Brainstem Leisions

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Brainstem Leisions

Lesions of the Brainstem

  • most frequently syndromes of arterial occlusion or circulatory insufficiency that involve the vertebrobasilar system.
  • Vascular Lesions of the Medulla
    • result from occlusion of the vertebral artery or its branches
      • anterior and posterior spinal arteries
      • posterior inferior cerebellar artery [PICA]).
  • Medial medullary syndrome
    • results from occlusion of the anterior spinal artery.
    • affected structures and resultant deficits
      • Corticospinal tract
        • contralateral hemiparesis of the trunk and extremities
      • Medial lemniscus
        • contralateral loss of proprioception, discriminative tactile sensation, and vibrationsensation from the trunk and extremities
      • Hypoglossal nerve roots (intra-axial fibers)
        • ipsilateral flaccid paralysis of the tongue
  • Lateral medullary syndrome (PICA syndrome)
    • is also called Wallenberg syndrome.
    • results from occlusion of the vertebral artery or one of its medullary branches (e.g., PICA).
    • affected structures and resultant deficits:
      • Vestibular nuclei (medial and inferior)
        • nystagmus, nausea, vomiting, and vertigo
      • Inferior cerebellar peduncle
        • ipsilateral cerebellar signs (dystaxia, dysmetria, dysdiadochokinesia)
      • Nucleus ambiguus of cranial nerve (CN) IX, CN X, and CN XI (somatic visceral efferent [SVE])
        • ipsilateral laryngeal, pharyngeal, and palatal paralysis (loss of the gag reflex [efferent
        • limb], dysarthria, dysphagia, and dysphonia [hoarseness])
      • Glossopharyngeal nerve roots (intra-axial fibers)
        • loss of the gag reflex (afferent limb)
      • Vagal nerve roots (intra-axial fibers)
        • neurologic deficits same as those seen in lesion of the nucleus ambiguus
      • Spinothalamic tracts
        • contralateral loss of pain and temperature sensation from the trunk and extremities
      • Spinal trigeminal nucleus and tract
        • ipsilateral loss of pain and temperature sensation from the face
      • Descending sympathetic tract
        • ipsilateral Horner syndrome (ptosis, miosis, hemianhidrosis, vasodilation, and apparent enophthalmos)
  • Vascular Lesions of the Pons
    • result from occlusion of the basilar artery or its branches
      • anterior inferior cerebellar artery [AICA]
      • transversepontine arteries
      • superior cerebellar artery
  • Medial inferior pontine syndrome
    • results from occlusion of the paramedian branches of the basilar artery.
    • affected structures and resultant deficits:
      • Abducent nerve roots (intra-axial fibers)
        • ipsilaterallateral rectus paralysis
      • Corticobulbar tracts
        • contralateral weakness of the lower face
      • Corticospinal tracts
        • contralateral hemiparesis of the trunk and extremities
      • Base of the pons (middle cerebellar peduncle)
        • ipsilaterallimb and gait ataxia
      • Medial lemniscus
        • contralateralloss of proprioception, discriminative tactile sensation, and vibration sensation from the trunk and extremities
  • Lateral inferior pontine syndrome (AICA syndrome)
    • results from occlusion of a long circumferential branch of the basilar artery, AICA.
    • affected structures and resultant deficits
      • Facial nucleus and intra-axial nerve fibers
        • ipsilateral facial nerve paralysis
        • loss of taste from the anterior two-thirds of the tongue
        • loss of the corneal and stapedial reflexes
      • Cochlear nuclei and intra-axial nerve fibers
        • unilateralcentral nerve deafness
      • Vestibular nuclei and intra-axial nerve fibers
        • nystagmus, nausea, vomiting, and vertigo
      • Spinal trigeminal nucleus and tract
        • ipsilateral loss of pain and temperature sensation from the face
      • Middle and inferior cerebellar peduncles
        • ipsilateral limb and gait dystaxia
      • Spinothalamic tracts
        • contralateral loss of pain and temperature sensation from the trunk and extremities
      • Descending sympathetic tract
        • ipsilateralHorner syndrome (ptosis, miosis, hemianhidrosis, vasodilation, and apparent enophthalmos)
  • Lateral midpontine syndrome
    • results from occlusion of a short circumferential branch of the basilar artery.
    • affected structures and resultant deficits:
      • Trigeminal nuclei and nerve root (motor and principal sensory nuclei)
        • completeipsilateral trigeminal paralysis, including:
        • Paralysis of the muscles of mastication
        • Jaw deviation to the paretic side (due to unopposed action of the intact lateralpterygoid muscle)
        • Facial hemianesthesia (pain, temperature, touch, and proprioception
        • Loss of the corneal reflex (afferent limb of CN V-1)
      • Middle cerebellar peduncle (base of the pons)
        • ipsilateral limb and gait dystaxia
  • Lateral superior pontine syndrome
    • results from occlusion of a long circumferential branch of the basilar artery, the superior cerebellar artery.
    • affected structures and resultant deficits:
      • Superior and middle cerebellar peduncles
        • ipsilateral limb and trunk dystaxia
      • Dentate nucleus
        • signs similar to those seen with damage to the superior cerebellar peduncle (dystaxia, dysmetria, and intention tremor)
      • Spinothalamic and trigeminothalamic tracts
        • contralateralloss of pain and temperature sensation from the trunk, extremities, and face
      • Descending sympathetic tract
        • ipsilateralHorner syndrome (ptosis, miosis, hemihidrosis, and apparent enophthalmos)
      • Medial lemniscus (lateral division [gracilis])
        • contralateral loss of proprioception, discriminative tactile sensation, and vibrationsensation from the trunk and lower extremity
  • Locked-in syndrome (pseudocoma)
    • results from infarction of the base of the superior pons
    • infarcted structures include the corticobulbar and corticospinal tracts,
    • results in quadriplegia and paralysis of the lower cranial nerves.
    • also may result from central pontinemyelinolysis.
    • Communication occurs only by blinking or moving the eyes vertically

 

    • Lesions of the Midbrain
      • result from
        • vascular occlusion of the mesencephalic branches of the posterior cerebral artery
        • aneurysms of the posterior circle of Willis.
        • tumors of the pineal region.
        • hydrocephalus.
    • Dorsal midbrain (Parinaud) syndrome
      • is frequently the result of a pinealoma or germinoma of the pineal region.
      • affected structures and resultant deficits:
        • Superior colliculus and pretectal area
          • paralysis of upward and downward gaze
          • pupillary disturbances
          • absence of convergence
        • Cerebral aqueduct
          • noncommunicating hydrocephalus
          • occuras a result of compression from a pineal tumor
    • Paramedian midbrain (Benedikt) syndrome
      • results from occlusion or hemorrhage of the paramedian midbrain branches of the posterior cerebral artery.
      • affected structures and resultant deficits:
        • Oculomotor nerve roots (intra-axial fibers)
          • completeipsilateraloculomotor nerve paralysis
          • eye abduction and depression because of the unopposed action of the lateral rectus(CN VI) and the superior oblique (CN IV) muscles
          • severe ptosis (paralysis of the levatorpalpebrae muscle)
          • ipsilateral fixed and dilated pupil (complete internal ophthalmoplegia)
        • Red nucleus and dentatorubrothalamic tract
          • contralateralcerebellar dystaxia with intention tremor
        • Medial lemniscus
          • contralateral loss of proprioception, discriminative tactile sensation, and vibrationsensation from trunk and extremities
    • Medial midbrain (Weber) syndrome
      • results from
        • occlusion of midbrain branches of the posterior cerebral artery
        • aneurysmsof the circle of Willis.
      • Associated structures and resultant deficits:
        • Oculomotor nerve roots (intra-axial fibers)
        • Corticobulbar tracts
          • contralateral weakness of the lower face (CN VII), tongue (CN XII), and palate (CN Corticospinal tracts
          • contralateral hemiparesis of the trunk and extremities
    • InternuclearOphthalmoplegia (INO)
      • is also known as medial longitudinal fasciculus (MLF) syndrome, which results from a lesion of the MLF.
      • Lesions occur in the dorsomedialpontinetegmentum
      • may affect one or both MLFs.
      • is a frequent sign of multiple sclerosis.
      • results in medial rectus palsy on attempted lateral gaze and monocular nystagmus in the abducting eye with normal convergence.
    • Jugular Foramen (Vernet) Syndrome
      • affects CN IX, CN X, and CN XI.
      • affected structures and resultant deficits:
          • Glossopharyngeal nerve (CN IX)
            • loss of the gag reflex (afferent limb)
            • loss of taste sensation in the posterior third of the tongue
            • unilateralloss of the carotid sinus reflex
          • Vagal nerve (CN X)
            • laryngeal paralysis with dysarthria, dysphagia, and dysphonia (hoarseness)
            • palatal paralysis with loss of the gag reflex (efferent limb)
          • Accessory nerve (CN XI)
            • weakness of the sternocleidomastoid and upper trapezius muscles (the shoulder droops)


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            This video is part of a playlist of videos on the internal structure of the brain stem. The playlist uses simplified sketches that are gradually drawn for the purpose of description.
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