Brainstem and Cranial Nerve Dysfunction

Brainstem Localization

Knowledge of the long tracts that ascend and descend through the brainstem and the locations of cranial nerve and other brainstem nuclei are critical for the localization of brainstem lesions. These can be considered along three important axes: rostral-caudal, dorsal-ventral, and medial-lateral. In general (with exceptions), the rostrocaudal direction reflects the different cranial nerve nuclei, the dorsal-ventral axis separates cranial nerve nuclei (dorsal) from long tracts passing through the brainstem (ventral), and the medial-lateral direction within each side of the brainstem separates motor (medial) from sensory (lateral) structures.

Localization of lesions affecting the brainstem is easier if a systematic approach is used. When faced with a difficult diagnostic problem, it is important to think systematically rather than relying on the many complicated brainstem syndromes. Important questions to ask include the following:

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  Is the lesion intra-axial or extra-axial?

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  What is the rostrocaudal location of the lesion?

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  Is the intraaxial lesion unilateral or bilateral?

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  What clinical conditions can produce damage in this localization?

Isolated single cranial nerve palsies are usually extra-axial, that is, not in the substance of the brainstem. Multiple cranial nerve palsies can still be caused by extraaxial disease. An intraaxial lesion is suggested by the combination of cranial nerve palsies and signs of damage to ascending and descending tracts. For example, an isolated CN VI palsy, which causes impaired abduction of the ipsilateral eye, is relatively common and can result from microvascular disease, trauma, and increased intracranial pressure, although it is often idiopathic. In contrast, a CN VI palsy combined with damage to the medial longitudinal fasciculus, which causes internuclear ophthalmoplegia, is caused by a lesion in the pons.

Rostrocaudal localization is most easily identified by carefully determining which cranial nerves are affected. For example, an oculomotor lesion with signs of intraaxial damage suggests a midbrain lesion, whereas glossopharyngeal and vagus damage suggests a medullary lesion.

Determination of whether the lesion is unilateral or bilateral requires understanding of which tracts are crossed and at which level. The descending corticospinal tracts cross in the medulla. The dorsal columns, which carry information about fine touch, vibration, and proprioception, ascend the spinal cord uncrossed, synapse in the nucleus gracilis and nucleus cuneatus in the medulla, and then cross as they ascend through the medulla, forming the medial lemniscus. The spinothalamic tract axons, which convey pain and temperature sensation, cross within the spinal cord segment and then ascend crossed in the cord. The spinothalamic tract stays lateral in the brainstem and ascends to the midbrain where it joins with the medial lemniscus to enter the thalamus.

Once the lesion has been determined to be intraaxial and the rostrocaudal and unilateral or bilateral localization has been made, individual syndromes can be considered. Specific etiologies are suggested by associated symptoms; for example, acute onset of a deficit suggests ischemic stroke, sudden onset of headache and vomiting suggests a hemorrhage, and a slowly progressive deficit suggests an expanding mass lesion.