Chronic lameness is a fairly common occurence in dogs and cats. Yet in many instances, the cause(s) are never fully elucidated. Most of the time we only treat the symptoms with analgesia, dietary modifications, "neutraceuticals" and/or, when appropriate, excercise restriction in order to make our patients comfortable. However, in fairness to fellow veterinarians and to clients, sometimes the clinical manifestations of lameness, in conjunction with age, breed (which narrow the list of probable causes), other health issues and client financial limitations makes a full diagnostic workup, which can be expensive, an academic excercise that does not alter the prognosis nor the treatment options. Nevertheless, I think I speak for most veterinarians and pet owners when I advocate a full diagnostic workup so that we are certain that the ameliorative treatment we provide does not mask an insidious and potentially serious underlying problem.
Acute onset lameness is most often precipitated by a traumatic event, though in the absence of a supportive history, metabolic, cardiogenic, vascular (thrombus?), infectious, neurological, neoplastic and immune-mediated causes must be seriously considered. Animals are frequently in dire pain and while addressing this it is imperative that the definitive diagnosis be established early to identify a potentially important underlying problem and to prevent the development of a progressive and potentially life-long affliction that jeopardizes the animal's quality of life.
The purpose of this page will be to provide a broad overview of small animal lamenesses, with illustrations if possible, that demonstrate anatomical and physiological relationships of those components which directly impact locomotion, namely the central and peripheral nervous systems, muscles, bones and joints and miscellaneous soft tissues. In addition, when appropriate, the physiological basis of metabolic, infectious, congenital and other more esoteric causes of lameness will be explained, hopefully in a manner that is readily understandable to any pet owner, as it should be. This project will take time and so, as has been the case often on this web site, "chapters" will be added one at a time over a period of days and perhaps weeks. I will certainly try to expedite the process as I am able.
Neurological Aspects of Locomotion
The first portion of this topic will try and cover the neuromuscular aspects of locomotion, so that you can appreciate how an injury or a disease process that may occur quite distant from the lame limb can be responsible for that lameness, nevertheless.
When muscle contracts in a coordinated manner, limbs move in a coordinated manner. Such motion (deemed "motor activity")--voluntary and involuntary--usually begins as electrical impulses originating in higher and lower motor centers in the brain. These impulses pass down the spinal cord in specific and highly organized tracts towards the target (second nerve then) muscle and ultimately initiate movement, as will be described. The spinal cord is housed and protected within a multiply segmented boney column--the vertebral column, sometimes referred to as the "backbone(s)". The spinal cord sits within this protective boney structure. Figure 1, though not of high resolution, illustrates this relationship: Vertebral column is divided into cervical (neck), thoracic (chest), lumbar (lower) and sacral (hip) segments.
Figure 1 The cord really sits within the vertebral column and can not be seen , but is drawn yellow here for illustration.
Notice that the nerve fibers actually leave the cord and pass from within the vertebral column to the "outside" through natural spaces between boney vertebral segments.
Figure 2 is a schematic illustration of what the cord would look like if half of each veterbral bone were removed (for visualization)
Figure 2 Notice that nerve roots eminate from cord and nerve fibers pass out of
Figure 3 represents the terminal portion of Figure 2..the end of the cord. Notice that the cord ends before the vertebral column ends but the nerves emininating from the terminal aspects of the cord continue within the boney vertebral canal and exit the vertebral column further away.
Figure 3: Magnification of Figure 2. Note the end of the cord and the
continuation of nerves within the vertebral column.
As the figures try to show, nerve roots eminate from the spinal cord all along its length. Specific roots form specific nerves. Branches of these connect (more appropriately "synapse") to the ends of separate nerve fibers that, in turn, stimulate an impuse in either another nerve or to various and very specific soft tissue structures. In the case of a limb muscle, the stimulation provided by the input electrical impulse that originated higher up (e.g. in the brain) causes changes in the movement of specific charged molecules in the cell membrane. This, in turn, stimulates exquisitely intricate chemical activity within the muscle cell that, eventually results in the shortening (contraction) of muscle fibers. If the muscle's tendon is attached to a bone, contraction of the muscle exerts force causing the bone to move in the general direction of contraction. The exact magnitude and direction of movement will depend on what other bone and soft tissue associations are concurrently involved.
The next figure (Figure 4) represents the cross-sectional view of the spinal cord and includes labels and arrows whose purpose is to illustrate the approximate location and direction and consequence of some electrical impulses generated from sensory (e.g. pain, touch, itch, stretch) stimuli ( yellow ). Notice that there is coexistence, divergence and even mixing of sensory pathways (i.e. a single touch to a point on a limb (a leg) elicits concurrent electrical pathways from limb-to-spine-to-brain and from limb-to-spine-to limb (...a reflex sensory-to-motor pathway). An example of the latter is the patella reflex: the knee ligament is gently tapped, stretching ligaments and tendons and sensory nerves within them; the impulse travels in the sensory (yellow) branches of the nerves to the spinal cord and stimulates the motor (blue) branch in the same segment of the spinal cord to send an impulse back to the muscles of the leg to "jerk" (kick). Note that the original stimulus also sends an impulse up the spinal cord towards the brain...thus the brain will know that the knee has been tapped. Upon close inspection of Figure 4, you see that this reflex can occur without any input from the brain (it is a simple arc); however, the motor fibers eminating from the brain intermingle with the motor fibers of the arc; it is, therefore possible (in fact quite probable) that the brain, which was also made aware of the stimulus, has some influence on some characteristic(s) of the reflex arc. This particular concept can be useful in physically localizing the presence of a neurological cause of lameness to a specific region of the spinal cord as well as assessing the severity of the problem.
Figure 4: Yellow=Sensory; Blue=Motor
(Back to sensory text)
So...it is important to realize that many kinds of lesions that perturb the spinal cord, the nerve roots and/or the sensory or motor nerves that connect to muscles, joints, bone and other tissues can result in abnormalities in gait or attitude that we label as "lameness". The next section will touch upon a specific example of this: intervertebral disk disease. Then the topic will digress to non-neurological causes of lamesness, such as inherited or acquired orthopedic syndromes--joint, bone, ligament---as well as other inherited, metabolic and infectious diseases that cause muscle weakness, lameness and/or pain (manifest as lameness). This is a big topic...I intend to slowly hone in on the information you need to help your pet...I simply want to be sure you have the foundation to fully appreciate it
:Cross-section of Verterbral Canal: Illustration of Intervertebral Disk.
Note bulging of ruptured or degenerated disk material (place cursor over image)
into spinal canal, with potential for pressure/damage to spinal cord
Figure 5 is a schematic representation of the relationships of spinal cord, boney vertebral canal, ligamentous support structure (the dorsal longitudinal ligament is shown here) and the corresponding intervertebral disc. The latter is composed of complex cartilage and, in theory, each serves as a buffer/cushon between the adjacent boney vertebrae.
In some animals, trauma or simple degenerative changes to cartilage result in the bulging or extrusion of disc material into the small canal containing the spinal cord. This exerts pressure on the cord, it's blood and nutrient supplies; inflammation and swelling ensues, and exacerbates the damage to the integrity of the cord and it's related structures, as well as the structures innervated by it. The net effect is loss of functionality, and too often, there is considerable pain. Afflicted animals may demonstrate weakness and abnormal gait (staggering, falling down) and even paralysis if damage is severe.
Treatment depends upon the severity of clinical signs and radiological findings. Medical management involves aggressive use of anti-inflammatory medications and alleviation of pain. Quite often, medical resolution is not possible and to prevent irreversible loss of neurological integrity, surgical intervention is required.
The next discussions will explore bone and joint abnormalities that can result in lamenesses; after that diseases of muscle!
A table is available to review which will be indexed for easy reference
Selected: Bone-Joint-Ligament Lamenesses
Hip Joint Basics
- This malady is, unfortunately, a too-common occurrence. It happens primarily to large breed dogs and is caused by complex genetics (polygenic) and environmental factors.
- It is usually a disease of young dogs (<2yrs) but can develop in older individuals, as well.
- The figure above, left, illustrates a normal hip joint (the "coxofemoral joint"). The uppermost aspect of the thigh bone (the femur) consists of an angled appendage (the femoral neck & head) at whose end there is a hemispheric component (the head) that normally fits into a hollowed/concave hemispheric space known as the acetabulum on the pelvis (hip bone).
- This arrangement (the "articulation" of the femoral head within the acetabulum) comprises the coxofemoral joint. It is stabilized by fibrous ligaments within and around the joint.
- When the leg moves, the femoral head is supported by and rotates within the acetabulum. Both the head and the acetabulum are coated with a slippery cartilage and the these are further surrounded with a thick, lubricating fluid which, together, provide an environment that prevents friction from leading to damage of structures and maximizes functionality. Ultimately, this prevents joint inflammation (arthritis) and pain.
- In order for this joint to function optimally, the femoral head must articulate at a precise angle appropriate for maximal weight bearing; malalignment of any of the participating structures resulting from inappropriate force, or angle of articulation as well as malformation of the head or the acetabulum will lead to degenerative joint disease, and, potentially life-long pain.
Definition and Causes
- Hip dysplasia is a laxity of the hip joint that develops between birth and skeletal maturity that can result in the abnormal alignment of articular surfaces. Hip dysplasia often leads to painful arthritis. Causes are multifactorial.
- Heredity: Many genetic determinants may, collectively, be responsible; the mechanism(s) which lead to clinical the manifestation of signs is complex and incompletely understood.
- Diet: The influence of diet on skeletal and joint anomalies has been discussed in considerable detail on this web site (see Large Breed Puppy Diet). Basically, rapid growth leads to large body mass. This results in greater stress forces on immature bone and growth plate cartilage. Consequently, microfractures within growth plates and exacerbation of (geneticaly predisposed) joint structure malalignments ensues.
- Excessive High-Impact Exercise: This may similarly affect joint and growth plate integrity.
- Clinical History:
- Young-Dog Syndrome: A young (4-12 months) large-breed canine with sudden decrease in activity or onset of hindlimb lameness may be associated with some loss of hip muscle mass.
- Older-Dog Syndrome: An older (>12 months) large-breed canine with insidious loss of rear limb muscle mass, shifting weight while standing (listing between left and right rear limbs), especially after exercise.
- Palpation of Coxofemoral Joint
- Barden Method
- Ortolani Sign: This is a complex series of moving leg through various ranges of motion while concurrently palpating the hip joint for signs of subluxation/laxity.
- Radiological Signs:
- Precise positioning for radiological evaluation of the hip joint usually requires heavy sedation or anesthesia.
- With standard positioning for the evaluation of the hip joint, there are accepted abnormal radiological signs that are consistent with the diagnosis of hip dysplasia. Evaluation of the shape and congruity of the femoral head with the acetabulum, evidence for abnormal wear of articular surfaces, as well as the presence of degenerative changes are some of the parameters examined.
- Conservative (Medical/Physical Therapy)
- Promote increased muscle mass. (Note that atrophy of thigh and pelvic muscles due to disuse [pain?] of hindlimb(s) actually exacerbates the stress on the hip joint and spreads an additional support burden on the remaining limbs)
- Correct Obesity
- Exercise is required to prevent muscle atrophy and may help in the management of obesity.
- Diet Modification (lower caloric density diet or fewer "treats". for example)
- Examples: On Mondays, Wednesdays and Fridays, go for leash walks, swimming (minimal stress to joint while building muscle mass) and mild retrieving...promote the "trot" rather than speed running (which is high impact).
- Such a regimen will make the dog sore....initially, during the first few weeks.
- Non-steroidal antiinflammatory medication (check with your veterinarian) could be given on Tuesdays and Thursdays (the "off" days) if needed.
- Obesity Management:
- Execise regimen, as described above
- Medical and laboratory evaluation to rule out underlying causes (e.g. hypothyroidism) of obesity.
- Surgical Options
- Triple Pelvic Osteotomy (TPO):
- This is a major surgical procedure in which the angle of the pelvis is changed to to better accomodate the head of the femur within the acetabulum.
- The TPO is ideally performed early (6-12 months of age) before the development of arthritis and degenerative joint disease.
- RULES OF THUMB: This procedure should NOT be done on any animal with degenerative joint disease or who is greater than 18 months of age.
- Total Hip Arthroplasty (THA):
- This procedure involves replacing the entire hip joint with an artificial hip joint (a similar procedure is performed in people.
- Reserved for clinically significant (PAINFUL!) arthritis and degenerative joint disease.
- NOT appropriate if there is significant muscle mass atrophy or if there is infection anywhere (e.g. dental disease/gingivitis, urinary tract, skin).
- Femoral Head and Neck Osteotomy (FHO):
- Involves excision of the articular components of the femur (the head and the "neck"[....the portion of bone that connects to the head of the femur]) and thus bypassing the normal hip joint by promoting the formation of a "false joint".
- This surgery promotes the generation of a fibrous capsule which, along with normal thigh and pelvic muscles, stabilizes and supports the limb and the pelvis. There is no articular surface, per se; hence, this is a "false joint".
Cranial Cruciate Ligament Avulsion
Stifle (Knee) Joint Basics
- The Stifle Joint's Range of Motion is illustrated in this figure
- The Stifle joint is stabilized by numerous ligaments, as well as the gastrocnemius and quadriceps tendons. Two small but extremely important ligmentous structures are found within the joint and each is specifically connected to strategic portions of bone thus providing strength, stability and integrity. They are the Cranial (Anterior) and Caudal (Posterior) Cruciate ligments. Together, they maintain the strict normal front-to-back alignment of the two major bones (the femur, or thigh bone, and the tibia, or shin bone). The following illustrations reveal the nature of this relationship under normal conditions and following rupture of the cranial cruciate ligament.
- During flexion of the joint, the cranial and caudal cruciate ligaments actually twist on each other; this prevents abnormal "inward" rotation of the tibia (relative to the femur).
- During extension, the cranial and caudal cruciate ligaments untwist; now stabilization and protection of the joint from abnormal rotation relies mainly upon the external (collateral) fibrous ligaments, each one connecting the femur to the tibia. There are two collateral ligaments: one on the inside (medial-facing the inner thigh) and one on the outside (lateral-the side easily seen in a standing dog) aspects of the stifle joint.
- A fibrocartilagenous pad...the meniscus...sits in the joint, tightly associated with the tibia and guides the normal articular motion; the meniscus is composed of lateral (toward the outside) and medial (towards the inside) components. The lateral meniscus is less rigidly attached than the medial meniscus.
- In addition to the smooth articular cartilage and viscous joint fluid which provide lubrication and minimize friction, the joint also contains a small amount of fat.
Causes of Cranial Cruciate Avulsion
- Excessive Forces: Most often, the result of running, frequent turning and shifting of direction, jumping; these type of activities result in severe forward-compressive or rotational forces on the tibia, respectively.
- When rupture follows excessive internal rotation of the tibia, a portion of the femur rubs over the meniscus, causing tears or actually rolling/folding the meniscus onto itself
- Degenerative changes: anatomical/ conformational anomalies result in inappropriate alignment of joint structures, inflammation then degenerative changes, including the weakening of internal ligamentous supports.
- Any inflammatory joint condition that results in degenerative joint disease weakens the ligamentous infrastructure and predisposes to rupture.
- Partial Ruptures: Sometimes only a portion of the cranial cruciate ligament is ruptured --i.e. some fibers are torn. In most, but not all instances, there is pain, swelling and inflammation and...ultimately, complete rupture ensues.
- Often in animals undiagnosed partial or complete rupture is followed by the deposition of fibrous tissue around the joint. This is Nature's way of trying to provide some stability. These animals are never normal and intermittently are non-weightbearing on the affected limb.
- In acute rupture, the animal is usually non-weightbearing, the stifle is swollen and painful.
- When there is chronic or old, partial tears, the joint capsule is thickened (increased fibrous tissue), the animal is painful or intermittently painful and lame or intermittently lame.
- Cranial Drawer Sign: With complete rupture, one is able to move the tibia forward (with respect to the femur)
- Tibia Compression Test: The application of force upwards, from the hock (ankle), parallel to the tibia, results in the forward displacement of the tibia (as in the Cranial Drawer Sign).
- Increased Joint Laxity: Abnormal internal rotation of the tibia.
- Other: Note...some animals with partial tears or longstanding cruciate ligament avulsion may not demonstrate any of the above-mentioned abnormal responses.
- Radiographs (X-rays): May visualize malalignment of tibia with respect to femur. May see signs of joint swelling, including displacement of joint fat. With time, may see evidence of degenerative joint disease.
- Magnetic Imaging (MRI): May actually be able to assess ligament integrity.
- Joint Fluid Analysis: Is useful in eliminating other causes of stifle joint disease.
- Arthroscopy: Provides direct visualization of all internal joint structures.
- Exploratory Arthrotomy: Provides the most direct method for assessing and concurrently repairing damage to the joint.
- Aggressive medical management: In very small dogs with acute injury, it is occassionally possible to effect resolution via:
- Strict Exercise Restriction and Joint Immobilization: At least 4-6 weeks of kennel confinement.
- Physical Therapy: Required for several months.
- Most Animals: require surgical intervention. There are over 100 different surgical procedures and the appropriate procedure is tailored to the unique needs of each patient.
- Post-Operative Exercise Restriction: At least 4-6 weeks of restricted activity, such as short leash walks to eliminate, etc.
- Physical Therapy: As described for medical management scenario.
- Prognosis: Is usually good with surgery (80%-90% return to normal function) but the success rate is less than 80% if there is concurrent damage to the meniscus.
Canine Eosinophilic Panosteitis
- Panosteits is a disease in which there is inflammatory and degenerative changes of the medullary (the medulla= the middle compartment of long (e.g. leg) bones.
- The medulla of bones is a soft tissue space surrounded by hard (cortical) bone; it contains marrow (fat and blood cell precurosrs).
- Viral: causes are presently unclear but there is considerable evidence that there is an underlying viral etiology. Some speculate that Canine Distemper infection or vaccination may each play an important role.
- Large/ Giant Breed Dogs:especially German Shepherds and Rottweillers.
- Young : Dogs are usually young--(5-12 months) but disease has been reported in animals as young as 2 months and as old as 7yrs
- Male Dogs: are more commonly affected than females.
- History includes:
- variable inappetance or anorexia
- Sudden Onset of Lameness without history of trauma
- Wax-Wane/Shifting: lamess is variable and may shift to different limbs
- Front Limbs more likely affected
- Not Affected By Rest or Exercise
- Physical Exam
- Intermittent Fever
- Pain on palpation of the bone (50% of patients)
- Tonsilitis: some animals have this concurrently
- Blood Evaluation may show elevated white blood cell counts--especially with elevated eosinophils (a type of white cell)---or results may be completely normal.
- X-Rays: radiographs of affected long bone(s) show variable changes in the density of the medullary cavity; the appearance varies with the phase (early, middle or late) of the disease.
- Supportive: management of pain is crucial--aspirin or other non-steroidal anti-inflammatory drug as needed during the painful (4-6 weeks) period.
- Resolution: the problem can persist for several months...but eventually will resolve.
(the above list of abnormalities is by no means complete...it is just a representative sampling. Future additions to this topic will focus on diseases of muscle....cn)
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