The intercostal muscles, as well as the abdominal and paraspinal muscles, are segmentally innervated. Intercostal motion during breathing implies neurologic integrity; a lack of motion implies involvement. The abdominal and paraspinal muscles can be similarly evaluated, for they are both segmentally innervated by T7-T12 (L1). To test for the integrity of their innervation, have the patient do a half sit-up as you palpate the anterior abdominal wall. As the patient sits up, note whether the umbilicus is pulled toward any of the four quadrants of the abdomen. If the umbilicus is pulled in one direction, the opposing flaccid muscles are denervated (Beevor’s sign) (Fig. 2-1). Note that the umbilicus is the dividing line between T10 above and T11 below. Obviously, this test should not be performed during the acute stages of thoracic lesions or with patients who have unstable spines.

Sensory innervation may be determined in accordance with the chart (Fig. 4-1). Special skin landmarks that mark sensory areas are as follows:

There is complete paralysis of the lower extremities, with the exception of some hip flexion from partial innervation of the iliopsoas (T12, L1-L3) (Fig. 4-2).

There is no sensation below the L1 sensory band, which extends over the proximal third of the anterior aspect of the thigh.

The patellar and Achilles tendon reflexes are absent when spinal shock is present. As spinal shock wears off, the reflexes become exaggerated.

The bladder (S2-S4) does not function. The patient cannot urinate in a stream. The anus is initially patulous, and the superficial anal reflex (S2-S4) is absent. As spinal shock wears off, the anal sphincter contracts and the anal reflex becomes hyperactive.

There is good power in hip flexion because the iliopsoas is almost completely innervated. The adductor muscles are partially innervated (L2-L4) and show diminished power. Although the quadriceps (L2-L4) are partially innervated, there is no clinically significant function. No other muscles in the lower extremity have innervation, and the unopposed action of the iliopsoas and adductors tends to produce a flexion and slight adduction deformity.

There is no sensation below the L2 sensory band, which ends two-thirds of the way down the thigh.

The patellar reflex receives innervation from L2 to L4, but the L2 contribution is small.

There is no voluntary control.

In addition to the iliopsoas and adductors, the quadriceps (L2-L4), although slightly weak, show significant power. No other muscle groups are functioning. Thus, the hip tends to become flexed, adducted, and externally rotated while the knee remains extended.

Sensation is normal to the level of the knee (L3 dermatome band).

The patellar reflex (L2-L4) is present, but decreased. The Achilles tendon reflex is absent.

There is no voluntary control.

Muscle function at the hip and knee is the same as in L3 neurologic lesions except that
quadriceps function is now normal. The only functioning muscle below the knee is the tibialis anterior (L4), which causes the foot to dorsiflex and invert.

In addition to the entire thigh, the medial side of the tibia and foot has sensation.

The patellar reflex (predominantly L4) is normal; the Achilles tendon reflex (S1) is still absent.

There is no voluntary control of either function.

The hip still has a flexion deformity, because the gluteus maximus does not function. Innervation of the gluteus maximus is derived from L5, S1 and S2. The gluteus medius (L1-S1) has partial function; it counteracts the action of the adductors. The quadriceps are normal.

The knee flexors function partially with the medial hamstrings (L5) present and the lateral hamstrings (S1) absent.

The foot dorsiflexors and invertors function. Because the plantar flexors and evertors are still absent, the foot tends to develop a calcaneus (dorsiflexion) deformity.

Sensation is normal in the lower extremity, with the exception of the lateral side and plantar surface of the foot.

The patellar reflex is normal. The Achilles tendon reflex is still absent.

There is no voluntary control of either function.

The hip muscles are normal, with the exception of slight gluteus maximus weakness. The knee muscles are normal. The soleus and gastrocnemius (S1, S2) are weak, and the toes show clawing as a result of intrinsic muscle weakness (S2, S3).

Sensation in the lower extremity is normal. There is perianal anesthesia.

The patellar and Achilles tendon reflexes are normal, because the S2 contribution to the Achilles tendon reflex is small.

There is still no voluntary control of either function.

Elicit the plantar response by running a sharp instrument across the plantar surface of the foot, and along the calcaneus and lateral border of the forefoot. Normally, in a negative reaction, the toes plantarflex. A positive reaction (Babinski’s sign) occurs when the great toe extends as the other toes splay (Fig. 4-3). This sign indicates an upper motor neuron lesion—a corticospinal tract involvement. To ascertain the level of the lesion, correlate this sign with other neurologic findings. In young infants, the presence of Babinski’s sign is normal rather than pathologic. However, this response should disappear by 12 to 18 months of age.

To elicit Oppenheim’s sign, run your finger along the crest of the tibia. Normally there should be no reaction at all, or the patient should complain of pain. Under abnormal circumstances, the reaction is the same as it is in plantar stimulation: the great toe extends as the other toes splay (Oppenheim’s sign) (Fig. 4-4). Oppenheim’s sign is not as reliable as Babinski’s sign and should be used as a confirmation of a positive Babinski’s sign.

The lack of the cremasteric reflex may be due either to the loss of the reflex arc or to an upper motor neuron lesion. However, absence of the reflex in association with the presence of a pathologic
reflex (Babinski’s or Oppenheim’s signs) supports the diagnosis of an upper motor neuron lesion.

To elicit the superficial cremasteric reflex, stroke the inner side of the upper thigh with the sharp end of a neurologic hammer. If the reflex is intact, the scrotal sac on that side will be pulled upward as the cremaster muscle (T12) contracts. If the cremasteric reflex is unilaterally absent, there is probably a lower motor neuron lesion between L1 and L2 (Fig. 4-5).

The possibility of cord return, and whatever partial functional recovery it may provide, depends on whether the lesion is complete or incomplete, whether the cord is completely severed or only partially severed or contused. Injuries in which no function returns over a 24-hour period are assumed to be complete lesions, where no return of cord function will occur. A complete neurologic examination is needed to confirm such a diagnosis. If, however, there is partial return of function in the initial period, the lesion is probably incomplete, and more function may eventually return. Function must return at more than one neurologic level to support such a diagnosis, however, because return at only one level may simply indicate that the nerve root at the level of the lesion has been partially damaged or contused. Such single-level return gives no indication as to whether the lesion below it is complete or incomplete. The recovery of this single nerve root is considered to be a root lesion (rather than a cord lesion) of the root originating just proximal to the injured portion of the cord. Functional return of muscle strength from such an injury may occur at any time; prognostication for root return is good as late as six months after the initial injury.