Recognizing key spinal cord syndromes

If your patient complains that she can't feel the hot water landing on her shoulders in the shower, would you know how to identify the lesion causing that symptom? In this video, from our Clinical Neurology Essentials course, you'll learn about the four key syndromes of spinal cord injury presentations and the little clues you should look for to help you recognize and localize a spinal cord pathology.

Confidently choose and perform the most appropriate neurologic examination for any patient! With our Clinical Neurology Essentials course, you'll learn and master basic and advanced examination skills, neuroanatomy, and the art of asking the right questions, so that you can interpret examination findings and localize pathologies with ease. Don't forget to register for a free trial account to access Chapter 1 of this course, now!

[00:00:00] There are a number of spinal cord syndromes which can occur in addition to the anterior and posterior artery syndromes discussed in the last lesson. Small central lesions might affect centrally crossing fibers of the spinothalamic tract. In these cases, there is loss of pain and temperature sensibility in affected dermatomes with preserved vibration and proprioception. This is

[00:00:30] known as dissociated sensory loss. This pattern of dissociated sensory loss is often seen with cervical cord syrinx. We previously encountered this pathology which is due to an enlargement of the central canal of the cord that fills with fluid and compresses tissues in the center of the cord. Patients may complain of being unable to feel the temperature of hot water in a shower on their shoulders. In large central cord

[00:01:00] lesions, there is loss of pain and temperature sensibility but there can also be loss of adjacent tracts and gray matter. At the segment involved, there are lower motor neuron signs due to anterior horn cell damage. Below that level, there is upper motor neuron damage due to damage of the corticospinal tracts. With some central core lesions because of this somatotopic patterns of sensory fibers, the sensory loss pattern might produce clinical phenomena

[00:01:30] of sparing sacral fibers from sensory loss. In contrast, lesions or masses externally compressing the cord seen for instance with spinal metastases often involve sacral spinothalamic tract fibers producing sacral anesthesia. This can be an important clue to extra-axial lesions or those outside of the cord versus intra-axial lesions or those inside the spinal cord.

[00:02:00] Lesions that produce large central cord syndrome are commonly seen with multiple sclerosis or tumors of the cord, such as Astrocytomas. Complete hemisection of the spinal cord produces what is known as Brow-Sequard's syndrome. The segment bearing the lesion shows lower motor neuron changes from damage to anterior horn cells. Below that segment, there is ipsilateral upper motor neuron paresis from damage to the

[00:02:30] lateral corticospinal tract. There is ipsilateral loss of proprioception, vibration and two-point discrimination below the lesion due to posterior column damage since these fibers do not cross into reaching the brainstem. There is ipsilateral anesthesia in sensory distribution of that segment due to involvement of fibers which enter the segment but have not yet crossed. Pain and temperature loss below the level of lesion

[00:03:00] is contralateral. Though pure hemi lesions are rare, understanding the ramifications will help with localization. This type of injury can be sustained with gunshot wounds, other penetrating injuries, tumors or hemorrhages. When complete cord transection occurs, total loss of sensation and motor control are seen below the level of the lesion. Lower motor neuron changes occur at the level of the lesion,

[00:03:30] and upper motor neuron changes are seen below. Early on after the injury, there is spinal shock and total flaccidity. Bowel and bladder control is lost, respiratory dysfunction occurs if the lesion is above C5 because of injury to the phrenic nerve which arises from C3 through C5 and innervates the diaphragm. Complete transection of the cord is most often seen at the major trauma but can also

[00:04:00] result from a penetrating injury, transverse myelitis, or tumors, or hemorrhages that cause compression of the cord. In combined degeneration which is previously referred to as posterolateral column syndrome, we see damage of the posterior columns and the lateral corticospinal tracts. Signs include the loss of proprioception and vibration sensation, as well as loss of motor function below the level of the

[00:04:30] lesion where we see in upper motor neuron picture. Because the spinothalamic tract is not affected, pain and temperature sensibility will be normal. Combined degeneration can occur acutely such as when someone abuses nitrous oxide or gradually due to absorption issues from pernicious anemia, copper deficiency also causes this rarely. Damage usually is reversible if treated early.

[00:05:00] In tabes dorsalis damage occurs in the large posterior route fibers destined for the posterior columns. The damage is often symmetrical affects most often the legs and is seen as loss of proprioception with sensory ataxia, deep pain and touch sensation can be involved as well, reflexes are lost, and hypotonia is seen due to loss of these fibers. The syndrome is characterized by lightning-like pain in the

[00:05:30] legs. Tabes dorsalis is most commonly caused by tertiary syphilis.