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      Deformative stress associated with an abnormal clivo-axial angle: A finite element analysis

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          Abstract

          Background:

          Chiari malformation, functional cranial settling and subtle forms of basilar invagination result in biomechanical neuraxial stress, manifested by bulbar symptoms, myelopathy and headache or neck pain. Finite element analysis is a means of predicting stress due to load, deformity and strain. The authors postulate linkage between finite element analysis (FEA)-predicted biomechanical neuraxial stress and metrics of neurological function.

          Methods:

          A prospective, Internal Review Board (IRB)-approved study examined a cohort of 5 children with Chiari I malformation or basilar invagination. Standardized outcome metrics were used. Patients underwent suboccipital decompression where indicated, open reduction of the abnormal clivo-axial angle or basilar invagination to correct ventral brainstem deformity, and stabilization/ fusion. FEA predictions of neuraxial preoperative and postoperative stress were correlated with clinical metrics.

          Results:

          Mean follow-up was 32 months (range, 7-64). There were no operative complications. Paired t tests/ Wilcoxon signed-rank tests comparing preoperative and postoperative status were statistically significant for pain, bulbar symptoms, quality of life, function but not sensorimotor status. Clinical improvement paralleled reduction in predicted biomechanical neuraxial stress within the corticospinal tract, dorsal columns and nucleus solitarius.

          Conclusion:

          The results are concurrent with others, that normalization of the clivo-axial angle, fusion-stabilization is associated with clinical improvement. FEA computations are consistent with the notion that reduction of deformative stress results in clinical improvement. This pilot study supports further investigation in the relationship between biomechanical stress and central nervous system (CNS) function.

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          Most cited references124

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          Quality of life measurement: bibliographic study of patient assessed health outcome measures.

          To assess the growth of quality of life measures and to examine the availability of measures across specialties. Systematic searches of electronic databases to identify developmental and evaluative work relating to health outcome measures assessed by patients. Types of measures: disease or population specific, dimension specific, generic, individualised, and utility. Specialties in which measures have been developed and evaluated. 3921 reports that described the development and evaluation of patient assessed measures met the inclusion criteria. Of those that were classifiable, 1819 (46%) were disease or population specific, 865 (22%) were generic, 690 (18%) were dimension specific, 409 (10%) were utility, and 62 (1%) were individualised measures. During 1990-9 the number of new reports of development and evaluation rose from 144 to 650 per year. Reports of disease specific measures rose exponentially. Over 30% of evaluations were in cancer, rheumatology and musculoskeletal disorders, and older people's health. The generic measures--SF-36, sickness impact profile, and Nottingham health profile--accounted for 612 (16%) reports. In some specialties there are numerous measures of quality of life and little standardisation. Primary research through the concurrent evaluation of measures and secondary research through structured reviews of measures are prerequisites for standardisation. Recommendations for the selection of patient assessed measures of health outcome are needed.
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            Chiari I malformation redefined: clinical and radiographic findings for 364 symptomatic patients.

            Chiari malformations are regarded as a pathological continuum of hindbrain maldevelopments characterized by downward herniation of the cerebellar tonsils. The Chiari I malformation (CMI) is defined as tonsillar herniation of at least 3 to 5 mm below the foramen magnum. Increased detection of CMI has emphasized the need for more information regarding the clinical features of the disorder. We examined a prospective cohort of 364 symptomatic patients. All patients underwent magnetic resonance imaging of the head and spine, and some were evaluated using CINE-magnetic resonance imaging and other neurodiagnostic tests. For 50 patients and 50 age- and gender-matched control subjects, the volume of the posterior cranial fossa was calculated by the Cavalieri method. The families of 21 patients participated in a study of familial aggregation. There were 275 female and 89 male patients. The age of onset was 24.9+/-15.8 years (mean +/- standard deviation), and 89 patients (24%) cited trauma as the precipitating event. Common associated problems included syringomyelia (65%), scoliosis (42%), and basilar invagination (12%). Forty-three patients (12%) reported positive family histories of CMI or syringomyelia. Pedigrees for 21 families showed patterns consistent with autosomal dominant or recessive inheritance. The clinical syndrome of CMI was found to consist of the following: 1) headaches, 2) pseudotumor-like episodes, 3) a Meniere's disease-like syndrome, 4) lower cranial nerve signs, and 5) spinal cord disturbances in the absence of syringomyelia. The most consistent magnetic resonance imaging findings were obliteration of the retrocerebellar cerebrospinal fluid spaces (364 patients), tonsillar herniation of at least 5 mm (332 patients), and varying degrees of cranial base dysplasia. Volumetric calculations for the posterior cranial fossa revealed a significant reduction of total volume (mean, 13.4 ml) and a 40% reduction of cerebrospinal fluid volume (mean, 10.8 ml), with normal brain volume. These data support accumulating evidence that CMI is a disorder of the para-axial mesoderm that is characterized by underdevelopment of the posterior cranial fossa and overcrowding of the normally developed hindbrain. Tonsillar herniation of less than 5 mm does not exclude the diagnosis. Clinical manifestations of CMI seem to be related to cerebrospinal fluid disturbances (which are responsible for headaches, pseudotumor-like episodes, endolymphatic hydrops, syringomyelia, and hydrocephalus) and direct compression of nervous tissue. The demonstration of familial aggregation suggests a genetic component of transmission.
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              Neuronal and glial apoptosis after traumatic spinal cord injury.

              Cell death was examined by studying the spinal cords of rats subjected to traumatic insults of mild to moderate severity. Within minutes after mild weight drop impact (a 10 gm weight falling 6.25 mm), neurons in the immediate impact area showed a loss of cytoplasmic Nissl substances. Over the next 7 d, this lesion area expanded and cavitated. Terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL)-positive neurons were noted primarily restricted to the gross lesion area 4-24 hr after injury, with a maximum presence at 8 hr after injury. TUNEL-positive glia were present at all stages studied between 4 hr and 14 d, with a maximum presence within the lesion area 24 hr after injury. However 7 d after injury, a second wave of TUNEL-positive glial cells was noted in the white matter peripheral to the lesion and extending at least several millimeters away from the lesion center. The suggestion of apoptosis was supported by electron microscopy, as well as by nuclear staining with Hoechst 33342 dye, and by examination of DNA prepared from the lesion site. Furthermore, repeated intraperitoneal injections of cycloheximide, beginning immediately after a 12.5 mm weight drop insult, produced a substantial reduction in histological evidence of cord damage and in motor dysfunction assessed 4 weeks later. Present data support the hypothesis that apoptosis dependent on active protein synthesis contributes to the neuronal and glial cell death, as well as to the neurological dysfunction, induced by mild-to-moderate severity traumatic insults to the rat spinal cord.
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                Author and article information

                Journal
                Surg Neurol Int
                SNI
                Surgical Neurology International
                Medknow Publications (India )
                2152-7806
                2010
                16 July 2010
                : 1
                : 30
                Affiliations
                Doctors Community Hospital, Georgetown University Hospital, United States
                [1 ]Computational Biodynamics LLC., Yale University, United States
                [2 ]Dartmouth-Hitchcock Medical Center, Georgetown University Hospital, United States
                [3 ]Bethesda MRI & CT, Georgetown University Hospital, United States
                [4 ]University of Alabama Medical Center, Georgetown University Hospital, United States
                [5 ]Kettering University, United States
                [6 ]Thomas Jefferson University Hospital, United States
                [7 ]Cleveland Clinic Foundation, United States
                Author notes
                *Corresponding author
                Article
                SNI-1-30
                10.4103/2152-7806.66461
                2940090
                20847911
                a3704fd1-635d-48f4-948d-25234402ec25
                © 2010 Henderson FC.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 15 March 2010
                : 25 May 2010
                Categories
                Original Article

                Surgery
                stretch myelopathy,finite element analysis,chiari malformation,craniocervical junction,deformative stress,clivo-axial angle

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