Defined as paralysis (no motor function) of one side of the body and can be indicative of upper motoneuron lesions. The most common cause however is a cerebrovascular accident (stroke).
Indicative of upper motoneuron corticospinal lesions, it is defined as weakness of the body on either the left or right side.
Fasciculation
This is where all of the muscles fibres a motor unit contract involuntarily and spontaneously, appearing as small ripples underneath the skin. It is caused by malfunctioning alpha motor neurones, which we rely on for voluntary movement, and is a sign of lower motoneuron lesions. [1][2]
Lower motoneuron associated terms:
Babinski Sign
(Extensor Plantar Reflex) This is a polysynaptic reflex whereby if the sole of the foot is stroked from heel to toe, the big toe dorsiflexes and the other toes fan outwards. This is normal in those up to 2 years of age. However, its presence in those older can be a sign of corticospinal (pyramidal) tract damage/lesions, either on one side or bilaterally. [3]
Clonus
Similar to fasciculation, except the contractions are much greater and often caused by a reflex, ranging from 3 to 7 Hz. The presence of a clonus (most commonly at the ankle) is an indicator of an upper motoneuron lesion/syndrome. [4][2]
Spasticity
(Muscular Hypertonicity) Muscles have increased tone and offer resistance/feel stiffer when moved. Deep tendon reflexes are exaggerated, such as the knee jerk reflex. Overall this is due to loss of inhibitory effects in the corticospinal pathway. [5]
OBJECTIVES
Describe the anatomy of the spinal cord.
Diagrams above [6]
To clarify, upper motoneurons are found within the spinal cord, while lower motoneurons branch off from the spinal cord and actually innervate the muscles.
Describe the function of the spinal cord tracts.
The ascending and descending tracts are located in the white matter of the spinal cord. Spinal nerves enter and exit via the grey matter. As you move down the spinal cord, the ratio of grey matter to white matter increases. The white matter houses myelinated axons, while the grey matter is home to the cell bodies and dendrites.
The corticospinal (pyramidal) tract is the descending tract made up of motor axons that deals with contralateral voluntary motor function. It decussates at the spinomedullary junction and originates from the primary motor cortex.
The dorsal column medial lemniscus pathway is an ascending tract that deals with ipsilateral sensations, including touch, vibration and proprioception, of the upper and lower limb. Input is from wide, myelinated axons (Aα and β afferents). The cuneate fasciculus for the arm is lateral to the gracile fasciculus for the leg. It crosses over in the medulla of the brainstem.
The spinothalamic tract is an ascending tract that deals with contralateral simple touch, temperature and pain. Input is from narrow, generally unmyelinated axons (Aδ and C fibres). These end at the dorsal horn, cross over at their spinal cord input level and then ascend to the thalamus.
The spinocerebellar tract is an ascending tract divided into two parts. The ventral part deals with proprioception for both legs. The dorsal part deals with ipsilateral proprioception. Its input is from Aα and β (Ia,Ib and II) afferents.[6]
What are the possible effects of damage to the spinal cord?
A lesion in a spinal nerve will result in loss of sensation to an individual dermatome, however lesions in peripheral nerves, will affect many dermatomes due to the "overlapping" nature of the peripheral nerves.
Lesions to the central core (syringomyelia) will cause bilateral loss of pain sensation and temperature discrimination.
Lesions to the entire spinal cord (transections) will naturally, result in complete bilateral loss of sensory and motor function.
Lesions to the spinothalamic tract will be identifiable by loss of pain, crude touch and temperature discrimination contralateral and below the level of the lesion.[6]
Lesions to either the left or right side of the spinal cord (hemisections) are known as Brown Sequard Syndrome. Patients with it present with ipsilateral hemiplegia and contralateral loss of pain sensation and temperature discrimination. Like the scenario, it is most often seen with cervical spine problems. It is rare that the spinal cord is perfectly hemisectioned. Often the lesions span various tracts on that side of the spinal cord, as visible with this patient.[7]
What tests are carried out?
Testing for pain involves a neurological pin, and pricking the patient multiple times around the test area to see if they feel the pain. A control is used in the form of the blunt end of the tool, as well as pricking the known unaffected parts of the body.
Testing for joint position sense / proprioception can be done by asking them to state whether their joint is flexed / extended while they are blindfolded.
Other tests include light touch, which can be tested for by stroking a piece of cotton wool over the desired area.
Temperature discrimination can be tested simply by dipping the patient's hands into either a bowl of warm or cold water. Note: doing so with warm water while they are asleep, will not result in them urinating unconsciously, bar the absence of bladder reflexes. (Credit: Mythbusters)
Vibration sensing involves tapping a tuning fork, placing the round base on the test area and asking them to tell you: (1) If they can feel it (2) When it stops vibrating. A time lapse in (2) may be indicative of pathology.[6]
Explain the symptoms.
The injury to the spinal cord, as it was above T6, sent him into immediate spinal (neurogenic) shock. This hyperpolarises the neurons below C5, as a result, he becomes areflexic and results in his inability to move skeletal muscles in his arms and legs. He also loses reflexes of the bladder, bowels and genitals, due to lack of stimulation to pre-ganglionic autonomic neurons. [8][2]
The burning in both arms is referred to as paraesthesia (pins and needles). This could be due to pressure on his arms, cutting off blood supply to the local nerves, spinal shock or nerve damage.
The left hemiplegia is caused by damage to the motor neurons in the ventral horn (ipsilateral flaccid paralysis... area on diagram), affecting limb and trunk muscles.
The right hemiparesis is caused by lesions to the corticospinal tract (ipsilateral spastic paresis).
Pain is dealt with by the spinothalamic tract, which crosses over at the specific spinal cord level, relevant to that dermatome. Hence lesion to the left spinothalamic tract at C5 to T1 will result in loss of pain sensation below the right shoulder.
The ASIA (American Spine Injury Association) scale is used to categorise the level of impairment one has from a spinal cord injury. [7]
Captain blue could be classified as C when he first enters the hospital as he has some, if weak, motor function to the arm. These movements are supplied from the C5-C8 spinal nerve levels, up to 3 levels below that of injury, and are therefore used in classification.
Overall I believe that Brown-Sequard syndrome best describes his symptoms given the locations of legion present.[9]
Was any treatment given to Captain Blue pre-surgery?
It is likely that he was given methylprednisolone - an anti-inflammatory glucocorticoid, to prevent further damage to the central nervous system. It is shown that its administration helps to improve future potential motor function of the patient. The recommended dose is 30 mg/kg IV, then an IV drip of 5.4 mg/kg/hr for 23 hours. [10]
Why were X-Rays Taken?
X-Rays meant the exact levels of damage to the spinal cord could be assessed and whether there were any bone fragments that presented a risk and how the spine would be adjusted in surgery. The overall aim is to reduce pressure on the spine and prevent further inflammation & damage.
Why was there an improvement in Captain Blue's condition?
The second paragraph describes the symptoms once the spinal shock has worn off.
More movement in the right arm and leg suggests recovery/repair of the left corticospinal tract, however not nearly enough to outgrow the Babinski sign still present on the left side.
Still no voluntary movement on the left side suggests recovery is very slow in the ventral horn. However some impulses are reaching the muscles, with the appearance of fasciculation of the left deltoid.
The presence of proprioception on both sides means that the dorsal column medial leminiscus and dorsal and ventral spinocerebellar tracts remained untouched by the lesion.
The absence of pain sensation on the areas mentioned is representative of the damage to the left spinothalamic tract from levels C5 and below.
What is the prognosis?
Captain Blue's recovery depends on how serious the injury is. For an injury at the C5 spinal level, it is possible that after much rehabilitation, he may regain functionality at a couple of spinal levels below, allowing him greater range of movement and more sensation in his arms.
This would include many members of a multi disciplinary team, such as physiotherapists, occupational health workers, nurse, psychologist, spinal cord specialist etc. He would be encouraged to be as independent as possible, requiring less nurse help over time and be able to eat/shave/brush his teeth by himself. It is possible that he will require a wheelchair. This will give him more mobility and thus more confidence, reducing the risk of depression that is so common when people's livelihoods are taken from them. The physiotherapists will also help prevent atrophy of workable muscles and try and build up strength in the weaker, yet still functioning muscles. Much like stroke recovery, tasks will progress from simple getting in and out of chairs to walking aided and then unaided.
He may be taking medication that will aid to reduce any pain he may be experiencing and to reduce the severity of clonuses and fasciculation, as well as to help with normal bladder and bowel function.
The one year mortality rate for (isolated) spinal cord injury is roughly 6%. At ten years this becomes around 80%. Of course this depends on age at time of injury. [11]
Captain Blue was also born in 2035, so perhaps there may be advances in spinal cord injury treatment by the time of incident. [12] Perhaps he will receive implants/use machines that can read his thoughts and translate them into movements of limbs that have lost their neural connections.
However, should any further recovery occur, it will be within the next five months. As of yet the CNS cannot fully recover as chemicals surround the axons in the CNS which inhibit growth and repair, unlike the PNS in which there are many neurotrophic factors that aid recovery of the nervous system. As is visible in the diagram, damage to the spinal cord results in formation of scar tissue, of which neurons are unable to pass through and unable to re-route themselves around any kind of lesion.
Diagram of spinal cord damage & repair [13]
1807 words
