Herron and Trippi  evaluated 24 patients, all with degenerative spondylolisthesis treated with laminectomy alone. At follow-up varying between 18 and 71 months after surgery, 20 out of the 24 patients reported a good result. Epstein  reported on 290 patients treated over a 25-year period. Excellent results were obtained in 69% and good results in 13%. These optimistic reports do not correlate with "return to competitive employment" rates, which for the most part are dismal in most spinal surgery series.In the past two decades there has been a dramatic increase in fusion surgery in the U.S.: in 2001 over 122,000 lumbar fusions were performed, a 22% increase from 1990 in fusions per 100,000 population, increasing to an estimate of 250,000 in 2003, and 500,000 in 2006. In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year. For patients with continued pain after surgery which is not due to the above complications or conditions, interventional pain physicians speak of the need to identify the "pain generator" i.e. the anatomical structure responsible for the patients pain. To be effective, the surgeon must operate on the correct anatomic structure, but is often not possible to determine the source of the pain. The reason for this is that many patients with chronic pain often have disc bulges at multiple spinal levels and the physical examination and imaging studies are unable to pinpoint the source of pain.
Cerebroretinal microangiopathy with calcifications and cysts (CRMCC) is a rare genetic disorder, which affects multiple organs. Its hallmarks are widespread progressive calcifications, cysts and abnormalities of the white matter of the brain, usually occurring together with abnormalities of the blood vessels of the retina. Additional features include poor prenatal growth, preterm birth, anemia, osteopenia and bone fractures, and gastrointestinal bleeding. It is caused by compound heterozygous mutations in the conserved telomere maintenance component 1 (CTC1) gene, but its exact pathophysiology is still not well understood. Cerebroretinal microangiopathy with calcifications and cysts is alternatively known as the Coats plus syndrome, a reference to its most typical ocular phenotype. Signs and Symptoms
Presentation
Before birth
A child who has inherited this disorder will grow slower than normal in the uterus before birth and typically will be born before term. The pregnancy can be complicated by gestational hypertension and pre-eclampsia. After birth
The majority of affected children present with symptoms and signs relating to the eyes such as leukokoria, redness, irritation and impaired vision, which result from retinal detachment and glaucoma. A minority present with seizures or spasticity. The time of onset of symptoms varies from infancy to adolescence. Because a child born before term will need to undergo screening for retinopathy of prematurity, some will have abnormalities in their retinal blood vessels detected when they have no symptoms yet. Brain
Neurologic symptoms and signs vary depending on the site of the brain abnormalities. Common symptoms are partial epilepsy, asymmetric spasticity, ataxia and cognitive impairment. The latter affects visuospatial and visuoconstructive skills first.