Spinal Cord

The spinal cord, as seen in cross section (Fig. 14), contains central grey matter and peripheral white matter. The grey matter contains many neuronail cell bodies and synapses. The white matter contains ascending and descending fiber pathways. The ascending pathways relay sensory information to the brain. The descending pathways relay motor instructions down from the brain. The number of synapses within a pathway is not very important to know clinically. However, it is vital to remember the sites of contralateral crossing over of the various pathways and also the location of the pathways within the white matter as seen in cross section (Fig. 14).

Posterior rool

Peripheral nerve

Posterior rool

Peripheral nerve

Str Spinal Chord Faciculus Gracilis

WHITE MATTER GREY MATTER

"Anterior root

WHITE MATTER GREY MATTER

"Anterior root

Fasciculus gracilis

Fasciculus cuneatus

Posterior horn

Anterior horn

Posterior horn

Spinothalamic Tract

Spinocerebellar tract Corticospinal tract

Spinothalamic tract

Spinocerebellar tract Corticospinal tract

Spinothalamic tract

Fig. 14 Major subdivisions of the spinal cord. The posterior columns consist of the fasciculus gracilis plus fasciculus cuneatus.

The Sites of Crossing Over

There are 3 main sensory systems entering the spinal cord:

1. Pain-temperature

2. Proprioception — stereognosis (see glossary)

3. Light touch

To avoid confusion, no sensory synapses will be drawn in figure 15. As a rule though, there is a tendency for sensory fibers to synapse just prior to crossing over (Fig. 16).

To thqlomut ond cftrqbrq cortex (Sentory)

Proprioception And Stereognosis Pathway

PAIN-

TEMPERATURE

PR0PRI0CEPTI0N-

STEREOGNOSIS

(CONSCIOUS)

Motor corta

PAIN-

TEMPERATURE

PR0PRI0CEPTI0N-

STEREOGNOSIS

(CONSCIOUS)

l<J .Corticoipfoal 1 trod < ¿-Spinocerebellar I

UNCONSCIOUS PROPRIOCEPTION

MOTOR (CORTICOSPINAL TRACT)

Fig. 15 Schematic view of the major ascending and descending pathways. UMN, upper motor neuron; LMN, lower motor neuron.

Sensory Pathways The Spinal Cord

PAIN- TEMPERATURE PROPRIOCEPTION- STEREOONOSS UGHT TOUCH (CONSCIOUS)

Fig. 16 Three major sensory pathways.

PAIN- TEMPERATURE PROPRIOCEPTION- STEREOONOSS UGHT TOUCH (CONSCIOUS)

Fig. 16 Three major sensory pathways.

The pathway for pain and temperature enters the spinal cord, crosses over to the opposite half of the cord almost immediately (actually within one or two spinal cord vertebral segments), ascends to the thalamus on the opposite side, and then moves on to the cerebral cortex. In reality many fibers end in the brain stem and never make it as far as the thalamus, but these will not concern us here. A lesion of the spinothalamic tract will result in loss of pain-temperature sensation contralateral^, below the level of the lesion.

The pathway for proprioception and stereognosis (also for the perception of vibration) initially remains on the same side of the spinal cord that it enters, crossing over at the junction between the spinal cord and brain stem. The synaptic areas just prior to this crossing are the nucleus cuneatus and nucleus gracilis (Fig. 16). Nucleus gracilis contains proprioceptive information from the lower part of the body, whereas nucleus cuneatus conveys information from the upper levels. Their corresponding spinal cord pathways are termed fasciculus gracilis (graceful, like a ballerina's legs) and fasciculus cuneatus (cunning, being closer to the brain). The fasciculus gracilis and fasciculus cuneatus are collectively termed the posterior columns (Fig. 14). A lesion of the posterior columns results in a decrease in conscious proprioception and stereognosis (also vibration sense) ipsilaterally below the level of the lesion. (Actually, the deficit is mostly in stereognosis, since conscious proprioception and vibration sense are to some extent represented in more lateral regions of the cord.)

The path for light touch combines features of the above two pathways. It partly remains uncrossed until it reaches the level of the brain stem, and partly crosses over at lower levels. This is why light touch typically is spared in unilateral spinal cord lesions; there are alternate routes to carry the information.

All the above sensory pathways eventually cross over and terminate in the thalamus. From there, they are relayed to the sensory area of the cerebrum. A lesion of the sensory area of the cerebral cortex may result in a contralateral deficit of all the above sensory modalities.

Proprioception-stereognosis has a conscious and an unconscious component. The conscious pathway, mentioned above, connects with the thalamus and cerebral cortex, enabling you to describe, for instance, the position of your limb. The unconscious pathway connects with the cerebellum (the cerebellum is considered an unconscious organ) as the spinocerebellar pathway

Posterior Spinocerebellar Tract
Fig. 17 The spinocerebellar and corticospinal tracts. S., superior cerebellar peduncle; M., middle cerebellar peduncle; I., inferior cerebellar peduncle. UMN, upper motor neuron; LMN, lower motor neuron.

and enables you to walk and perform other complex acts subconsciously without having to think which joints are flexed and extended (Fig. 17). (In this book where it is stated that a patient presents with "proprioceptive loss," this refers to loss of conscious proprioceptive sensation, as tested by asking the patient to describe the position of a limb.)

Unlike the other sensory pathways, which cross contralaterally, the spinocerebellar primarily remains ipsilateral. In general, one side of the cerebellum connects with the same side of the body. Thus cerebellar lesions tend to produce ipsilateral malfunctioning, whereas cerebral lesions result in contralateral defects.

There are three main connections between the cerebellum and the brain stem—the superior, middle and inferior cerebellar peduncles, which connect with the midbrain, pons, and medulla, respectively. The spinocerebellar pathways enter the cerebellum via the superior and inferior peduncles (Fig. 17).

The motor (corticospinal) pathway is relatively simple. It extends from the motor area of the cerebral cortex down through the brain stem, crossing over at approximately the same level as the medial lemniscus (at the junction between brain stem and spinal cord), (Figs. 15,17). (There is an uncrossed component that will not concern us here.)

The corticospinal pathway synapses in the anterior horn (motor grey matter) of the spinal cord just prior to leaving the cord. This is important, for motor neurons above the level of this synapse (connecting the cerebral cortex and anterior horn) are termed upper motor neurons (UMN), whereas those beyond this level (the peripheral nerve neurons) are termed lower motor neurons (LMN). These terms are actually somewhat misleading and probably would better have been phrased as first order motor neurons (UMN) and second order motor neurons (LMN), as either of these categories may have axons that lie in the upper or lower part of the body. Upper and lower motor neuron injuries result in different clinical signs. Although both result in paralysis, they differ as follows:

Upper MN Defect spastic paralysis no significant muscle atrophy fasciculations and fibrillations not present hyperreflexia

Babinski reflex may be present

Lower MN Defect flaccid paralysis significant atrophy fasciculations and fibrillations present hyporeflexia

Babinski reflex not present

Cross Sectional Location of the Pathways

Figure 14 illustrates the position of the sensory and motor pathways in cross section.

For unknown reasons various disease processes affect different portions of the spinal cord. Amyotrophic lateral sclerosis (Fig. 18A) is characterized by a combination of upper and lower motor neuron signs—muscle weakness, atrophy, fibrillations, and fasciculations combined with hyperreflexia. The lesion involves both the anterior horns (motor) of the grey matter (causing a lower motor neuron lesion) as well as the corticospinal tracts (resulting in an upper motor neuron lesion).

Tertiary syphilis (tabes dorsalis) includes propioceptive loss and pain (posterior root irritation), particularly affecting the lower extremities. The lesion involves the posterior columns of white matter (Fig. 18B) and may extend to the posterior roots and root ganglia.

In pernicious anemia (Fig. 18C), there is proprioceptive loss and upper motor neuron weakness. The lesion involves the posterior columns and corticospinal tracts.

Polio attackes the anterior horn cells (Fig. 18D) leading to lower motor neuron involvement, with weakness, atrophy, fasciculations, fibrillations, and hyporeflexia.

Patients with Guillain-Barre syndrome (Fig. 18E) experience sensory and lower motor neuron loss because of peripheral nerve involvement.

Certain muscle groups may be affected more than others in an upper motor neuron lesion. In the typical cerebral hemisphere stroke secondary to carotid artery occlusion, the patient develops decorticate posturing, characterized by flexion of the wrist and elbow and extension (straightening) of the

ANTERIOR WHITE C0MM3SURE (Crowing poln-1»mp. titer«)

Fig. 18 Lesions sites in classical diseases. A. Amyotrophic lateral sclerosis (Lou Gehrig's disease). B. Tertiary syphilis. C. Pernicious anemia. D. Polio. E. Guillain-Barre. F. Syringomyelia.

Pernicious Syphilis

ANTERIOR WHITE C0MM3SURE (Crowing poln-1»mp. titer«)

Fig. 18 Lesions sites in classical diseases. A. Amyotrophic lateral sclerosis (Lou Gehrig's disease). B. Tertiary syphilis. C. Pernicious anemia. D. Polio. E. Guillain-Barre. F. Syringomyelia.

ankle and knee. In midbrain strokes, the posturing is similar, except that the elbow is extended (decerebrate posturing). The mechanisms apparently involve injury to other motor pathways (extrapyramidal) outside the corticospinal (pyramidal) system. "Pure" lesions of the corticospinal tract result predominantly in difficulty with skilled movements of the distal aspect of the extremities.

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