The noises phobia is common in canine. It is an extreme fear to a defined stimulus characterized by sensitization, anticipation and flight. It is result of the interactions biological, genetic and environmental, being classified in specific or post-traumatic. The physic and psychopathology involve numerous cortical structures, limbic and shaft brain, with participation of innate, learned and emotional components. The clinical signs consist reactions of unjustified fear in front of an identifiable stimulus. Diagnosis is based on clinics approaches and the treatment appeals to therapies and drugs.
The phobia limited to a reduced group of stimuli as the fireworks, thunders, shots or explosions is the most common of the specific phobias in canine, being of slightly frequent presentation in felines. In contrast to the indispensable survival fear of the individual and the species, the phobia is a pathological behavior of excessive fear that has lost its adaptive character. Nevertheless, the limit between an intense normal fear and a specific slight phobia is not completely clear.
The phobia is an extreme, excessive and persistent fear unleashed by a definite stimulus (or group of narrowly related stimuli) normally presented in the environment and without real danger. It is accompanied by the sensitization processes, anticipation and avoidance, provoking a clinical significant discomfort that interferes with the normal behavior.
Sexual differences do not appear its incidence. For some authors the fear might have an average or high hereditably and this would predispose that certain breeds or familiar lines develop a phobia. In the unit of clinical ethology of the Hospital School of Veterinary Medicine of the University of Buenos Aires the phobias corresponded to 10,50 % of the disorders of behavior diagnosed in 190 patients. Nevertheless we suppose that a great percentage of phobic animals are not taken to consultation or are bad diagnosed in the clinical consultation.
It is a clear example of interactions between biological, genetic and environmental factors. The cause is not completely clarified, nevertheless the majority of the times we can classify according to its origin in specific or posttraumatic. There are reports of excessive fear with rigidity and inhibition in certain dog breeds. Nevertheless up to the moment, it has not been possible to demonstrate a genetic origin due to the absence of scoreboards or of controlled studies where it is possible to indicate the environmental influence. The specific or otogenic phobia begins in the juvenile stage. Traumatic situations or previous unleashing negative experiences associated with the above mentioned stimuli are identified. Nevertheless there are other involved factors. Deficit of the development for sensory isolation, is absent in the mechanisms of adjustment and inadequate socialization. Early inadequate experiences with aggressive learning when escaped from a novel stimulus. Presence of physical, etiologic pathology or combination of both. These phobias are the most difficult to control. On the other hand the posttraumatic phobia is restored after a sensibly accident or traumatic experiences associated with the stimulus in question. For example animals that observed or were near to an explosion. They do not present a typical beginning age.
In the phobic response, numerous cortical, limbic and structures from the cerebral stem participate. They are principally important the locus ceruleus (LC), rafe back nucleus, hypothalamus, tonsil, hippocampus and frontal cortex. The central role corresponds to the noradrenergic system that seems to suffer a deregulation without neuropathologic injury, but also other systems of intimately related neurotransmitters are compromised. The noradrenergic route has its origin in the LC, principal noradrenergic nucleus of the base of the brain that sends connections to the frontal cortex, limbic system and spinal cord principally. It is the one in charge of the wide scale of physiological, etiological and emotional responses. The struggle or flight reaction is coordinated in turn by the axis hypophysis--hypothalamus--adrenal with liberation of the stress hormones. An increase of the thalamic transmission that accompanies the activation of the LC can lead to hyperalertness and hyperreactivity and by trigeminal route, the fear expressions are generated. The catecholamines act on beta-adrenergic recipients increasing the long term memory of the negative events, with an adaptive purpose. It is suspected that the tonsil recognizes the alarm that comes from the LC and instantaneously it remembers fears learned in the past. The central nucleus of the tonsil is a rich internal network of synapses that seems to be the place for the determined fear. Also it receives sensorial information coming from the thalamus. This can happen by direct connection between two structures or indirectly from the thalamus across the sensory auditory cortex. The direct tract does not communicate detailed information about the stimuli, but it is quick. Something very important in life threaten situations. The indirect tract involves an area of the cortex that interprets the sensory information and then it sends relevant signs to the tonsil. It is slower but it allows a more detailed interpretation of the event. This are the routes of conduction that settle down during the therapy but in the presence of a very stressful situation, the internal circuits of the tonsil are the ones in charge of the making the phobia acute. During the response of fear, in the presence of indicative signs of threat the tonsil through connections with the hypothalamus, dorsal motor nucleus of the vagus, parabraquial nucleus, LC and paraventricular nucleus, takes part in the autonomic activation responsible for hypereflex signs of fear and anxiety. Then the increase of reactivity of the LC and of the tonsil play an important roll in the phobias. The hippocampus is another major structure of the limbic system involved in the memory storage and it has connections with the tonsil and hypothalamus. In stress situation dopamine is liberated in a selective form by the neurons of the mesocortical route (frontal) and mesolimbic (amygdaloidal) stimulating the alertness and the exploratory conduct. The dorsal rafe nucleus, principal serotoninergic central nucleus, increases its activity by stress or anxiety, disabling the adaptive and social conduct. The increase of the serotoninergic activity in the hippocampus area is seem to be related to previous experiences. The GABA, an important inhibiting central neurotransmitter, modifies the sympathetic and serotoninergic tone, the one who collaborates in its anxiolytic effects. The GABA blockade produces anxiety and increase the respiratory and cardiac frequency. Also it is involved in the glutamate and aspartate recipients sensitization phenomena. The formation of new synapses pieces sustains the memorization of the response to the sensibilizing stimulus. The functional studies realized with positrons emission scanner (PET and SPECT) seem to indicate an increase of noradrenaline liberation from the LC, stimulating the parahippocampus neurons.
The fear innate component is of vital importance for the species. Nevertheless this phylogenetic fear can evolve to a clinical form of phobia after adverse experiences during the ontogenic development. The favorable stimuli appear in agreeable contexts in the presence of the ancestors. Whereas the dangers appear in adverse situations. The different stimuli will then behave like sensibilizers (neophobias) or habituation according to the circumstances, intensity and frequency of presentation. The response depends also partly on the socialization, previous experience and medical and emotional condition of the individual. The exhibition to a frequent stimulus, of low intensity, in an open situation, in an individual with good sensory and etiological development drives to the habituation. If the stimulus is occasional and intense as thunders, shots or fireworks, it produces a physiological response of fear. Nonetheless if it has no consequences, after several exhibitions the habituation takes place and it stops answering. On the other hand if it associates to aversive experiences (pursuit or punishment), without possibility of escaping (closed situation), in animals with poor environmental stimulation or during the stage of the development, then, it transforms in a phobogenic stimulus, though it does not present a real danger, generating an amplified response (intensification of the fear). The negative experience is memorized by deep and lasting effects on the conduct. This pathological process named sensitization is the one that leads to the constitution of a phobia and consists of the absence of habituation in front of a threatening stimulus without real danger with a disorganized response for fear that is intensified and loses its adaptive character. Every new exhibition worsens the picture, being the more and more painful experience. This process does not depend only on external factors as the intensity and the frequency of exhibition, but also on development perturbations on having diminished the threshold of response to the fear. In some cases a phobia of high intensity is established after only one exhibition that not necessarily represents physical trauma as it does emotionally. Though the explanation of this phenomenon partly would be by means of the classic conditioning, it does not allow to justify completely the natural phobias. On having eliminated the undetermined associate stimulus, the response does not diminish gradually and persists for years. The operating conditioning clarifies a bit more the situation when it explains that the fear that the stimulus generates leads the organism in doing everything possible for attenuating or eliminating the potential threat, learning conducts of avoidance and flight. This avoidance pattern remains stable a lot of times as a result of the reinforcement produced when the tension is diminished. Even more when it receives the owner's attention with the intention of calming it by caressing or giving food. Therefore, the avoidance also defrosts a central role in the phobias and remains fixed and instrumental as a stable symptom for its effectiveness. This explanation continues being insufficient and can be questioned in some other aspects. The anticipation frequently accompanies the sensitization and generates excessive fear before the presence of the phobogenic stimulus and in response to secondary associate stimuli that precede the original one, like atmospheric pressure, wind, rain or lightings. It appears as result of the hyperalertness and hyperreactivity that generate an automatic response that excludes the possibility of a cognitive evaluation. Only if the tension is sufficiently limited can recover the control and take a conscious decision about the characteristics and the consequences of the event. In some cases they can appear other stimuli or situations similar but be away in time and space as engine, electrical appliances or constructions noises, which they pass to the development of complex phobias by means of the generalization mechanism. We might suppose that the fear subjective conscience, an important component of the emotional response, is present in the company animals. This is difficult but impossible to demonstrate scientifically. But it is possible to interpret it across the observation of conduct changes that suggest it.
It is characterized by the presence of the identifiable stimulus, alone or multiple but homogeneous as thunders, fireworks, shots and explosions (strong noises). Opposite to the exhibition to this phobogenic stimulus unchains a typical excessive fear reaction characterized by: deambulation, flight, to hide, shacking, attachment to the owner and down position (tail between legs, low head, semiflexed members, ear pavilions back). The most intense reactions are accompanied by groans, sialorrhea, tachycardia, tachypnea, mydriasis, hyperalertness, hyperstesia, hypermotility, excavation, barrier destruction (doors, windows, grills) and pheromone alarm discharge. Also there can appear enuresis, vomiting, diarrhea and fear aggression. The anticipation phenomenon appears opposite to heterogeneous stimuli associated temporarily with the primary stimulus, as changes of atmospheric pressure, ionization, odors, wind and lightning, and accompanied by the avoidance behavior. These typical responses of fear correspond to the noradrenergic activation and secondarily the dopaminergic, causing a great clinical discomfort with inhibition of the normal behaviors. With this complete clinical signs the necessary and sufficient conditions for a diagnosis consistent on a extreme response, active avoidance, intense escaping, anxiety associated with the sympathetic activation, concomitant tachypsiquia with decrease of the pain sensibility or to social stimuli and a pattern of invariable response opposite to the repeated exhibition.
It is usual for it to be immediate and generally the same owner realizes it, describing clearly the signs. The noise that generates the process is intense and unmistakable. Anyway it is necessary to establish a diagnostic criteria based on clearly definite targets parameters. 1) Excessive fear for the presence or anticipation of a specific sonorous stimulus. 2) immediate response of excessive fear characterized by sympathetic activation. 3) The stimuli are avoided or are supported by intense fear including immobilization, hypermotility, hyposensibility to the pain or to social stimuli. 4) Rules of invariable responses to repeated exhibitions. 5) The avoidance and anticipation interfere with the normal behavior or provoke a clinical significant discomfort. The records of PET and SPECT yet are not of clinical use.
It is necessary to do it with the anxiety, the hierarchic conflicts and the response of normal fear of an intense, unexpected and slightly habitual stimulus.
Favorable with patience and sufficient motivation of the owners. On the other hand in patients with anxiety, public intense response, with lot of evolution time, difficult event to reproduce artificially and of natural avoidance, the healing possibility is practically none. Nevertheless, it is possible to control the symptoms in the expositions.
While the desensibilization is done, the patient must not be exposed to the natural stimulus, since in this case, the successful grade of habituation gets lost. Counterconditioning it by means of the administration of food rations or a section of social game in association to the absence of response to the stimulus. To apply a disruptive stimulus as a bell or spray, in the appetizing phase of the response and orientated it to a different activity. Flood exposing it to the noise at an intensity over the response range and not to be removed until the symptoms disappear and it calms down, and only in cases of slight phobias and of recent appearance. Controlled exhibition in front of the stimulus to an intensity that, still over the range of abnormal response, the patient can support and be controlled in sure and effective way until relaxation, increasing the exhibition gradually.
It is necessary to choose the compound according to the clinical picture.
Alprazolam (0,12-0,25 mg/kg/6-8 hrs PO) with more anxiolytic action than the diazepam, given one or two hours before. Chlorazepate (0,5-1 mg/kg/8-12 hrs PO) with a longer half life. Clonazepam (0,1-0,5 mg/kg/8-12 hrs PO). Propanolo1 (0,5-2 mg/kg/8 hrs PO) it blocks de beta-adrenergic activity reducing the anxiety physical symptoms and has certain serotoninergic effect. C1omipramine (1-2 mg/kg/12 hrs PO) anti-depressive with anxiolytic action. Acetylpromazine (0,1-0,5 mg/kg PO) does not reduce the anxiety but it can be sufficiently sedative to avoid lesions.
To favor a correct sensory development, to do an early stimulation exhibiting to the puppy or juvenile to the biggest quantity of possible stimuli in suitable contexts, to allow a suitable socialization heterospecific, to avoid traumatic experiences and not to reinforce the responses of normal fear when are presented.
1. Askew, H. R.: Treatment ofBehavior Problem in Dogs and Cats: A Guide for tha Small Animal Veterinarian. 28 ed., London, Black:well Science, 2004.
2. Beaver, B. V.: Canine Behavior: A Guide for Veterinarians. Philadelphia. Saunders, 1999.
3. Dodman, N. H.; Shuster,L.: Psicofarmacología de los Desórdenes de Conducta Animal. Buenos Aires, Intermédica. 1999.
4. Hart, B. L.; Hart, L. A.: Canine and Feline Behavioral Tberapy. Philadelphia, Lea & Febiger, 1985.
5. Houpt, K. A: Domestic Animal Behavior for Veterinarians and Animal Scientis. 3a. Edic. Ames, Iowa State University Press, 1998.
6. Landsberg, G.; Hunthausen, W.; Ackerman, L.: Handbook of Behavior Problems of the Dog and Cal 28 ed.,Philadelphia. Saunders, 2003.
7. Manteca Vilanova. X.: Etología Clínica Veterinaria del perro y del gato. 38 ed., Barcelona. Multimédica, 2003.
8. Mentzel, R. E.; Atgibay, T. l.: Apresenta_ao de doen_as comportamentais em pequenos animais. XXV ANCLIVEPA 19 al 23 de mayo de 2004. Gramado, Brasil.
9. Overall, Karen L.: Clinical Behaviornl Medicine Small Animals. Sí. Louis, Mosby, 1997.
10. Pageat, P.: Patología del Comportamiento del Perro. Barcelona, Pulso, 2000.
11. Voith, V. L.; Borchelt, P.L.: Readings in CompanionAnimal Behavior. Trenton, VLS, 1996.