Approach to differentiating lesions (brainstem): Clinical sciences

Brainstem lesions, or simply injuries to the midbrain, pons, or medulla, can result in various signs, because many important structures and pathways reside in the brainstem, including cranial nerves and nuclei, the reticular activating system, the respiratory centers, as well as the motor, somatosensory, cerebellar, and sympathetic pathways.

Now, if your patient presents with a chief concern suggestive of a brainstem lesion, first, perform an ABCDE assessment to determine if they are unstable or stable.

If unstable, stabilize the airway, breathing, and circulation. In some cases, you might even have to use intubation and start mechanical ventilation.
Next, obtain IV access, consider starting IV fluids, and don’t forget to put your patient on continuous vital sign monitoring and cardiac telemetry. Finally, if needed, be sure to manage high intracranial pressure.

Now, let’s go back to the ABCDE assessment and take a look at stable individuals.

In this case, your first step is to obtain a focused history and physical examination. Keep in mind that symptoms and physical exam findings will depend on the lesion location and the part of the brainstem that’s affected. In other words, symptoms could include confusion, changes in vision, facial droop and numbness, hearing loss, and trouble swallowing or speaking. Also, some individuals might report weakness or numbness in the arms or legs.

Now, switching gears and moving on to physical exam findings. An injury to the reticular activating system will result in altered mental status and a decreased level of consciousness. Next, oculomotor nerve involvement in the midbrain will result in sluggish or nonreactive pupils and ptosis; while an injury to the midbrain or pons could also result in impaired extraocular movements. Additionally, injuries of the pons, where the trigeminal and facial nerve nuclei reside, can result in facial numbness and, or, weakness.

Next, a lesion to the cochlear nerves at the pontomedullary junction can cause hearing loss, while injury to the glossopharyngeal and vagus nerves in the medulla would impair gag and cough reflexes. Injuries of the nuclei of spinal accessory nerves, which also reside in the medulla, will result in weakness of the sternocleidomastoid and trapezius muscles; while an injury of the hypoglossal nerve will cause the tongue to deviate towards the side of the lesion when protruded. Finally, lesions of the corticospinal tracts can cause limb weakness, while injuries of the somatosensory pathways can result in sensory loss.

With these findings, consider a brainstem lesion, so your next step is to assess the location of brainstem injury based on the clinical presentation.

Alright, first, let’s take a look at individuals who are presenting with impaired eye adduction.

In this case, consider a midbrain lesion because the oculomotor nerve, or cranial nerve III, controls almost all muscles responsible for eye movements. The two exceptions are the superior oblique, which is innervated by the trochlear nerve, and the lateral rectus, which is controlled by the abducens nerve.

Next, assess for ptosis, meaning, check if there’s involvement of the levator palpebrae superioris muscle. If present, assess for contralateral weakness.

Now, the presence of ptosis and contralateral weakness is suggestive of cranial nerve III palsy. In this case, history will reveal double vision that is worse when looking at close objects due to impaired convergence of the affected eye. On examination, you will notice that the affected eye is deviated laterally and inferiorly or in other words, “down and out,” at rest. This occurs due to unopposed actions of the superior oblique and lateral rectus muscles. Additionally, there will be impaired eye adduction, elevation, and depression. With these findings, diagnose a cranial nerve III palsy.

Now, here's a clinical pearl to keep in mind! If you see a pupil-involving cranial nerve III palsy, rule out an aneurysm of the posterior communicating artery! Pupillary dilatation should make you think of a compressive lesion, because the parasympathetic fibers that innervate the pupillary sphincter run along the outer surface of the nerve.

On the flip side, if both ptosis and contralateral weakness are present, the presentation is consistent with Weber syndrome. This syndrome occurs due to a lesion, most often a stroke, that affects cranial nerve III fascicles and the cerebral peduncle in the midbrain, which contains the corticospinal tracts.

Alright, let’s switch gears and discuss a patient who has impaired eye adduction, with no ptosis. In this case, consider internuclear ophthalmoplegia, due to an injury to the medial longitudinal fasciculus, or MLF. The MLF coordinates lateral gaze by connecting the abducens nucleus to the medial rectus subnucleus of the contralateral oculomotor nucleus. This results in simultaneous abduction of one eye and adduction of the other.

The history could reveal risk factors for stroke, like diabetes or hypertension; or a history of multiple sclerosis, while the physical exam will show nystagmus of the abducting eye on lateral gaze and impaired adduction of the other eye. With these findings, diagnose internuclear ophthalmoplegia.

Now, let’s move on to patients with impaired eye abduction.

Since abduction is mediated by the abducens nucleus and nerve, consider a pontine lesion. Next, assess for weakness to determine the extent of the lesion. If there is no weakness present, consider a cranial nerve VI palsy.

In this case, the exam will reveal medial deviation of the affected eye at rest due to the unopposed action of the medial rectus, as well as impaired abduction on lateral gaze. With these findings, diagnose cranial nerve VI palsy.

On the flip side, if you identify hemiplegia, consider Millard-Gubler syndrome. In these individuals, there's a lesion of the ventral pons that affects the cranial nerve VI fascicles and the corticospinal tracts, causing contralateral limb weakness. The fascicles of the facial nerve, cranial nerve VII, can also be affected!

As a result, on exam, you will notice medial deviation of the affected eye at rest with impaired eye abduction, as well as ipsilateral lower motor neuron facial palsy. There is also contralateral limb weakness. With these findings, diagnose Millard-Gubler syndrome.