More brainstem lesions

aka Neurological Mind-boggler 004

Here are some scenarios to try out Gates’ Brainstem Rules of 4 (original figures and re-imagined images)


Scenario 5

You are examining a patient with sudden onset right-sided weakness. These are your clinical examination findings:

  • weakness of the right upper and lower limbs.
  • weakness of the left face
  • failure of abduction of the left eye
  • loss of vibration and proprioception in the right upper and lower limbs.

Where is the lesion?

Answer and interpretation
  • weakness of the right upper and lower limbs:
    • motor (corticospinal pathway) localises the lesion to the contralateral medial brainstem
  • weakness of the left face:
    • involvement of the face means the lesion must be at or above the upper pons; the coexistent involvement of CN6 (see below) suggests involvement of the left CN7, which accounts for ipsilateral weakness (i.e. affecting the left face)
  • failure of abduction of the left eye:
    • indicates CN6 involvement, localising the lesion to the ipsilateral pons.
    • (sparing of CN3 and CN12 means the midbrain and medulla are not involved)
  • loss of vibration and proprioception in the right upper and lower limbs:
    • confirms localisation of the lesion to the contralateral medial brainstem

Site of the lesion: left medial pons.

Interestingly, the facial nerve runs a strange course – it loops around medial to the CN6 nucleus from its own laterally situated CN7 nucleus. Thus a CN7 palsy tends to coexist with a CN6 lesion despite the CN7 nucleus being in the lateral pons.


Scenario 6

You are examining a patient with sudden onset intermittent double vision (diplopia). These are your clinical examination findings:

  • failure of adduction past the midline (movement towards the nose) of the left eye and leading eye (right) nystagmus on looking laterally to the right. Normal eye movements on looking to the left.
  • The patient is hypertensive. There is no hemiparesis and further examination is unremarkable.

Where is the lesion?

Answer and interpretation
  • This finding suggests a unilateral left-sided internuclear ophthalmoplegia, which localises the lesion to the ipsilateral medial longitudinal fasciculus (MLF). The MLF connects CN3 in the midbrain and the contralateral CN6 in the pons.
  • The MLF is not usually affected when there is hemiparesis as it lies further back in the brainstem relative to the motor (corticospinal) pathway.
  • Unilateral internuclear ophthalmoplegia can result from a lacunar infarct — but always remember the possibility of multiple sclerosis.

Site of the lesion: left medial longitudinal fasciculus (connects CN3 in the midbrain and contralateral CN6 in the pons).


The next two scenarios turn up some exceptions to the Brainstem Rules of 4…

Scenario 7

You are examining a patient with a right-sided Horner syndrome. These are your clinical examination findings:

  • right-sided Horner’s syndrome.
  • right-sided limb ataxia.
  • left-sided total loss of sensation.

Where is the lesion?

Answer and interpretation
  • right-sided Horner’s syndrome:
    sympathetic pathway localises the lesion to the ipsilateral lateral brainstem.
  • right-sided limb ataxia:
    spinocerebellar pathway localises the lesion to the ipsilateral lateral brainstem.
  • left-sided total loss of sensation:
    Spinothalamic pathway localises the lesion to the contralateral lateral brainstem. furthermore, the lesion can be localised to the midbrain because there is total loss of sensation. In the midbrain, the medial lemniscal pathway is actually situated more laterally, ventral to the spinothalamic pathway – ie. the two pathways come together… a somewhat tricky exception to the Rules of 4!

Site of the lesion: Right dorsolateral midbrain.

An extensive lesion that also involves CN3 is known by the delightful name of Nothnagel syndrome.


Scenario 8

You are examining a patient with a ‘down and out’ right eye with pupillary dilatation. These are your clinical examination findings:

  • right-sided impaired adduction, supradduction and infradduction of the ipsilateral eye with a dilated pupil.
  • left-sided limb ataxia.

Where is the lesion?

Answer and interpretation
  • right-sided impaired adduction, supradduction and infradduction of the ipsilateral eye with a dilated pupil:
    • CN3 lesion localises the lesion to the ipsilateral medial midbrain.
  • left-sided limb ataxia:
    • usually this indicates ipsilateral spinocerebellar pathway involvment (a lateral structure). However, in this case we know that the midbrain is affected (CN3 palsy) and the red nucleus lies in the medial midbrain just lateral to the CN3 nerve fascicle.
    • Damage to the red nucleus interrupts the ‘dentatorubrothalamic tract’ from the opposite cerebellar hemisphere causing cerebellar signs in the limbs opposite to the CN3 lesion — and throws another spanner in the works of the Brainstem Rules of 4…

Site of the lesion: Right medial midbrain.

The clinical manifestations of this lesion (affecting the CN3 nucleus or its fascicle as well as the red nucleus) is known as Benedikt syndrome.


References

Neurological Mind Boggler 700

CLINICAL CASES

Neurological Mind-boggler

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

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