The cerebral hemispheres are where the motor pathways originate, and where the somatosensory pathways terminate. The left cerebral hemisphere controls the motor functions of the right side of the body, and the right cerebral hemisphere controls the motor functions of the left side of the body. This crossed system is maintained in other modalities including the somatosensory and visual pathways: If the left hemisphere controls the right side of the body, it makes sense that it would need somatosensory information about the right side of the body and visual information about the right side of the world.

There are three main clinically relevant tracts for motor and somatosensory function for the body—one motor and two sensory—that span the brain, brainstem, and spinal cord:

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  Motor: The corticospinal tracts send motor information from the cortex to the spinal cord as the name suggests.

  
  
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  Sensory: The anterolateral (or spinothalamic) tracts and dorsal (or posterior) column pathways bring sensory input from the spinal cord to the brain by way of the brainstem. The names of these pathways refer to their anatomic positions within the spinal cord.

In this chapter, the anatomy of these pathways will be described, providing a foundation for localizing symptoms of weakness and sensory changes, and also laying out anatomic landmarks in the brain, brainstem, and spinal cord that will serve as points of orientation as additional pathways are described in subsequent chapters.

The corticospinal tracts are the final output of the motor system, conveying the action plan to the alpha motor neurons of the anterior horns of the spinal cord, which, in turn, relay the signals to move the muscles by way of peripheral nerves (Fig. 4–1). The corticospinal tracts are sometimes referred to as the pyramidal system (since they travel for part of their course in the medullary pyramids). The extrapyramidal system includes the basal ganglia and cerebellum, which participate in circuits with the motor cortex and are involved in action initiation and coordination (see Chs. 7–8).

Each corticospinal tract begins in the motor cortex, which is located in the precentral gyrus (immediately anterior to the central sulcus). The motor cortex is organized by the region of the body it controls: face lateral, hand and arm superior to this, and leg and foot most medial (with arm and leg representations connected at the shoulder/hip such that the hand is most lateral and the foot most medial with the arm and leg between).

The cell bodies from layer 5 of the motor cortex give rise to axons that travel in the subcortical white matter (specifically in the posterior limb of the internal capsule), then in the ventral/anterior brainstem (cerebral peduncles of the midbrain, basis pontis of the pons, and medullary pyramids of the medulla). At the junction of the medulla and the cervical spinal cord (cervicomedually junction), the corticospinal tracts cross (decussate), such that the corticospinal tract that began in the left hemisphere descends on the right side of the spinal cord and the corticospinal tract that began in the right hemisphere descends on the left side of the spinal cord.

Once in the spinal cord, the main clinically relevant corticospinal tracts are situated posterolaterally. In the spinal cord, the axons that have traveled all the way from the contralateral motor cortex synapse on alpha motor neurons in the anterior horns of the spinal cord gray matter. Axons of the alpha motor neurons leave the ventral/anterior spinal cord via ventral roots and enter peripheral nerves to travel to muscles.

For clinical purposes, the pyramidal motor system can be considered as a two-neuron system. First-order neurons have their cell bodies in the motor cortex (precentral gyrus), and their axons travel through the internal capsule, brainstem, and spinal cord (the corticospinal tract). Second-order neurons have their cell bodies in the anterior horn of the spinal cord, and their axons travel through nerve roots and peripheral nerves. The neurons of the central nervous system (CNS) component in the brain/brainstem/spinal cord (i.e., the corticospinal tract) are referred to as upper motor neurons, and the neurons of the peripheral nervous system (PNS) component (anterior horn of the spinal cord through the ventral roots into peripheral nerves) are referred to as lower motor neurons.

Because of the crossing (decussation) of the corticospinal tracts at the cervicomedullary junction, unilateral corticospinal tract lesions in the brain or brainstem cause contralateral weakness, whereas unilateral spinal cord lesions cause ipsilateral weakness. Lesions in individual roots and nerves cause weakness in the particular muscle(s) that they supply.

Upper Motor Neuron Lesions Versus Lower Motor Neuron Lesions

Understanding the differences in the clinical signs caused by upper motor neuron lesions (CNS) versus lower motor neuron lesions (PNS) is an essential component of the assessment of weakness. With upper motor neuron lesions, all of the signs go up: reflexes are “up” (increased: hyperreflexia), tone is “up” (increased: spasticity), and the big toe may go up when stroking the bottom of the foot (Babinski sign).

With lower motor neuron lesions, nearly all of the signs are lowered: diminished or absent reflexes (hyporeflexia or areflexia), decreased (flaccid) tone, decreased muscle bulk (atrophy), toes downgoing (no Babinski sign). Abnormal muscle twitches called fasciculations can occur with diseases affecting lower motor neurons. Fasciculations are an example of a sign of increased activity due to lower motor neuron dysfunction, and are therefore an exception to the “up” and “low” mnemonic for signs associated with pathology of upper and lower motor neurons (Table 4–1).

Another upper motor neuron sign is the Hoffmann sign, which can be thought of as a Babinski sign for the upper extremity. To see if a Hoffmann sign is present, the examiner holds the patient’s hand by the middle finger with one hand, and uses the other hand to quickly flick the tip of the middle finger (as if snapping one’s fingers, but with the patient’s finger between). If a Hoffmann sign is present, the fingers and thumb will flex. As with the Babinski sign, this sign is indicative of upper motor neuron (CNS) dysfunction.

A very important clinical point is that some of the classic upper motor neuron findings such as increased tone and hyperreflexia are often not present acutely after a CNS insult and take time to emerge. For example, with weakness caused by acute stroke or acute spinal cord trauma, the affected limb(s) will usually be flaccid and areflexic in the acute setting. Upper motor neuron signs emerge over time. Therefore, it may be more challenging to distinguish between upper and lower motor neuron causes of weakness in the acute setting. An upgoing toe (Babinski sign) may be present acutely (although not always), and when it is, can help point toward a CNS etiology of weakness.

Pronator drift is another indication of upper motor neuron pattern weakness: when the arms are held outstretched with the palms up and fingers spread (as if holding a tray), the hand may begin to close and the arm may begin to pronate and drift downward if upper extremity weakness is due to CNS/upper motor neuron pathology. (With parietal lesions, the affected arm may drift upward due to impaired proprioception.) Unlike the upper motor neuron signs described above that may not be present acutely (since it is a reflection of the pattern of weakness).

When an upper motor neuron lesion causes weakness without causing complete paralysis, a distinct pattern of weakness may be seen in which the upper extremity extensors are weaker than the flexors, and the lower extremity flexors are weaker than the extensors. In other words, the arm is stronger when flexing the elbow compared to extending the elbow, and the leg is stronger when extending the knee compared to flexing the knee. This pattern can be remembered by recalling the posture of a patient with long-standing upper motor neuron injury (e.g., prior stroke): the arm, wrist, and fingers are flexed and pronated close to the body, whereas the lower extremity is extended at the knee with the foot plantarflexed and needs to be circumducted when the patient walks. This posture demonstrates that the stronger flexors of the arm have overcome the weaker extensors, and the stronger extensors of the leg have overcome the weaker flexors. As with pronator drift, this upper motor neuron pattern of weakness can be present acutely (as opposed to hyperreflexia and increased tone, which generally take time to emerge, as described above). Note that a radial nerve palsy will affect the triceps, wrist/finger extensors, and supinator, and can thus mimic an upper motor neuron lesion and vice versa (see Ch. 16).