The spinal cord is one of the most important and most sensitive organs in the body. If it is traumatized, its cells will not regenerate; injuries usually result in permanent damage. Therefore, the spinal cord is protected in a very special fashion. It goes through a bony canal within the spine; it is surrounded by protective bone everywhere except over the disks. This extreme protection reflects its importance and its fragility.

Disks are rubber-like cushions between the vertebrae. They allow the back to move up and down and sideways without allowing contact between the bones of the spinal column.

What does it mean for a disk to rupture, and how does it happen?

The disk is composed of two parts. The outer covering is much like a thick shell. It is comprised of tough fibers that protect and contain the central part. It is thinnest at the top; this thin area is located just below the spinal cord. The central part of the disk has the consistency of thick tooth paste; it is much softer than the outer part.

When the outer shell degenerates, it allows the central part of the disk to escape. This is called a disk rupture or a ruptured disk. Since the shell is thinnest near the spinal cord, disk material that escapes almost always goes upward, putting pressure on the cord. Because the spinal cord is encased within its bony canal, it cannot move away from the pressure and it becomes pinched.

Degenerative disk disease causes spontaneous degeneration of the outer part of the disk, resulting in escape of the central part. It is not related to injury, although trauma can cause disks to rupture. It is also not related to age. Most dogs with degenerative disk disease are 3-7 years old. It is just a spontaneous event that is most likely controlled by genetic factors. Certain breeds, notably the Dachshund, Poodle, Pekinese, Lhaso Apso, and Cocker Spaniel have a high incidence of disk disease. Other breeds, such as the German Shepherd and Doberman Pinscher, also have disk disease but with a lower incidence. Many breeds never have degenerative disk disease.

Most owners report that a disk rupture occurred following some traumatic event, such as a relatively small jump or fall. Although this act is frequently blamed for the disk rupture, if the disk had not already been degenerating, the rupture would not have occurred.

CNS disease is a broad term used to describe a number of conditions causing inflammation of the central nervous system (CNS).

Depending on which part of the CNS is inflamed, can be more precisely divided into meningitis (inflammation of the meninges), encephalitis (inflammation of the brain) and myelitis (inflammation of the spinal cord). Each condition can occur primarily on its own but it is usually combined with at least one of the other two (meningo-encephalitis, meningo-myelitis).

What are the causes of inflammatory CNS disease?
Causes of inflammatory CNS disease can be either infectious or non-infectious. Infectious causes are probably the least common and can be due to viral (Distemper in dogs, feline-infectious peritonitis, FIV), bacterial, protozoal (Toxoplasma, Neospora) or fungal agents. Non-infectious causes are more common and include breed-specific disorders of Yorkshire terrier, Maltese, Pug, as well as presumed immune-mediated disorder (Granulomatous Meningo-Encephalitis also known as GME).

The later is probably the most common cause of inflammatory CNS disease in dogs. Why the immune system suddenly becomes 'over-excited' and decides to inflame the CNS remains a mater of speculation. Other rare non-infectious causes include pre- (inflammation that will turn into cancer with time) and para- (cancer outside of the nervous system having distant effect - in that case inflammation of the brain) neoplastic disorder.

What are the signs of inflammatory CNS disease?
The signs of inflammatory CNS disease vary according to which part of the CNS is inflamed (brain, spinal cord and/or meninges).

When meningitis occurs on its own, pain, stiffness of the gait, reluctance to move the neck and hunched-up back are the most common signs. Fever is only seen in less than half of the cases and its absence can therefore not be used to discard the possibility of meningitis. Encephalitis and myelitis are associated with neurological signs reflecting which part of the nervous system is inflamed.

Caudal Occipital Malformation Syndrome (COMS) is the canine analog of human Chiari type I malformation. The disorder is a congenital anomaly of the caudal occipital region of the skull that leads to overcrowding of the caudal fossa and compression of the cervicomedullary junction at the level of the foramen magnum. Both direct bony compression and progressive meningeal hypertrophy in the region of the dorsal cervicomedullary junction are thought to lead to abnormalities of cerebrospinal fluid (CSF) flow dynamics. These CSF flow changes often lead to fluid accumulation within the spinal cord (i.e., syringohydromyelia). Clinical signs of central nervous system (CNS) dysfunction referable to the brain and/or spinal cord can result from COMS.

Although the cause of COMS is unknown, it is suspected to be a genetically transmitted developmental disorder of the occipital bone mesoderm. In patients with COMS, there tends to be some level of cerebellar compression, as well as constriction of the cervicomedullary junction in the vicinity of the foramen magnum. With chronic bony compression at the cervicomedullary junction, and probable turbulent CSF flow and pressure changes in this region, it is thought that the underlying meninges become hypertrophied with time. Such hypertrophy has been documented in both humans with Chiari type I malformation and dogs with COMS. There are numerous theories to explain the development and propagation of syringohydromyelia cavities in patients with COMS. An in-depth discussion of these theories (e.g., “water-hammer” effect, “suck”, “slosh”, “ball-valve” effect) is beyond the scope of this presentation. Common to all of these theories is obstruction of normal CSF flow at the level of the cervicomedullary junction.

Degenerative joint disease (osteoarthritis) results from destruction of the cartilage that protects the bones that make up the joint. Cartilage destruction can be the result of normal stress on abnormal joints or abnormal stress on normal joints. Hip dysplasia, a malformation of the hip sockets, is one example of normal stress on abnormal joints. Constant jumping over obstacles, stretching or tearing ligaments during strenuous exercise, or injuries in a fall or accident are examples of abnormal stress on normal joints.

Degenerative joint disease can be further subdivided into primary disease for which no known cause is evident and secondary disease for which a cause can be pinpointed. Among the causes of secondary degenerative joint disease are hip dysplasia, patella luxation (loose kneecaps), osteochondritis dissecans (OCD, the development of cartilage “flaps” in the joints when bone development is disturbed), trauma and ruptured cruciate (knee) ligaments. Secondary degenerative joint disease can sometimes be prevented or halted by surgical repair of the joint before arthritis progresses.

Degenerative arthritis may not manifest until the dog has had years of abnormal stress. Since cartilage has no nerves, the damage can progress with no outward signs until the joint is severely compromised and the lubricating fluid has thinned and lost its ability to protect the bone surfaces.