Answers to Clinical Cases

1. Ventricular enlargement is a consequence of loss of neural tissue. Because the volume of the skull is fixed, as brain tissues decrease in volume due to a neurodegenerative process, there is a corresponding increase in ventricular volume.

2. The cerebral cortex and hippocampal formation are severely affected. By contrast, brain stem structures are not.

1. Both the dorsal column-medial lemniscal pathway and the corticospinal tract decussate within the ventral portion of the medulla. Without these decussations, the two sides of the ventral medulla become somewhat separated. CSF is present where the decussating axons should be. Axons important for coordinating eye movements normally decussate in the dorsal pons. Without this decussation, the two sides of the dorsal pons also become somewhat separate, as revealed by the presence of CSF and the formation of a shallow sulcus.

2. No, the corpus callosum is an example of a structure with intact decussating axons.

1. The proximal portion of the middle cerebral artery became occluded. This affected both deep branches to subcortical white matter and superficial branches supplying the cerebral cortex.

2. Since all descending motor control axons converge within the internal capsule, damage to this structure alone can produce the major limb and facial motor signs seen in this patient.

1. Mechanoreceptive axons ascend within the dorsal columns, including those for touch, vibration sense, and limb proprioception. It is unclear why the patient's touch sense was spared.

2. The ability to maintain an upright posture depends, in part, on lower limb proprioception. Without limb proprioception, vision can partially substitute. Therefore, when this patient closes his eyes, he is deprived of this compensating modality and, in consequence, he looses his balance.

1. Anterolateral system axons decussate just ventral to the central canal, where the syrinx originates. This is why they are damaged first. Mechanoreceptive axons are located farther dorsally, affording them some protection initially.

2. Limb motor neurons are located ventrolateral to the syrinx. As with the dorsal mechanoreceptive axons, motor neurons are initially afforded protection by their distance from the initial site of syrinx development. Eventually the syrinx expands to affect a significant portion of the ventral horn.

1. The posterior inferior cerebellar artery, or PICA, supplies the dorsolateral medulla. This was infarcted in the patient. The territory supplied by PICA receives little or no collateral circulation from other arteries, which makes this region of the medulla particularly vulnerable to ischemia. Whereas only a wedge-shaped infarcted region is revealed on the MRI, it is likely that the entire territory is affected because of the paucity of collateral circulation.

2. PICA occlusion destroys the spinal trigeminal tract and nucleus at this level and caudal. These structures carry information about trigeminal protective senses on the ipsilateral side. By contrast, PICA occlusion damages the ascending anterolateral system fibers, which carry information from the contralateral limbs and trunk.

1. See Figure 7–17C.

2. The infarction involved more than only the primary visual cortex on the medial occipital lobe surface. The optic radiations were also damaged.

3. The posterior parietal lobe, necessary for attending to stimuli, and the lateral occipital cortex, important for visual spatial function, were not affected by occlusion of the posterior cerebral artery.

1. Unilateral hearing loss occurs because the acoustic neuroma impedes conduction of signals from auditory structures to the brain stem. Impairment in pons and cerebellar function, due to compression by the neuroma, likely explains the gait instability. Impairment in conduction of facial muscle control signals by the seventh (facial) nerve, because of compression by the neuroma, leads to mild flattening of the left nasolabial fold.

2. There is no impairment of the middle ear ossicles with an acoustic neuroma, hence preservation of air conduction.

1. Taste buds in different locations on each side of the tongue are innervated by different peripheral nerves. Damage to multiple nerves, with very different peripheral locations, must occur for complete taste loss on one side of the tongue. By contrast, a single central lesion can disrupt taste information transmission to the thalamus and cortex.

2. The taste pathway, unlike other sensory pathways, is ipsilateral.

3. The central tegmental tract transmits taste information to the thalamus. A nearby structure, the parabrachial nucleus, is also involved in visceral and chemical sensations. The function of this nucleus also could be affected.

1. Because the ascending pain pathway, the anterolateral system, decussates caudal to the lesion, the affected axons originated from the contralateral side. The ascending tactile pathway, the dorsal column, is an ipsilateral spinal path; it decussates in the medulla. The affected axons are on the same side as the lesion.

2. The anterolateral system decussates as it ascends. Neurons contributing to this pathway at the level of the lesion do not reach the affected side until 1-2 segments rostrally. Therefore, they bypass the injury.

3. The key motor pathway damaged by the lesion, the corticospinal tract, decussates rostral to the lesion, in the medulla. The damaged axons control muscles on the side of the spinal injury. This same side is also affected by damaged to the dorsal columns.

1. Based on changes in signal on the MRIs, the location of the infarction is in the ventral pons, close to the midline. This is within the territory of paramedian and short circumferential branches of the basilar artery (see Figure 3–3B2).

2. Lower facial muscle control is mediated by a contralateral corticobulbar projection, as is limb muscle control. Therefore, after unilateral lesion of the corticobulbar and corticospinal tracts, there is loss of control of these muscles. By contrast, upper facial muscles and trunk muscles receive more bilateral control, so that after unilateral lesion, there is some residual, redundant, control.

3. After damage to the corticospinal tract, there are plastic changes that result in increased contralateral deep tendon reflexes. This results in abnormal limb posture, increased muscle tone, and difficulty in controlling the weakened limb. Usually these changes present weeks after the injury, but in this patient they occurred immediately after the injury. Further, these changes are most common after damage to the corticospinal tract during development, such as in cerebral palsy, and after spinal cord injury, and less frequent after adult stroke.

1. This is due to a lesion of the left abducens nucleus. Abducens motor neurons are lesioned, which prevents left eye abduction. Further, there may be a slight adduction because of the unopposed action of the medial rectus muscle (Figure 12–1A, top). The right eye fails to adduct because internuclear neurons connecting the left abducens nucleus with the right oculomotor nucleus are lesioned.

2. This is due to a lesion of the MLF on the left side. This interrupts the signal to activates the right medial rectus muscle; hence, the right eye does not adduct.

1. Romberg sign (see Chapter 4) is the inability of a person to stand upright when his or her eyes closed. There is swaying and a lost balance. It is due to loss of lower extremity proprioceptive. In Friedreich ataxia there is a loss of lower extremity proprioceptive because of degeneration of large-diameter mechanoreceptive afferents.

2. This is a classical posture use by patients with cerebellar disease. It is likely a strategy to provide better stability in maintaining an upright posture, in the face of impaired limb proprioception and motor control.

1. The action of the basal ganglia on each side is to influence control on contralateral musculature. Basal ganglia output is directed to ipsilateral thalamus and motor cortex, which, in turn, controls contralateral muscles. Brain stem output would also be expected to primarily affect contralateral limb control, likely by contralateral reticulospinal projections.

2. Lenticulostriate branches of the middle cerebral artery supply the subthalamic nucleus.

1. A branch of the posterior inferior cerebral artery (PICA) was affected. Since the total territory of PICA was not infarcted, the occlusion was most likely that of a more distal branch.

2. (1) loss of ipsilateral facial pain: spinal trigeminal tract and nucleus; (2) contralateral pain loss: anterolateral system; and (3) ataxia: climbing fibers from the olive, dorsal spinocerebellar tract, cuneocerebellar tract, and other fibers of the inferior cerebellar peduncle; (4) hoarse voice: nucleus ambiguus and consequent paralysis of ipsilateral laryngeal muscles; (5) ipsilateral ptosis: descending hypothalamic fibers that regulate the sympathetic nervous system control of the tarsal muscle.

1. The temporal lobe serves diverse functions. The superior temporal gyrus is key to audition and language. The middle and inferior temporal gyri are important for visual perception. The temporal pole and medial temporal lobe contain limbic association cortex. The temporal pole, corresponding to Brodmann's area 38, is important in personality. This is the part damaged in the patient. This area has extensive interconnections with other limbic system cortical regions as well as the amygdala.