Psychomotor Epilepsy Catalepsy and Narcolepsy

Epilepsy in cases of bizarre or unusual behavior occurring with little or no warning, one should suspect the possibility of a biological pathology involving the brain. psychomotor seizure activity (limbic epilepsy) often presents with psychosomatic symptoms, like chronic vomiting or diarrhea (Reisner, 1991), and various behavioral signs. Although behavior problems associated with fear and aggression are typically viewed as learned patterns, some such patterns may be (in part or whole) the behavioral manifestation of seizure activity in the hypothalamus, limbic system, or temporal lobes (Aronson, 1998). The amygdala is particularly sensitive to seizure activity, perhaps an etiologically significant factor in the development of some forms of panic disorder and generalized anxiety. Holliday and coworkers (1970) studied 70 cases of canine motor epilepsy presenting with varying degrees of severity and duration. As the result of interviews taken with owners, they detected a number of behavioral sequelae occurring co-morbidly with epilepsy in dogs, suggesting the possibility of a limbic system or temporal lobe involvement:

Behavioral signs of varying duration and form were common before or after a generalized seizure or sometimes pre- and postictally. The behavioral abnormalities consisted of: wandering in circles, restlessness, somnolence, apparent blindness, viciousness, inappropriate barking, attacking inanimate objects, terror-stricken behavior, inappetence, voracious appetite, generalized trembling, champing of the jaws, licking movements, and behaviour as if one ear were painful. such changes usually lasted a few hours at most, but were occasionally present for 3—4 days. In a few dogs the behavioral signs were the most prominent abnormality, appearing at times in the absence of generalized tonic-clonic seizures. (1970:283)

Unfortunately, such pathology is difficult to diagnose through conventional EEG tests done to verify somatomotor epilepsy. one way to determine whether a particular case is precipitated by underlying limbic seizure activity is to compare the differential effects of epileptogenic drugs and antiepileptic drugs on the expression of the behavior in question. Borchelt and Voith (1985) have described a case involving a male Lhasa apso that, when presented with food, would begin eating, lift his head, growl, and whirl about attacking the surrounding area. The bizarre, poorly directed, species-atypical character of the behavior prompted a pharmacological test. It was found that the dog's aggressive behavior could be kindled by injecting him intravenously with chlorpromazine regardless of the social context or ongoing environmental stimulation. On the other hand, if the dog was given an oral dose of diazepam before eating, he ate peacefully without exhibiting any aggressive behavior.

Dodman and colleagues (1992) have reported three cases of what they term episodic dyscontrolsyndrome (aggression), all of which appear to be associated with limbic seizure activity. The dogs (a Chesapeake Bay retriever, cocker spaniel, and English springer spaniel) exhibited fairly well-directed, although inappropriate and exaggerated, species-typical aggressive behavior. The episodes of aggression were found to be associated with several features that suggested limbic seizure activity. It was noted that the dogs exhibited various premonitory mood changes in the directions of increased irritability and depression, several autonomic signs (excessive salivation, pupillary dilation and glazing of the eyes, and vomiting), and intense aggressive behavior at a high frequency under low or no apparent provocation. All of the dogs proved responsive to phenobarbital therapy—a confirmatory indicator of seizure activity.


Catalepsy is a condition in which dogs lose muscular control over the body, with full or partial collapse. Under full cataleptic loss of voluntary control, dogs may fall into a trancelike condition during which the limbs exhibit a plastic rigidity remaining in the form they are placed (Fox, 1968). A common example of catalepsy is tonic immobility, a phenomenon that is widespread in the animal kingdom and that may have a biological self-preservative function when an animal is faced with environmental threat (Gallup and Maser, 1977). The behavior has been described as feigning death or protective inhibition. A very familiar example of the behavior is exhibited by the opossum, a marsupial that uses tonic immobility as a primary mode of defense against predation. Cataleptic tonic immobility can be induced in a variety of ways: "The conditions for induction have included eye contact, pressure on body parts, repetitive stimulation, inversion, and restraint" (Crawford, 1977:89). Dogs that are abruptly rolled on their sides, following a brief struggle, are often absorbed into a state of tonic immobility. Tonic immobility might be part of a parasympathetic rebound effect in response to intense sympathetic arousal. Another interpretation conceptualizes tonic immobility and catalepsy as a response to conflict provoked by incompatible motivations between active and passive defensive mechanisms; that is, when an animal is threatened with imminent physical danger during which escape is not possible and attack is equally ineffectual, the outcome may be cataleptic immobility. Gran din (1992) has argued that the induction of tonic immobility is an elemental part of some taming processes in animals (e.g., wild horses), claiming that the firm touch calms while the light touch excites. She has designed a squeeze machine for the treatment of autistic and hyperactive children, claiming that physical pressure promotes a lasting sense of calmness and well-being. This may be relevant to the beneficial effects of forced lateral recumbency on some dogs. Dogs exposed to such restraint for several minutes are often significantly calmer when finally released.


Narcolepsy is a sleep disorder that, in humans, is associated with catalepsy and the rapid onset of sleep. In dogs, it appears to be genetically determined, with breeds such as the Doberman pinscher, miniature poodle, and black Labrador retriever most often exhibiting the disorder (Voith, 1979). The condition is incurable. During episodes of narcolepsy, affected dogs move rapidly from an active state into a state of muscular weakness and collapse while apparently remaining in a trancelike conscious state. The onset of narcoleptic episodes is frequently associated with feeding times, during periods of general excitement, during or just after elimination, and sometimes during sexual activity. Regarding such attacks, Foutz and colleagues write,

These attacks are frequently precipitated by the excitement of approaching desired goals, such as food, a play object or companion, or sexual activity. Some breeds such as Labradors often experience cataplexy more frequently when playing and exercising than when eating. Unpleasant experiences such as pain (caused by a hypodermic injection), fear, or parturition, do not appear to specifically elicit attacks. Cataplexy also appears to occur spontaneously. Very young puppies do not appear to be significantly responsive to food, but play activities are major precipitants for attacks.

Pavlov (1927/1960:319) appears to be describing narcolepsy when he writes concerning a highly inhibited dog that could not bear even a short delay of conditional reinforcement without becoming "drowsy and even fall[ing] asleep over its plate while taking the food."

Although the causes of narcolepsy are not definitively known, recent advances point to a dysfunction associated with the cholinergic innervation of the pontine reticular formation (PRF). Catalepsy associated with narcolepsy may result from the abnormal activation of these cholinergic mechanisms associated with the induction of REM (rapid eye movement) sleep. A colony of narcoleptic Doberman pinschers has been isolated and is currently being subjected to various experimental manipulations in an effort to determine the causal mechanisms involved. Reid and coworkers (1994) have directly measured ACh activity in the PRF via probes implanted into the pons of narcoleptic dogs. They have found a definite relationship be tween narcoleptic episodes and increased levels of extracellular ACh in the PRF of affected dogs. Interestingly, baseline levels of ACh in the PRF did not differ between controls and narcoleptic dogs.

The diagnosis of narcolepsy can be confirmed by EEG or by injecting narcoleptic dogs with imipramine. Reportedly, affected dogs quickly recover from the attack after being injected with the drug (Voith, 1979). In severe cases, CNS stimulants (d-ampheta-mine and methylphenidate) are sometimes prescribed to control the disorder (Foutz et al., 1980). Narcolepsy in dogs is often left untreated, since treatment is problematical (Hart, 1980). Medication with CNS stimulants may produce a variety of undesirable side effects and produce increasing tolerance over time.

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  • ulpu
    Can dogs have catalepsy?
    7 years ago
  • Lisa
    How is catalepsy different from epilepsy?
    6 years ago
  • mohammad
    Is limb rigidity typical in a narcoleptic dog?
    6 years ago
  • wolfgang
    Can dogs be trained to detect cataleptic seizures?
    4 years ago
  • margaret
    What causes canine catalepsy?
    3 years ago

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