Anatomy clinical correlates: Spinal cord pathways

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Anatomy clinical correlates: Spinal cord pathways

M1 Beweging

M1 Beweging

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Transcript

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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!

Okay, 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, it’s made up of both grey and white matter.

Grey matter is found in the centre 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 grey 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 the 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 tracts: 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 the spinocerebellar 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 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 disk 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 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 C1 and C3, then there’s no function below the level of the head and a ventilator is needed to maintain respiration.

If transection happens between C4 and C5 then the individual will suffer quadriplegia, meaning they have no function of their upper and lower limbs or trunk, however they can still breath on their own since the phrenic nerve is spared.

If transection happens between C6 and C8, then there’s still a complete loss of trunk and lower limb function, however some movements of the upper limb will be intact, allowing for functions such as feeding or using a wheelchair.

If transection happens between T1 and T9, 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 T10 and L3, then there will be some level of dysfunction of the lower limbs resulting in difficulties with walking and ambulation.

Now, unlike a complete lesion of the spinal cord, which causes bilateral loss of function of the structures below the lesion, a hemilesion, which is a 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 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 tracts crossover 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 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 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 ascends 1 or 2 spinal segments above the level where the 1st 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, typically cross over right away.

So, since these fibres all cross over within the spinal cord, a hemilesion 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 1-2 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 is 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 1-2 levels below the lesion there is a complete sparing of crude touch, pressure, pain and temperature.

To sum up, during a hemi-section, on the ipsilateral side of the lesion, there will be 1) at the level of the lesion there is loss of all sensory sensation 2) Below the lesion complete loss of fine touch, two point discrimination, vibration, and proprioception, where 1-2 levels starting below the lesion there is complete sparing of crude touch, pressure, pain and temperature 3) there will be lower motor neuron signs such as flaccid paralysis at the level of the lesion 4) upper motor neuron signs below the level of the lesion, and 5) on the contralateral side, at the level of the lesion and below there is loss of pain and temperature where 1-2 levels starting below the lesion there is loss of crude touch and pressure.

Of note, hemisection at T1 may result in ipsilateral horner syndrome. Alternatively, damage to the spinal cord can also be a result of ischemia.

Sources

  1. "Human Biology and Health" Pearson Prentice Hall (1992)
  2. "Exploring Psychology" Worth Publishers (2009)
  3. "Encyclopedia of Human Genetics and Disease" ABC-CLIO (2012)
  4. "Central Pattern Generator for Locomotion: Anatomical, Physiological, and Pathophysiological Considerations" Frontiers in Neurology (2013)
  5. "A case of spinal cord decompression sickness presenting as partial Brown-Sequard syndrome" Neurology (1997)
  6. "DEATH BY DECAPITATION" The American Journal of the Medical Sciences (1889)
  7. "Stroke and dementia risk: A systematic review and meta‐analysis" Alzheimer's & Dementia (2018)
  8. "Neuropathic osteoarthropathy of the shoulder secondary to syringomyelia" Diagnostic and Interventional Imaging (2021)
  9. "Neurofilaments in motor neuron disorders: towards promising diagnostic and prognostic biomarkers" Molecular Neurodegeneration (2020)
  10. "Acute arterial occlusion" StatPearls Publishing (2021)