A Classical Syndrome
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The syndromes of the spinal cord can be grouped into three classes: pure motor, pure sensory, and combined motor and sensory syndromes. The Brown-Sequard syndrome, which was described right here in the good old USA at the Medical College of Virginia/Virginia Commonwealth University, by Dr. Sequard Brown (who would later amend his name to Brown-Sequard in honor of his mother), is one clinical entity that is classified under combined motor and sensory syndromes. This implies that it is characterized by both motor and sensory deficits (because motor as well as sensory tracts are affected).
The lesion is a hemisection of the spinal cord, which commonly results from trauma, particularly from motor vehicle accidents. Though it is very rare in clinical practice, it serves as a perfect review for spinal cord functions and is highly regarded because of its utility in the teaching of the principle of lesion localization.
It affects the corticospinal, spinothalamic and the posterior column tracts, along with the anterior horn cells, on one side. The Table below summarizes the most important structures affected and the corresponding symptoms:
|Ipsilateral upper motor neuron symptoms (spastic hemiparesis, Babinski sign) below the lesion
|Ipsilateral lower motor neuron symptoms (flaccid paralysis)
|Ipsilateral loss of proprioceptive and discriminatory sensation
|Hypothalamospinal tract transection rostral to T2
|Horner syndrome (ptosis, miosis and anhidrosis)
|Lateral spinothalamic tract
|Contralateral loss of pain and temperature
Imagine a patient who has sustained a left-sided hemisection (such as shown in the illustration below):
Figure 1. Localization of clinical deficits in Brown-Sequard syndrome; sensory deficits are in color.
The corticospinal tract and dorsal column signs and symptoms are on the left and the spinothalamic deficits are on the right. Recall that the corticospinal tract and dorsal column pathway cross at the caudal medulla; therefore, a lesion of them below the decussation produces ipsilateral symptoms related to these tracts. However, because the lateral spinothalamic tract crosses in the spinal cord, the deficits related to this tract (i.e., anesthesia) is contralateral.
This is illustrated with the image below:
Figure 2. A simplistic schematic showing a left spinal cord hemisection producing Brown-Sequard syndrome. The direction of impulse conduction is indicated by the arrows and the lesion is indicated by the dark black line. The descending lateral corticospinal tract is shown in blue, the ascending lateral spinothalamic tract in green and the ascending dorsal column-medial lemniscus (DCML) pathway in red. Signs related to the corticospinal tract and the DCML are on the left side (ipsilateral) because the lesion is below the medullary crossing point. However, spinothalamic sensory signs are contralateral (on the right) because the spinothalamic tract crosses in the spinal cord. Lesions of this tract on the left side of the cord prevent conduction of pain and temperature information from the right side of the body from being transmitted to the somatosensory cortex.
Now, herewith an explanation of the illustration you just saw. If you follow the direction of impulse conduction of the three pathways (i.e., from the origin to the destination), you will understand the following:
Because the descending corticospinal tract crosses in the medulla, a lesion of this tract in the spinal cord results in ipsilateral upper moto neuron (UMN) deficits below the level of the lesion.
Also, because the ascending dorsal column tract crosses at the medulla, a lesion in the spinal cord results in ipsilateral loss of dorsal column modalities (proprioception, discriminative and vibratory sensation) below the level of the lesion.
However, a lesion of the ascending lateral spinothalamic tract results in contralateral loss of pain and temperature below the level of the lesion because this tract crosses inside the spinal cord as it takes off. This means that, had it not been for the early crossing of the spinothalamic tract in the spinal cord, all findings in spinal cord hemisection would have been ipsilateral below the level of the lesion. Conversely, had all three tracts crossed in the lower medulla, all spinal cord lesions of these tracts would have produced ipsilateral deficits, and a lesion at the medulla or above would have produced contralateral deficits.
Above the medulla, a lesion of these tracts results in contralateral deficits because, at this point, all three have crossed. Thus, the issue becomes simplified in the brain stem and above because, at that level, lesions of all the tracts are contralateral. This is why Brown-Sequard is so useful in the teaching or understanding of lesion localization.
Also, keep in mind that, because the descending hypothalamospinal axons that innervate the intermediolateral cell column end in the spinal cord at the T1-T2 spinal roots level, any hemisection of the spinal cord rostral to T2 level will present with Horner syndrome (ptosis, miosis and anhidrosis).
The figure below depicts clinical deficits resulting from lesions of tracts and structures of the spinal cord. Now, our question of the day is, which disease causes the findings in this picture? Which structure(s) is/are affected in this syndrome?
Figure 3. Another classic spinal cord syndrome. Can you name it?
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