Nerve root deficit

If reduction really improves the sagittal balance and rate of fusion, it may result in the risk of neurological complications, particularly L5 nerve root deficit. 

From a combination of personal communications with the treating surgeons and a literature review, it appears that one common complication of attempting to reduce L5 onto SI for patients with spondyloptosis is postoperative L5 nerve root deficit. An additional more serious, but commonly described, complication is iatrogenic cauda equina syndrome with loss of... 

In the last twenty years, 27 of these procedures were performed for severely functionally handicapped patients. No patients without severe symptoms were operated. Twenty-one of the patients had had no previous surgery. Six had had multiple previous attempts to achieve stabilization, reduction and decompression for very severe disability. Most of them had had pre-operative or post-operative cauda equina syndrome as well as L5 nerve root deficit. 

One multiply operated patient who had pre-operative cauda equina syndrome twice, does wear a bilateral drop foot brace for L5 nerve root deficit though she no longer takes any narcotic medication. She was deeply habituated on narcotics prior to the surgical procedure. 

Permanent or temporary deficits of spinal cord function are caused either by cord ischemia after arterial hypotension, or by cord compression due to an epidural or subdural hematoma or infection, or injury to the spinal cord and nerve roots as a consequence of needle puncture, introduction of a catheter, or chemical irritation. 

Patients may experience a sudden onset of low back pain with bending or lifting an object or a more gradual onset of low back pain. The pain may radiate into a lower extremity, frequently following the course of the sciatic nerve. Depending on the nerve root involved and the severity of the herniation, there may be sensor) or reflex changes or motor weakness. Neurologic-deficit helps differentiate radiculopathy from referred pain. 

The diverse physiological actions of capsaicin described in the previous sections have motivated numerous, equally diverse, in vivo and in vitro studies in search of biochemical correlates. The most attention, however, has been focused on the sensory system since a direct effect of capsaicin on sensory nerves has been suspected for a long time. More recent observations of capsaicin-induced sensory neuron degeneration in neonatal animals have added further impetus to determine the resultant neurochemical deficits of this lesion. It is perhaps fortunate that the small type B neurons of dorsal root ganglia which appear anatomically to succumb to capsaicin after both neonatal and adult treatment are also among the neurons for which putative neurotransmitter markers have been identified. Accordingly, these markers, two of which are the peptides somatostatin and substance P, have provided both a means to assess the neurotoxic potential of capsaicin, and to some extent relate anatomical with neurochemical investigations. For the sake of coherence the biochemical aspects of some reports cited in the previous sections are discussed here. The major conclusions in these reports will be summarized in Section 13. 

---