Chapter 9: The Brainstem and Cranial Nerves

The three levels of the brainstem from superior to inferior are the midbrain, pons, and medulla. The midbrain is just inferior to the bilateral thalami, and the medulla transitions inferiorly into the cervical spinal cord. Most simply, the brainstem can be thought of as a “spinal cord for the head and neck”: Just as the spinal cord has sensory information coming in and motor information going out for the extremities and torso, the brainstem has sensory information coming in and motor information going out for the head and neck. In addition to somatic sensory information, however, the brainstem also receives vestibular, auditory, taste, and visceral sensory information. Motor functions of the brainstem include control of ocular, pupillary, facial, laryngeal, pharyngeal, and visceral musculature.

Understanding the brainstem requires a general framework for what is there and where it is. As far as what is in the brainstem, there are five general categories of structures:

1. The descending motor pathways for the extremities and torso (corticospinal tracts; see Ch. 4)

2. The ascending somatosensory pathways from the extremities and torso (dorsal columns and spinothalamic tracts; see Ch. 4)

3. The cranial nerve nuclei and associated structures

4. Connections with the cerebellum (the cerebellar peduncles; see Ch. 8)

5. The reticular activating system and ascending neurotransmitter-specific projection pathways: substantia nigra (dopamine), locus coeruleus (norepinephrine), median raphe nuclei (serotonin), pedunculopontine nuclei (acetylcholine)

As points of orientation for where structures are in the brainstem, the following principles apply at all three levels of the brainstem (Fig. 9–1):

• The corticospinal tracts run in the anterior (ventral) aspect of the brainstem.

• The somatosensory pathways for the extremities and torso move a bit over the course of their ascent, but are most often posterior (dorsal) within the brainstem (with the exception of the mid-medulla, where the medial lemnisci are medial and extend anteriorly; see Ch. 4).

• The cranial nerve nuclei are all posterior (dorsal).

  • In general, the motor cranial nerve nuclei are closest to the midline, and their cranial nerves emerge medially/anteriorly (CN 4 is an exception in that it exits posteriorly).

    • The motor cranial nerve nuclei innervating skeletal muscle are at the midline: CNs 3, 4, and 6 (innervating extraocular muscles) and CN 12 (innervating tongue muscles).

    • The motor cranial nerve nuclei innervating branchial muscles are more lateral: CN 7 (facial muscles), CN 5 (jaw muscles), and CNs 9 and 10 (muscles of the larynx/pharynx)

  • The sensory and special sensory cranial nerve nuclei are all more lateral than the motor cranial nerve nuclei: sensory nuclei of CN 5, vestibular and cochlear nuclei (CN 8), and nucleus solitarius (for taste and visceral sensation)

• The cerebellar peduncles all arise from the posterior/dorsal brainstem (logically, since the cerebellum is posterior to the brainstem)

• The ascending neurotransmitter-specific projection pathways are found throughout the brainstem, but the reticular-activating system involved in maintaining arousal and consciousness reside in the upper pons and midbrain.

The Cranial Nerve Nuclei

The 12 cranial nerves can be divided into three groups of four that mostly correspond to the three brainstem levels with a few exceptions denoted by asterisks:

• Midbrain: 1*-2-3-4

• Pons: 5*-6-7-8*

• Medulla: 9-10-11*-12

The exceptions are as follows:

• CN 1 and CN 11 do not connect with the brainstem.

• CN 5 has nuclei at all three levels of the brainstem (although its fibers enter at the level of the pons as would be expected from the pons = 5*-6-7-8* schema; see Ch. 13).

• For CN 8, the vestibular nuclei are in the medulla and the cochlear nuclei are at the pontomedullary junction.

• CN 2 can be considered a partial exception: Although CN 2’s main projections are the visual pathways, which do not project to the brainstem (see Ch. 6), the afferent limb of the pupillary light reflex is communicated by CN 2 to the midbrain as would be expected by the midbrain = 1*-2-3-4 schema.

The Cerebellar Peduncles

The three cerebellar peduncles nearly correspond to the three levels of the brainstem, with one exception (point 3 below; see also Fig. 8–3).

1. The inferior cerebellar peduncles connect the medulla to the cerebellum.

2. The middle cerebellar peduncles connect the pons to the cerebellum.

3. Although things would have been simpler if the superior cerebellar peduncles connected to the midbrain to give one pair of cerebellar peduncles per brainstem level, the superior cerebellar peduncles connect the cerebellum to the upper pons (en route to connections with the midbrain and thalamus).

The Arterial Supply of the Brainstem

The vascular supply of the brainstem corresponds to its three levels, with one pair of circumferential arteries per level of the brainstem (Fig. 9–2):

1. Superior cerebellar arteries (SCAs) for the midbrain (though the superior midbrain is supplied by the PCAs)

2. Anterior inferior cerebellar arteries (AICAs) for the pons

3. Posterior inferior cerebellar arteries (PICAs) for the medulla

These arteries all have “cerebellar” in their names since they not only supply the brainstem, but also the cerebellum posterior to it. Most commonly, the SCAs and AICAs arise from the basilar artery and the PICAs from the vertebral arteries. The anterior spinal artery arises from the vertebral arteries and supplies the medial medulla and anterior spinal cord. At the level of the pons and midbrain, the midline basilar artery supplies the medial brainstem through penetrating branches.

Tables 9-1, 9-2, 9-3, and 9-4 summarize the structures of the brainstem (Table 9-1), the afferent and efferent limbs of the brainstem reflexes (Table 9-2), the cranial nerve functions, associated nuclei, and skull foramina of entry and exit (Table 9-3), and the cranial nerve nuclei (Table 9-4). Individual cranial nerves and their associated pathways are discussed in more detail in Chapters 10-14.

Crossed Signs Due to Brainstem Lesions

Recall that the corticospinal tracts do not cross until the cervicomedullary junction, the dorsal column pathways cross in the medulla, and the spinothalamic tracts cross in the spinal cord (see Ch. 4). Therefore, throughout most of the brainstem, lesions lead to contralateral weakness and/or sensory symptoms in the extremities. However, with the exception of CN 4, all cranial nerves project ipsilaterally. Therefore, unilateral lesions of the brainstem cause ipsilateral sensory and/or motor symptoms in the face, but contralateral symptoms in the body (crossed signs). For example, a lesion affecting the left pons would cause ipsilateral (left-sided) facial weakness (CN 7) and contralateral (right-sided) arm/leg weakness (not-yet-crossed corticospinal tract).

Medial Versus Lateral Brainstem Syndromes

As discussed above, the descending corticospinal tracts are anterior and medial throughout the three levels of the brainstem, and the motor cranial nerve nuclei for skeletal muscle (CN 3, CN 4, CN 6, CN 12) are posterior and medial and their associated cranial nerves exit anteriorly and medially (with the exception of CN 4, the only cranial nerve that exits posteriorly) (Fig. 9-3). The sensory and special sensory cranial nerve nuclei are dorsolateral in the brainstem. Therefore, lesions of the medial brainstem cause predominantly motor symptoms and signs, whereas lesions of the dorsolateral brainstem cause predominantly sensory and special sensory symptoms and signs. Since the cerebellar peduncles are positioned on the dorsal/dorsolateral aspects of the brainstem (and the cerebellum is just posterior to the brainstem and supplied by the same circumferential arteries), dorsolateral brainstem pathology may cause cerebellar symptoms (e.g., ataxia, nausea/vomiting; see Ch. 8).

For example, in the medulla, the schema to recall the relevant cranial nerve nuclei is “9-10-11*-12,” but we must remove CN 11 (an exception), and add the spinal nucleus of CN 5 (pain and temperature sensation in the face; see Ch. 13) and the vestibular nuclei of CN 8. CN 12 innervates skeletal muscle, and so its nuclei are medial with the bilateral CN 12 exiting anteriorly and medially. The branchial motor nuclei associated with CN 9 and CN 10 are dorsolateral to the CN 12 nucleus. The spinal nucleus of CN 5 and the special sensory vestibular nuclei (CN 8) are dorsolateral to the nuclei of CN 9 and CN 10. Therefore, unilateral medial medullary infarction causes ipsilateral tongue weakness (CN 12) and contralateral extremity weakness (due to involvement of the not-yet-crossed corticospinal tract). In contrast, lateral medullary infarction causes ipsilateral loss of facial pain/temperature sensation (spinal tract and nucleus of CN 5) and contralateral pain/temperature sensation loss in the extremities (due to involvement of the already-crossed anterolateral tract) as well as vertigo (vestibular nuclei), nausea/vomiting and ataxia (inferior cerebellar peduncle and cerebellum), dysarthria and dysphagia (nucleus ambiguus), and ipsilateral Horner’s syndrome (descending oculosympathetic pathway; see. Ch. 10). This constellation of findings in lateral medullary infarction is called Wallenberg’s syndrome. Medial medullary infarction is caused by occlusion of the anterior spinal artery, and lateral medullary infarction is caused by occlusion of the vertebral artery or PICA.

When brainstem syndromes are caused by stroke, a lateral syndrome generally suggests occlusion of a circumferential artery (SCA, AICA, PICA), whereas a medial syndrome generally suggests occlusion of a penetrating branch of the vertebrobasilar system (or the anterior spinal artery at the level of the medulla). Pathophysiologically, a distal occlusion of a circumferential artery can suggest embolism as the mechanism, whereas a more medial stroke in the territory of a penetrating branch from one of the vertebral arteries or the basilar artery can suggest atherosclerosis (see Ch. 19).

Locked-in Syndrome

In locked-in syndrome, the patient is awake and conscious, but cannot move or communicate with the exception of blinking and vertical gaze. The portion of the reticular-activating system responsible for maintaining consciousness and arousal is in the dorsal pons (pontine tegmentum) and midbrain. Ventral pontine lesions (e.g., basilar artery thrombosis, pontine hemorrhage, central pontine myelinolysis) cause loss of all motor function controlled by the pons (resulting in quadriplegia, bilateral facial weakness, horizontal gaze palsy), but the patient may still be awake and able to blink and look vertically if the dorsal pons, midbrain, and structures superior to it (i.e., thalami, cerebral hemispheres) are spared. (In basilar thrombosis, these regions can be perfused by collateral flow through the posterior communicating arteries to the posterior circulation distal to the occlusion). It is important to distinguish the locked-in state from coma, since a locked-in patient is conscious (as compared to a comatose patient, who is not).