Approach to differentiating lesions (brainstem): Clinical sciences

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Introduction 0:00–0:30

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.

Unstable Patient 0:30–1:10

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 ABCD assessment and take a look at stable individuals.

Stable Patient 1:10–3:21

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 non reactive 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.
All right. First, let's take a look at individuals who are presenting with impaired eye adduction.

Cranial nerve III palsy 3:21–5:11

In this case, consider a midbrain lesion because the oculomotor nerve or cranial nerve. Three 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 is involvement of the levator palpebrae, superioris muscle if present, assess for contralateral weakness.
Now, the presence of ptosis and absence of contralateral weakness is suggestive of cranial nerve. Three 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, three palsy. Now, here's a clinical pearl to keep in mind, if you see a pupil involving cranial nerve, three 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, three fascicles and the cerebral peduncle.

Weber syndrome 5:11–5:34

In the midbrain which contains the corticospinal tracts. All right, let's switch gears and discuss a patient who has impaired eye adduction with no ptosis.

Internuclear ophthalmoplegia 5:34–6:32

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 obducens nucleus to the medial rectus subnucleus of the contralateral oculomotor nucleus.
This results in simultaneous abduction of one eye and abduction 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 abduction of the other eye.
With these findings diagnose internuclear ophthalmoplegia. Now let's move on to patients with impaired eye abduction.

Cranial nerve VI palsy 6:32–7:13

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 six palsy.
In this case, the exam will reveal medial deviation of the affected eye at rest due to unopposed action of the medial rectus as well as impaired abduction on lateral gaits.
With these findings diagnosed cranial nerve six palsy on the flip side. If you identify hemiplegia, consider millard Goler syndrome.

Millard-Gubler syndrome 7:13–7:58

In these individuals, there's a lesion of the ventral pons that affects the cranial nerve, six fascicles and the corticospinal tracts causing contralateral limb weakness, the fascicles of the facial nerve cranial nerve seven 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 Goler syndrome. Finally, if you identify quadriplegia on examination, there is a bilateral injury to the ventral pons and you should consider locked in syndrome, which is usually due to a basilar artery stroke.

Locked-in syndrome 7:58–8:45

On exam, you will find an awake patient who is unable to speak on command. The patient can blink and move their eyes vertically but not horizontally.
In addition to quadriplegia, these patients will have bilateral facial weakness with these exam findings diagnose locked in syndrome.
Patients with locked in syndrome due to a pontine lesion remain awake and alert because the reticular activating system located in the midbrain is spared.
Next, let's discuss patients with intact extraocular movements, meaning the lesion has spared cranial nerves 34 and six, which are in the midbrain and pons.

Lateral medullary syndrome 8:45–10:35

In this case, you should consider a medullary lesion more specifically lateral or medial medullary syndrome. To differentiate between the two, be sure to assess for Horner Syndrome, which includes the presence of ipsilateral ptosis, miosis and anhidrosis.
If present. There is involvement of the descending sympathetic fibers that pass from the hypophthalmus through the lateral medulla, meaning that the patient likely has lateral medullary syndrome, which is also known as Wallenberg Syndrome.
Due to the involvement of the vestibular nuclei. The patient will usually report nausea, vomiting and dizziness or vertigo history will also reveal hiccups a hoarse voice and difficulty swallowing.
On examination, you will notice nystagmus and a decreased gag reflex on the side of the Horner Syndrome. Next, you will identify a decreased pain and temperature sensation on the side of the face with the Horner Syndrome due to injury to the spinal trigeminal nucleus and decreased pain and temperature sensation on the contralateral side of the body and limbs from injury to the spinothalamic tract.
Also, there will be limb ataxia, ipsilateral to the Horner syndrome due to the inferior cerebellar peduncle involvement at this point.
Diagnose lateral medullary syndrome, which most commonly occurs due to vertebral or posterior inferior cerebellar artery infarction.
On the other hand, if your patient has intact extraocular movements and no Horner syndrome, consider medial Medullary syndrome.

Medial medullary syndrome 10:35–11:35

In this case, history will reveal slurred speech, trouble swallowing and unilateral limb weakness and numbness, which often results in difficulty walking and balancing on exam.
Due to involvement of the hypoglossal nucleus or fascicles. You will notice a tongue deviation towards the side of injury.
Next from injury to the corticospinal tract. There will be contralateral arm and leg weakness and due to the injury to the medial lemniscus, there will be contralateral loss of proprioception and vibration sense.
With this combination of findings, diagnose medial medullary syndrome, which usually occurs due to vertebral or anterior spinal artery infarction.
Finally, let's discuss individuals with impaired extraocular movements, facial droop and tongue deviation. In this case, you should think of a process affecting cranial nerves in the midbrain pons and medulla.

Leptomeningeal carcinomatosis 11:35–12:58

In other words, you should consider a meningeal process as the underlying cause. Since infiltration of the meningeal spaces or the cerebrospinal fluid that resides, there can affect any surface area of the brainstem.
Next, further evaluate history and physical exam findings to assess the underlying cause. The most important ones include leptomeningeal carcinomatosis and subarachnoid hemorrhage.
First, let's focus on leptomeningeal carcinomatosis, which is associated with progressive neurologic deficits, progressive headache, possibly with a known history of malignancy or constitutional symptoms like fatigue and weight loss.
With these findings, you should consider leptomeningeal carcinomatosis or cancer infiltrating the leptomeninges to confirm the diagnosis, send cytology of the cerebrospinal fluid.
And if cytology shows the presence of malignant cells, diagnose leptomeningeal carcinomatosis. On the other hand, in subarachnoid hemorrhage, your patient will typically report a sudden onset of neurologic deficits and severe headache, possibly with a known cerebral aneurysm.

Subarachnoid hemorrhage 12:58–13:25

With these findings consider subarachnoid hemorrhage. So be sure to obtain a head ct if the imaging reveals blood in the subarachnoid space, diagnose subarachnoid hemorrhage.
All right, as a quick recap brainstem lesions or simply injuries to the midbrain pons or medulla can result in various signs including circulatory and respiratory instability, cranial nerve dysfunction, motor weakness, sensory loss in coordination and altered consciousness.

Review 13:25–14:18

Now based on the clinical presentation, you can determine the lesion location. Impaired eye adduction suggests a midbrain lesion, impaired eye abduction suggests a pontine lesion while intact ocular movements should make you think of medullary lesions.
Finally, if there are impaired extraocular movements, facial droop and tongue deviation, consider meningeal processes.