Haus-Great news

[Gina Heitz <brier@oregonsbest.com>]

We are home from the Neuro consult and it seams as though the FCE diagnosis 
is most probable and we are on the road to recovery.  With the improvements 
Haus has made everyone is encouraged and a complete recovery is quite 
possible.  So what is FCE?  Here you go:

But first I want to tell you all he really is improving.  He walked up the 
ramp when we got home into the house. :-)))  And jumped up onto the couch 
as to say gee it's good to be home....  Amazing and yes very encouraging

Fibrocartilaginous Infarction: Compliments of:  Dr. Clemmons 
<http://pawcare.com/rclemmons/para.htm>

Even though animals do not suffer from the same degree of vascular disease 
as human beings, infarction of the spinal cord with fibrocartilaginous 
material is not uncommon. It occurs in any breed of dogs, but is most 
common in large breeds, such as Great Danes, Labrador retrievers and German 
Shepherds. Although both arteries and veins can be affected, most commonly 
it is the venous system of the spinal cord which is obstructed, leading to 
a hemorrhagic infarction. It is believed that herniation of the nucleus 
pulposus takes place either into the vertebral body or the venous sinuses 
within the spinal column. Since the vertebral body represents a vascular 
space communicating with the spinal venous system, the material gains 
access to the spinal veins. These veins do not have valves, allowing the 
fibrocartilaginous material to flow up and down the spinal column. When 
intra-thoracic pressure increases, this material can be back-flushed into 
small penetrating spinal cord veins. When the intra-thoracic pressure 
returns to normal, the veins collapse trapping the material and leading to 
excessive venous pressure upstream to the occlusion. The venules rupture 
leading to a hemorrhagic infarction. The pattern of infarction usually 
affects a quadrant of the spinal cord, although initial signs may affect 
more of the spinal pathways due to inflammation and spinal cord swelling. 
The infarction can occur anywhere along the spinal cord, but the causal 
cervical and mid- to lower lumbar spinal cord segments appear to be most 
frequently involved.


The presence of spinal cord infarction should be suspected whenever a 
patient presents with acute onset of paresis or paralysis which is markedly 
asymmetrical and there is no evidence of hyperpathia. Vascular disease is 
generally acute and non-progressive. In addition, the spinal cord contains 
pain pathways, but no pain receptors. As such, strict diseases within the 
spinal cord without meningeal involvement are usually not painful. Most of 
the other diagnostic tests will be within normal limits. Occasionally, 
there will be evidence of hemorrhage on CSF analysis. Spinal radiographs, 
do not demonstrate the disease, but may reveal other evidence of spinal 
column degeneration. Myelography will be normal or demonstrate mild 
intramedullary swelling. In a small number of cases (where the vascular 
occlusion is secondary to a systemic disease), the minimum data base will 
show evidence of the systemic disease.

The treatment of spinal cord infarction is that for acute spinal cord 
injury, using methylprednisolone at 30 mg/kg initially. This is followed by 
15 mg/kg every 8 hours for the first 24-48 hours. Then, oral prednisolone 
is begun at 0.5 mg /kg every 12 hours for 5 days. I continue prednisolone 
at 0.5 mg/kg every other day, in the morning, for up to another 2 weeks. 
Many cases will improve dramatically within the first week, although they 
will still improve over several months. If there has been no improvement in 
the first week, re-examination and additional tests may be indicated. Since 
usually only a quadrant of the spinal cord is affected, the patient will 
improve most on the unaffected side. Reorganization will usually allow 
these patients to function adequately. Spinal cord infarction from 
fibrocartilaginous material is a sporadic problem and, usually, does not 
reoccur.