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A 70-year-old man is seen in the emergency department with an infarct in the posterior inferior cerebellar artery. He demonstrates loss of pain and temperature sensation on the right side of the body and the left side of the face. He appears unsteady on his feet and falls toward the left. Due to his symptoms and the blood vessel involved, which one of the following presentations would you also expect to find?
Hoarseness
A patient presents with left-sided hemiplegia; loss of fine touch & vibration sensation on the left side of the body; and deviation of the tongue, when protruded, toward the right. A lesion of which arterial supply most likely caused the paralysis observed in this patient?
Right-sided branches of the anterior spinal artery
A 65-year-old female presents at the emergency department with sudden onset right-sided ataxia accompanied by dizziness and nausea. There is mild right-sided facial palsy & numbness.
Cerebellar examination shows dysmetria and dysdiadochokinesia on the right upper extremity. She is unable to do heel to shin to knee test (assesses lower limb coordination) on the right. When asked to sit on the bed unassisted, she falls to her right side. On walking, she has a wide-based gait and falls to the right. What is the artery that is most likely affected in this patient?
Anterior inferior cerebellar artery
A 62-year-old man suffers a basilar artery occlusion, preventing blood supply to the paramedian basilar arterial branches that supply a portion of the brainstem. Which of the following constellation of signs would he most likely to display?
Inability to abduct the right eye + muscle weakness in the upper and lower left limbs as well as the right side of the face.
Brainstem Structures
•Ascending sensory tracts
•Descending motor tracts
•Descending autonomic pathways
•Cerebellar peduncles
•Cranial nerve nuclei and nerves
Brainstem vascular syndromes
•The most common cause of brainstem vascular syndromes is ischemic stroke.
•Combinations of structures affected by a lesion will vary by case
All potential structures may not be affected
Signs will vary based upon severity & extent of the lesion
•The hallmark of a brainstem lesion/syndrome is:
Ipsilateral cranial nerve deficit and
Contralateral body deficit (weakness, sensory loss, or ataxia)
•T1 weighted MRI – fatty tissue is bright
•T2 weighted MRI – water is bright
•Diffusion Weighted MRI – water molecule Brownian motion is bright
Midline arterial zone structures
•Cranial nerve somatic motor nuclei:
Midbrain: Oculomotor, Trochlear
Pons: Abducens
Medulla: Hypoglossal
•Cranial nerve roots emerging near the median plane.
•Medullary pyramids.
•Medial corticospinal fibers/tracts .
•Medial longitudinal fasciculus.
•Medial lemniscus.
Lateral arterial zone structures
Cranial nerve general sensory and visceral motor nuclei:
Pons: Trigeminal, Motor Nucleus of V, Facial
Medulla: Trigeminal, Vestibular, Nucleus ambiguus, Dorsal vagal, Solitary nucleus
Cranial nerve roots emerging more laterally .
Spinothalamic tracts.
Ventral trigeminal tract.
Cerebellar peduncles.
The greatest number of vascular injuries in the brainstem involve arteries of the lateral zone
4 midline structures beginning with “M”
1.Motor pathways (CST)
Contralateral weakness of the arm and leg.
2.Medial lemniscus
Contralateral loss of vibration and proprioception in the arm and leg.
3.Medial longitudinal fasciculus
Ipsilateral loss of coordinated eye movements (internuclear ophthalmoplegia).
4.Motor nuclei and nerves
Ipsilateral loss of the cranial nerve that is affected (III, IV, VI, or XII).

4 “side” structures beginning with “S”
1.Spinothalamic tract
Contralateral alteration of pain and temperature affecting the arm and leg, rarely the trunk
2.Sensory nucleus of CN V
Ipsilateral alteration of pain and temperature of the face in the distribution of CN V
3.Sympathetic tract
Ipsilateral Horner’s syndrome (partial ptosis and miosis)
4.Spinocerebellar tracts
Ipsilateral ataxia of the arm and leg

Internuclear ophthalmoplegia
•Internuclear ophthalmoplegia is an ocular movement disorder caused by a lesion of the medial longitudinal fasciculus.
•A lesion of the medial longitudinal fasciculus can produce impaired horizontal conjugate eye movements.
•It is characterized by:
•Impaired adduction of the ipsilateral eye.
•Nystagmus of the abducting eye due to a compensatory response trying to overcome the weakness of the adducting eye
Horner’s syndrome
•Cervical Sympathetic Pathway from the hypothalamus descends through the cervical spinal cord.
•Fibers synapse on preganglionic sympathetic cells that project to the superior cervical ganglion.
•The superior cervical ganglion innervates the dilator pupillae muscles, the superior tarsal muscle of eyelid, and the sweat glands of the face.
•Lesions that interrupt these pathways produce ipsilateral Horner’s syndrome:
•Miosis: Constricted pupil.
•Ptosis: Droopy eyelid.
•Anhidrosis: Lack of facial sweating.
“4” Cranial Nerves above the pons
•Midbrain
CN III – Oculomotor
All extraocular muscles except lateral rectus (abduction) and superior oblique (intorsion, depression, and abduction)
Upper eyelid (levator palpebrae)
Edinger-Westphal Nucleus
Pupillary constriction
Accommodation
•CN IV – Trochlear
Superior oblique (intorsion, depression, and abduction of the eyes)
“4” Cranial Nerves at the pons
CN V – Trigeminal
Mastication
Facial sensation
CN VI – Abducens
Lateral rectus (abduction of the eyes)
CN VII – Facial
•Facial expression
•Lacrimation and salivation
•Orbicularis oculi (closing the eyes)
•Stapedius (modulated auditory volume)
CN VIII – Vestibulocochlear
•Hearing
•Balance
“4” Cranial Nerves below the pons
CN IX – Glossopharyngeal
•Taste, swallowing, salivation
•Phonation
•Monitor chemo- and baroreceptors
CN X – Vagus
•Taste, swallowing
•Phonation
•Monitor chemo- and baroreceptors
•Parasympathetics to thoracoabdominal viscera
CN XI – (Spinal) Accessory
•Sternocleidomastoid and trapezius for head turning and shoulder shrugging
CN XII – Hypoglossal
•Tongue movement
Midbrain
Cranial Nerve Nuclei and Nerve Roots:
CN III: Oculomotor (inferior oblique, medial rectus, superior rectus, & inferior rectus)
CN IV: Trochlear (superior oblique)
Blood Supply:
Posterior cerebral artery (PCA) and penetrating branches.
Structures:
Edinger-Westphal nucleus: Pupillary constriction & lens accommodation.
Medial longitudinal fasciculus: Conjugate horizontal eye movements.
Medial lemniscus: Sensory pathway for fine touch, vibration, & proprioception.
Red nucleus: Flexors, arm swing, & fine motor control of the hands.
Substantia nigra: Modulates movement.
Cerebral peduncles: House descending motor tracts.
Pons
Cranial Nerve Nuclei and Nerve Roots:
CN V: Trigeminal (motor and sensory of the face)
CN VI: Abducens (lateral rectus)
CN VII: Facial (muscles of facial expression)
CN VIII: Vestibulocochlear
Blood Supply
Medial: Basilar Artery & Paramedian Branches.
Lateral: Anterior Inferior Cerebellar Artery (AICA).
Structures
Superior Vestibular nucleus: Inputs to CN III & IV.
Spinal trigeminal tract & nucleus: Pain & temperature of the face.
Medial longitudinal fasciculus: Conjugate horizontal eye movements.
Medial lemniscus: Sensory pathway for fine touch, vibration, & proprioception
Descending corticospinal tracts: Voluntary movement of the body.
Spinothalamic tracts: Pain & temperature of the body.
Medulla
Cranial Nerve Nuclei and Nerve Roots
CN IX: Glossopharyngeal (larynx/pharynx/soft palate).
CN X: Vagus (larynx/pharynx/soft palate; Horner’s syndrome).
CN XI: (Spinal) Accessory.
CN XII: Hypoglossal (movement of the tongue).
Blood Supply
Medial: Anterior Spinal Artery & Penetrating Branches.
Lateral: Posterior Inferior Cerebellar Artery (PICA).
Structures
•Corticospinal tracts/pyramids: Voluntary movement of the body.
•Medial lemniscus: Sensory pathway for fine touch, vibration, & proprioception.
•Spinal trigeminal nucleus and tract: Ipsilateral loss of pain & temperature in face
•Lateral spinothalamic tract: Contralateral loss of pain & temperature in body
•Inferior cerebellar peduncle: Ipsilateral cerebellar signs/nystagmus.
Benedikt Syndrome (Paramedian Midbrain Syndrome) with red nucleus
Classic Presentation, Sudden Onset:
•Hemiparesis of contralateral upper and lower limbs with UMN signs
•Hemiparesis of contralateral lower muscles of facial expression (corticobulbar fibers supply the facial motor nucleus bilaterally – except the lower motor neurons supplying perioral muscles).
•CN III palsy: Ipsilateral eye deviates down and out. There is paresis of all extraocular muscles except the Lateral Rectus (abductor) and the Superior Oblique (abductor and depressor). Thus, the affected eye will be abducted and depressed.
•Diplopia
•Dilation of ipsilateral pupil (if preganglionic parasympathetic axons from the Edinger-Westphal Nucleus are affected)
•Ipsilateral ptosis (again, yet another feature of CN III palsy).
•Contralateral intention tremor and ataxia (cerebellar inputs to the red nucleus)
Weber Syndrome (Medial Midbrain Syndrome) without red nucleus
Classic Presentation, Sudden Onset:
•Hemiparesis of contralateral upper and lower limbs with UMN signs
•Hemiparesis of contralateral lower muscles of facial expression (corticobulbar fibers supply the facial motor nucleus bilaterally – except the lower motor neurons supplying perioral muscles).
•CN III palsy: Ipsilateral eye deviates down and out. There is paresis of all extraocular muscles except the Lateral Rectus (abductor) and the Superior Oblique (abductor and depressor). Thus, the affected eye will be abducted and depressed.
•Diplopia
•Dilation of ipsilateral pupil (if preganglionic parasympathetic axons from the Edinger-Westphal Nucleus are affected)
•Ipsilateral ptosis (again, yet another feature of CN III palsy).
Ventral Pontine Syndrome (Locked-in Syndrome)
Classic Presentation, Sudden Onset:
•Presents as a collection of bilateral motor & sensory signs, sometimes supplemented by CN V-VIII dysfunction.
•Quadriplegia + bilateral corticobulbar signs with vertical gaze & eyelid retraction preserved (dorsally located oculomotor circuitry remains intact).
•Consciousness is preserved (reticular formation is spared).
•Patients with classical or incomplete forms are still able to communicate.
Lesion: Can result from severe infarct or pontine hemorrhage of the basilar artery.
1.Presents as a collection of bilateral motor & sensory signs, sometimes supplemented by CN V-VIII dysfunction.
Quadriplegia + bilateral corticobulbar signs with vertical gaze & eyelid retraction preserved (dorsally located oculomotor circuitry remains intact).
2.Consciousness is preserved (reticular formation is spared).
3.Patients with classical or incomplete forms are able to communicate via ocular movements. An EEG may also be used to assess consciousness.