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).
Axial diffusion-weighted MRI of medial and lateral medullary infarction: A: Left medial medullary infarction. B: Left lateral medullary infarction.
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).
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).