Caudal Basal Pontine Syndrome
Caudal basal pontine syndrome, which is associated mainly with the paramedian branches of the basilar artery, affects mainly the descending corticospinal tract and root fibers of CN VI if the lesion extends far enough medially. The effects of such a lesion would typically produce contralateral hemiplegia and signs of paralysis of CN VI (loss of lateral gaze in the eye on the side ipsilateral to the lesion).
Rostral Basal Pontine Syndrome
Occlusion of portions of the paramedian branches of the basilar artery, which affects the rostral half of the basilar pons (rostral basal pontine syndrome), will most likely affect axons of sensory and motor components of the trigeminal nerve and the corticospinal tract. The common deficits would presumably include a contralateral hemiplegia (corticospinal tract deficit) and ipsilateral loss of facial sensation and ability to chew (CN V deficits).
Rostral Pontine Tegmental Syndrome
Rostral pontine tegmental syndrome is associated mainly with occlusion of the long circumferential branches of the basilar artery. The structures affected include the sensory and motor nuclei of CN V, medial lemniscus, spinothalamic tracts, reticular formation, and, if the lesion extends far enough laterally, the cerebellar afferent fibers contained in the middle cerebellar peduncle. The deficits associated with this syndrome would typically include ipsilateral loss of sensation to the face and ability to chew (CN V deficits); contralateral loss of pain, temperature, Horner’s syndrome, and conscious proprioception from the body (spinothalamic and medial lemniscal deficits); and, possibly, ataxia of movement (due to disruption of the cerebellar afferent fibers).
Other Related Syndromes of the Pons
In addition to the syndromes just described, others have been characterized, and several of them are noted here.
The Locked-ln Syndrome
After a large infarct of the basilar pons, there is significant loss of functions associated with both the corticobulbar and corticospinal tracts in locked-in syndrome. As a result, there is a paralysis of most motor functions, including the limbs (corticospinal loss), and functions associated with motor cranial nerves (corticobulbar loss), other than the ability to blink one’s eyes and display vertical gaze. Consequently, the patient can only communicate by blinking or moving his or her eyes.
The Medial Tegmental Syndrome
If the lesion is restricted to the medial aspect of the pons, the likely targets will include the nucleus of the abducens nerve (CN VI), the fibers of the facial nerve (CN VII), which pass over the nucleus of CN VI, and, possibly, the medial lemniscus in the medial tegmental syndrome. The consequent loss of functions will include an ipsilateral facial paralysis, loss of lateral gaze on the side ipsilateral to the lesion, and contralateral loss of conscious proprioception and discriminative touch if the lesion extends sufficiently ventral to involve the medial lemniscus.
The One-and-a-Half Syndrome
If there is a discrete lesion of the dorsomedial tegmentum, which involves the nucleus of CN VI, the pontine (lateral) gaze center of the paramedian pontine reticular formation,and the MLF, the patient will display one’and’a'half syndrome that includes a combination of lateral gaze paralysis (CN VI) coupled with an internuclear ophthalmoplegia (an inability to gaze to the side of the lesion). Thus, the patient cannot move the ipsilateral eye horizontally, and the contralateral eye can only be abducted, usually resulting in nystagmus of that eye.
Clinical Case
History
On an intern’s first night on call in the hospital, a nurse asked the intern to come to the room of an elderly patient named Seymour, who suddenly appeared to have become comatose. Except for a history of vascular disease and an inability to stop smoking, there did not seem to be any clues to the cause of the man’s coma.
Examination
The intern examining Seymour noticed that he appeared at first to stare straight ahead and blinked when the intern asked him to do so. When asked to blink twice or keep his eyes closed, he was also able to comply. However, he was unable to follow any commands involving other parts of his body. Seymour was unable to speak or move his arms or legs. He was able to move his eyes in the direction of the intern when he spoke. The intern asked Seymour to blink twice if he understood the commands but was unable to move, and he complied. His arms and legs appeared to be paralyzed, and when the lateral portion of the plantar surface of both his feet were scratched, the great toes dorsiflexed with an upward fanning of the remaining toes.
Explanation
Seymour has locked-in syndrome, a syndrome of infarction of the medial half of the basilar pons supplied by the basilar artery.This area contains the corticospinal and corticobulbartracts, and infarction of this area causes paralysis of most, if not all, motor functions, including bilateral paralysis of the face and body as well as loss of voice. Often, the tegmentum of the pons (i.e„ reticular formation) is spared, thus preserving consciousness and sensation.Therefore,the patients who suffer an infarction of this type will appear to be comatose but remain alert. One of the first descriptions of this syndrome can be found in The Count of Monte Cristo, by Alexandre Dumas, written in 1844.The character, Monsieur Noirtrier de Villefort, lost the use of his voice and limbs; he was able to communicate by the use of eye-blinks and went as far as to dictate a will in this manner.The condition, as described by Dumas, occurred suddenly and was probably the result of a vascular accident.
SUMMARY TABLE
Major Fiber Tracts and Nuclear Groups of the Pons and Cerebellum
|
Name of Structure |
Function |
Effects of Lesions |
|
|
Fiber Tracts: Pons |
|
|
Pyramidal tract (includes small component of the corticobulbar tract) |
Mediates voluntary control of movement of the limbs and motor functions of CN IX, X,and XII |
Upper motor neuron paralysis affecting the limbs and disruption of motor functions associated with CN IX,X,and XII |
|
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 |
Ascending component is present at this level only: Regulates position of the eyes in response to vestibular input |
Impaired adduction of eye contralateral to lesion; nystagmus |
|
Descending tract of CNV (in caudal pons only) |
First-order neuron mediating somatosensory (especially pain and temperature) sensation from the head to brain |
Loss of pain and temperature sensation from the ipsilateral head region |
|
Lateral spinothalamic tract |
Mediates pain and temperature sensation from the body |
Loss of pain and temperature sensation from the opposite side of the body |
|
Trapezoid body |
Mediates auditory signals from cochlear nuclei to the superior olivary nucleus |
Likely partial CNS auditory deficits |
|
Rubrospinal tract |
Facilitates flexor motor neurons |
Unknown, because pure rubrospinal tract lesions have not been reported |
|
Medial reticulospinal tract |
Facilitates muscle tone via their actions upon alpha and gamma motor neurons |
Specific lesions of this pathway have not been reported but, in theory, loss of such inputs from this pathway to spinal cord might produce hypotonia (see Chapters 19 and 23) |
|
Transverse pontine fibers |
Mediates fibers from deep pontine nuclei to cerebellum as part of a two-neuronal pathway linking the cerebral cortex with cerebellar cortex |
Largely unknown, but lesions of this pathway would likely affect coordination of purposeful movements associated with cerebellar functions |
|
Nuclear Groups: Pons |
||
|
Vestibular nuclei (lateral and superior) |
Transmits vestibular inputs to spinal cord, cranial nerve nuclei mediating eye movements (i.e., CN VI, IV, and III), and to cerebellum |
Nystagmus; impaired adduction of eye contralateral to lesion; possible ataxia due to loss of input to cerebellum |
|
Deep pontine nuclei |
Origin of transverse pontine fibers that pass through middle cerebellar peduncle to cerebellar cortex, mediating inputs from cerebral cortex to cerebellar cortex |
Largely unknown, but lesions of this pathway would likely affect coordination of purposeful movements associated with cerebellar functions |
|
Reticular formation |
Nuclei and fibers mediating varieties of functions such as sleep and wakefulness, sensory, motor, and autonomic functions |
Mainly loss of consciousness |
|
Abducens nucleus (CN VI) |
Mediates lateral movement of the ipsilateral eye |
Inability of ipsilateral eye to abduct, producing strabismus (inability of both eyes to focus on the same object) |
|
Name of Structure |
Function |
Effects of Lesions |
|
|
Nuclear Groups: Pons |
|
|
Facial nucleus and nerve (CN VII) |
Motor nucleus mediates facial expression; superior salivatory nucleus (parasympathetic innervations of salivatory, pterygopalatine, lacrimal, and palatine glands) |
Loss of ipsilateral facial expression and diminished salivatory function |
|
Main sensory nucleus (CNV) |
Second-order neuron mediating somatosensory sensation from the head regions to thalamus and then to cerebral cortex |
Loss of somatosensory sensation from the head on the side ipsilateral to the lesion |
|
Motor nucleus (CN V) |
Mediates muscles of mastication (and jaw-closing reflex) |
Loss of jaw-dosing reflex |
|
Mesencephalic nucleus (CNV) |
Mediates unconscious (from mainly muscle spindles of the jaw) to cerebellum and motor nucleus of CN V, contributing to monosynaptic jaw-closing reflex |
Loss or disruption of jaw-closing reflex |
|
Nucleus locus ceruleus and raphe nuclei |
Origin of major norepinephrine and serotonin innervations of the CNS, respectively |
Disruption of sleep and wakefulness and varieties of other functions, in particular, those associated with control over emotional behavior |
|
Solitary nucleus |
Mediates cardiovascular functions and also serves as a relay nucleus for taste impulses to the thalamus |
Disruption of cardiovascular regulation and taste sensation |
|
Cerebellum |
||
|
Anterior, posterior, and flocculonodular lobes |
Three lobes of cerebellum which receive selective inputs from spinal cord (mainly from anterior lobe), brainstem (anterior and posterior lobe), vestibular structures (flocculonodular lobe), and cerebral cortex (mainly posterior lobe) for regulation of balance, coordinated movements, and muscle tone |
Depending upon the regions affected, lesions may cause loss of balance, hypotonia, or loss of coordination of movements |
|
Middle cerebellar peduncle |
Transmits inputs arising from the contralateral deep pontine nuclei to cerebellar cortex (comprising a disynaptic pathway from the cerebral cortex to cerebellar cortex) |
Largely unknown, but lesions of this pathway would likely affect coordination of purposeful movements associated with cerebellar functions |
|
Superior cerebellar peduncle |
Major efferent pathway of cerebellar cortex whose axons target the red nucleus and thalamus (ventrolateral nucleus) |
Believed to disrupt coordinated movements associated with functions of the cerebellum |
|
Dentate, interposed, and fastigial nuclei |
Deep cerebellar nuclei; dentate and interposed nuclei project through superior cerebellar peduncle,targeting the red nucleus and thalamus, respectively (presumably for coordination of movements); fastigial nucleus projects to lower brainstem neurons, such as reticular formation and vestibular nuclei for regulation of muscle tone and balance (see Chapter 21 for further details) |
Loss of functions associated with cerebellum (i.e., coordination of movements, nystagmus, ataxia of movement, hypotonia) |
CNS = central nervous system; CN = cranial nerve.
