Neuroscience '04 at RWJMS Course Director, Richard S. Nowakowski, Ph.D. (e-mail: neuro@umdnj.edu) Department of Neuroscience and Cell Biology Robert Wood Johnson Medical School
Answers for CLINICAL PROBLEM SOLVING: Brainstem Lesions

CASE A: Answers

1. The symptoms result from damage to specific structures as follows:
   1. left vestibular nuclei (also vestibulocerebellar interconnections via the inferior cerebellar peduncle),
   2. left inferior cerebellar peduncle,
   3. nucleus ambiguus,
   4. efferent axons of cranial nerves IX and X,
   5. left solitary tract and nucleus, (Note this might be seen only as "diminished taste sensation" rather than a "loss" of taste.)
   6. left spinal nucleus and tract of V,
   7. left lateral spinothalamic tract,
   8. descending central autonomic fibers (originating in the reticular formation and hypothalamus) passing through the brainstem tegmentum on the left (exact location unclear).
2. The lesion is in the dorsolateral portion of the rostral (open) medulla on the left side. This constellation of symptoms is known as lateral medullary syndrome (or Wallenberg's Syndrome).
3. Lateral medullary syndrome is the most common of the medullary syndromes and is frequently the result of thrombosis of the posterior inferior cerebellar artery (PICA) or the vertebral artery from which the PICA arises.

CASE B: Answers

1. The symptoms result from damage to several structures as follows:
   1. the right abducens (VI) nerve or nucleus (innervating the lateral rectus muscle), leaving the medial rectus unopposed;
   2. the medial longitudinal fasciculus (interconnecting the IIIrd, IVth and VIth nuclei);
   3. the right facial (VII) nerve or nucleus; (N.B. The asymmetry in both upper and lower quadrants suggests lower motor neuron involvement, because the upper motor neuron (corticobulbar) input to the VIIth nucleus is bilateral to the neurons which innervate the forehead; thus an upper motor neuron lesion is likely to produce asymmetry in the lower quadrant only.)
   4. the corticospinal tract originating in the right hemisphere; considered alone, the lesion could occur anywhere from the precentral gyrus, through the internal capsule, cerebral peduncle, ventral pons and medulla on the right or in the left dorsolateral funiculus of the upper spinal cord; however, based on the cranial nerve symptoms, it can be localized to the right side of the brainstem, above the pyramidal decussation;
   5. the right medial lemniscus; similar loss could result from lesion of the dorsal columns in the upper spinal cord or dorsal column nuclei on the left; however, the cranial nerve symptoms indicate damage of the medial lemniscus itself.
2. Because of the internal strabismus and impaired conjugate eye movements, the woman sees double when both eyes are open. Closing one eye to eliminate the diplopia is a common reaction.
3. This is an infarction of the pons on the right side at the level of the facial colliculus. A paramedian infarction would involve the MLF, abducens nucleus and nerve, fascicles of the VIIth nerve, and possibly the medial lemniscus. Involvement of the corticospinal tract in this patient suggests a basal infarction that encroaches on more lateral portions of the basal pons as well. Corticospinal tract involvement is more prominent in basal infarctions of the pons, while conjugate gaze is more frequently spared. Unilateral loss of function of the VIth and VIIth nerves accompanied by contralateral hemiplegia constitutes Millard-Gubler Syndrome, while involvement of only cranial nerve VI with contralateral hemiplegia is Raymond's Syndrome. However, because the axons of the pyramidal tract are dispersed in the basal pons, the hemiplegia may be incomplete in either. In Foville's Syndrome the infarction extends even more laterally and includes ipsilateral facial numbness and paralysis, Horner's syndrome, conjugate gaze palsy and deafness in addition to the VIth nerve palsy and contralateral hemiplegia. The facial weakness resulting from pontine lesions can be very complex, depending on the extent of damage to upper and lower motor neurons.

CASE C: Answers

1. The symptoms result from damage to specific structures as listed below, and the time course of the development of the symptoms suggests the presence of a slow-growing tumor.
   1. left cochlear (VIII) nerve,
   2. left vestibular (VIII) nerve,
   3. left sensory V and left motor VII,
   4. sensory root of the left trigeminal (V) nerve,
   5. motor root of the left trigeminal (V) nerve,
   6. left facial (VII) nerve,
   7. left facial (VII) nerve,
   8. cerebellar peduncles and cerebellum and/or vestibular (VIII) nerve. (Could be either side, but since other symptoms are on the left, the left side should be the strongest suspect.)
2. This is a large acoustic neuroma in the cerebello-pontine angle on the left side of the brainstem which has begun to compress the cerebellum and brainstem. This kind of tumor generally arises from the Schwann cells on the vestibular division of the VIIIth nerve and enlarges (often very slowly, perhaps over 10 - 20 years!) to put increasing pressure on the facial and trigeminal nerves, then on cerebellar peduncles, cerebellum and underlying brainstem nuclei. The first symptoms detected are usually auditory and involve a progressive loss of hearing, sometimes preceded by a period of tinnitus. One of the most reliable symptoms is impairment of the corneal reflex, since the trigeminal afferent axons of that reflex arc (unlike the other cranial nerves in the region) are particularly sensitive to the mechanical stresses imposed by the tumor. Other tumors of the cerebellopontine angle follow a different clinical sequence.

CASE D: Answers

1. The specific symptoms are caused by involvement of structures as follows:
   1. Corticospinal tract axons originating from the right hemisphere; the lesion could be anywhere along the pathway from cortex through the internal capsule, cerebral peduncle, ventral brainstem on the right to dorsolateral funiculus of the upper spinal cord on the left. Note that "paresis" is a partial or incomplete paralysis and is sometimes used to describe a general weakness or loss of strength.
   2. Corticospinal tract axons originating from the right hemisphere PLUS corticobulbar and/or bulbospinal pathways in the right side of the brainstem and/or left side of the upper spinal cord. These pathways are adjacent to each other in the internal capsule and cerebral peduncle and also in the lateral funiculus of the spinal cord.
   3. Corticospinal tract axons originating from the right hemisphere; the lesion could be anywhere along the pathway from cortex through the internal capsule, cerebral peduncle, ventral brainstem on the right to dorsolateral funiculus of the upper spinal cord on the left.
   4. Corticobulbar projections to the left motor nucleus of the VIIth nerve; these axons originate in the right hemisphere and travel in close proximity with the corticospinal tract, through the internal capsule and cerebral peduncle on the right, then crossing to the opposite side at the level of the VIIth nerve nucleus. N.B. a lesion of the left VIIth nerve or nucleus would produce a weakness in both upper and lower quadrants of the left side of the face; sparing of the upper quadrant suggests an upper motor neuron lesion, since the corticobulbar innervation for the upper face is bilateral.
   5. Fascicles of the right oculomotor (III) nerve exiting between the cerebral peduncles cause a complete IIIrd nerve palsy or oculomotor ophthalmoplegia: strabismus with consequent diplopia (double vision), ptosis, dilation of the pupil, downward, abducted position of the eye, and loss of accommodation.
   6. right optic tract.
2. The lesion is located in the ventral region of the midbrain on the right side and involves the cerebral peduncle (containing the corticospinal and corticobulbar tracts), the IIIrd neve, and the optic tract. Complete IIIrd nerve palsy in combination with contralateral hemiplegia including the face constitutes Weber's syndrome and can result from basal infarction of the midbrain. In this patient, the optic tract was also involved, producing blindness in the left visual field (vs the left eye).
3. The apparent discrepancy between the patient's complaint and the actual visual field deficit is common and illustrates the importance of visual field testing.