A 56-year-old man presented to the emergency department for evaluation of chest pain radiating to the back. He was diagnosed with a type A aortic dissection and proceeded to the operating room for emergent open repair. Following the procedure, the patient is brought to the post-operative care unit for further monitoring. During the patient’s postoperative assessment, he reports thoracic back pain and an inability to move the bilateral lower extremities. The patient's temperature is 98.6.0 °C (37 C °F), pulse is 30/min, respirations are 24/min, blood pressure is 195/95 mmHg, and O 2 saturation is 97% on room air. Pinprick testing demonstrates bilateral loss of pain sensation below the xiphoid process. The patient has preserved proprioception, vibratory sense, fine touch, and two-point discrimination. Which of the following best describes the underlying etiology of this patient’s clinical presentation?

The spinal cord is made up of millions of neurons whose axons and cell bodies are constantly transmitting information between our brain and the rest of our body.

In doing. So, the spinal cord acts as an amazing information highway allowing our brain and body to work together to interact with the world around us.

But what happens when this information highway is disrupted or damaged? Well, injury to the spinal cord leads to a variety of classic clinical conditions with predictable deficits which we will explore in this video.

So let's get to it. Ok.

Spinal cord pathways0:35–2:18

Before we move on to spinal cord injuries, let's freshen up our knowledge of the spinal cord itself. Zooming in on a cross section of the spinal cord.

You'll see it's made up of both gray and white matter. Gray matter is found in the center of the spinal cord and has two dorsal or posterior horns that contain sensory neuron cell bodies and two ventral or anterior horns that contain motor neuron cell bodies surrounding the gray matter is white matter which consists of the axons of various neurons.

They are organized into tracts that carry information to and from the brain. There are four main sensory pathways ascending the spinal column.

First, there's a spinothalamic tract which is divided into two parts. The lateral tract carries sensory information for pain and temperature.

While the anterior tract carries information for crude touch and pressure. Next, there are two dorsal column tracks.

The fasciculus gracilis, which carries sensory information from the lower trunk and legs. And the fasciculus cuneatus which carries sensory information from the upper trunk and arms.

These tracts both carry sensations such as two point discrimination, vibration, fine touch and proprioception. Then there's a spino cerebellar tract which has an anterior and posterior part.

These are ascending pathways from the spinal cord to the cerebellum and carry proprioceptive information from the body. Finally, the major motor pathways descending down the spinal column are the anterior and lateral corticospinal tracts which are descending tracts that allow us voluntary movement of the limbs.

Spinal cord compression and transection2:18–4:01

Spinal cord injuries can happen because of a number of different causes. First, the spinal cord can undergo compression or increased pressure such as from a protruding intervertebral disc or osteophytes.

And this can produce sensory and motor symptoms in the area innervated by that particular spinal segment. In more severe cases, the spinal cord may undergo transection leading to the loss of all sensation and voluntary movement inferior to the site of the lesion.

Let's take a closer look at the effects of spinal cord transection. The higher the level the transection occurs at the more function is lost if transection happens between C one and C three, then there's no function below the level of the head and the ventilator is needed to maintain respiration.

If transection happens between C four and C five, then the individual will suffer quadriplegia, meaning they have no function of their upper and lower limbs or trunk.

However, they can still breathe on their own. Since the phrenic nerve is spared.

If transection happens between C six and C eight, then there's still a complete loss of trunk and lower limb function. However, some movements of the upper limb will still be intact allowing for functions such as feeding or using a wheelchair.

If transection happens between T one and T nine, the individual becomes paraplegic. So there's paralysis of both lower limbs.

While upper limb function remains intact. In this case, the amount of trunk control varies with the height of the lesion, meaning the higher the lesion, the more severe the deficits are, if transection happens anywhere between T 10 and L3, then there will be some level of dysfunction of the lower limbs resulting in difficulties with walking and ambulation.

Brown-Sequard syndrome4:01–7:32

Now, unlike a complete lesion of the spinal cord, which causes bilateral loss of function of the structures below the lesion.

A hemileia, which is the lesion to only one side of the spinal cord, also known as Brown Sequard syndrome will spare certain functions on each side of the body depending on the side of the lesion the most common cause is a penetrating trauma like a gunshot injury or stab wound in the back.

But a large spinal cord tumor can also lead to this syndrome. A complete hemisection would result in damage to multiple neural tracts while sparing others.

When we consider each tract, we have to think about what happens to that motor or sensory modality at the level of the lesion and below the level of the lesion, we also need to think about which side of the body will be affected.

Since the tracks cross over at different locations. For example, a complete hemisection on the right hand side would result in the following.

First, there'd be damage to the dorsal column on the right side which will lead to the loss of fine touch, two point discrimination, vibration and proprioception in the right side of the body, which is ipsilateral to the side of the lesion.

The loss of these sensory modalities would occur at the level of the injury and below it. Second, the anterior horn will be damaged resulting in a lower motor neuron lesion at that particular level.

Remember the lower motor neurons synapse with the upper motor neurons of the descending tracts such as the corticospinal tract damage to the anterior horn cells will lead to lower motor neuron signs such as ipsilateral flaccid paralysis and hypoactive deep tendon reflexes at the specific spinal level of the lesion.

Third, damage to the lateral corticospinal tract passing through that spinal level results in upper motor neuron signs on the ipsilateral side of the lesion below the level of the lesion.

These signs include things such as spastic paralysis, hyperactive deep tendon reflexes and a positive babinski reflex. Finally, there's damage to the spinothalamic tract.

The spinothalamic tract is a bit different though, because fibers of the anterior tract which carries crude touch and pressure will actually ascend one or two spinal segments above the level where the first order neurons enter and then cross over to the opposite side of the spinal cord.

In contrast, the fibers of the lateral tract which carry pain and temperature cross over right away. So, since these fibers all cross over within the spinal cord, a hemileia on the right side of the spinal cord will cause loss of these sensory modalities.

On the left side, the level that's affected though will change a bit. This means on the contralateral side, 1 to 2 levels, starting below the lesion, there is a loss of crude touch and pressure due to anterior tract damage and at the level of the lesion and below, there's loss of pain and temperature due to lateral tract damage.

Furthermore, on the ipsilateral side of the lesion, the lateral spinothalamic tract which synapse at that level and the anterior spinothalamic tract fibers that have not crossed yet will both be damaged.

So at the level of the lesion on the ipsilateral side, there will be complete loss of all sensory sensation. But starting 1 to 2 levels below the lesion, there is a complete sparing of crude touch, pressure, pain and temperature to sum up during a hemisection.

Brown-Sequard syndrome summary7:32–8:29

On the ipsilateral side of the lesion, there will be one at the level of the lesion, loss of all sensory sensation. Two below the lesion, complete loss of fine touch, two point discrimination vibration and proprioception where 1 to 2 levels starting below the lesion, there is complete sparing of crude touch, pressure, pain and temperature.

Three, there will be lower motor neuron signs such as flaccid paralysis at the level of the lesion. Four, upper motor neuron signs below the level of the lesion and five on the contralateral side at the level of the lesion.

And below there's loss of pain and temperature where 1 to 2 levels starting below the lesion, there's loss of crude touch and pressure of note, hemisection at T 1 may result in ipsilateral Horner syndrome.

Alternatively, damage to the spinal cord can also be a result of ischemia. Now remember that the spinal cord gets its blood supply from branches of the vertebral, ascending cervical deep cervical intercostal lumbar and lateral sacral arteries.

Ischemia8:29–10:45

One of the major arteries supplying the spinal cord is the anterior spinal artery, which is formed by branches of the vertebral arteries running longitudinally down and supplying the anterior two thirds of the spinal cord with the posterior one third of the spinal cord being supplied by the posterior spinal arteries, occlusion of the anterior spinal artery can be iatrogenic such as during surgery for aortic aneurysm repair.

Or it may also occur as a complication of trauma, aortic dissection, thrombosis, embolism, vasculitis, and severe hypotension.

Normally above the level of T eight. The anterior spinal artery arises from branches of the vertebral arteries.

While below the level of T eight, it's mainly supplied by the artery of avic, which is a branch of the aorta. This means the area below the level of T eight is particularly vulnerable during aneurysm repair.

As a result, anterior spinal artery occlusion can result in anterior cord syndrome. This is characterized by three aspects.

First, there's damage to the anterior horn causing lower motor neuron injury at the level of the lesion which results in muscle paralysis and atrophy.

Second, there's damage to the lateral corticospinal tracts which result in paralysis below the lesion and subsequent upper motor neuron signs such as spasticity and hyperreflexia over a few days to weeks.

And third, there's damage to the spinothalamic tract on both sides of the cord which results in bilateral loss of pain, temperature, crude touch and pressure below the level lesion bear in mind though that this does not affect the dorsal columns as they are supplied by the posterior spinal arteries.

So, fine touch, two point discrimination, vibration and proprioception will be spared if you need a breather. After all that you're in luck.

Quiz10:45–11:01

So, can you identify the ascending and descending spinal tracts on this image up. Next, let's talk about some other conditions that can affect the ascending and descending tracts of the spinal cord.

Syringomyelia11:01–12:40

First, there's Syringomyelia a lesion of the central spinal cord. This is a cystic cavity or syrinx within the central canal of the spinal cord which contains cerebrospinal fluid that gradually expands the cause of Syringomyelia isn't well understood, but it is most commonly associated with a congenital condition called chiari malformation.

Type one, some acquired conditions that can cause Syringomyelia are things like spinal cord tumors or trauma. Normally, cerebrospinal fluid would flow through the four ventricles of the brain.

And after the fourth ventricle, the fluid either flows into the subarachnoid space or moves down into the central canal.

In chiari malformations, cerebellar displacements of structures such as the cerebellar tonsils occurs and blocks these openings.

The expanding cyst in Syringomyelia usually causes compression of the anterior white commissure. First.

This is where the fibers of the spinothalamic tract cross over on their way to bringing sensory information to the brain.

Symptoms of this compression would result in bilateral symmetrical loss of pain and temperature sensation depending on the spinal cord level.

The compression is at certain dermatomes will be affected. It's more likely to affect the upper extremities but can occur anywhere if the cyst expands further, it can compress the ventral horns.

This can result in flaccid paralysis of muscles innervated by that spinal cord level as the synapses of the lower motor neurons are affected.

Next up, there's tabes dorsalis which is caused by tertiary syphilis. With tabes dorsalis, there's demyelination and degeneration of the dorsal columns and dorsal roots of the spinal cord.

Tabes dorsalis12:40–13:29

Typically tabes dorsalis results in a loss of the sensations of two point discrimination, vibrations, fine touch and proprioception.

Without the sensations of vibration and proprioception, the individual will often stumble in the dark and have difficulty in coordination while walking, also known as sensory ataxia.

Another telltale sign is a positive Romberg sign which is a test of proprioception where the person stands with their feet, close together, arms to the sides and the eyes closed, which results in unsteadiness.

The dorsal columns can also be affected by vitamin b12 or cobalamin deficiency, which can result from autoimmune gastritis, tapeworms or prolonged vegan diets with no B12 supplementation and results in neurological dysfunction called subacute combined degeneration or SCD.

Subacute combined degeneration13:29–14:33

The main sites of involvement are the spinocerebellar tract resulting in ataxia and recurrent falls. The lateral corticospinal tracts causing spastic paralysis, increased, deep tended reflexes and the babinski reflex and the dorsal columns causing loss of position and vibration sensation and sensory ataxia, which can lead to a positive Romberg sign.

Patients may also develop a smooth erythematous, shiny tongue referred to as atrophic glossitis. A good way to remember that is by thinking of SCD as spinocerebellar corticospinal and dorsal columns.

Amyotrophic lateral sclerosis14:33–15:06

Then there's amyotrophic lateral sclerosis or a SS which is a motor neuron disorder that affects both the upper and lower motor neurons of the corticospinal and corticobulbar pathways throughout the body.

This can result in upper motor neuron signs such as spastic paralysis. With hyperactive deep tendon reflexes and positive babinski sign.

The medulla and spinal cord also undergo degeneration causing lower motor neuron signs such as muscle atrophy, hypoactive deep tendon reflexes and fasciculations.

Review15:06–16:17

Ok. Now, for a quick recap, spinal cord injuries can be caused by compression or pressure of spinal nerve root ischemia or transection.

There can be complete transection of the spinal cord as well as a hemisection of the spinal cord, which results in brown sequard syndrome.

Anterior cord syndrome occurs with a loss of blood supply from the anterior spinal artery affecting the anterior two thirds of the spinal cord.

With central cord lesion, specifically Syringomyelia fluid builds up within the central canal causing compression of the anterior white commissure of the spinothalamic tract with tes dorsalis caused by tertiary syphilis.

There's demyelination and degeneration of the dorsal columns and dorsal roots of the spinal cord resulting in a loss of the sensations of two point discrimination, vibrations, fine touch and proprioception.

With vitamin b12 deficiency. There can be subacute combined degeneration involving the spinocerebellar tract.

The corticospinal tracts and the dorsal columns with a s both the upper and lower motor neurons of the corticospinal and corticobulbar pathways are affected