B. Brain
6. Central Nervous System Pathways
Up to this point, the diverse functional gray regions in the brain and spinal cord have been identified. In order for the nervous system to work, an extensive circuitry has been established to interconnect areas throughout the central nervous system.
We have just described the intrinsic white matter circuitry within the cerebrum: the associational, commissural, and subcortical fibers. The subcortical fibers consist of a multitude of axonal pathways that provide afferents to the cerebrum and efferents from the cerebrum.
Many names are used for pathways within the central nervous system, including fasciculus (bundle), lemniscus (ribbon), peduncle (stalk), and tract (trail). Many of the pathways also have a name that indicates its function (e.g., the optic tract con-nects the eyes and visual regions, the corticospinal (Chapter 9, Fig. 9.6) tract runs from the cortex to the spinal cord, and the corticonuclear (Chapter 9, Fig 9.7) tract connects the cerebral cortex to the cranial nerve nuclei). Unfortunately, the majority of the pathways have names that give no clue to function (e.g., the medial longitu-dinal fasciculus, lateral lemniscus, and cerebral peduncle). The major tracts and their role in the central nervous system are discussed in Chapter 6. For each path-way, the student needs to learn the following:
1. Cells of origin
2. Location of the tract in the brain 3. Site of termination of pathway 4. Function.
As an example of function within the central nervous system we will now use a functionally very significant region that provides volitional motor control to the muscles of the body: the motor–sensory cortex.
7. Motor–Sensory Cortex (Fig. 1.6)
This cortex is found around the central sulcus that separates the frontal from the parietal lobe. It has six layers. Figure 1.6 identifies the vertically oriented central sulcus, which is surrounded by the precentral/motor strip and postcentral/sensory
cortex. This region controls the skeletal muscles in the body that permit us to under-take so many tasks. In order to perform a skilled motor task, one is dependent on precise sensory input, so we will first describe the sensory portion of this circuit.
Sensory Information from the Foot to the SensorimotorCortex
In the sensory system, three different neuronal groupings are traversed before the sensory information reaches the cerebral cortex from the periphery: the primary, secondary, and tertiary neurons. The sensory information of importance for precise movement originates from stretch receptors in the muscles, tendons, and joints of the hand and is encoded as electrical impulses that detail the contraction status of the muscles, tendons, and joints. The cells of origin, the primary cell bodies, are in the large sensory ganglia attached to the lumbar and sacral segments of the spinal cord. The information is carried in by the dendrite of the primary sensory cell and its axon enters the central nervous system and ascends uncrossed and ipsilaterally in the posterior column of the cord until the medullospinal junction. In the medul-lospinal junction second-order nerve cells appear in the posterior column, the grac-ile nucleus. The axons from the primary neurons synapse on this nucleus. The axons of the second-order axons cross the midline and ascend contralaterally in one of the major ascending white matter pathways (the medial lemniscus) into the tha-lamus of the diencephalon where they synapse on the third-order neurons in the ventral posterior lateral nucleus, which then send fibers ipsilaterally onto the foot region on the upper end and medial surface of the postcentral gyrus.
Motor Control of the Foot from the Motor–Sensory Cortex
In the motor system, two distinct neuronal groups are necessary for a movement:
one in the motor cortex of the cerebrum (the upper motor neuron) and the other in the spinal cord or brain stem (the lower motor neuron). Motor control to the foot is carried centrifugally by the corticospinal pathway. The corticospinal path-way to the foot originates from layer V on the medial surface of the motor cortex of the precentral gyrus and to a lesser degree in the postcentral gyrus. Before exiting the gray matter, the fibers are covered with myelin and descend on the same side through the internal capsule, cerebral peduncle, pons, and medullary pyramid. The corticospinal fibers cross (decussate) to the other side of the brain in the medullospinal junction and enter the lateral column of the spinal cord.
Fibers to the musculature of the leg descend to lower lumbar and sacral levels and synapse in either the intermediate region of the gray matter of the spinal cord or directly on the ventral horn cells. The axons from the ventral horn cell leave the central nervous system form the peripheral nerves that synapse on the motor end-plates of the muscles in the leg, which produce the contraction. The actual initia-tion of the movement is from the prefrontal and premotor region of the frontal lobe (see Chapter 9).
Interruption of the corticospinal pathway or destruction of the motor cortex pro-duces upper motor neuron paralysis with increased reflex tone and spasticity, whereas injury to the spinal cord ventral horn cells produces lower motor neuron paralysis and atrophy of the muscle and decreased reflex tone (Table 1.6).
In summary, it takes three orders of sensory neurons to provide the information to the cerebral cortex and two levels of motor neurons to produce a hand movement in response to the sensory information. Note that the sensory information ascends and crosses over, whereas the motor information descends and crosses so that the same side is represented in the cerebral cortex. Of course, the hand movement also needs a conscious decision to be made, which is what the cerebral cortex working as a unit does. The following Case History illustrates the effects of a lesion in the leg region of the motor strip on movement.
Case History 1.1 (Fig. 1.9)
This 45-year-old right-handed, married, white female, mother of four children was referred for evaluation of progressive weakness of the right lower extremity of 2 years’ duration. This weakness was primarily in the foot so that she would stub the toes and stumble. Because she had experienced some minor nonspecific back pain for a number of years, the question of a ruptured lumbar disc had been raised as a possible etiology. The patient labeled her back pain as “sciatica” but denied any radiation of the back pain into the leg. She had no sensory symptoms, and no blad-der symptoms. Six months before the consultation, the patient had transient mild weakness of the right leg that lasted a week. The patient attributed her symptoms to “menopause” and depression, and her depression had improved with replace-ment estrogen.
Neurological examination: Neurological examination revealed that the patient’s mental status was normal and the cranial nerves were all intact. There was a mini-mal drift down the outstretched right arm, and there was significant weakness in the right lower extremity with ankle dorsiflexion and plantar flexion was less than 30%
of normal. Inversion at the ankle was only 10–20% of normal. Toe extension was 50% of normal and there was minor weakness present in the flexors and extensors at the knee. In walking, the patient had a foot drop gait and had to overlift the foot to clear the floor. Examination of the shoes showed greater wear at the toes of the
Table 1.6 Comparison of upper motor neuron to lower motor neuron lesion Upper motor neuron lesion (UMN) Lower motor neuron lesion LMN Lesion in Motor Cortex or Corticospinal tract Lesion in ventral horns or ventral rootlets Reflexes: Increase (2+ normal), 3+, or 4+ Reflexes; Decrease or are absent (+1 or 0) Babinski (extensor plantar response)
Muscles spastic (sign of injury to Muscles: Limb Flacid Fasciculations,
corticospinal) lead to atrophy
right shoe, with evidence of scuffing of the toe. The patient’s deep tendon stretch reflexes were increased at the patellar and Achilles tendons on the right. In addi-tion, reflexes in the right arm at the biceps, triceps, and radial periosteal were also slightly increased. The plantar response on the right was extensor (sign of Babinski) and the left was equivocal. All sensory modalities were intact. Scoliosis was present with local tenderness over the lumbar, thoracic, and cervical vertebrae, but no ten-derness was present over the sciatic and femoral nerves.
Comments: It was clear that the symptoms and signs were not related to com-pression of the lumbar nerve roots by a ruptured disc. Such a comcom-pression (lumbar radiculopathy) would have produced a lower motor neuron lesion, a depression of deep tendon stretch reflexes, lumbar radicular pain in the distribution of the sciatic nerve and tenderness over the sciatic nerve, no increase in reflexes in the upper or lower extremities, and no sign of Babinski. The fact that reflexes were more active in both upper and lower extremities on the right, with the sign of Babinski on the right, suggested a process involving the corticospinal tract. The fact that the weak-ness was greatest in the foot suggested a meningioma involving the parasagittal motor cortex where the foot area is represented.
Clinical Diagnosis: With these clinical considerations in mind, an MRI of the patient’s head was obtained and the MRI confirmed the clinical impression of a meningioma in the right cerebral hemisphere. This tumor was successfully removed by the neurosurgeon, with an essentially complete restoration of function.
Fig. 1.9 Meningioma in the left cerebral hemisphere (From EM Marcus and J Jacobson, Integrated neuroscience, Kluwer, 2003)