Canine and Feline Epilepsy. Luisa De Risio

Чтение книги онлайн.

Читать онлайн книгу Canine and Feline Epilepsy - Luisa De Risio страница 23

Автор:
Жанр:
Серия:
Издательство:
Canine and Feline Epilepsy - Luisa De Risio

Скачать книгу

M. (2011) Identification of clinically used drugs that activate pregnane X receptors. Drug Metabolism and Disposition: the Biological Fate of Chemicals 39, 151–159.

      Sisodiya, S.M., Lin, W.R., Harding, B.N., Squier, M.V. and Thom, M. (2002) Drug resistance in epilepsy: expression of drug resistance proteins in common causes of refractory epilepsy. Brain 125, 22–31.

      Spector, R. (2000) Drug transport in the mammalian central nervous system: multiple complex systems. A critical analysis and commentary. Pharmacology 60, 58–73.

      Tishler, D.M., Weinberg, K.I., Hinton, D.R., Barbaro, N., Annett, G.M. and Raffel, C. (1995) MDR1 gene expression in brain of patients with medically intractable epilepsy. Epilepsia 36, 1–6.

      Trepanier, L.A., Van Schoick, A., Schwark, W.S. and Carrillo, J. (1998) Therapeutic serum drug concentrations in epileptic dogs treated with potassium bromide alone or in combination with other anticonvulsants: 122 cases (1992-1996). Journal of the American Veterinary Medical Association 213, 1449–1453.

      Vincent, A., Irani, S.R. and Lang, B. (2010) The growing recognition of immunotherapy-responsive seizure disorders with autoantibodies to specific neuronal proteins. Current Opinion in Neurology 23, 144–150.

      Volk, H.A. and Löscher, W. (2005) Multidrug resistance in epilepsy: rats with drug-resistant seizures exhibit enhanced brain expression of P-glycoprotein compared with rats with drug-responsive seizures. Brain 128, 1358–1368.

      Volk, H.A., Burkhardt, K., Potschka, H., Chen, J., Becker, A. and Löscher, W. (2004a) Neuronal expression of the drug efflux transporter P-glycoprotein in the rat hippocampus after limbic seizures. Neuroscience 123, 751–759.

      Volk, H.A., Potschka, H. and Löscher, W. (2004b) Increased expression of the multidrug transporter P-glycoprotein in limbic brain regions after amygdala-kindled seizures in rats. Epilepsy Research 58, 67–79.

      Volk, H.A., Arabadzisz, D., Fritschy, J.M., Brandt, C., Bethmann, K. and Löscher, W. (2006) Antiepileptic drug-resistant rats differ from drug-responsive rats in hippocampal neurodegeneration and GABA(A) receptor ligand binding in a model of temporal lobe epilepsy. Neurobiology of Disease 21, 633–646.

      Volk, H.A., Matiasek, L.A., Luján Feliu-Pascual, A., Platt, S.R. and Chandler, K.E. (2008) The efficacy and tolerability of levetiracetam in pharmacoresistant epileptic dogs. The Veterinary Journal 176, 310–319.

      von Klopmann, T., Rambeck, B. and Tipold, A. (2007) Prospective study of zonisamide therapy for refractory idiopathic epilepsy in dogs. Journal of Small Animal Practice 48, 134–138.

      Voss, L.J., Jacobson, G., Sleigh, J.W., Steyn-Ross, A. and Steyn-Ross, M. (2009) Excitatory effects of gap junction blockers on cerebral cortex seizure-like activity in rats and mice. Epilepsia 50(8), 1971–1978.

      Waldbaum, S. and Patel, M. (2010) Mitochondria, oxidative stress, and temporal lobe epilepsy. Epilepsy Research 88, 23–45.

      Weissl, J., Hülsmeyer, V., Brauer, C., Tipold, A., Koskinen, L.L., Kyostila, K., Lohi, H., Sauter-Louis, C., Wolf, M. and Fischer, A. (2012) Disease progression and treatment response of idiopathic epilepsy in Australian Shepherd dogs. Journal of Veterinary Internal Medicine 26, 116–125.

      Wessmann, A., Volk, H.A., Parkin, T., Ortega, M. and Anderson, T.J. (2012) Living with canine idiopathic epilepsy: A questionnaire-based evaluation of quality of life. Journal of Veterinary Internal Medicine 26, 1.

       Luisa De Risio Neurology/Neurosurgery Unit, Centre for Small Animal Studies, Animal Health Trust, Newmarket, UK

      A seizure (or ictus) has been defined as ’a transient occurrence of signs due to abnormal excessive or synchronous neuronal activity in the brain’ (Fisher et al., 2005). The clinical manifestations of a seizure are sudden and transient and depend on location of onset in the brain, patterns of propagation and a variety of other factors (see Chapter 1). Seizures can affect one or more of the following functions: sensory, motor, and autonomic activity, consciousness, emotional state, memory, cognition or behaviour (Fisher et al., 2005). The seizure (or ictus) may be preceded by a prodrome (or prodromal phase), which can be characterized by anxiety, restlessness, increased affection, withdrawal, aggressiveness, or vocalization, and by an aura, which is the initial manifestation of a seizure. The prodrome can occur hours to days before the seizure, the aura generally lasts seconds. The aura has been described in people as a subjective sensation, such as dizziness, tingling, and anxiety at the start of a seizure. In animals it may manifest as increased or decreased attention seeking, stereotypical sensory or motor behaviour (e.g. licking, pacing) or autonomic manifestations (e.g. salivating, vomiting, urinating). The ictus is the seizure itself and, in most cases, it lasts only a few minutes. The post-ictal period occurs soon after the seizure (or ictus) and may last seconds to days. Clinical manifestations include disorientation, aggressive behaviour, restlessness, pacing, lethargy, deep sleep, hunger, thirst, defecation, urination, ataxia, proprioceptive deficits and decreased or absent menace response with or without actual blindness.

      Epilepsy has been defined as an enduring disorder of the brain that is characterized by recurrent seizures (Blume et al., 2001; Fisher et al., 2005). As there are many causes of chronic recurrent seizures, epilepsy is not a specific disease but rather a group of heterogeneous conditions. However, not all seizures are associated with epilepsy. For instance, a seizure can be the reaction of a normal brain to a transient insult, such as intoxication or metabolic disorder. If seizures no longer occur when the metabolic or toxic disorder resolves, the patient is not considered to have epilepsy.

      A classification of seizures and epilepsies is important as clinical manifestations and aetiologies of seizures vary considerably. A standardized and uniform classification of seizure and epilepsy would allow consistency in the use of diagnostic terms, improve communication among clinicians and methods of evaluating treatment, and facilitate comparison of clinical cases and scientific studies.

      Classification of seizures and epilepsies in veterinary medicine is largely based on its human counterpart and focuses on seizure phenomenology and aetiology (Schwartz-Porsche, 1994; Podell et al., 1995; Berendt and Gram, 1999; Licht et al., 2002; Podell, 2004). The main limitations of the veterinary classification are that: (i) recognition of seizure occurrence and clinical manifestations is largely dependent on the pet-owner’s observation; (ii) electroencephalographic (EEG) data are usually not available; and (iii) no agreement has been reached for a standardized terminology in veterinary medicine. Therefore, the veterinary literature on this subject is often confusing with regard to definitions and interpretations. In addition, as in human medicine, seizure classification is an ongoing process and therefore updating is necessary.

      This chapter will initially present the definitions and classifications of seizure and epilepsy in human medicine that are relevant in order to understand how terminology and classification have been developed and could evolve in veterinary medicine. Subsequently the focus will be on proposed veterinary terminology and classification.

       Classification of Seizures and Epilepsies in Human Medicine

      In human medicine, the International League

Скачать книгу