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Seizures
/content/chapter/10.22233/9781910443125.chap8
Seizures
- Author: Michael Podell
- From: BSAVA Manual of Canine and Feline Neurology
- Item: Chapter 8, pp 117 - 135
- DOI: 10.22233/9781910443125.8
- Copyright: © 2013 British Small Animal Veterinary Association
- Publication Date: January 2013
Abstract
The approach to and treatment of seizure disorders in small animals is similar in many respects to the treatment of various other ailments in veterinary medicine: an antecedent historical problem arises, a proper diagnosis is made to confirm the condition, and therapy is initiated to treat the underlying disease or signs of the disease. This chapter reviews clinical signs, lesion localization, pathophysiology, differential diagnosis, neurodiagnostic investigation, treatment.
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Figures
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8.2
Abnormal origins of (a) generalized, (b) focal and (c) focal progressing to generalized seizure discharges. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA. © 2013 British Small Animal Veterinary Association
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8.2
Abnormal origins of (a) generalized, (b) focal and (c) focal progressing to generalized seizure discharges. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA.
/content/figure/10.22233/9781910443125.chap8.fig8_3
8.3
Lesion localization for seizure disorders. The forebrain comprising the cerebrum and diencephalon is highlighted. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA. © 2013 British Small Animal Veterinary Association
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8.3
Lesion localization for seizure disorders. The forebrain comprising the cerebrum and diencephalon is highlighted. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA.
/content/figure/10.22233/9781910443125.chap8.fig8_4
8.4
Glutamate receptors in the CNS generally responsible for excitation of associated neurons. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA. © 2013 British Small Animal Veterinary Association
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8.4
Glutamate receptors in the CNS generally responsible for excitation of associated neurons. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA.
/content/figure/10.22233/9781910443125.chap8.fig8_5
8.5
The neuronal circuitry in the cerebrum responsible for feed-forward inhibition. An imbalance in the levels of excitation and inhibition can lead to seizure discharges. (Modified from
March 1998
). Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA. © 2013 British Small Animal Veterinary Association
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8.5
The neuronal circuitry in the cerebrum responsible for feed-forward inhibition. An imbalance in the levels of excitation and inhibition can lead to seizure discharges. (Modified from
March 1998
). Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA.
/content/figure/10.22233/9781910443125.chap8.fig8_6
8.6
Recruitment of groups of neurons undergoing a paroxysmal depolarizing shift can be responsible for extension of the seizure focus. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA. © 2013 British Small Animal Veterinary Association
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8.6
Recruitment of groups of neurons undergoing a paroxysmal depolarizing shift can be responsible for extension of the seizure focus. Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA.
/content/figure/10.22233/9781910443125.chap8.fig8_9
8.9
GABAA receptor in the CNS generally responsible for increasing local chloride levels and causing a surrounding inhibition. The receptor can be bound by barbiturates (BBT) and benzodiazepines (BZD). Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA. © 2013 British Small Animal Veterinary Association
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8.9
GABAA receptor in the CNS generally responsible for increasing local chloride levels and causing a surrounding inhibition. The receptor can be bound by barbiturates (BBT) and benzodiazepines (BZD). Illustration created by Allison L. Wright, MS, CMI, Athens, Georgia, USA.
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8.13
Algorithm for use of phenobarbital and potassium bromide (KBr) in the dog. a The dose of phenobarbital should be increased by 10–25%. b The dose of phenobarbital should be cautiously increased or a second drug, such as KBr, should be given. The formula used to calculate the phenobarbital dose adjustments is as follows: (Desired concentration/Actual concentration) × total mg phenobarbital per day = Oral daily dose of phenobarbital (mg). Css = steady-state concentration. © 2013 British Small Animal Veterinary Association
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8.13
Algorithm for use of phenobarbital and potassium bromide (KBr) in the dog. a The dose of phenobarbital should be increased by 10–25%. b The dose of phenobarbital should be cautiously increased or a second drug, such as KBr, should be given. The formula used to calculate the phenobarbital dose adjustments is as follows: (Desired concentration/Actual concentration) × total mg phenobarbital per day = Oral daily dose of phenobarbital (mg). Css = steady-state concentration.
Supplements
Complex partial seizure (automatism)
3-year-old male Boston Terrier with paroxysmal episodes of stereotypical licking and turning movements. Note that the dog does not actually lick itself during the episode. (See page 119 in the Manual)
Focal motor seizure
2-year-old neutered Maltese bitch with continuous facial muscle movements and normal level of consciousness. (See page 119 in the Manual)
Generalized tonic–clonic seizure
4-year-old male neutered Border Collie with a more classical generalized tonic–clonic epileptic seizure seen in many dogs. (See page 119 in the Manual)
Myoclonic and atonic seizures
2-year-old neutered Australian Sheltie bitch with a myoclonic and atonic seizure disorder. Myoclonic movements are characterized by rhythmic contraction–relaxation of the head and neck muscles. The atonic seizure is characterized by the sudden ‘drop’ attack at the end of the clip. (See page 119 in the Manual)
Status multiple seizure types
5-year-old male neutered German Shepherd Dog with continuous seizure activity characterized by both myoclonic movements of the head and neck, and ‘drop’ attacks. This dog also suffered from generalized tonic–clonic seizures. (See page 118 in the Manual)