Steroid responsive

Follow-up appointments will be very important and absolutely necessary with a diagnosis of steroid-responsive meningitis-arteritis. Your veterinarian will determine the schedule of the return visits which will depend on how well your furry family member responds to the treatment. The follow-up will mean repeat blood tests and analysis of the CSF until the veterinarian can see that the markers have returned to normal. This could mean appointments every 4 to 6 weeks for several months. It is imperative that you keep the appointments and do not discontinue the medication even though you may think your dog is feeling better. It should be noted that many pets will need a prescription for gastroprotectants; if you see any side effects from the long-term therapy such as blood in the stool or vomiting, or if you are concerned in any way with your pet’s health, contact the clinic without delay. With SRMA there is a potential for relapse, meaning that continued contact with your veterinarian will be recommended.

The exact etiopathogenesis of SRMA is unknown ( Tipold 2000 ). Activated T cells have been demonstrated in dogs with SRMA, indicating potential contact with an antigenic stimulus; however, no bacterial or viral agents have been identified to date ( Tipold and others 1996 ). A Th2-mediated immune response is most likely, based on the presence of high CD4:CD8a ratios and a high proportion of B cells in peripheral blood and CSF. A Th2-mediated immune response is further supported by the expression of low levels of Th1-response-related cytokines (IL-2, IFN-γ) and upregulation of Th2 cytokines (IL-4) in blood and CSF in dogs with the acute form of SRMA ( Schwartz and others in press ). This Th2-mediated immune response leads to an upregulation of the humoral immune response and excessive IgA production ( Schwartz and others 2008b ).

This would occur most likely through each cell shrinking in size in response to the energy deficit (and/or in extreme situations from some cells dying via either apoptosis or necrosis, depending on location). [4] This may occur as a result of there not being enough ATP to maintain cellular functions: notably failure of the Na/K ATPase, resulting in a loss of the gradient to drive the Na/Ca antiporter which normally keeps Ca +
2 out of cells so that it does not build to toxic levels that will rupture cell lysosomes leading to apoptosis. An additional feature of a low energy state is failure to maintain axonal transport via Dynein/Kinesin ATPases, which in many diseases results in neuronal injury to both the brain and/or periphery. [5]

A 14-year-old boy, without any preceding history of trauma, meningoencephalitis or seizures, was admitted in a comatose state. A similar episode of loss of consciousness 2 months prior with normal neuroimaging and electroencephalogram (EEG) had been followed by behavioral alterations. A year previously, during evaluation for increased appetite and poor weight gain, he was noted to have small goitre with thyroid-stimulating hormone (TSH) mIU/L, T3 nmol/L, and T4 nmol/L. Routine hemogram, blood biochemistry, thyroid function tests including free hormone levels, ultrasonography thyroid and magnetic resonance imaging were normal. EEG showed diffuse slowing of all waves. Cerebrospinal fluid showed no pleocytosis and electrophoresis showed oligoclonal band. Viral studies and serum N-methyl-D-aspartate receptor antibody levels were negative. Anti-thyroid peroxidase (Anti-TPO) antibodies were raised. Intervention was with intravenous dexamethasone 4 mg every 6 h for 1 week followed by tapering schedule of oral prednisolone over 6 months.

Steroid responsive

steroid responsive

A 14-year-old boy, without any preceding history of trauma, meningoencephalitis or seizures, was admitted in a comatose state. A similar episode of loss of consciousness 2 months prior with normal neuroimaging and electroencephalogram (EEG) had been followed by behavioral alterations. A year previously, during evaluation for increased appetite and poor weight gain, he was noted to have small goitre with thyroid-stimulating hormone (TSH) mIU/L, T3 nmol/L, and T4 nmol/L. Routine hemogram, blood biochemistry, thyroid function tests including free hormone levels, ultrasonography thyroid and magnetic resonance imaging were normal. EEG showed diffuse slowing of all waves. Cerebrospinal fluid showed no pleocytosis and electrophoresis showed oligoclonal band. Viral studies and serum N-methyl-D-aspartate receptor antibody levels were negative. Anti-thyroid peroxidase (Anti-TPO) antibodies were raised. Intervention was with intravenous dexamethasone 4 mg every 6 h for 1 week followed by tapering schedule of oral prednisolone over 6 months.

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