Janda's classification of muscle imbalances
Throughout Janda's observations of patients with neurological disorders and chronic musculoskeletal
pain, Janda found that the typical muscle response to joint dysfunction is
similar to the muscle patterns found in upper motor neuron lesions, concluding that
muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle
tightness or spasticity is predominant. Often, weakness from muscle imbalance results
from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness
varies between individuals, but the pattern rarely does. These patterns lead to
postural changes and joint dysfunction and degeneration. Janda identified three stereotypical patterns associated with distinct chronic pain
syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes
are characterized by specific patterns of muscle weakness and tightness that cross
between the front and the back of the body.
Upper-crossed Syndrome:
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle
crossed syndrome. In UCS, tightness of the upper trapezius
and levator scapula on the dorsal side crosses with tightness of the pectoralis major
and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of
the middle and lower trapezius. This pattern of imbalance creates joint dysfunction,
particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral
joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change
in morphology. Specific postural changes are seen in UCS, including forward head
posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted
shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These
postural changes decrease glenohumeral stability as the glenoid fossa becomes more
vertical due to serratus anterior weakness leading to abduction, rotation, and winging
of the scapulae. This loss of stability requires the levator scapula and upper trapezius
to increase activation to maintain glenohumeral centration (Janda 1988).
lower-crossed Syndrome:
Lower-crossed Syndrome (LCS) is also referred to as distal or pelvic crossed syndrome. In LCS, tightness of the thoracolumbar extensors on the dorsal
side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep
abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius.
This pattern of imbalance creates
joint dysfunction, particularly at
the L4-L5 and L5-S1 segments, SI
joint, and hip joint. Specific postural
changes seen in LCS include anterior
pelvic tilt, increased lumbar lordosis,
lateral lumbar shift, lateral leg rotation,
and knee hyperextension. If
the lordosis is deep and short, then
imbalance is predominantly in the
pelvic muscles; if the lordosis is shallow
and extends into the thoracic
area, then imbalance predominates
in the trunk muscles.
Janda identified two subtypes
of LCS: A and B.
Patients with LCS type A use more
hip flexion and extension movement
for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These
individuals compensate with a hyperlordosis limited to the lumbar spine and with a
hyperkyphosis in the upper lumbar and thoracolumbar segments.
Janda's LCS type B involves more movement of the low back and abdominal area.
There is minimal lumbar lordosis that extends into the thoracolumbar segments,
compensatory kyphosis in the thoracic area, and head protraction. The COG is
shifted backward with the shoulders behind the axis of the body, and the knees are
in recurvatum.
Deep stabilizing muscles responsible for segmental spinal stability are inhibited
and substituted by activation of the superficial muscles (Cholewicki, Panjabi, and
Khachatryan 1997). Tight hamstrings may be compensating for anterior pelvic tilt or
an inhibited gluteus maximus. LCS also affects dynamic movement patterns. If the hip
loses its ability to extend in the terminal stance, there is a compensatory increase in
anterior pelvic tilt and lumbar extension. This compensation creates a chain reaction
to maintain equilibrium, in which the increased pelvic tilt and anterior lordosis increase
the thoracic kyphosis and cervical lordosis (see chapter 3).
In adults, muscle imbalance begins distally in the pelvis and continues proximally
to the shoulder and neck area. In children, this progression is reversed, and muscle
imbalance begins proximally and moves distally.
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