Introduction:
A spondylolisthesis leads to an instability of the spine. The result is additional
burden on the m.erector spinae and the intracellular organell (here: Mitochondria).
In this study histological muscle findings are evaluated in spondylolisthesis in
comparison prolapsed intervertebral discs.
So far myopathological findings have not been investigated for both patient
groups.

Question:
What muscular changes and what long-term damage does
spondylolisthesis lead to?

Material and methods:
Altogether 23 patients with spondylolisthesis (m: 14; f: 9) and
14 patients with prolapsed intervertebral discs were examined
and operatively treated.
•  Operative therapy:
      - in case of spondylolisthesis: PLIF
      - in case of prolapsed intervertebral discs: discectomy,
•  muscle biopsy,
•  histological and electro-microscopic examination of m.erector spinae,
•  genom analysis,
•  incorporation of clinical and chemical laboratory findings.

Results:
The clinical comparison of patients with spondylolisthesis (a)
to patients with prolapsed intervertebral discs (b) shows:
•  no difference in age,
•  no dominance of professions with forced positions,
•  no familial frequency of spinal-disease,
•  no substantial differences in the duration of complaints,
•  no familial frequency of myopathy and generalised mitochondrial disease,
•  no pathological chemical laboratory or genetic findings,
•  differences in the spinal segments:

The myohistological examination in both patient goups shows
for patients with spondylolisthesis:

Discussion:
The result show that long-term, persistant muscular stress exists through
instability in the spine. The muscular stress leads to an increase in the
energy metabolism of mitochondria in the muscle (2). A mitochondrial
lassitude followes this compensation. The muscular performance decreases (1).
As a result, there is an interference of mitochondria, it s  morphology (4)
and it s metabolism performance (ATP) (3).
The instability of the spine cannot be compensated at this stage (5).
The spinal sliding progresses as a result of the
“local stress- and metabolic-induced exhaustion mitochondriopathy”
of the m.erector spinae.

Refences:
1. Jerusalem, F. J.., Zierz, St.: Muskelerkrankungen. 1991 Georg Thieme, Stuttgart-New York.
2. Junqueira, L.. C., Carneiro, J.: Histologie. 1991 Springer Verlag, Berlin, Heidelberg, New York, London,
    Paris, Tokyo, Hong Kong, Barcelona, Budapest.
3. Reichmann, H., Rohkamm, R., Ricker, K., Mertens, H. G.: Mitochondriale Myopathien DMW 1988,
    113. Jg., Nr. 3.
4. Walter, G. F.:Neuromuskuläre Mitochondriopathie. 1981 Gustav-Fischer, Stuttgart-New York.
5. Wieben, K., Falkenberg, B.: Muskelfunktion. 1991 Georg Thieme Verlag Stuttgart-New York.