1. 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

2. No Disclosures

3. Purpose To demonstrate brain stem anatomy through a series of brain stem strokes and correlating location with symptoms.

4. 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.

5. 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.

6. Case 1 Symptoms : Contralateral(Left) sided weakness body and face. Contralateral(Left) sided ataxia. Axial DWI though the mid Pons Sagittal T1 with axial DWI plane superimposed in blue. What is the most common symptom for a large paramidline stroke of the basis pontis in addition to contralateral weakness? Basis pontis Tegmentum

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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. Corticospinal and corticobulbar Frontal lobe corticopontine Corticopontine from occipital, parietal, and temporal lobes.

13. 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.

14. 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. Basis pontis Tegmentum

15. 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

16. 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. Spinal trigeminal nucleus Chief sensory trigeminal nucleus

17. 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.

18. 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.

19. Case 5 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. Superior midbrain: level of the superior colliculi.

20. 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.

21. 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 Inferior midbrain at level of the inferior colliculi

22. 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. Brachium conjunctivum CN 4 nucleus Superior midbrain at level of superior colliculi Inferior midbrain at level of the inferior colliculi

23. 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.

24. CN 7 Nucleus Spinal nucleus of CN7 CN 6 nucleus 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.

25. CN 7 Nucleus Spinal nucleus of CN5 CN 6 nucleus 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.

26. 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

27. 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 3 rd 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

28. 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. MLF

29. 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.

30. 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. Nucleus Ambiguus Tractus solitarius CN 5 spinal nucleus Vestibular Nuclei Hypoglossal nucleus Dorsal motor nucleus of the vagus nerve Trigeminothalamic tract Dorsal spinocerebellar tract

31. 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. Nucleus Ambiguus Tractus solitarius CN 5 spinal nucleus Vestibular Nuclei Hypoglossal nucleus Dorsal motor nucleus of the vagus nerve Trigeminothalamic tract Dorsal spinocerebellar tract

32. 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. Nucleus Ambiguus Tractus solitarius CN 5 spinal nucleus Vestibular Nuclei Hypoglossal nucleus Dorsal motor nucleus of the vagus nerve Trigeminothalamic tract Dorsal spinocerebellar tract

33. Thank You

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