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.
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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).
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.
Lesions to spinocerebellar tracts
- Lesions of the spinocerebellar tracts (lateral funiculus) present with loss of muscle coordination (ataxia).
- However, the spinocerebellar pathways are unlikely to be damaged in isolation – there is likely to be additional injury to the descending motor tracts. This will cause muscle weakness or paralysis, and usually masks the loss of muscle coordination.
- Ataxia = loss of muscle coordination
Effects of Upper and Lower Motor Lesions on Muscles of Facial expression
Bell’s palsy
- This diagram illustrates the impact of an UMN lesion (lesion A) and a LMN lesion (lesion B) on the activity of the muscles of facial expression.
- UMN lesion (A) results in weakness in lower facial muscles only, as LMNs innervating the upper facial muscles receive bilateral input from motor cortex
- LMN lesion results in paralysis of both upper and lower facial muscles on the side of the lesion, a condition known as Bell’s palsy.
Unilateral UMN lesion for
V - trigeminal
XI - spinal accessory
XII - hypoglossal nerve
- It also turns out that crossed and uncrossed corticonuclear input to the motor nuclei for CN V, XI and XII is not equal.
- The preponderance of input to these nuclei is crossed.
- This woman had tongue weakness caused by damage to corticonuclear fibers in the internal capsule. Left lingual paresis (tongue deviates to the left) was evident and was found to be due to small hemorrhage in the internal capsule. Note that the clinical presentation is indistinguishable from that of a LMN lesion
- Therefore, while paralysis of muscles innervated by these nuclei is unlikely given a unilateral UMN lesion, there can be contralateral muscle weakness (paresis).
Paramedian and short circumferential arteries supply the medial and/or anterior territory; long circumferential arteries supply the lateral territory.
There is a systematic positioning of cranial nerve nuclei by type.
There is a systematic positioning of cranial nerve nuclei by type.
Medial lesions mostly affect GSE nuclei and fibres.
Lateral lesions affect SVE and sensory nuclei and fibres from nuclei of any type that run laterally
In addition, Important tracts are also preferentially affected:
Medial/Anterior: medial lemniscus (blue) corticospinal/nuclear tracts (red)
Lateral: spinothalamic tract (green)
Lateral medullary syndrome - Wallenberg’s Syndrome
This is the most common of brainstem lesions encountered clinically.
As shown in the drawing, this is clearly a lesion affecting the lateral compartment of the medulla.
The signs of this syndrome are:
- Dizziness, vertigo (loss of balance) due to damage of vestibular nuclei (a SSA nucleus)
- Dysphagia, hoarseness and difficulty swallowing, absent gag reflex due to damage of the nucleus ambiguus and CN IX fibres projecting to solitary nucleus.
***A quick note about the gag reflex:
The afferent (or sensory) limb is carried by CN IX (GVA) to the lower part of the solitary nucleus The efferent (or motor) limb is carried by CN X (SVE) from nucleus ambiguus.
- Some ipsilateral loss of pain and temperature sensation on the face (damage to spinal V tract
and nucleus, GSA) - Contralateral loss of pain and temperature sensation on the body (damage to the
spinothalamic tract, GSA) - Horner’s syndrome: damage of the sympathetic tract
- Ataxia, loss of coordination of voluntary muscle function (damage of the inferior cerebellar peduncle)
Medial medullary syndrome
Key loss of function includes:
- Deviation of the tongue to the side of lesion (damage of CN XII nucleus or fibres, GSE)
- Contralateral loss of discriminative touch & conscious proprioception (body) (medial lemniscus damage)
- Contralateral spastic (UMN lesion) paralysis (body) (pyramidal tract damage)
Lateral pontine syndrome
- Many of the features are similar to lateral medullary syndrome:
1. Dizziness, loss of balance (damage to vestibular nuclei and fibres of CN VIII)
2. Ipsilateral loss of pain and temperature sensation in the face (damage of spinal V tract and nucleus, GSA)
3. Contralateral loss of pain and temperature sensation (spinothalamic tract damage)
NOT SHOWN! Horner’s syndrome and ataxia (damage of hypothalamospinal fibres and
cerebellar peduncles, respectively)
- Damage of CN VII fibres or motor nucleus (SVE) leading to ipsilateral paralysis of the upper and lower face and loss of corneal reflex.
- Damage of CN VIII fibres & cochlear nucleus (SSA) leading to ipsilateral hearing loss.
***A quick note about the corneal or “blink” reflex.
Afferent (sensory) limb: CN V (main sensory nucleus, GSA)
Efferent (motor) limb: CN VII (facial motor nucleus, SVE)
Medial pontine syndrome
- Contralateral spastic hemiparesis (body) (corticospinal tract)
- Contralateral loss of touch and proprioception (body) (medial lemniscus)
- Loss of lateral rectus function (abducens nucleus, GSE)
- Ipsilateral paralysis of the upper and lower face, loss of corneal reflex (SVE fibres from CN VII motor nucleus)
Millard Gubler Syndrome - Anterior pontine syndrome
- Bilateral spastic hemiparesis (body) (corticospinal tract)
could produce contralateral UMN lesion signs CN XII (corticonuclear tract) - Bilateral loss of touch and proprioception (body) (medial lemniscus)
In some cases the lesion can extend to affect fibres of:
- CN VI (GSE, lateral rectus paralysis), or even
- CN VII (SVE, muscles of facial expression, corneal reflex)
Weber’s Syndrome - Medial midbrain syndrome
- Ipsilateral loss of eye muscle function; ipsilateral loss of pupillary light reflex (GSE and GVE CN III fibres)
- Contralateral spastic hemiparesis (corticospinal fibres).
The jaw-jerk reflex is mediated by a monosynaptic connection between the mesencephalic trigeminal nucleus and the trigeminal motor nucleus. This connection is usually suppressed by corticonuclear input to the trigeminal motor nucleus.
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