Level of the Superior Colliculus
Tectum
In the rostral half of the midbrain, the tectum is formed by the superior colliculus, which has replaced the inferior col-liculus (Figs. 12-5 and 12-6). The superior colliculus receives retinal inputs. Its projections to the cervical spinal cord via the tectospinal tract presumably serve to produce reflex movements of the head and neck in response to sensory inputs. It contributes to the regulation of oculomotor responses and, in particular, mediates tracking movements of objects as they move through the visual field (i.e., horizontal conjugate gaze).
Tegmentum
There are few overt morphological changes in the appearance of the PAG at the level of the superior colliculus relative to that of the inferior colliculus. Just below the PAG lies the oculomotor nuclear complex (CN III), which has now replaced the trochlear nucleus (Fig 12-5). The oculomotor nerve, which includes both GSE and general visceral efferent components, passes through the red nucleus and exits in a ventromedial position within the midbrain. The somatomotor component includes nerve bundles that innervate the medial, inferior, and superior rectus muscles as well as the inferior oblique and levator palpebrae muscles. Thus, the somatomotor components of this cranial nerve are essential for most vertical eye movements, medial deviation of the eyes, and elevation of the eyelid.
Another major change that takes place at this level is that the red nucleus begins to replace the superior cere-bellar peduncle. The red nucleus is present throughout the rostral half of the midbrain and extends into the caudal diencephalon (Fig. 12-5). It plays an important role in motor functions. The axons supply all levels of the spinal cord and facilitate the discharge of flexor motor neurons. The red nucleus also influences cerebellar activity by projecting its axons to the inferior olivary nucleus, which, in turn, supplies the contralateral cerebellar cortex.
An additional new feature of the tegmentum is the presence of an important source of dopaminergic fibers that supply much of the forebrain, other than the striatum. These dopaminergic cells are located in the ventromedial aspect of the tegmentum, called the ventral tegmental area, adjacent to the position occupied by the pars com-pacta of the substantia nigra (Fig. 12-5).
Other features of the tegmentum remain essentially similar to those found at the level of the inferior colliculus. Ascending sensory pathways (i.e., medial lemniscus and trigeminothalamic and spinothalamic fibers) are situated in the lateral aspect of the tegmentum. Likewise, the sub-stantia nigra remains essentially unchanged at this level. The reticular formation is also present throughout this level of the tegmentum and extends to the rostral limit of the midbrain.
Crus Cerebri
The crus cerebri appears similar at all levels of the mid-brain, and the topographical arrangement of the descending fibers remains the same as described earlier for the level of the inferior colliculus.
At the far rostral aspect of the midbrain, several morphological changes begin to appear. On the dorsal aspect of this level of the midbrain, the superior colliculus is replaced by a large mass of cells called the pretectal region (or area). This region constitutes part of the circuit for the pupillary light reflex, which is a reflex that causes constriction of the pupil when the eye is exposed to light. This reflex involves the activation of retinal fibers (in response to light) that make synaptic contact with neurons in the pretectal region, which, in turn, project to the nucleus of CN III. Preganglionic parasympathetic neurons of the Edinger-Westphal nucleus send their axons in CN III and then synapse with postganglionic neurons in the ciliary ganglion, which innervate the pupillary constrictor muscles of the pupil. It is via this reflex pathway that, when light is shone into the eye, the pupil constricts (i.e., pupillary light reflex).
This parasympathetic component also innervates the ciliary muscle, which, when contracted, causes a release of the suspensory ligament of the lens; the result is an increase in the curvature of the lens. When this parasympathetic component, together with the somatic motor component of CN III, is activated, an accommodation reaction for near vision takes place.
Other morphological changes that may be noted at this level include the presence of the posterior commissure, which is situated just dorsal to the PAG. It contains fibers that arise from various nuclei, including the pretectal region, which synapse with cranial nerve nuclei that control extraocular eye muscles. Such connections coordinate movements of the two eyes.
Because this level of the brainstem constitutes a transitional region between the midbrain and diencephalon, it is not surprising that several structures associated with the diencephalon begin to appear in sections at this level. Three thalamic nuclei are evident that appear to sit over the midbrain like a tent. The largest of these structures is called the pulvinar, which is a massive nucleus that forms a large part of the posterior thalamus and which lies dorsolateral to the pretectal region and superior colliculus. Two other nuclei include: the medial geniculate nucleus, which is part of the auditory relay system and located lateral to the tegmentum, and the lateral geniculate nucleus, which is part of the visual relay pathway and located lateral to the medial geniculate nucleus.
Clinical Considerations
The most common disorders of the midbrain result mainly from vascular lesions of branches of the posterior cerebral artery but may also derive from tumors such as those situated in the region of the pineal gland.
Weber’s Syndrome
Weber’s syndrome is characterized by an ipsilateral oculomotor paralysis, coupled with a contralateral upper motor neuron paralysis. The specific oculomotor deficits may include a dilated, unresponsive pupil, a drooping eyelid, and an eye that deviates downward. This disorder typically results from a vascular lesion that affects the medial aspect of the cerebral peduncle at the level of the superior colliculus and the root fibers of the oculomotor nerve.
Benedikt’s Syndrome
In Benedikt’s syndrome, the patient exhibits an ipsilateral paralysis of the oculomotor nerve as well as a tremor of the opposite limb, coupled with possible somatosensory loss in the contralateral side of the body. This disorder also results from a vascular lesion that affects root fibers of the oculomotor nerve and the region of the red nucleus, including the superior cerebellar peduncle and adjoining portions of the medial lemniscus and, possibly, the spinothalamic tracts. The tremor may result from damage to the superior cerebellar peduncle or to fibers of the basal ganglia that pass close to the red nucleus or, perhaps, even damage to the red nucleus itself. Sensory loss is likely due to damage to the medial lemniscus and spinothalamic tracts.
Gaze Palsy (Parinaud’s Syndrome)
Gaze palsy results from a vascular lesion or a pineal tumor and involves the dorsal aspect of the midbrain, including the pretectal area and region of the posterior commissure. The patient presents with an upward gaze paralysis,possible nystagmus with downward gaze, light-near dissociation, large pupil, abnormal elevation of the upper lid, and paralysis of accommodation.
Clinical Case
History
Mark is a 35-year-old man without prior history of any neurological dysfunction. For several days, some of his friends thought that his left pupil was somewhat dilated, and for a day or so, he was perhaps developing a "lazy eye," in which he had difficulty in opening the eye. He ignored the comments and did not seek medical advice. While driving, he noticed that he had some difficulty seeing; he experienced double vision, and, while swerving to avoid hitting a tree that he believed suddenly"came out of nowhere," he collided with a tree that he didn’t see at all on his left side. While he was waiting for the ambulance, he thought that perhaps he had hurt his right leg because he had difficulty moving it.
Examination
After arriving at the emergency room, a neurologist was called in because of the damage to Mark’s left eye and right leg.The left eye was found to deviate to the left. When Mark attempted to look toward the right, his left eye remained deviated to the left and somewhat inferiorly.The pupil in that eye did not react when a flashlight was shone into it.The left side of Mark’s mouth did not elevate as much as the right side when he was asked to smile, but his forehead remained symmetric when he raised his eyebrows. Both his right arm and leg were slightly weak, and when the lateral aspect of the plantar surface of his right foot was scratched, the great toe dorsiflexed and the other toes fanned upwards. When this maneuver was repeated on the left side, the toes deviated downward. Mark was immediately sent for a magnetic resonance imaging scan (MRI) of his head.
Explanation
Mark has Weber’s syndrome,a lesion involving the midbrain in which the outflow tract of the third cranial nerve is compromised as well as are the corticospinal and corticobulbar tracts running through the cerebral peduncle. The MRI scan revealed an aneurysm (out-pouching of the artery, often congenital in origin) of the posterior communicating artery pressing on the left cerebral peduncle and outflow tract of the left third nerve.
Cranial nerve III innervates four of the six extraocular muscles, which move the eyes. Unopposed actions of the superior oblique and lateral rectus muscles, the only two muscles that the third nerve doesn’t innervate, cause the eye to remain in a "down-and-out" position. Pressure from the aneurysm on the third nerve fibers originating ftom the Edinger-Westphal nucleus causes the pupil to be nonreactive.The pressure on the cerebral peduncle causes the classic upper motor neuron findings, such as facial palsy with sparing of the forehead due to bilateral central innervation of this area, weakness, and Babinski sign on the right foot.
Weber’s syndrome may also occur as a stroke syndrome, resulting from occlusion of the interpeduncular branches of the posterior cerebral artery, a tumor pressing on this area, or a multiple sclerosis plaque.
SUMMARY TABLE
Major Fiber Tracts and Nuclear Groups of the Midbrain
|
Name of Structure |
Function |
Effects of Lesions |
|
|
Fiber Tracts |
|
|
Cerebral peduncle |
Contains corticobulbar,corticospinal,and corticopontine fibers |
Upper motor neuron paralysis affecting the limbs; disruption of motor functions associated with cranial nerve function (pseudobulbar palsy,see Chapter 19) |
|
Medial lemniscus |
Transmits conscious proprioception, pain, and temperature from the body and limbs to the thalamus (and then to cerebral cortex) |
Loss of conscious proprioception and some pain and temperature from the body and limbs; some ataxia of movement |
|
Medial longitudinal fasciculus |
Terminal endings of ascending component is present at the caudal level of midbrain; regulates position of the eyes in response to vestibular input |
Impaired adduction of eye contralateral to lesion; nystagmus |
|
Lateral spinothalamic and trigeminothalamic tracts |
Mediates pain and temperature sensation from the opposite side of body and head region |
Loss of pain and temperature sensation from the opposite side of the body and mostly the opposite side of the head |
|
Nuclear Groups |
||
|
Periaqueductal gray |
Site of descending sympathetic fibers to lower brainstem autonomic neurons; site of descending fibers mediating inhibition of pain (see Chapter 15); regulation of emotional behavior, including fear,flight, anxiety, rage behavior) |
Disruption of sympathetic regulation within the CNS (possible development of Horner’s syndrome); disruption of expression of selected forms of emotional behavior such as rage, flight, and fear; disruption of the pain inhibitory pathway, most likely leading to more intense feelings following nociceptive stimulation |
|
Superior cerebellar peduncle |
Contains ascending fibers from cerebellum to red nucleus and thalamus |
Ataxia; presumed loss of coordinated movements |
|
Red nucleus |
Gives rise to rubrospinal tract that facilitates flexor motor neurons of the contralateral side |
Largely unknown, but lesions of this pathway would likely affect coordination of purposeful movements associated with cerebellar functions |
|
Reticular formation (including some raphe neurons and ventral tegmental neurons) |
Nuclei and fibers mediating varieties of functions such as sleep and wakefulness, sensory, motor, and autonomic functions; raphe neurons are serotonergic and project to much of the CNS; ventral tegmental neurons are dopaminergic and project to much of the forebrain |
Mainly, loss of consciousness; disruption of processes associated with regulation of emotional behavior, which may result in conditions such as anxiety, depression, and related disorders (see Chapter 28 for details) |
|
Trochlear nerve (CN IV) |
Mediates lateral movement of the ipsilateral eye |
Diplopia, especially when downward gaze is attempted |
|
Oculomotor nucleus and nerve (CN III) |
Contains both general somatic efferent, innervating all extraocular eye muscles except superior oblique (for movement of the eye) and general visceral efferent neurons innervating ciliary ganglion and muscle and radial (constrictor) muscles of eye for control of accommodation and pupillary light reflexes, respectively |
Loss of ability to direct eye medially as well as considerable loss of up and down movement; disruption of papillary light and accommodation reflexes |
|
Name of Structure |
Function |
Effects of Lesions |
|
|
Nuclear Groups |
|
|
Inferior colliculus |
Auditory relay nucleus mediating auditory signals to the medial geniculate nucleus of thalamus |
Some CNS hearing loss |
|
Superior colliculus |
Receives some visual inputs from optic tract fibers; descending fibers form tectospinal tract, which plays a role in tracking movements of the eys and reflex movements of head and neck |
Largely unknown |
|
Substantia nigra |
Contains both dopaminergic (pars com-pacta) and GABAergic neurons (pars reticulata). Dopaminergic neurons project to neostriatum and GABAergic neurons project to thalamus, both of whose projections contribute to regulation of motor functions |
Loss of dopamine neurons in substantia nigra results in Parkinson’s disease |
CNS = central nervous system; CN = cranial nerve; GABA = gamma-aminobutyric acid.
