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consequently the foot deviates into eversion. The result is flattening of the longitudinal
arch and development of a flat foot with valgus deformity. If this deformity exists
bilaterally, 'Charlie Chaplin' type of gait may develop. In cases where spasticity of the
plantar flexors of foot and toes is predominant, the patient has difficulty in placing the
foot firmly on the ground, and as a result of the overaction of the long flexors the toes
drag along the ground. This is particularly apparent when the patient walks without shoes.
Analysis of the spastic paraplegic or paraparetic patient's total body movement by the
medical attendant, in co-operation with the physiotherapist, will serve as a basis for the
choice of the most suitable techniques to restore or improve the patient's walking
capability. Other factors which have to be considered in the assessment of gait, especially
in complete cord lesions, are for what purpose the gait is required and how far it is
practical.
The training should be started in parallel bars in front of a mirror to establish a new
pattern of gait under visual guidance, and walking on elbow crutches should not be
started until the patient has overcome the hip extension, adduction and circumduction
movement of the legs, as well as the forward and sideways tilting of the body. In extension
and adduction spasticity, auto-assisted exercise on the Stoke Mandeville bed-bicycle
often has a relaxing effect, as a preliminary, to the walking in parallel bars or on crutches
in promoting flexion of hips and knees. Another useful method in this respect is walking
exercise in a heated swimming pool, and relaxing of the extension-adduction spasticity
can be achieved by preliminary passive movements of the legs given by the physio
therapist. Certain paraplegics with strong extensor spasms learn to turn them to good
use by standing and walking on them without calipers in parallel bars and deliberately
provoking contractions of the latissimus dorsi. When relaxation of the extensor group
occurs and knee flexion is imminent, the patient braces himself, and by this manoeuvre
the pull, which the latissimus dorsi exerts on the pelvis, serves as a strong afferent impulse
to initiate the extensor response of gluteal muscles, hamstrings and quadriceps. Some
paraplegics with complete mid-thoracic lesion were able to walk several lengths of the
parallel bars without assistance, and thus regain relief and a sense of well-being from
stretching their bodies and holding the upright position. Above all, the resulting relaxa
tion of their spasticity may last for several hours (see also Chapter on Spasticity).
The ataxic gait.
The term 'ataxic gait' presupposes that the patient is able to walk but
that his gait is unsteady and he has difficulty in keeping the equilibrium of his trunk. The
underlying cause of ataxia is either involvement of cerebellar pathway or damage to the
posterior columns or posterior roots. In spinal cord lesions, we have to deal mainly with
the latter cause. In incomplete lesions of the spinal cord, the damage of the neural
elements may only involve the posterior column tracts or—more frequently—it is
combined with the damage of the pyramidal tracts. In cauda equina lesions, the damage
of the posterior roots may also be in the foreground of the clinical symptomatology.
Unlike cerebellar ataxy, the ataxy based on the loss of posterior column sensibility
increases when the patient walks in the dark or has to close his eyes (Romberg sign).
Moreover, there is hypotonia of his muscles if there is no additional damage to the pyra
midal tracts. The patient walks by widening his base, and the loss of postural sensibility
