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].
