a pulmonary pattern suggestive of mild diffuse pneumonia was observed. Treatment was performed with sulfamethoxazole and trimethoprim, and the dog's condition improved slightly. Discussion: Based on lower motor neuron findings, the neurologic lesion was localized in the nerve roots, peripheral nerves, neuromuscular junctions, or muscles. The most important diseases in the list of differential diagnoses were immune-mediated or infectious polyradiculoneuritis (toxoplasmosis, neosporosis), myasthenia gravis, toxic polyneuropathy (botulism, chronic organophosphate poisoning), and paraneoplastic polyneuropathy. Among these differential diagnoses, polyradiculoneuritis is one of the most common. It is an idiopathic inflammatory disease. Exposure to raccoon saliva (in the U.S.), vaccination, or infection have been proposed as precipitating causes, but the triggers of this disease remain unknown. Serology for neosporosis was negative, while IgG titers for toxoplasmosis were 1:4096. In a previous study, dogs with acute polyradiculoneuritis were more likely to have T. gondii IgG serum antibody titers than dogs without neurologic signs. Infection with the protozoa T. gondii and N. caninum can cause intense polyradiculoneuritis in dogs accompanied by myositis, especially in puppies. One treatment trial was based on the administration of sulfonamide-trimethoprim with pyrimethamine, whose efficacy in the treatment of toxoplasmosis in dogs has also been reported in the literature. Neurologic deficits improved slightly, and there is a possibility that certain signs may not disappear completely because of the permanent damage caused by inflammation of the nervous system, as observed in the present case. The case had the limitation that it was not possible to perform other laboratory tests to demonstrate histopathologically the presence of Toxoplasma gondii organisms in muscles or nerves. Recovery of normal function is less likely in protozoan polyradiculoneuritis than in noninfectious polyradiculoneuritis. Thus, in the present case, the main suspicion was polyradiculoneuritis secondary to toxoplasmosis. Although it is a rare condition, it is important to consider toxoplasmosis in dogs with LMN-type tetraparesis or tetraplegia.

Meningomielite eosinofílica provavelmente associada à toxoplasmose em um gato / Eosinophilic meningomyelitis probably associated with toxoplasmosis in a cat

Background: The cerebrospinal fluid (CSF) of healthy cats presents up to 5 cells/µL, with predominance of mononuclear cells and the presence of more than 1% eosinophils is rare and should always be considered an abnormal finding. There is no consensus on the term eosinophilic pleocytosis, as it is used to indicate the presence of more than 10 eosinophils/µL or more than 10% of the total leukocytes. The increase in eosinophils in the CSF may result from infectious, inflammatory, neoplastic and idiopathic diseases. The objective of this paper is to report a case of marked pleocytosis in CSF, with 84% eosinophils, probably due to toxoplasmosis, in a cat with paraparesis and diffuse spinal pain. Case: A mixed breed female cat, neutered, adult and domiciled in a rural area was presented due to gait abnormalities in the pelvic limbs that started one day before presentation. The general physical examination was unremarkable. On neurological examination it was observed asymmetric deficit of postural reactions in pelvic limbs, patellar reflex normal to increased and pain elicited on palpation of the thoracic and lumbar spine. Based on these findings, the neurological syndrome was classified as thoracolumbar, but with diffuse pain, and the main differential diagnoses were inflammatory/ infectious and neoplastic diseases. The leukogram showed eosinophilia and the serum biochemistry showed no significant changes. Serological assays for feline immunodeficiency virus and feline leukemia virus were negative. Analysis of cerebrospinal fluid (CSF) identified marked pleocytosis with 84% eosinophils and increase in protein concentration. Myelography showed no compressive or expansive changes. Fungal culture for CSF cryptococcosis was negative. Serum immunofluorescence antibody titer for Toxoplasma gondii (IgG) was 1:256. There was a marked improvement after treatment with sulfametoxazole/trimethoprim and pyrimethamine and after 3 weeks of treatment, there was almost complete recovery of neurological signs and after 9 months the cat was neurologically normal. Discussion: The most common causes of acute-onset thoracolumbar spinal cord syndrome in cats, with diffuse pain on spinal palpation, are meningomyelitis of inflammatory/infectious origin, such as feline infectious peritonitis (FIP) and neoplasms such as lymphoma. Other meningomyelitis of inflammatory origin, such as infectious and immune-mediated meningomyelitis of unknown origin are considered uncommon in cats. Although the clinical, systemic and neurological signs of FIP and toxoplasmosis may have similarities, in the present case FIP was not considered responsible for the observed signs, as the evolution of the case and the analysis of the CSF tend to be different. The peripheral eosinophilia, the cytological analysis of the CSF, characterized by marked eosinophilic pleocytosis, associated with a positive titer for toxoplasmosis, good response to treatment and improvement in the neurological condition, with survival for more than 9 months after treatment, rules out the possibility of FIP. Neurological signs observed in the absence of systemic signs are more common in cases of protozoan reactivation, which probably occurred in the present case. The possibility of toxoplasmosis in the patient in this report was reinforced by the fact that the animal came from a rural area. Eosinophilia of CSF is most commonly associated with parasitic infections, although it can be caused by a variety of infectious agents, but in the cat of the present report, the marked eosinophilic pleocytosis was likely due to toxoplasmosis, which is a rare occurrence in this specie. In conclusion, toxoplasmosis should be considered in the differential diagnosis of focal spinal cord lesions in cats. The identification of laboratory findings as well as the appropriate therapy favored the good evolution of the condition.