The Parson Russell Terrier is a healthy breed overall, with relatively few serious health issues. The Parson Russell Terrier Association of America, as the AKC Parent Club for Parsons, serves as caretaker and protector of the breed. To fulfill that role, we need to be proactive about health issues that are related to the health and welfare of the Parson Russell Terrier.
Below is a list compiled from the AKC Canine Health Foundation with regards to the Parson Russell Terrier and health issues they can have.
- Atopic Dermatitis
- Congenital Deafness- can be Unilateral or Bilateral
- Cryptorchidism-Failure for one or both testicles to descend into the scrotum.
- Legg-Calve Perthes Disease- (LCP)- results when the blood supply to the femoral head is interrupted resulting in avascular necrosis, or the death of bone cells. On-set 4 to 7 months of age
- Late On-Set Ataxia-(LOA)- Incoordination of gait and lack of balance, onset 6 months to 1 year
- Mast Cell Tumors
- Patellar Luxation
- Primary Lens Luxation-(PLL)
- Spinocerebellar Ataxia - (SCA) with or without Myokemia and Seizures- On set as early as 10 weeks
Please additional pages for specific information regarding the above conditions
DEVELOPMENT DNA TEST FOR LATE ONSET ATAXIA
Late onset ataxia (LOA) in the Parson Russell terrier (PRT) and Jack Russell terrier (JRT) is a disease of incoordination of gait and lack of balance. The onset age for the disease is usually between 6 months and 1 year of age, when owners may start to notice that their dog is showing changes in gait pattern (often weaving of the hind limbs) and some difficulty balancing. The disease is progressive and affected dogs become increasingly uncoordinated with difficulty balancing, which makes moving around and everyday tasks such as going up and down stairs difficult. There is no treatment or cure for LOA and affected dogs are often euthanized, typically around two years after onset, on humane grounds as their quality of life diminishes. The Animal Health Trust canine genetics research group has identified the mutation causing LOA.
The AHT also offer a test for Spinocerebellar Ataxia with or without Myokymia and Seizures for the Parson Russell terrier (PRT) and Jack Russell terrier (JRT) known as the SCA test, please see below under Other forms of ataxia for details.
CLEAR: These dogs have two normal copies of DNA and are likely to be clear of LOA. The results of our research suggest that there may be other causes of ataxia in the breed so we cannot exclude the formal possibility that clear dogs could develop a genetically different form of ataxia due to other mutations that are not detected by this test.
CARRIER: These dogs have one copy of the LOA associated mutation and one normal copy of DNA. These dogs will not develop LOA themselves as a result of the LOA mutation but they will pass the mutation on to approximately 50% of their offspring. The results of our research suggest that there may be other causes of ataxia in the breed so we cannot exclude the formal possibility that carriers could develop a genetically different form of ataxia due to other mutations that are not detected by this test.
AFFECTED: These dogs have two copies of the LOA associated mutation and have a very high chance of developing LOA.
The test will effectively reduce the number of LOA cases in the PRT. We encourage owners to keep us updated on the health of dogs they have tested. We are particularly interested to hear from owners of dogs that:
- are clinically affected with ataxia but that do not have two copies of the mutation,or
- are over 4 years old and remain free from ataxia despite having two copies of the mutation.
This information will help us to monitor the effectiveness of the test, to possibly refine the test in the future if necessary and to start to investigate additional cause(s) of ataxia in PRTs and JRTs.
Other forms of ataxia
Spinocerebellar Ataxia (SCA) with or without Myokymia and Seizures The mutation for this condition was identified by the University of Missouri and a DNA test is available both through the Animal Health Trust and University of Missouri. Affected dogs also show signs of cerebellar ataxia as early as 2-6 months of age. At post-mortem examinations, degeneration can be found in the areas of the spinal cord that carry information to the cerebellum, hence the term spino-cerebellar ataxia. The coordination difficulties also progress, but in addition other signs can develop. The majority of cases also develop myokymia, an involuntary twitching of the muscles. The myokymia also becomes progressively worse with age and can result in episodes of generalized muscle spasms and over-heating. In addition, a small percentage of dogs with SCA have true epileptic seizures, some as young as 10 weeks of age. Most dogs with SCA are also euthanized young due to poor quality of life.
Neonatal Granuloprival Ataxia (NGA)
Another form of ataxia called Neonatal Granuloprival Ataxia (NGA) is also hereditary but the mutation has not yet been identified. As the name implies, coordination difficulties in dogs with NGA are apparent from the time they begin to walk, which clearly distinguishes it from the other forms. In these dogs, an area of the cerebellum called the granular layer degenerates. There is currently no test for this condition.
Both the University of Missouri and the Animal Health Trust have found a small number of dogs reported as suffering from cerebellar ataxia which began after weaning age that do not have either of the known mutation. This may represent another form of hereditary ataxia or they may represent an acquired cause of the disease.
The Animal Health Trust and the University of Missouri have discovered different mutations which cause similar, but distinct forms of the disease in Jack/Parson Russell Terriers. We are working to investigate those cases of ataxia which do not have either of the known mutations.
We would like to thank all the Breed Clubs and individuals who have contributed financially to this research and to all the Parson Russell terriers and their owners who have contributed DNA and information to this research.
LOA/SCA Tests are available from AHT
LOA-test approx $62.00 (40 GBP)
SCA-test approx $62.00 (40 GBP)
SCA Tests are also available from OFFA
PLL Tests available from OFA
PLL Test from AHT
PLL-test $54.00 (35 GBP)
Additional information regarding specific conditions known to affect the Parson Russell Terriers
Allergies, also known as hypersensitivities, are acquired overreactions by a dog’s immune system to something that it perceives as being foreign and potentially dangerous, called an “allergen.” Common canine allergens are food ingredients, pollens, grasses, weeds, plants, flea and tick saliva, mites, chemical cleaners, detergents and other household products, plastics, drugs, carpet fibers and cigarette and cigar smoke. Allergies often cause skin problems, ear irritation and gastrointestinal upset. Affected dogs may scratch, lick or bite at irritated skin areas, creating sores that can become infected. The constant head shaking and scratching from “allergic ears” can cause blood-filled blisters, called hematomas, on the bottom of the ear flaps. Dogs with allergies can develop significant behavioral changes because of the inescapable discomfort associated with their condition. - See more at: http://akcchf.petwave.com/Dogs/Health/Allergies.aspx#sthash.VsYAmMKo.dpuf
Atopy, also called allergic inhalant dermatitis, atopic dermatitis, atopic eczema and immune-mediated skin hypersensitivity, is a common genetically-influenced disease that makes dogs react to things that normally don’t cause skin problems. The triggers of atopic reactions are called allergens. These can be anything that causes the immune system to overreact. One dog may be overly sensitive to weed pollen in the air, while its littermate may be allergic to touching grass. Common allergens are pollen, grasses, weeds, trees, mold, dust, dust mites, grains, chemicals, fertilizers, wool and feathers. Most affected animals are allergic to more than one thing. Atopic dogs get itchy when they come into contact with something that overstimulates their immune system. At first, symptoms may be mild. Many dogs eventually start scratching and biting at their skin and become extremely distraught. This causes skin sores and infections, making the dog miserable. Atopy usually is controllable with medicine and lifestyle changes. Veterinary and owner attention are necessary to keep the dog comfortable. - See more at: http://akcchf.petwave.com/Dogs/Health/Atopy.aspx#sthash.OggpK8Ws.dpuf
GENETICS AND INHERITANCE OF CANINE DEAFNESS
Dr. George M. Strain, Louisiana State University Comparative Biomedical Sciences, School of Veterinary Medicine, Baton Rouge, Louisiana 70803
Congenital deafness in dogs (or other animals) can be acquired [caused by intrauterine infections, ototoxic drugs like gentamicin, liver disorders, or other toxic exposures before or soon after birth] or inherited. Inherited deafness can be caused by a gene defect that is autosomal dominant, recessive, sex-linked, or may involve multiple genes (more on this later). It is usually impossible to determine the cause of congenital deafness unless a clear problem has been observed in the breed, or carefully planned breedings are performed. In this article I will discuss what is currently known about the genetics of deafness in dogs so that breeders can make the best informed decisions possible when attempting to reduce or eliminate deafness.
Congenital deafness has been reported for approximately 80 breeds, with the list growing at a regular rate (see list of Dog Breeds with Reported Congenital Deafness); it can potentially appear in any breed but especially those with white pigmentation. Deafness may have been long-established in a breed but kept hidden from outsiders to protect reputations. The disorder is usually associated with pigmentation patterns, where the presence of white in the hair coat increases the likelihood of deafness. Two pigmentation genes in particular are often associated with deafness in dogs: the merle gene (seen in the Collie, Shetland Sheepdog, Dappled Dachshund, Harlequin Great Dane, American Foxhound, Old English Sheepdog, and Norwegian Dunkerhound among others) and the piebald gene (Bull Terrier, Samoyed, Greyhound, Great Pyrenees, Sealyham Terrier, Beagle, Bulldog, Dalmatian, English Setter). However, not all breeds with these genes have been reported to be affected. The deafness, which usually develops in the first few weeks after birth while the ear canal is still closed, usually results from the degeneration of part of the blood supply to the cochlea (the stria vascularis). The nerve cells of the cochlea subsequently die and permanent deafness results. The cause of the vascular degeneration is not known, but appears to be associated with the absence of pigment producing cells (melanocytes) in the blood vessels. All of the function of these cells are not known, but one role is to maintain high potassium concentrations in the fluid surrounding the hair cells of the cochlea; these pigment cells are critical for survival of the stria. Deafness in the Doberman, which is also accompanied by vestibular (balance) disturbance, results from a different mechanism, where hair cell death is not the result of degeneration of the stria. Deafness may also occur later in life in dogs from other causes such as toxicities, infections, or injuries, or due to aging (presbycusis); these forms of deafness almost never have a genetic cause in animals and thus do not present a concern in breeding decisions.
The prevalence of congenital deafness in different breeds is seldom known because of the limited number of studies (see table on Breed-Specific Deafness Prevalence In Dogs). In the Dalmatian, where the incidence is highest, 8% of all dogs in the US are bilaterally deaf and 22% are unilaterally deaf. In the English Setter, English Cocker Spaniel, Australian Cattle Dog, and Bull Terrier, where fewer numbers of dogs have been hearing tested, the incidence appears to be about one third to one half that of Dalmatians. Unilateral or bilateral deafness is found in 75% of all white Norwegian Dunkerhounds, but the incidence in normal-color dogs is unknown. Other breeds with a high incidence are the Catahoula and Australian Shepherd. The incidence of all types of deafness in the general dog population is low, reported to be 2.56 to 6.5 cases per 10,000 dogs seen at veterinary school teaching hospitals, but these data predate the availability of hearing testing devices and so are much lower that actual values. Recognition of affected cases is often difficult, because unilaterally deaf dogs appear to hear normally unless a special test (the brainstem auditory evoked response, BAER) is performed; facilities to perform the BAER are usually only available at veterinary schools (see list of BAER Testers). It should be noted that a unilaterally deaf dog can be as great a genetic risk for transmission of deafness to its offspring as is a bilaterally deaf dog.
The method of genetic transmission of deafness in dogs is usually not known. There are no recognized forms of sex-linked deafness in dogs, although this does occur in humans. The disorder has been reported to have an autosomal recessive mechanism in the Rottweiler, Bull Terrier, and Pointer, but this suggestion is not reliable because the reports were before the availability of BAER testing and the ability to detect unilaterally deaf dogs. References usually state that deafness transmission in most other breeds is autosomal dominant, but this is false, as will be discussed below. Pigment-associated inherited deafness is not restricted to dogs. Similar defects have been reported for mice, mink, pigs, horses, cattle, cats, and humans. Deafness in blue-eyed white cats is common and is known to be passed on as an autosomal dominant defect. Blue eyes, resulting from an absence of pigment in the iris, is common with pigment-associated deafness but is not, in and of itself, an indication of deafness or the presence of a deafness gene; however, in several breeds dogs (Dalmatian, English Setter, English Cocker Spaniel, Bull Terrier) with blue eyes are statistically more likely to be deaf. Waardenburg's syndrome, a human condition, presents with deafness, a stripe of white in the hair and beard, blue or different colored eyes (even in blacks and asians), no pigment behind the retina, and minor structural deformities around the nose and eyes. This is an autosomal dominant disorder with incomplete penetrance, which means that individuals that inherit the disorder may not show all components of the syndrome - i.e., they may not be deaf. Incomplete penetrance of a defect greatly complicates the determination of mode of inheritance. At present there is no documentation that incomplete penetrance is a factor in any canine deafness.
In simple Mendelian genetics, each dog carries two copies of each gene, one from each parent. The possible outcomes of breedings can be demonstrated with tables showing the genotype of both parents and the possible combinations in their offspring. If deafness is carried as a theoretical simple autosomal recessive gene (d), the breeding of two hearing carriers (Dd) (Table 1) will result, on average, in 25% affected dogs (dd), 50% hearing carriers (Dd), and 25% free of the defect (DD). The breeding of a carrier to a dog free of the defect (Table 2) will result in no affected dogs but 50% carriers and 50% free. The breeding of an affected dog to a carrier (Table 3) will result in 50% affected, 50% carriers, and no free. Finally, the breeding of an affected dog to a dog free of the defect (Table 4) will result in 100% carriers and no affected or free.
If instead the deafness is carried as a simple autosomal dominant gene (D), the breeding of an affected dog (Dd) to a free dog (dd) (Table 3) would result on average in 50% affected and 50% free. Dogs with the genotype DD would be unlikely to occur unless two deaf dogs had been bred. All of the above assumes that incomplete penetrance is not acting. If more than one gene (recessive and/or dominant) is involved in producing the deafness, the possible combinations become much more complicated. In humans more than 50 different autosomal recessive or dominant deafness genes or loci have been identified. The children of two deaf parents with two different recessive deafness can be unaffected but carry both genes. If deafness in dogs results from more than one recessive gene, the possible outcomes of breedings are more numerous and determination of the mechanisms of transmission will be difficult.
As stated above, deafness is often associated with the merle (dapple) gene, which produces a mingled or patchwork combination of dark and light areas. This gene (M) is dominant so that affected dogs (Mm) show the pattern, which is desirable in many breeds. However, when two dogs with merle are bred, 25% will end up with the MM genotype (i.e., Table 1). These dogs usually have a solid white coat and blue irises, are often deaf and/or blind, and are sterile. Breeders of these dogs breeds know not to breed merle to merle. In this case the deafness is neither dominant nor recessive, but is linked to a dominant gene that disrupts pigmentation and secondarily produces deaf dogs.
Genetic transmission of deafness in dogs with the piebald (sp) and extreme white piebald (sw) pigment genes, such as the Dalmatian, is less clear. These genes affect the amount and distribution of white areas on the body. Deafness in Dalmatians does not appear to be autosomal dominant, since deaf puppies result from hearing parents. It does not appear to be a simple recessive disorder: we have bred pairs of deaf Dalmatians and obtained bilaterally hearing and unilaterally hearing puppies, when all should have been deaf if the disorder was recessive. These findings might be explained by a multi-gene cause, the presence of two different autosomal recessive deafness genes, or a syndrome with incomplete penetrance. Further studies (in progress) will be required to determine the mechanisms. Several candidate genes known to cause pigment-related deafness in humans or mice have been eliminated as the possible cause of pigment-associated deafness in Dalmatians. Whole-genome screens will hopefully identify the cause in this and other breeds.
Recent studies have shown that deafness in Dobermans, which do not carry the merle or piebald genes, results from direct loss of cochlear hair cells without any effects on the stria vascularis. Vestibular (balance) system signs, including head tilt and circling, are seen, and the deafness is transmitted by a simple autosomal recessive mechanism. A similar pathology has been described for the Shropshire Terrier.
So what should breeders do when deafness crops up? The most conservative approach would be to not breed the affected animal and not repeat the breeding that produced deafness. It is frequently recommended (i.e. Dalmatian Club of America) that bilaterally deaf puppies should be euthanized, since they make poor pets, are difficult to train, are prone to startle biting, frequently die from misadventure (cars), and require excessive care. There is considerable controversy on this point, and there is no question that many people have successfully raised deaf dogs. For every story of a problem deaf dog there seems to be a story of one that was successfully raised. Unfortunately, there is no way to predict how a deaf puppy will turn out. Unilaterally deaf dogs can make good pets but should not be bred. When deafness is uncommon in a breed, affected dogs should not be bred, but this does not mean that all related dogs are a risk and must be retired from breeding. An understanding of simple autosomal recessive and dominant patterns, as explained above, can allow the breeder to make better informed decisions and likely avoid future deaf animals without sacrificing a breeding line that has been shaped over many years. However, extreme caution must be used when line breeding of dogs related to deaf dogs, whether the deafness is unilateral or bilateral. To make these decisions in an informed manner for breeds with known deafness, it is important that advantage be taken of hearing testing facilities at veterinary schools. Unilaterally deaf dogs cannot be detected by other means, and these dogs will pass on their deafness genes.
CERF AND THE OFA
To help breeders locate important screening information with less effort, the Canine Eye Registry Foundation (CERF) has graciously agreed to allow the OFA to display some of its data. In order for CERF results to appear on the OFA site each dog must have:
An existing OFA record
A current CERF exam
Identical registration name and number information registered with each organization (in order to establish the database links).
CERF will transmit this data to the OFA on a monthly basis. There will be a brief lag between the time the CERF exam is conducted, the time the results appear on the CERF website, and the time they appear on the OFA website.
The OFA will only accept Normal CERF results directly from CERF. Owner submissions will only be accepted for Abnormal CERF results that the owner wishes to display on the OFA website. The addition of this information is designed to provide a maximum amount of health screening information in a single location. Please refer to the CERF website itself if questions arise regarding the existence or validity of a particular dog's CERF number.
CERF was founded by a group of concerned, purebred owner/breeders who recognized that the quality of their dog's lives were being affected by heritable eye disease. CERF was then established in conjunction with cooperating, board certified, veterinary ophthalmologists, as a means to accomplish the goal of elimination of heritable eye disease in all purebred dogs by forming a centralized, national registry.
The CERF Registry not only registers those dog's certified free of heritable eye disease by members of the American College of Veterinary Ophthalmologists (A.C.V.O. ), but also collects data on all dogs examined by A.C.V.O. Diplomates. This data is used to form the CERF data base which is useful in researching trends in eye disease and breed susceptibility. Not only is this data useful to clinicians and students of ophthalmology, but to interested breed clubs and individual breeders and owners of specific breeds.
While CERF maintains its own database, the OFA and CERF have a positive working relationship, and CERF shares data electronically with the OFA. Once a month, CERF sends the OFA an update file containing all dogs which have been issued a CERF eye clearance. Based on matching registration numbers, all dogs on the CERF file with existing OFA records have their CERF data imported into the OFA database, and the CERF results appear on the OFA website.
For more information on CERF, please visit their website: http://www.vmdb.org/cerf.html
Cataracts: An Overview
Cataracts are the clouding or darkening of the lens of an eye. The lens functions as the focusing body in the eye. When malfunctions occur an increased amount of proteins accumulate in the eye and the lens becomes cloudy or opaque. Cataracts are classified a number of ways such as the age at which they appear, the cause of them, or the severity of the cataract. Classifications for the age of onset are congenital (present at birth), juvenile (present early in life), and senile (present later in life). Classifications for the severity of the cataract are incipient (one small spot), immature (covers most of the lens), mature (covers the entire lens), and hypermature (dehydration of the cataract). In cases with incipient cataracts the dog's vision is normally not hindered. With immature cataracts the dog's vision is slightly blurry. When a dog has mature cataracts vision is lost. With hypermature cataracts a mature cataract loses water and protein and basically shrivels up. This can leave clear spots in which vision may be regained but only if the rest of the eye is still functional. One may think a hypermature cataract is a good thing because the cataract is "clearing up" but in fact this process can cause more damage to the eye than a mature cataract can.
Cataracts are one of the most common eye problems in dogs today, and although they are common you should not confuse them with nuclear sclerosis. Nuclear sclerosis is a hardening of the lens which occurs normally in ageing dogs. When this happens, the eye itself becomes a blue like color, similar to the look of a cataract, but does not impede the vision of the dog. Your veterinarian will be able to tell the difference between cataracts and nuclear sclerosis. While nuclear sclerosis does not require treatment cataracts normally do.
Primary Lens Luxation-PLL
Lens subluxation/luxation: partial (subluxation) or complete displacement of the lens from the normal anatomic site. Lens luxation may result in elevated intraocular pressure (secondary glaucoma) causing vision impairment and pain and/or retinal detachment.
Legg-Calve-Perthes Disease (LCP) is a disorder of hip joint conformation occurring in both humans and dogs. In dogs, it is most often seen in the miniature and toy breeds between the ages of 4 months to a year.
LCP results when the blood supply to the femoral head is interrupted resulting in avascular necrosis, or the death of the bone cells. Followed by a period of revascularization, the femoral head is subject to remodeling and/or collapse creating an irregular fit in the acetabulum, or socket. This process of bone cells dying and fracturing followed by new bone growth and remodeling of the femoral head and neck, can lead to stiffness and pain.
LCP is believed to be an inherited disease, although the mode of inheritance is not known. Because there is a genetic component, it is recommended that dogs affected with LCP not be used in breeding programs.
Definition of Mast Cell Tumors
Mast cell tumors, also called mastocytomas, mast cell sarcomas or MCTs, are common cancerous accumulations of cells that form nodular skin masses. Normal mast cells are involved in inflammatory and allergic reactions. Why they aggregate into tumors in some dogs isn’t well-understood. The fact that certain breeds have a higher incidence of mast cell tumors suggests a genetic component. These tumors are most common in older dogs. About 50% of mast cell tumors are malignant, which means that they tend to progressively worsen and without treatment ultimately result in death. Mast cell tumors usually show up as isolated lumps on the skin, although they occasionally appear in cauliflower-like clusters. They often metastasize to the spleen, liver, bone marrow, lymph nodes and other skin sites. Most affected dogs show no symptoms of irritation or illness. Still, owners should have any lumps on their dog examined by a veterinarian.
THE LUXATING KNEE
What is Patellar Luxation?
The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position.
Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are 8 weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb.
Patellar Luxation Categories
Patellar luxations fall into several categories:
1 Medial luxation; toy, miniature, and large breeds
3 Lateral luxation; toy and miniature breeds
5 Lateral luxation; large and giant breeds.
7 Luxation resulting from trauma; various breeds, of no importance to the certification process.
Numbers 1, 2 and 3 are either known to be heritable or strongly suspected.
Medial Luxation in Toy, Miniature, and Large Breeds
Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation. Patellar luxation should be considered an inherited disease.
Three classes of patients are identifiable:
1 Neonates and older puppies often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.
3 Young to mature animals with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.
5 Older animals with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as result of minor trauma or because of worsening of degenerative joint disease pain.
Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may be touched to the ground every third or fourth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance (genu varum) with the feet turned inward and with most of the weight transferred to the front legs.
Permanent luxation renders the quadriceps ineffective in extending the stifle. Extension of the stifle will allow reduction of the luxation in grades 1 and 2. Pain is present in some cases, especially when chondromalacia of the patella and femoral condyle is present. Most animals; however, seem to show little irritation upon palpation.
Lateral luxation in small breeds is most often seen late in the animal's life, from 5 to 8 years of age. The heritability is unknown. Skeletal abnormalities are relatively minor in this syndrome, which seems to represent a breakdown in soft tissue in response to, as yet, obscure skeletal derangement. Thus, most lateral luxations are grades 1 and 2, and the bony changes are similar, but opposite, to those described for medial luxation. The dog has more functional disability with lateral luxation than with medial luxation.
In mature animals, signs may develop rapidly and may be associated with minor trauma or strenuous activity. A knock-knee or genu valgum stance, sometimes described as seal-like, is characteristic.
Sudden bilateral luxation may render the animal unable to stand and so simulate neurological disease. Physical examination is as described for medial luxation.