Download Series of Brain Stem Strokes with Anatomic and

Series of Brain Stem Strokes with
Anatomic and Clinical Correlation
Paul Aldinger, DO
Mark Buehler, MD
Terrence Lewis, MD
Zack Rost, MD
Mohamad Bazerbashi, MD
Roy Schneider, MS
University of Toledo
Toledo, OH
Control #: 1025
Poster #: eP-47
No Disclosures
Purpose
To demonstrate brain stem anatomy through a
series of brain stem strokes and correlating
location with symptoms.
• Anatomy of the brainstem is complex. It
contains white matter tracts that connect
the spinal cord, cerebellum, and
supratentorial brain as well cranial nerve
nuclei.
• These structures relate to one another in
an anatomically confined space and
therefore focal lesions of the brainstem
may cause dramatic and varied symptoms
based on those anatomic relationships.
• In the following slides a series of 8
brainstem strokes accompanied by key
images and patient symptoms will be
presented.
• Questions and a discussion of each case
will follow.
Case 1
Basis pontis
Tegmentum
Sagittal T1 with axial DWI
plane superimposed in blue.
Axial DWI though the mid Pons
Symptoms:
•
•
Contralateral(Left) sided weakness body and face.
Contralateral(Left) sided ataxia.
What is the most common symptom for a large paramidline
stroke of the basis pontis in addition to contralateral
weakness?
• A syndrome of contralateral weakness and contralateral ataxia is the most
common consequence of paramidline infarcts of the pontine basis.
• Contralateral weakness is caused by involvement of the corticospinal and
corticobulbar tracts [yellow]. The corticospinal tracts cross at the caudal
medulla. The corticobulbar tracts crossover at the level of individual cranial
nerve nuclei with some exception.
• Facial weakness in this case does not include the muscles of mastication
innervated by the trigeminal nerve(CN 5). The motor nucleus of CN 5
receives fibers from the bilateral brainstem and cortex so muscles of
mastication will be unaffected by lesions proximal the nucleus itself.
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•
•
•
Ataxia is caused by involvement of corticopontine fibers [pink], pontine nuclei,
and pontocerebellar fibers [green].
Cerebellopontine fibers [pink] synapse on pontine nuclei. Pontine nuclei give
rise to cerebellopontine fibers [green]. Cerebellopontine fibers decussate in the
pons and travel through the contralateral middle cerebellar peduncle.
The cerebellum affects coordination on the ipsilateral side of the body, so
lesions of the pontine basis usually cause contralateral ataxia.
Ipsilateral ataxia is also possible because of decussating corticopontine fibers
may be affected after they cross.
• Infarcts of the pons and medulla are most often paramedian and
don’t cross the midline.
• This is because the involved paramedian penetrating branches of
the basilar and distal vertebral arteries don’t cross the midline.
• Isolated unilateral strokes of the basis pontis usually have a
relatively good prognosis.
Case 2
What is the most likely combination of
symptoms caused by this stroke?
A) Contralateral weakness and ipsilateral ataxia.
B) Contralateral weakness and contralateral ataxia.
C) Ipsilateral weakness and ipsilateral ataxia.
D) Contralateral weakness and contralateral
numbness.
•
•
•
This infarct caused contralateral weakness sparing the face and contralateral
ataxia.
It affected corticospinal fibers [yellow] and corticopontine fibers [pink] just like in
the prior case and therefore produced very similar symptoms.
It affected the tracts more rostrally in the right cerebral peduncle of the midbrain.
Corticospinal and
corticobulbar
Frontal lobe corticopontine
Corticopontine from
occipital, parietal,
and temporal lobes.
•
•
•
•
Corticopontine fibers from the occipital, parietal, and temporal lobes travel through the lateral
portion of the peduncle [pink].
Corticospinal and corticobulbar fibers [yellow] are in the central portion of the peduncle.
Coroticopontine fibers from the frontal lobes are in the medial part of the peduncle and are
not shown.
There is likely no facial weakness because, though both in yellow, corticobulbar fibers pass
more medially in the peduncle than corticospinal fibers.
Case 3
Symptoms:
Left sided numbness including face.
What sensation is unlikely to be affected by this
infarct?
A) Vibration and fine touch to the face.
B) Temperature, crude touch, and pain to the face.
C) Vibration and fine touch to the body.
D) Temperature, crude touch, and pain to the body.
Basis pontis
Tegmentum
•
•
•
•
Numbness in the contralateral body is likely caused by involvement of the medial
lemniscal pathway [blue] and trigeminothalamic pathway [red].
In the pons they travel in the tegmentum, posterior to the corticospinal tract and
pontine nuclei in the basis pontis.
The trigeminothalamic tract carries crude touch, temperature, and pain sensation.
It crosses from the contralateral side in the spinal cord.
The medial lemniscal tract carries vibration, fine touch, and proprioception. It
crosses over from the contralateral side in the caudal medulla.
Spinal trigeminal nucleus
•
•
•
•
Numbness in the contralateral face is likely caused by involvement of the
trigeminothalamic pathway.
Secondary neurons carrying crude touch, pain, and temperature originate from
the spinal trigeminal nucleus(CN 5) [light blue].
They cross from the contralateral side at the level they originate in the CN 5
nucleus and travel in the trigeminothalamic tract. The trigeminothalamic tract
courses adjacent to the medial lemniscal tract [blue] and therefore would be
affected by this infarct.
The spinal trigeminal nucleus [light blue] extends from the caudal medulla to the
mid pons.
Spinal trigeminal nucleus
Chief sensory trigeminal nucleus
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•
•
Secondary neurons carrying fine touch and vibration also join the trigeminothalamic
tract, but only some of them cross over. They ascend bilaterally to the thalamus.
Therefore fine touch and vibration sensation to the face are unlikely to be affected
by this infarct. That is why it is rare to lose all sensation to one side of the face with
a brainstem lesion.
The secondary neurons for fine touch and vibration originate in the chief sensory
trigeminal nucleus in green. It is more focal than the long spinal trigeminal nucleus
residing in the mid pons at the superior extent of the spinal trigeminal nucleus.
Case 4
What are the most likely symptoms caused by this infarct?
A) Contralateral limb weakness and ipsilateral body sensory loss.
B) Ipsilateral limb weakness and ipsilateral body sensory loss.
C) Ipsilateral limb weakness and contralateral body sensory loss.
D) Contralateral limb weakness and contralateral body sensory loss.
•
•
•
•
•
This infarct in the anterior medulla caused contralateral weakness and
contralateral sensory loss.
It is affecting the corticospinal tract carrying motor neurons [yellow] and the
medial lemniscus carrying fine touch, vibration, and proprioception [blue].
Both tracts cross at the caudal medulla below the level of this infarct so the
contralateral body was affected.
Contralateral weakness and contralateral sensory loss are the two most
common symptoms caused by medial medullary infarcts.
The cranial nerve nuclei reside more posteriorly in the medulla and therefore
were unaffected.
Case 5
Superior midbrain: level of the superior
colliculi.
Symptoms:
• Diplopia with right eye down and out.
What additional symptom would be most likely?
A) Ipsilateral ataxia.
B) Contralateral weakness.
C) Contralateral ataxia.
D) Contralateral sensory loss.
•
•
This stroke caused a pure oculomotor nerve(CN 3) palsy causing the ipsilateral
eye to deviate down and out, as well as contralateral ataxia.
The eye deviates down out because of unopposed action of the lateral rectus and
superior oblique muscles in the presence of palsies of the other ocular muscles.
Could the pure CN 3 palsy have been caused by a lesion of only
the CN 3 nucleus?
No. The cranial nerve 3 nucleus is composed of several paramidline
subnuclei each serving different functions.
• The superior rectus is innervated by a contralateral subnucleus.
• The levator palpebrae is innervated by bilateral subnuclei.
• The medial rectus, inferior rectus, and inferior oblique are innervated by
ipsilateral subnuclei.
So some combination of CN 3 subnuclei and CN 3 tract involvement is most
likely.
Brachium conjunctivum
CN 4
nucleus
Superior midbrain at level of superior
colliculi
•
•
Inferior midbrain at level of the inferior
colliculi
Contralateral ataxia could have been caused by involvement of cerebellorubral
and cerebellothalamic fibers.
Theses are the main output pathways of the intermediate and lateral aspects of
the cerebellar hemispheres. They are responsible for limb coordination and motor
planning respectively for half of the body ipsilateral to that cerebellar hemisphere.
Brachium conjunctivum
CN 4
nucleus
Superior midbrain at level of superior
colliculi
•
•
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Inferior midbrain at level of the inferior
colliculi
Cerebellorubral and cerebellothalamic fibers travel through the superior cerebellar
peduncle to cross in the brachium conjuctivum seen as laterally oriented green
fibers in the DTI image.
This stroke affected them above their crossover at the brachium conjunctivum as
they synapse with or travel around the red nucleus which is located superior to the
brachium conjuctivum and anterior to the CN 3 nucleus.
The combination of CN3 palsy and contralateral ataxia is called Claude syndrome.
Case 6
Symptoms:
• Left facial drop.
• Paresis of both eyes on leftward gaze.
What structures are involved?
A) Medial longitudinal fasciculus and facial motor nucleus.
B) Medial longitudinal fasciculus and tract of the facial nerve.
C) Tract of the abducens nerve and facial motor nucleus.
D) Tract of the facial nerve and motor nucleus of the abducens nerve.
CN 7 Nucleus
Spinal nucleus of CN7
CN 6 nucleus
•
•
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Weakness of left eye lateral movement is caused by
involvement of the abducens(CN 6) nucleus in yellow.
Weakness of right eye medial movement occurs because CN
3 nuclei need the contralateral CN 6 nuclei to tell them what
to do with the medial rectus muscles.
If CN 6 is infarcted then the contralateral medial rectus will
not function.
However, the contralateral medial rectus will still function to
make the eyes converge on a near object.
CN 7 Nucleus
Spinal nucleus of CN5
CN 6 nucleus
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•
•
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Weakness of the left face is being caused by involvement of the
tract of the facial nerve(CN 7).
CN 7 fibers travel posteriorly looping around CN 6 nucleus before
exiting at the pontomedullary junction.
They are therefore often affected by lesions that affect the CN 6
nucleus.
The looping CN 7 tract and its relation to CN 6 nucleus is depicted
in the illustration on the left.
Case 7
Symptoms:
Right sided internuclear ophthalmoplegia(INO)
What are the symptoms of right internuclear ophthalmoplegia?
A) Impaired right eye adduction and nystagmus of left eye on left lateral gaze.
B) Impaired right eye adduction and nystagmus of left eye on right lateral gaze.
C) Impaired left eye adduction and nystagmus of right eye of left lateral gaze.
D) Impaired left eye adduction and nystagmus of left eye on left lateral gaze
MLF
•
•
INO is caused by lesions of the medial longitudinal fasciculus(MLF) [green]
between the CN 6 nuclei in the pons and CN 3 nuclei in the brainstem.
The MLF is a tract near midline the lies just ventral to the 3rd ventricle and
cerebral aqueduct with ascending and descending fibers. It extends from the
cervical spinal cord to CN 3 nuclei. Lesions below the CN 6 nuclei cause no
known syndrome.
MLF
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•
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INO is caused by damage to fibers traveling from the CN 6 nuclei to the
contralateral CN 3 nuclei. These fibers cross over immediately to the contralateral
MLF at the level where they originate from the CN 6 nuclei.
As described in the prior case, input from CN 6 is need by CN 3 in order to control
the medial rectus muscle. This input travels in the MLF.
In right INO the right MLF is damaged. The right medial rectus therefore will not
adduct the right eye on left lateral gaze.
The left eye will move alone on left lateral gaze. The left eye will then experience
nystagmus because of mechanism trying to bring it into alignment with the right
eye.
Case 8
Symptoms:
Left sided ataxia.
Decreased sensation left side of face.
Decreased sensation right side of body.
What additional symptoms can occur in Wallenberg's
Syndrome?
A) Vertigo/nausea/nystagmus, dysphagia, ipsilateral Horner’s Syndrome.
B) Ipsilateral tongue weakness, dysphagia, contralateral decreased facial sensation.
C) Vertigo/nausea/nystagmus, ipsilateral hearing loss, contralateral weakness,
dysphagia, ipsilateral Horner’s syndrome.
D) Ipsilateral hearing loss, dysphagia, vertigo.
Trigeminothalamic tract
Tractus solitarius
Nucleus Ambiguus
CN 5 spinal nucleus
Hypoglossal nucleus
Vestibular Nuclei
Dorsal spinocerebellar
tract
Dorsal motor nucleus of
the vagus nerve
•
•
Wallenberg’s syndrome, also know as lateral medullary syndrome, causes
ipsilateral loss of facial sensation, contralateral loss of body sensation, ipsilateral
ataxia, vertigo/nausea/ataxia, and dysphagia/hoarseness.
Its is the most common classically named stroke syndrome of the brainstem and
possibly the only one that is common enough to be clinically relevant.
Trigeminothalamic tract
Tractus solitarius
Nucleus Ambiguus
CN 5 spinal nucleus
Hypoglossal nucleus
Vestibular Nuclei
Dorsal spinocerebellar
tract
Dorsal motor nucleus of
the vagus nerve
•
•
•
•
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The current case included only ipsilateral decreased facial sensation, contralateral
decreased body sensation, and ipsilateral ataxia.
Lateral medullary infarcts commonly don’t include all the features of Wallenberg’s
syndrome.
Ipsilateral decreased facial sensation is from involvement of the CN 5 spinal nucleus
which serves crude touch, pain, and temperature sensation.
Contralateral decreased body sensation is from involvement of the trigeminothalamic
tract which serves crude, touch, pain, and temperature sensation.
Ipsilateral ataxia is from involvement of the dorsal spinocerebellar tract which enters
the cerebellum through the inferior cerebellar peduncle and does not cross at any
point.
Trigeminothalamic tract
Tractus solitarius
Nucleus Ambiguus
CN 5 spinal nucleus
Hypoglossal nucleus
Vestibular Nuclei
Dorsal spinocerebellar
tract
Dorsal motor nucleus of
the vagus nerve
•
•
•
•
If the current infarct was larger it could have affected multiple adjacent structures
and caused the complete Wallenberg’s syndrome.
Ipsilateral Horner’s syndrome(miosis, ptosis, anhidrosis) is caused by involvement
of descending sympathetic fibers which travel adjacent to the trigeminothalamic
tract.
Dysphagia is caused by involvement of the nucleus ambiguus which contains the
motor neurons for the pharynx and larynx primarily through the vagus nerve.
Vertigo/nausea/nystagmus is caused by involvement of the vestibular nuclei.
Thank You
Sources
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