Right-Handed Girls With Rt-Ais Measured Using Holtain Equipment Have Upper Arm Length Asymmetry (Right-Minus-Left) Which Is: 1) Relatively Longer On Scoliosis Curve Convexity; 2) Significantly Associated With Scoliosis Curve Severity (Cobb Angle And Apical Vertebral Rotation); And 3) Transient, Decreasing With Age And Years After Menarche [1,2]. The Aim Is To Test Whether The Right Upper Arm Length Relative Overgrowth And Spinal Deformity Severity Were Associated With Right Or Left Upper Arm Length Size-For-Age. 94 Right-Handed Girls With Rt-Ais, Age 11–18 Years, (Mean Cobb Angle 46 Degrees, Range 10–102 Degrees), Were Evaluated Using A Harpenden Anthropometer For Upper Arm Length Asymmetry, Plotted Against Right And Left Upper Arm Length Standard Deviation Scores (Sds), Calculated From 378 Normal Girls, Age 11–18 Years.Aim:
Method:
In patients with adolescent idiopathic scoliosis (AIS), anomalous extra-spinal left-right skeletal length asymmetries in upper limbs, periapical ribs, and ilia beg the question as to whether these bilateral asymmetries are connected in some way with pathogenesis. The upper arm and iliac length asymmetries correlate significantly with adjacent spinal curve severity respectively in thoracic and lower (thoracolumbar and lumbar) spine. In lower limbs, skeletal length asymmetries and proximo-distal disproportion are unrelated to spinal curve severity. Overall, these observations raise questions about mechanisms that determine skeletal bilateral symmetry of vertebrates in health and disorder, and whether such mechanisms are involved in the cause of this disease. We investigated upper arm length (UAL) asymmetries in two groups of right-handed girls aged 11–18 years, with right thoracic adolescent idiopathic scoliosis (RT-AIS, n=98) from preoperative and screening referrals (mean Cobb angle 45°) and healthy controls (n=240). Right and left UAL were measured with a Harpenden anthropometer of the Holtain equipment, by one of four observers (RGB, AAC, RKP, FJP). UAL asymmetry was calculated as UAL difference, right minus left, in mm. Repeatability of the measurements was assessed by technical error of the measurement (TEM) and coefficient of reliability (R).Introduction
Methods
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%).
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 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].
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
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 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].
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
Between 1993 and 1998, 16 consecutive hips in 12 patients (3M, 9F) with a mean age of 22 yrs (14–38 yrs), and mean time of symptom onset from surgery of 35 mths (9–60 mths) underwent Z-plasty of the iliotibial band for snapping hip. At mean follow-up of 36 mths (15–60 mths), all 16 hips (12 patients) were free of snapping whilst 14 hips (11 patients) experienced complete relief of symptoms. All patients considered the procedure successful and worthwhile, and there were no complications. We conclude that, in select patients who experience painful snapping of the hip because of a tense iliotibial band that has failed non-operative measures, iliotibial band lengthening by Z-plasty has been successful at improving or completely abolishing hip pain and snapping.
Many surgical approaches at decompression have been attempted for the thoracic outlet syndrome (TOS), but only the transaxillary and supraclavicular routes carry the best outcomes. More recently, a selective and tailored approach via the supraclavicular route has been favoured. We performed a retrospective review between 1978 and 1998, and report the outcome of the ‘’two surgeon approach’’ for TOS via the supraclavicular method. An orthopaedic and vascular surgeon jointly conducted 30 operations for disabling symptoms relating to TOS in 27 patients (21F, 6M), mean age of 29 yrs (range 18–63 yrs), having performed the preoperative assessment in conjunction with a neurologist. In all cases, it was essential that patient selection for surgery was determined on clinical grounds rather than the presence of a cervical rib. Anterior scalenectomy was performed via the supraclavicular route except in one case where the infraclavicular route was utilised. Additional surgical procedures were carried out according to the underlying abnormalities, i.e. excision of cervical rib or band or medial scalenectomy. The first rib was always spared. At mean follow-up of 37 mths (range 3-228 mths), 26/30 sides (87%) had excellent or good results. The results were fair or poor in three cases where scalenec-tomy alone was performed. There were no major complications and no patients required a re-operation. 24 patients (89%) returned to their previous lifestyle or occupation. Our results suggest that, with a multidisciplinary assessment and two-surgeon team, good to excellent surgical outcomes can be achieved via the supraclavicular route without resection of the first rib. Instead of the current practise of routine transaxillary first rib resection, we recommend decompression via this approach with further procedures tailored to the abnormality identified.