The possibility that AIS aetiology involves undetected neuromuscular dysfunction is considered likely by several workers [1,2]. Yet in the extensive neuroscience research of idiopathic scoliosis certain neurodevelopmental concepts have been neglected. These include [3]:
a CNS body schema (“body in the brain”) for posture and movement control generated during development and growth by establishing a long-lasting memory, and pruning of cortical synapses at puberty. During normal development the CNS has to adapt to the rapidly growing skeleton of adolescence, and in AIS to developing spinal asymmetry from whatever cause. Examination of publications relating to the CNS body schema, parietal lobe and temporo-parietal junction [4,5] led us to a new concept: namely, that a delay in maturation of the CNS body schema during adolescence with an early AIS deformity at a time of rapid spinal growth results in the CNS attempting to balance the deformity in a trunk that is larger than the information on personal space (self) already established in the brain by that time of development. It is postulated that this CNS maturational delay allows scoliosis curve progression to occur – unless the delay is temporary when curve progression would cease. The maturational delay may be primary in the brain or secondary to impaired sensory input from end-organs [6], nerve fibre tracts [2,7,8] or central processing [9,10]. The motor component of the concept could be evaluated using transcranial magnetic stimulation [11].
In subjects with lumbar, thoracolumbar or pelvic tilt scoliosis no pattern of structural leg length inequality has been reported [1]. Forty-seven girls of 108 consecutive adolescent patients referred from routine scoliosis school screening during 1996–1999 had lower spinal scoliosis – lumbar (LS) 17, or thoracolumbar (TLS) 30 (mean Cobb angle 16 degrees, range 4–38 degrees, mean age 14.8 years, left curves 25). The controls were 280 normal girls (11–18 years, mean age 13.4 years). Anthropometric measurements were made of total leg lengths (LL), tibiae (TL) and feet (FL) by one observer (RGB) and asymmetries calculated for LL, TL and FL, as absolutes and percentage asymmetries of right/left lengths. There are no detectable changes of absolute asymmetries with age for LL, TL or FL in scoliotic or normal girls. Asymmetries are found in scoliotic girls compared with normals with relative lengthening on the right for each of LL (0.95%) and TL (0.99%) (each p<
0.001), but not FL (0.38%).
The side distribution of single spinal curves in our school screening referrals for 1988–99 (n=218) suggests that the mechanism(s) determining curve laterality for the upper spine differs from those for the lower spine. We address here the laterality of right thoracic AIS. In the search to understand the aetiology of AIS some workers focus on mechanisms initiated in embryonic life including a disturbance of bilateral symmetry. The
Most workers consider that ribcage changes in AIS are secondary to spinal deformity. Others claim that ribs are pathogenic in curve initiation or aggravation. In 117 consecutive patients referred from school screening in 1996–99 and routinely scanned by ultrasound, 24 had thoracic and 33 thoracolumbar scolioses (right 37, left 20; mean age 14.9 years, range 12–18 years, girls 44 postmenarcheal 37, boys 13). On anteroposterior standing radiographs, Cobb angle (CA), apical vertebral rotation (AVR, Perdriolle) and apical vertebral translation (AVT from the T1-S1 line) were measured (mean &
range: CA 19°, 6–42°; AVR 15°, 0–39°; AVT 17 mm, 0–38 mm). Real-time ultrasound in the prone position recorded laminal rotation (LR) and rib rotation (RR) segmentally and the spine-rib rotation difference (SRRD) as LR
Primary Cobb angle, Secondary Cobb angle, Coronal C7-midsacral plumb line, Apical Vertebra Translation (AVT) of primary curve, AVT of the secondary curve, Upper instrumented vertebra (UIV) translation, UIV tilt angle, Lower instrumented vertebra (LIV), 8) LIV tilt angle Apical Vertebra Rotation (AVR) of the primary curve, Sagittal C7-posterior corner of sacrum plumb line T5-T12 angle, T12-S1 angle, shoulder height difference. The percentage improvements for each were noted. Correlation was sought between Total SRS score, each of the five individual domains and various radiographic parameters listed above by quantifying Pearson’s Correlation Coefficient (r).
Several workers consider that the aetiology of adolescent idiopathic scoliosis (AIS) involves undetected neu-romuscular dysfunction. During normal development the central nervous system (CNS) has to adapt to the rapidly growing skeleton of adolescence, and in AIS also to developing spinal asymmetry from whatever cause. A new etiologic concept is proposed after examining the following evidence:
anomalous extra-spinal left-right skeletal length asymmetries of upper arms, ribs, ilia and lower limbs suggesting that asymmetries may also involve vertebral body and costal growth plates; growth velocity and curve progression in relation to scoliosis curve expression; the CNS body schema, parietal lobe and temporoparietal junction in relation to postural mechanisms; and human upright posture and movements of spine and trunk. The central of four requirements is maturational delay of the CNS body schema relative to skeletal maturation during the adolescent growth spurt that disturbs the normal neuro-osseous timing of maturation. With the development of an early AIS deformity at a time of rapid spinal growth the association of CNS maturational delay results in postural mechanisms failing to balance a lateral spinal deformity in an upright moving trunk that is larger than the information on personal space (self) established in the brain by that time of development. It is postulated that CNS maturational delay allows scoliosis curve progression to occur – unless the delay is temporary when curve progression would cease. The concept brings together many findings relating AIS to the nervous and musculoskeletal systems and suggests brain morphometric studies in subjects with progressive AIS.
In schoolchildren screened for scoliosis about 40% have minor, non-progressive, lumbar scolioses secondary to pelvic tilt with leg-length and/or sacral inequality [1] not reported with preoperative thoracic curves [2]. Forty-nine of 108 consecutive adolescent patients referred from routine scoliosis school screening during 1996–1999 had lower spinal scoliosis with measurable radiological sacral alar and hip tilt angles – lumbar scoliosis 18, thoracolumbar scoliosis 31 (girls 41, boys 8, mean Cobb angle 16 degrees, range 4–38 degrees). In standing full spine antero-posterior radiographs measurements were made of Cobb angle and pelvic asymmetries as sacral alar and iliac heights (left minus right). From anthropometric measurements derivatives were calculated as ilio-femoral length (total leg length minus tibial length) and several length asymmetries, namely: ilio-femoral length asymmetry, total leg length inequality and tibial length asymmetry (all left minus right). Ilio-femoral length asymmetry correlates significantly with sacral alar height asymmetry (girls negatively r= − 0.456, p=0.002, boys positively r=0.726 p=0.041) but not iliac height asymmetry (girls p=0.201) from which three types are identified. Total leg length inequality but not tibial length asymmetry in the girls is associated with sacral alar height asymmetry (r= − 0.367 p=0.017 &
r=0.039 p=0.807 respectively). Interpretation is complicated by total leg lengths each including some ilium in which there is asymmetry [3]. But lack of association between ilio-femoral length asymmetry and iliac height asymmetry suggests that the femoral component is more important than iliac component in determining the associations between sacral alar height asymmetry and each of ilio-femoral length asymmetry and total leg length inequality.
Sacral alar height asymmetry and leg length asymmetries. The evidence suggests that sacral alar height asymmetry is not secondary to the leg length inequalities at least in most girls (negative correlations) and is more likely to result from primary skeletal changes in femur(s) and sacrum. Sacral alar height asymmetry and Cobb angle. Scoliosis progression and iliac height asymmetry [3] appear to need factors additional to those that determine ilio-femoral length asymmetry – for in the girls Cobb angle is associated with both sacral alar height asymmetry and iliac height asymmetry (each p<
0.001) but not with either ilio-femoral length asymmetry (p=0.249) or total leg length inequality (p=0.650). The additional factors may be biomechanical [4], and/or biological in the trunk [5] and central nervous system [6].
Patterns of extra-spinal skeletal length asymmetry have been reported for upper limbs [1] and ribcage [2] of patients with upper spine adolescent idiopathic scoliosis. This paper reports a third pattern in the ilia. Seventy of 108 consecutive adolescent patients referred from routine scoliosis school screening during 1996–1999 had lower spine scoliosis – lumbar (LS), thoracolumbar (TLS), or pelvic tilt scoliosis (PTS). Radiologic bi-iliac and hip tilt angles were both measurable in 60 subjects: LS 18, TLS 31, and PTS 11 (girls 44, boys 16, mean age 14.6 years). Cobb angle (CA), apical vertebral rotation (AVR) and apical vertebral translation from the T1-S1 line (AVT) were measured on standing full spine radiographs (mean Cobb angle 14 degrees, range 4–38 degrees, 33 left, 27 right curves). Bi-iliac tilt angle (BITA) and hip tilt angle (HTA) were measured trigonometrically and iliac height asymmetry calculated as BITA minus HTA (corrected BITA=CBITA) and directly as iliac height asymmetry. Iliac height is relatively taller on the concavity of these curves (p<
0.001). CBITA is associated with Cobb angle, AVR and AVT (each p<
0.001).
In idiopathic scoliosis the detection of extra-spinal left-right skeletal length asymmetries in the upper limbs, ribs, ilia and lower limbs [1–7] begs the question: are these asymmetries unconnected with the pathogenesis, or are they an indicator of what may also be happening in immature vertebrae of the spine? The vertebrate body plan has mirror-image bilateral symmetries (mirror symmetrical, homologous morphologies) that are highly conserved culminating in the adult form [8]. The normal human body can be viewed as containing paired skeletal structures in the axial and appendicular skeleton as a) separate left and right paired forms (e.g. long limb bones, ribs, ilia), and b) united in paired forms (e.g. vertebrae, skull, mandible). Each of these separate and united pairs are mirror-image forms – enantiomorphs. In idiopathic scoliosis, genetic and epigenetic (environmental) mechanisms [9–11] may disturb the symmetry control of enantiomorphic immature bones [12–13] and, by creating left-right endochondral growth asymmetries, cause the extra-spinal bone length asymmetries, and within one or more vertebrae create growth conflict with distortion as deformities (= unsynchronised bone growth concept) [14].
The mean pre-operative cephalic (cervico-thoracic) Cobb angle of 37.1degrees, corrected to 22 degrees, with progression to 26.6 degrees. The mean pre-operative caudal (lumbar) Cobb angle of 26.4degrees, corrected to16.2 degrees, this later progressed to 20.6 degrees. Coronal plane translation measured 1.68 cm at latest follow up [range 0.5–5.1cm]. The thoracolumbar longitudinal growth measured a mean of 8.81cm (approx0.8 cm/year) with a recorded lengthening of 2.54 cm (approx 0.23cm/year) in the instrumented segmented. Half the patients did not require further surgery.
Left-right skeletal length asymmetries in upper limbs related to curve side have been detected with adolescent thoracic idiopathic scoliosis (AIS). In school screening referrals with thoracic scoliosis we find apical vertebral rotation (AVR, Perdriolle) is associated significantly with upper arm length asymmetry. Sixty-nine of 218 consecutive adolescent patients referred routinely during 1988–1999 had
To determine the quantitative adherence and biofilm development of P. acnes on titanium compared to surgical steel. To assess the subsequent effect of penicillin, the therapeutic drug of choice, on mature P. acnes biofilms.
High correlation was revealed between postoperative decompensation and derotation of lumbar apical vertebrae (P=0.62, p<
0.001) with a critical value of 40%. A 2x2 table showed that in patients with lumbar apical vertebral derotation of less than 40% specificity was 90% with regard to postoperative decompensation.