Diffusion-weighted imaging in kainic acid-induced complex partial status epilepticus in dogs

Hasegawa, Daisuke; Orima, Hiromitsu; Fujita, Michio; Nakamura, Shinichirou; Takahashi, Koji; Ohkubo, Seiji; Igarashi, Hironaka; Hashizume, Kazuyoshi

doi:10.1016/s0006-8993(03)03041-5

Cited by 50 publications

(51 citation statements)

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“…9 On the other hand, some hippocampal lesions have been identified in dogs with intractable idiopathic epilepsy, [31][32][33][34] and epileptic brain damage can be caused by status epilepticus. 12,13 Dogs in this study with qualitative MR hippocampal changes had findings similar to those in humans with hippocampal sclerosis. The characteristics of hippocampal sclerosis include hippocampal atrophy and hyperintensity on T2W and FLAIR images, and hypointensity on T1WI images.…”

Section: Discussionsupporting

confidence: 66%

“…There was no difference in the hippocampus volume ratio in dogs with status epilepticus/cluster seizures vs. dogs without. Based on this and other studies, 12,13,[31][32][33][34] temporal lobe epilepsy and hippocampal atrophy may occur in dogs, but at a lower frequency than in humans.…”

Section: Discussionmentioning

confidence: 78%

“…10,11 Epileptic brain damage accompanied by hippocampal lesions have also been reported in experimental epileptic models in dogs. 12,13 Thus, whether pathologic changes of the hippocampus, including temporal lobe epilepsy and hippocampal sclerosis, occur in canine epilepsy is controversial. Furthermore, no reports have described hippocampal volumetry in epileptic dogs.…”

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confidence: 99%

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Clinical Magnetic Resonance Volumetry of the Hippocampus in 58 Epileptic Dogs*

Kuwabara

Hasegawa

Kobayashi

et al. 2010

Veterinary Radiology &Amp; Ultrasound

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Hippocampal atrophy, which is a component of hippocampal sclerosis and recognized commonly in human intractable epilepsy, is controversial in canine epilepsy. We examined the hippocampal volume in 58 epileptic dogs and 35 control dogs using magnetic resonance (MR) images, and calculated the relative hippocampal volume asymmetry of the right and left hippocampus. Subjectively, there were visible MR imaging abnormalities in seven of the 58 epileptic dogs (12%). The hippocampel volume asymmetric ratio of epileptic dogs (5.84 AE 4.47%) was significantly greater than that of control dogs (1.62 AE 0.88%). Using a cutoff threshold asymmetric ratio of 6% that is indicated in human epilepsy, 28 epileptic dogs (48%) were characterized as having unilateral hippocampus atrophy. The hippocampal volume asymmetry ratio cannot be used to detect bilateral atrophy. In conclusion, although less frequent than that observed in human epilepsy patients, hippocampal atrophy may occur in canine epilepsy. r

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 78%

mentioning

confidence: 99%

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Clinical Magnetic Resonance Volumetry of the Hippocampus in 58 Epileptic Dogs*

Kuwabara

Hasegawa

Kobayashi

et al. 2010

Veterinary Radiology &Amp; Ultrasound

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“…For the chronic phase group, four animals were examined at approximately 72 hr (the end of CPSE) and 2 months after the onset of CPSE [5]. Two dogs were treated with PBS instead of KA, and were used as controls for the chronic group (PBS group).CSF sampling: The CSF samples used in this study were identical to those used in the previous studies [5,6]. CSF was collected by cisternal puncture under light general anesthesia using thiopental.…”

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confidence: 99%

Kinetics of Glutamate and .GAMMA.-Aminobutyric Acid in Cerebrospinal Fluid in a Canine Model of Complex Partial Status Epilepticus induced by Kainic Acid

Hasegawa

Matsuki

Fujita

et al. 2004

The Journal of Veterinary Medical Science

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ABSTRACT. An imbalance of excitatory and inhibitory transmitters in the brain has been suggested to cause epileptic seizures. In this study, we investigated the kinetics of glutamate (GLU) and γ-aminobutyric acid (GABA) in cerebrospinal fluid (CSF-GLU and CSF-GABA, respectively) using a high performance liquid chromatography (HPLC) in a canine model of complex partial status epilepticus (CPSE) induced by the microinjection of kainic acid (KA) into the unilateral amygdala. During the acute phase (3, 6, 12 and 48 hr after the onset of CPSE), CSF-GLU was significantly increased, while CSF-GABA was decreased, although not significantly. In the chronic phase, both CSF-GLU and CSF-GABA were significantly lower than normal at 72 hr after the onset of CPSE, and their levels returned to normal at 2 months. Results of the present study demonstrate that CSF-GLU is gradually increased in relation with seizure severity, and suggested the possibility that CSF-GABA was consistently decreased during CPSE induced by KA in dogs. KEY WORDS: cerebrospinal fluid, GABA, glutamate, kainic acid, status epilepticus.J. Vet. Med. Sci. 66(12): 1555-1559, 2004 It is well accepted that glutamate (GLU) and aspartate (ASP) are the main excitatory amino acids in the brain, while γ-aminobutyric acid (GABA) functions as an inhibitory neurotransmitter [9,15]. An imbalance between excitatory and inhibitory amino acids has been hypothesized as a possible mechanism for epileptic seizures, thus amino acid analysis in the cerebrospinal fluids (CSFs) has been employed for understanding the pathogenesis of epilepsy. Numerous articles reported concentrations of GLU and GABA in the CSF and/or brain tissues in human epileptic patients and/or experimental animal models, which were quite inconsistent [2-4, 7-9, 12, 15, 18]. On the other hand, in veterinary medicine, only a few reports deal with amino acid concentrations in the CSF [1,11,16,17]. Podell and Hadjiconstantinou [16,17] reported the concentrations of GLU and GABA in the CSF from dogs with idiopathic epilepsy, suggesting a diagnostic potential for the amino acid analysis.Previously, we reported the clinical, electrophysiological and pathological characteristics of a canine model of complex partial status epilepticus (CPSE) induced by a microinjection of kainic acid (KA) into the unilateral amygdala [5]. We also conducted further studies of this model using magnetic resonance imaging (MRI) [6]. These reports clearly demonstrated that our canine KA-induced CPSE model is valuable for investigating the status epilepticus-induced brain damage (excitotoxicity theory), as well as for characterizing the specificity of epilepsy in the dog. In this study, to examine the relationship between CPSE and neurotransmitters, we characterized the kinetics of GLU and GABA in the CSF (CSF-GLU and CSF-GABA, respectively) in the KA-induced CPSE-model dogs. MATERIALS AND METHODSThis study was performed in conformity with the Animal Care and Use Committee of Nippon Veterinary and Animal Science University.Normal animals: ...

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“…Further, more severe lesions, i.e. irreversible lesions, may result in necrotic and/or atrophic lesions and may extend to the hippocampi [10,11]. The first MRI of this case was obtained at 2 weeks after the cluster Fig.…”

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confidence: 98%

Long-Term Survival in a Dog with Anaplastic Oligodendroglioma Treated with Radiation Therapy and CCNU

et al. 2012

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ABSTRACT. A 9 year-old, neutered, male French Bulldog showing cluster seizures was diagnosed with a glioma in the right piriform cortex by MRI. Hypofractionated radiation therapy (RT) was performed using a linear accelerator. Although the lesion had involuted significantly at 2 months after RT, recurrence was observed at 4 months after RT. Chemotherapy was started using CCNU (60 mg/m 2 every 6-9 weeks) and was continued for one year. Follow-up MRI revealed involution of the lesion and the intervals of CCNU were increased to every 9-14 weeks. Two years after the first presentation, the dog suffered status epilepticus, followed by deficits of left sided postural reaction with cognitive dysfunction. The dog died on day 910, and histopathological diagnosis confirmed anaplastic oligodendroglioma. KEY WORDS: canine, CCNU, MRI, glioma, radiation therapy.doi: 10.1292/jvms.12-0058; J. Vet. Med. Sci. 74(11): 1517-1521, 2012 Gliomas such as oligodendrogliomas and astrocytomas are relatively common intracranial and intraparenchymal tumors in dogs [19]. In contrast to meningiomas, gliomas may be treated with megavoltage radiation therapy (RT) and/or chemotherapy (nitrosoureas) because of their location and infiltration [2,7,15,18]. Several reports have documented the results and prognosis of gliomas treated with RT [3,4] and chemotherapy [6,8,9]. However, detailed descriptions of individual cases are very limited.Here, we describe the long-term survival (2 years and 6 months) of a dog with glioma (final diagnosis: anaplastic oligodendroglioma) that was treated with megavoltage RT and CCNU (lomustine) therapy.A 9 year-old, 13.0 kg, neutered male French Bulldog presented with a complaint of cluster seizures that had started 2 weeks earlier. The seizures consisted of focal seizures (mastication, salivation, and vomiting) with secondary generalization. Although the neurological examination was normal and the seizures were controlled by phenobarbital (PB) (2 mg/kg, PO, BID), magnetic resonance imaging (MRI) was performed to evaluate intracranial disease. Cranial MRI (1.5 Tesla) revealed a lesion showing hyperintensity on T2-weighted (T2W) and fluid-attenuated inversion recovery (FLAIR) images, and hypointensity on T1-weighted (T1W) images without contrast enhancement (on gadolinium enhancement (Gd-) T1W) in the right piriform area (piriform cortex and amygdala) with mild mass effect (Fig. 1A, 1B). From these MRI findings, a glioma, likely a low-grade astrocytoma or oligodendroglioma, was diagnosed clinically (day 0).Because of the location of the lesion and by the owner's request, megavoltage radiation therapy (RT) using a 4 MV X-ray linear accelerator was started on day 14. The radiation treatment area was planned with software based on CT images. The lesion was treated with hypofractionated radiation that was 6 Gy per fraction from 4 directions (0°, 90°, 180° and 270°) once a week for 6 weeks (total 36 Gy). During the period of RT, no clinical signs, including seizures, occurred under PB therapy, and no problems associated with...

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Diffusion-weighted imaging in kainic acid-induced complex partial status epilepticus in dogs

Cited by 50 publications

References 26 publications

Clinical Magnetic Resonance Volumetry of the Hippocampus in 58 Epileptic Dogs*

Clinical Magnetic Resonance Volumetry of the Hippocampus in 58 Epileptic Dogs*

Kinetics of Glutamate and .GAMMA.-Aminobutyric Acid in Cerebrospinal Fluid in a Canine Model of Complex Partial Status Epilepticus induced by Kainic Acid

Long-Term Survival in a Dog with Anaplastic Oligodendroglioma Treated with Radiation Therapy and CCNU

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