Abnormal behavior in dogs can have a variety of medical causes; it can also reflect underlying problems of a psychological nature. Your veterinarian follows a systematic diagnostic approach in searching for medical causes when a pet exhibits unusual or unacceptable behavior. This includes:
Diagnostics steps (1) through (3) are usually completed first; additional tests such as steps (4) through (6) are performed as indicated. If these test results prove to be negative, a veterinary behavior consultant or qualified pet behavior therapist should evaluate the dog.
Inheritance has been shown to play an important part in the behavior of both animals and humans. The genetic influence on behavior disorders rarely accounts for more than half of the phenotypic expression of behavioral differences. Each of the multiple genes involved has small effect on the behavior. Newer techniques in molecular biology should permit the identification of the genetic DNA marker sequences responsible for behavioral variation.
However, behavior is the most complex phenotype because it not only reflects the functioning of the whole organism, but it is dynamic and changes in response to environmental influences. With respect to animal behavior, applied behavioral genetics first was studied several thousand years ago because animals were bred and selected for their behavior as much as their conformation. The results can be attested to by the dramatic differences in behavior and physique among various dog breeds. Today these breeds have a great range of genetic and behavioral variability.
In recent years, many investigators have noted the sudden onset of behavioral changes in dogs around the time of puberty. Many of these dogs also had begun to show the seasonal effects of allergies to inhalants and ectoparasites such as fleas, followed by the onset on skin and coat disorders, including pyoderma, allergic dermatitis and intense itching.
A typical history starts out with a quiet, well mannered and sweet natured puppy. The dog is outgoing, has attended puppy training classes to prepare for obedience, working or show events, and comes from a reputable breeder with no history of behavioral problems.
However, at the onset of puberty, which varies from seven months to a year, sudden major changes in personality are observed. Typical signs may include incessant whining, nervousness, schizoid behavior, fear in the presence of strangers, hyperventilation, undue sweating, occasional disorientation and failure to be attentive. These can progress to sudden unprovoked aggressiveness with other animals and with people, especially children.
The owners may attribute the problems to the sex hormonal changes accompanying puberty or just the uncertainties of adolescent development. Often these animals are neutered, which appears to alleviate the behavioral problems, specifically the aggression, for varying lengths of time. For a significant proportion of these animals, however, neutering does not alter the symptoms and they intensify progressively to the point that the adult can be described as flaky, unable to handle any kind of stress, frantically circling, hyperventilating and not able to settle down. Animals used for field work and tracking often fail to follow the scent, whereas those in obedience training may lose the scent articles. Their powers of concentration are often very short and so dogs that were training very successfully at obedience appear to lag behind in a disinterested fashion. With all of these changes in behavior, the problem of most concern is unwarranted aggression. When large breeds are affected, it poses a significant hazard to family members, friends, and strangers.
In some cases affected animals do not show aggression, but become very shy and fearful to the point that they are social outcasts and do not make acceptable house pets. These animals clearly are not suitable of for show, obedience or working purposes. Some of these dogs will show extremely submissive behavior, roll over and urinate upon being approached.
The third group of dogs showing aberrant behavior consists of those that experience seizure or seizure-like disorders beginning in puberty and continuing to midlife. These are dogs that appear perfectly healthy outwardly and have normal hair coats and energy, but suddenly experience seizures for no apparent reason. The seizures are often spaced several weeks to months apart, and occasionally they appear in a brief epileptic-form cluster. In come cases the animals become aggressive and attack those around them shortly before or after having one of these seizure episodes.
The number of dogs showing various types of abnormal behavior in these three classical modes (aggression, extreme shyness or seizure-like activity) has been increasing over the last decade. Veterinary colleagues have remarked that in recent years some young dogs have become completely unacceptable because of bizarre, sudden behavioral changes. Consequently, we began to examine these animals by using the stepwise diagnostic approach outlined previously. The importance of performing complete laboratory profiles on the blood and urine, with specific emphasis on thyroid hormonal function, was stressed.
We are surprised to find that in many of the cases studied, significant abnormalities were found in the thyroid profile. Some cases also had changes in the liver enzyme patterns, specifically with abnormal increases in pre and post-meal bile acids and elevated gamma glutamyl transferase levels. About 10 percent of these young dogs had abnormalities of the liver profile and a few also had changes in renal function. For the majority, however, the primary abnormality was attributable to abnormal thyroid function. This thyroid dysfunction would classically express high levels of T3 (tri-iodothyronin) and T4 (l-thyroxine) autoantibodies with an artifactual, apparent elevation of total T3 level. It would not be uncommon to find circulating total T3 levels that read as much as 3,000 to 5,000 nanograms per deciliter. While not all of the affected animals had documented evidence of T3 and T4 autoantibodies, some of these had positive antithyroglobulin antibody tests. In either event, the diagnosis was confirmed as autoimmune thyroiditis.
The autoimmune thyroid disease present in these patients apparently is inducing some type of physiological change in the cellular level, which leads to their aberrant behavior. This supposition can be made with some assurance because treatment of thyroiditis of these dogs with appropriate doses of thyroid replacement hormone given twice daily, along with a one-month tapering course of low-dose corticosteroids, has successfully reversed the behavioral problems within four to eight weeks. Dramatic changes in behavior have been recognized in a few cases as early as after ten days of therapy.
By contrast, it usually takes five to seven months of thyroid replacement therapy to effect complete disappearance of the circulating antithyroid antibodies. These dogs should be maintained for life on the appropriate dose of thyroid hormone, which may need to be adjusted periodically.
Another subset of affected dogs consists of those that do not have a demonstrable antithyroid profiles that are clearly abnormal. In these cases, levels of total T4 and t3, free T4 and free T3 are usually well below the lowest limits of the adult normal ranges or are in the low normal or borderline ranges. The latter situation is of particular significance in your dogs nine to 15 months of age. When these dogs are treated with standard doses of thyroid replacement therapy (0.1 milliliter per ten pounds of body weight) the clinical signs associated with abnormal behavior rapidly resolve.
To date more than 25 animals have been diagnosed as having thyroid imbalance as the major, if not exclusive, cause of their behavioral abnormalities. Some of these animals have been followed for as long as three years and are still exhibiting normal behavior. Animals on therapy have returned successfully to obedience activities, completed championships and undertaken field and tracking work.
Here are two case studies as examples:
In the first, a four year old male Akita weighing 110 pounds, suddenly attacked his owner and bit her in the face. The dog had been owned by the same family since early puppyhood and had been a remarkably even-tempered, well-behaved and non-aggressive pet with people and other animals. After seeking the advice of two veterinary clinicians and a major teaching hospital, the owner was about to give up in despair because no physical abnormalities could be found.
She was referred to us by an Akita rescue group, as this pattern of behavioral change has been associated with thyroid dysfunction in the breed. A complete thyroid panel was suggested and the dog was found to by hypothyroid. Thyroid therapy was initiated on a twice-daily basis. The dog's exemplary temperament returned and he has not shown any unusual behavior for over a year.
In the second, a nine-month old male Shetland Sheepdog from excellent show-quality bloodlines suddenly became frantic and fearful. acting intermittently, as if his vision were impaired, he attached a toddler in the owners' home. A complete physical examination was given and laboratory testing done; a routine check of rT4 was borderline normal. The dog's abnormal behavior appeared to resolve, but soon reappeared.
After a second attack, the dog had a complete thyroid profile done at Michigan State University's Animal Health Diagnostic Laboratory. The total T4 was 44 nmol/l, total T3 was 0 nmol/l, free T4 was 2 pmol/l, free T3 was > 20 pmol/l, T4 autoantibody was 18 and T3 autobody was 85. The referring veterinarian did not realize that the results were consistent with autoimmune thyroiditis and the dog was not treated. Two months later the dog attacked another person and a second thyroid profile was sent to the MSU laboratory. The second profile showed a total T4 of 29 nmol/l, total T3 of 0 nmol/l, free T4 of 25 pmol/l, free T3 of > 20 pmol/l, T4 autoantibody of 48 and T3 autoantibody of 91. Consultation with our group was then made.
The dog had a previous history of facial demodectic mange; because corticosteroids are not recommended with demodecosis, the treatment consisted of a full therapeutic dos of T4 thyroid supplement of 0.1 milligram per ten pounds and a one-third does of T3 thyroid supplement a 1 microgram per pound, both given twice daily. The rationale for treating with both T4 and T3 supplements in this case was to attempt to normalize the thyroid axis as quickly as possible to avoid danger to family members. At the time of this writing the dog's behavioral aggression has subsided.
For those animals that show occasional seizure disorders, thyroid medication alone usually will suffice. Anticonvulsant medication is needed along with the thyroid therapy to control cases with more severe seizure clusters. The anticonvulsants of choice would be phenobarbital or alternatively sodium bromide, particularly if the patient has abnormalities of liver function.
Because many of these animals have autoimmune disease, concomitant medical management includes voiding environmental factors that can further challenge the immune system. This means placing the animal on a hypoallergenic "natural" diet preserved with vitamins E and C (e.g. lamb and rice based, lower protein kibble without added chemical preservatives); avoiding drugs such as the pontentiated sulfonamide antibiotics and monthly heartworm preventives that may adversely affect the immune system in these susceptible dogs; and withholding vaccination boosters until the thyroid function is balance properly and the behavioral abnormalities are resolved. If animals are due for annual vaccine boosters during this period, vaccine antibody titers for distemper and parvovirus can be determined.
If your otherwise healthy young or adult dog experiences sudden behavioral changes, you should consult your vet and check for an underlying thyroid imbalance as show by:
In our experience, the most predictive thyroid test parameters to identify these cases are (1) and (2), because the thyroid-stimulating hormone response test just measures thyroid reserve, which remains adequate in the early stages of thyroid disease.
Thank you Dr. W. Jean Dodds for allowing me to reprint this on my site.
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