Module 28 - Spinal Cord and Brainstem Lesion Flashcards
What are some important differences between upper and lower motor neuron lesions?
- There are characteristic differences between upper and lower motor neuron lesions.
- Upper motor neuron lesions produce contralateral loss of function (when the lesion is above the pyramidal decussation) and ipsilateral loss of function (when the lesion is below the decussation).
- Upper motor neuron lesions produce spastic or rigid paralysis. Lower motor neuron lesions lead to flaccid paralysis.
- Deep tendon reflexes are increased after upper motor neuron lesions but are absent in the case of lower motor neuron lesions.
- In the case of UMN lesions, an abnormal reflex can appear – the Babinski sign.
- Muscle atrophy is less, or develops slowly, in the case of UMN lesions but faster and severe in the case of LMN lesions.
- Lastly, muscle fasciculations and fibrillations only occur in the case of LMN lesions.
Why do UMN lesions produce spastic or rigid paralysis?
LMNs are usually under the control of UMNs, limiting the impact of reflexes. When this control is lost, by an UMN lesion, the influence of reflexes increases. This is why UMN lesions produce spastic or rigid paralysis; even though a limb can be unresponsive, when moved externally (e.g. during physical exam) the limbs feels rigid and moves in a jerky manner and deep tendon reflexes are enhanced. This is because as the limb moves, proprioceptors are activated producing reflex responses in the spinal cord, pathways unaffected by the UMN lesion.
What happens to reflexes with a LMN lesion?
In the case of a LMN lesion, the innervation to the muscle is lost, so even reflex activity is lost. This can also lead to the Babinski sign – where stimulation of the sole of the foot produces an extensor plantar response rather than the normal plantar response.
Why does atrophy happen with LMN syndrome?
Muscles receive trophic factors from LMNs. Loss of LMNs therefore leads to atrophy (muscle wasting).
True or false: Fasciculations and fibrillations are present with UMN lesions?
FALSE = Damaged LMNs can become spontaneously active, producing fasciculations (muscle twitches that are visible) or, when damage is severe, fibrillations (individual muscle fibre contractions, detected by electrophysiology).
What is the difference between fasciculations and fibrillations?
Damaged LMNs can become spontaneously active, producing fasciculations (muscle twitches that are visible) or, when damage is severe, fibrillations (individual muscle fibre contractions, detected by electrophysiology).
Where does the blood supply come from for the primary motor cortex?
- Loss of blood supply is a common cause of upper motor neuron lesions.
- The blood supply to the primary motor cortex comes from the middle and anterior cerebral arteries.
Most of the primary motor and somatosensory area is supplied by the ________ cerebral artery.
Most of the primary motor and somatosensory area is supplied by the middle cerebral artery.
The region of the primary motor and somatosensory area related to the lower limb is supplied by the __________ cerebral artery.
The region of the primary motor and somatosensory area related to the lower limb is supplied by the anterior cerebral artery.
The blood supply to the internal capsule by the _____________branches of the middle cerebral artery.
Note also the importance of the blood supply to the internal capsule by the lenticulostriate branches of the middle cerebral artery.
An ischemic stroke affecting even a small region can produce significant loss of motor and sensory function by damaging axons passing through the ________ capsule. Note that the middle cerebral artery is more or less contiguous with the internal carotid. Therefore, an embolus that travels through the carotid system is likely to pass into the middle cerebral artery: about ________ of all ischemic strokes occurs in the middle cerebral artery territory.
- An ischemic stroke affecting even a small region can produce significant loss of motor and sensory function by damaging axons passing through the internal capsule.
- Note that the middle cerebral artery is more or less contiguous with the internal carotid.
- Therefore, an embolus that travels through the carotid system is likely to pass into the middle cerebral artery: about two-thirds of all ischemic strokes occurs in the middle cerebral artery territory.
There are two sources of blood supply to the spinal cord: superiorly, from the _____________; posteriorly, from ______________(off aorta). Both give rise to distinct (paired) posterior and (single) anterior spinal arteries.
There are two sources of blood supply to the spinal cord: superiorly, from the vertebral arteries; posteriorly, from segmental arteries (off aorta). Both give rise to distinct (paired) posterior and (single) anterior spinal artery
Why is it clinically significant if the blockage of a spinal artery happens in the anterior or posterior spinal artery?
- This is clinically significant because it means that blockage of the anterior spinal artery (or branches thereof) would tend to lead damage to the anterior/lateral white matter and anterior gray matter; blockage of posterior spinal arteries tend to lead to damage of posterior white and gray matter.
What are the key spinal cord structures?
- The posterior columns, white matter carrying discriminative touch and conscious proprioception
- The lateral corticospinal tract, white matter carrying axons from UMNs that target anterior horn cells
- The spinothalamic tract, white matter carrying pain and temperature information that crosses at the anterior white commissure
*RECALL for the Horner’s syndrome:
Recall that the sympathetic nervous system arises from pre-ganglionic neurons in the lateral horn of spinal cord levels T1-L2/L3…
…and that the preganglionic sympathetic neurons are influenced by descending projections from the hypothalamus (hypothalamospinal tract) located in the lateral funiculus.
IMAGE
Transverse Cord Lesion at a single level of the spinal cord
- All the key white matter tracts are affected on both sides of the cord.
- Loss of function and associated structures that are affected
- Bilateral loss of motor function → damage to lateral corticospinal tracts
- Bilateral loss of somatosensation → damage to posterior columns and spinothalamic tracts
- This loss is depicted by the color coded regions on the image of a person showing loss of motor (red), pain and temperature (green) and touch (blue).
Brown-Séquard syndrome - Hemicord lesions at a single level of the spinal cord
- There will be ipsilateral loss of motor function → due to loss of the lateral corticospinal tract on one side
- Ipsilateral UMN lesion signs
- There will be ipsilateral loss of touch and proprioception → due to loss of the posterior columns
- There will be contralateral loss of pain and temperature → loss of the spinothalamic tract on one side.
- *NOTE
- Because of Lissauer’s tract (spans a few levels in the spinal cord), loss of pain and temperature sensation may not match exactly the level of the lesion.
- Whereas loss of discriminative touch does match the level of the lesion.
- Recall that Lissauer’s (posterolateral) tract allows pain and temperature afferents to travel up or down 1-3 segments, synapsing on posterior horn cells above and below.
- For example, a hemi-lesion at the L4 spinal cord level could spare the L4 dermatome (afferents have travelled up to L3 or even L2 spinal cord level via Lissauer’s tract before crossing).
- Again the loss is depicted by the color-coded regions on the image of a person showing loss of motor (red), pain and temperature (green), and touch (blue). Imagine how strange It must be to have muscle weakness and loss of touch on one side and loss of pain and temperature sensation on the other side!
Central cord lesion (small affecting multiple levels of the spinal cord
- This lesion affects multiple levels of the spinal cord.
- Bilateral loss of pain and temperature over the dermatomes that correspond to the range of spinal cord levels affected.
- The example provided shows the classic “cape distribution” loss of pain and temperature sensation, as seen with small central cord lesions affecting cervical spinal cord (C4-C6).
Damage to what structure explains the bilateral loss of pain and temperature sensation?
Anterior white commissure
What other white matter tract would be affected given the lesion indicated?
Looks like some damage to the posterior columns; some loss of discriminative touch and proprioception
Posterior cord syndrome (at a single level of the cord)
- Loss of posterior spinal artery blood supply to the spinal cord can lead to posterior cord syndrome.
- This would lead to bilateral loss of touch and position sense below the level of the lesion (posterior columns).
Anterior Cord Syndrome (at a single level of the cord)
- Loss of anterior spinal artery supply can lead to anterior cord syndrome.
- This leads to bilateral loss of motor function → lateral corticospinal tract
Bilateral loss of pain and temperature sense → spinothalamic tract = below the level of the lesion.
Horner’s Syndrome
- Lesions of the lateral funiculus at L2/L3 and above will damage the hypothalamospinal tract, resulting in loss of sympathetic function. This leads to a condition called Horner’s Syndrome.
- Unilateral lesions produce ipsilateral loss of function!!!
- Key features of Horner’s syndrome include:
- Anhydrosis = decreased sweating; due to loss of innervation of sweat glands in skin (head and body)
- Miosis = constricted pupil; due to loss of innervation of pupil dilator muscle (parasympathetic- driven constrictor dominates)
- Partial ptosis = a weak, droopy eyelid; due to loss of innervation of the superior tarsal muscle (a smooth muscle adjoining the levator palpebrae superioris muscle that helps to raise the upper eyelid)
Damage to the lateral funiculus above S2-S4
- Damage to the lateral funiculus above S2-S4 will lead to loss of sacral parasympathetic outflow that drives pelvic parasympathetics.
- This can lead to loss of function:
- Urinary incontinence – lack of voluntary control over bladder emptying (normally drives detrusor muscle and inhibits internal urethral sphincter)
- Bowel incontinence – loss of control of internal anal sphincter
- Constipation – reduced motility in the distal 1/3 of the large intestine
- Loss of sexual function (e.g. erection).
