* This chapter is adapted from Zorowitz RD: Infratentorial stroke syndromes and Harvey RL: Cerebral stroke syndromes. In Stein J, Harvey RL, Winstein CJ, et al, editors: Stroke recovery and rehabilitation , ed 2, New York, 2015, Demos Medical Publishing.
The neurologic examination in acute care confirms the diagnosis of stroke and localizes the injury. In the rehabilitation setting, the lesion location is usually known, such that the neurologic examination focuses on identifying expected physical, communicative, and cognitive impairments characteristic of a particular stroke syndrome and on determining their impact on functional activity. Understanding stroke syndromes helps target the examination, which improves the practitioner’s efficiency and the accuracy of neurologic assessment.This chapter covers common clinical stroke syndromes that occur in brain regions above and below the tentorium. The syndromes described are those typical of arterial and branch occlusions rather than hemorrhagic rupture.
Supratentorial (Cerebral) Neuroanatomy
The two cerebral hemispheres are divided into four lobes: frontal, parietal, occipital, and temporal ( Figure 44-1 ).
The frontal lobe is separated from the parietal lobe by the central sulcus. All behavioral motor output originating in the frontal lobe, including mobility, object manipulation, directional eye movement, and verbal expression, are assisted by the basal ganglia and cerebellum. In contrast, processing of all visual, auditory, and somatosensory input is integrated in the thalamus, parietal, occipital, and temporal lobes. There are also significant interconnections between primary motor cortex and somatosensory cortex, premotor and ventral motor areas, as well as connections from the thalamus to the motor cortex and from the motor cortex to the basal ganglia, superior and inferior colliculi, and cerebellum.
Cortical Areas of the Frontal Lobe
Primary Motor Cortex (M1)
The primary motor (M1) cortex is located in the precentral gyrus, anterior to the central sulcus in both hemispheres. It is somatotopically organized in the form of the classic “homunculus,” where motor control for the feet is located in medial frontal regions; shoulder, arm, and hand are located along the superior lateral convexity; and face, tongue, and throat are located along the inferior convexity and the operculum ( Figure 44-1 ). Lesions of the M1 cortex result in hemiplegia, often without spastic dystonia.
Broca Area
Named after Paul Broca (1824-1880), the Broca area is one of the two primary cortical language areas. The Broca area is located in the inferior lateral convexity and within the operculum of the dominant (usually left) frontal lobe. Lesions in this area result in impaired oral motor communication characterized by nonfluent speech production, apraxic errors, and problems with syntax. The Broca area is also important for facilitating the production of motor activity given on verbal command. In addition, lesions in the Broca area may also result in mild to moderate loss of auditory comprehension, specifically that of the syntax of complex sentences, and limb apraxia of both right and left limbs.
Frontal Eye Fields
The frontal eye fields are cortical areas in the prefrontal area of the frontal lobe that are important in directional and exploratory eye movements. Each hemisphere contains two eye fields, the “eye field of the dorsomedial frontal cortex,” and the other, located dorsolaterally, is the “frontal eye field”. A unilateral lesion of either eye field will cause a gaze preference and often head-turning toward the side of the lesion, away from the hemiplegic side. Patients with such lesions will have reduced saccadic gaze and visual pursuit toward the contralateral visual field. In addition, injury to the nondominant (usually right) prefrontal area impairs exploratory eye movements to the left and contributes to the attentional deficits seen in neurologic neglect syndrome. Head and eye turning associated with nondominant prefrontal lesions is often more persistent, whereas that associated with dominant lobe lesions usually resolves within days to a few weeks.
Primary Cortical Sensory Areas
Primary Somatosensory Cortex (S1)
The postcentral gyrus is located anteriorly in the parietal lobe, behind the central sulcus, and contains primary somatosensory representation. Similar to M1, it is somatotopically organized with roughly the same organization anatomically as the primary motor cortex. Lesions in S1 result in loss of two-point discrimination and stereognosis in contralateral body. If subcortical sensory structures, such as sensory tracts and thalamus, are also involved, there may also be loss of pain, temperature, and joint position sense.
Primary Visual Cortex
Located on the medial surface of the occipital lobe, within the longitudinal fissure, is the calcarine or primary visual cortex. Unilateral hemispheric lesions of the visual cortex result in a contralateral homonymous hemianopsia. Symptoms of homonymous hemianopsia are also associated with lesions involving subcortical structures of the temporal lobes because the visual tracts extend from the ventral posterior lateral thalamus, radiate posterolaterally into the temporal lobes, and then arch medially to the occipital cortex ( Figure 44-1 ).
Primary Auditory Cortex
The primary auditory cortex is located on the superior temporal gyrus in the temporal lobe. This is also known as Heschl’s gyrus and is more prominent in the dominant hemisphere. Auditory cortex mediates pure tone recognition and is tonotopically organized by sound frequency. A lesion on or near Heschl’s gyrus does not result in deafness, but in the dominant hemisphere can cause complex auditory perceptual problems, such as pure word deafness.
Cortical Sensory Association Areas
Posterior Parietal Cortex
The posterolateral parietal area integrates neural information from somatosensory, visual, and auditory cortices to construct a cohesive perception of three-dimensional space and the body’s position within the surrounding environment. Lesions in the left parietal cortex usually may cause only transient right hemineglect syndrome, but lesions in the right parietal cortex may cause clinically significant left hemineglect syndrome. In addition, lesions in the right parietal hemisphere may cause visual perceptual deficits resulting in spatial disorientation. Clinically, these patients are unable to draw figures accurately, cannot use blocks to build a simple structure (known as constructional apraxia ), and are challenged to orient their clothing to their body while dressing (known as dressing apraxia ).
Wernicke Area
Named after Carl Wernicke (1848-1905), the Wernicke area is located posterior to Heschl’s gyrus in the dominant hemisphere. The Wernicke area processes spoken and written symbolic language into meaning and comprehension. Along with the Broca area, the Wernicke area participates in a larger network for processing language. Lesions in the Wernicke area result in impaired language comprehension and a fluent aphasia mixed with multiple paraphasic errors. Patients with Wernicke aphasia typically lack insight about their comprehension deficits.
Angular Gyrus
Immediately posterior to the Wernicke area is the angular gyrus, which receives visual input from the occipital lobe and the posterior inferior temporal lobe and mediates the processing of written language. Lesions of the angular gyrus can cause alexia.
Subcortical Structures
Posterior Limb of the Internal Capsule
The anterior portion of the posterior limb, beginning at the genu, contains fibers of the corticospinal tract that descend from the M1 cortex. These fibers pass between the thalamus and the globus pallidus into the cerebral peduncle, and then into the midbrain as the ventral crus cerebri ( Figure 44-1 ). The posterior limb of the internal capsule is somatotopically organized with face, hand, arm, and shoulder anterior to trunk, thigh, leg, and foot. Lesions in the internal capsule result in contralateral hemiplegia.
Thalamus
Located between the third ventricle and the posterior limb of the internal capsule, the thalamus functions as a sensory hub for somatosensory, visual, and auditory input ( Figure 44-1 ). Lesions can result in mild hemiplegia or hemiataxia, sensory deficits, pain syndromes, mild aphasia, and neglect syndrome.
Arcuate Fasciculus
The arcuate fasciculus is a cortical-cortical white matter tract that passes reciprocally between the Wernicke and Broca areas along an arched pathway. Lesions along the arcuate fasciculus can cause problems with repetition of language as well as limb apraxia bilaterally.
Corpus Callosum
The corpus callosum is a large arch-shaped bundle of white matter connecting the two cerebral hemispheres ( Figure 44-1 ). Depending on the location of the lesion, infarcts of the corpus callosum can result in a number of clinical manifestations attributable to disconnections between the right and left hemispheres.
Cerebrovascular Anatomy
Circle of Willis
In 1664, Thomas Willis provided the first complete description of the cerebral arterial circle, now commonly known as the circle of Willis . The circle is supplied by three intracranial arteries: the right and left internal carotid arteries anteriorly, and the basilar artery posteriorly ( Figure 44-2 ). The internal carotid arteries enter the circle of Willis at the point where the posterior communicating arteries (PComAs) branch posteriorly. The anterior choroidal artery (AChA) then branches before the internal carotids bifurcate into the middle cerebral artery (MCA) and the anterior cerebral artery (ACA). The basilar artery bifurcates into both posterior cerebral arteries (PCAs). The circle is completed by anastomosis of the PComA with the PCA and the anterior communicating artery (AComA) with both ACAs ( Figure 44-2 ).
The “typical” anatomy of the circle is only present in 35% of humans. Anatomic variations are numerous, including hypoplastic portions of the circle as well as the absence of the PComA on one side. In the presence of atherosclerotic disease of an internal carotid, retrograde blood flow from the external carotid artery through the ophthalmic artery may provide collateral flow. Leptomeningeal arteries may also provide another helpful but limited source of collateral blood supply to the cerebral cortex.
Anterior Choroidal Artery
The AChA is a major deep perforating artery that supplies the optic tract, globus pallidus, anterior hippocampus, and parts of the thalamus, including a branch to the lateral geniculate nucleus. In addition, the AChA provides blood supply to the deep white matter of the temporal lobe. As the “AChA” name implies, the terminal branches supply the choroid plexus of the temporal horn.
Anterior Cerebral Artery
The A1 segment of the ACA extends in an anteromedial direction to the anastomosis of the AComA. The A2 segment continues from the AComA along the medial frontal lobe within the medial longitudinal fissure between the cerebral hemispheres ( Figure 44-3 ). It then passes superiorly and posteriorly around the corpus callosum to supply the medial frontal lobe, the corpus callosum, the cingulate gyrus, the paracentral lobule, and portions of the medial parietal lobe. Tributaries from the ACA transverse over the convexity of the cerebral hemisphere and anastomose with tributaries from the MCA in a watershed region.
The recurrent artery of Heubner (RAH) is the largest of a group of the lenticulostriate arteries that supply the basal ganglia, intervening internal capsule, and other surrounding white matter. The RAH originates from the A1 or proximal A2 segment of the ACA. The RAH supplies the anterior caudate nucleus, anterior third of the putamen, tip of the outer segment of the globus pallidus, and anterior limb of the internal capsule. Within the dominant hemisphere, the RAH also supplies subcortical tissue near the Broca area.
Middle Cerebral Artery
The MCA supplies the largest volume of the cerebral hemisphere, including the basal ganglia, internal capsule, and visual radiations from the thalamus. The M1 segment courses from the carotid bifurcation laterally toward the insular cortex, along which it supplies a series of lenticulostriate branches to subcortical structures. At the insular cortex, the MCA divides into upper and lower divisions. The M2 segment constitutes the upper- and lower-division branches within the Sylvian fissure. The M3 segment includes the branches to the opercula, and the M4 are the branches overlying the cerebral convexities ( Figure 44-3 ).
The superior division of the MCA supplies the frontal operculum, the lateral convexity of the frontal lobe, and variably the parietal lobe. The inferior division of the MCA supplies the temporal operculum, lateral convexity of the temporal and occipital lobes, and variably the parietal lobe.
Posterior Cerebral Artery
The P1 segment constitutes the section from the basilar artery to the branch of the PComA. The P2 segment courses posterolaterally to supply the medial occipital lobe within the longitudinal fissure, the posterior corpus callosum, and the medial temporal lobes, including portions of the hippocampi. Branch tributaries pass over the convexity of the cerebral hemisphere and anastomose in a watershed region with MCA tributaries. Other tributaries within the longitudinal fissure anastomose with those of the ACA in the medial parietal lobe ( Figure 44-3 ).
Cerebral Stroke Syndromes
Ischemic infarcts can occur in all or a portion of a vascular bed supplied by an artery, depending on whether the occlusion is incomplete or total. Atherosclerotic or small-vessel disease can affect the quality of tissue perfusion in watershed regions of major arteries. Given the history and evidence on imaging of an infarct within a certain vascular distribution, the clinician should look for all components associated with a particular syndrome even though the patient may in fact exhibit varying degrees of signs and symptoms.
Carotid Artery Syndromes
Infarcts can occur from an occlusive carotid thrombus or thromboembolism to distal cerebral arteries (most usually the MCA). Watershed infarcts in the distal MCA distribution can occur, presenting with partial contralateral hemiplegia and a sensory deficit affecting the shoulder more than the hand and leg. Carotid thrombosis will often present with a transient ischemic attack (TIA), which usually lasts only minutes but by definition can last up to 24 hours. Amaurosis fugax, a transient monocular blindness, is a symptom typically caused by thromboembolism from the carotid to the ophthalmic artery with immediate thrombolysis. Often described as a “curtain dropping over the eye and rising again,” amaurosis fugax more often presents as a visual obscuration, clouding, or fogginess variably affecting the whole or part of the visual field in one eye. Completed strokes from carotid thrombosis rarely result in both ipsilateral monocular blindness and contralateral hemiplegia.
Anterior Choroidal Artery Syndrome
Ischemic injury in the territory of the AChA will cause a contralateral hemiplegia because of injury to the posterior limb of the internal capsule. Hemianopsia can also occur, depending on what structures are involved. Injury to the optic tract can result in a contralateral hemianopsia and reduced pupillary reaction. A lesion to the geniculocalcarine tract in the medial temporal lobe can also cause contralateral hemianopsia. If the lateral geniculate nucleus is injured, a contralateral hemianopsia with median horizontal sparing can occur and is diagnostic of an AChA occlusion. Visual sparing in the horizontal plane results because a portion of the lateral geniculate is supplied by the lateral choroidal artery. Dominant injuries of the AChA usually cause no language deficit, but nondominant injuries may cause a left hemineglect syndrome.
Anterior Cerebral Artery Syndrome
ACA strokes constitute only 3% or fewer of all strokes. Still, patients with ACA strokes have complex physical and cognitive deficits and usually require comprehensive neurorehabilitation services. Patients with unilateral ACA infarcts will have contralateral hemiplegia worse in the leg and shoulder than in the arm, hand, and face, as a result of injury to the medial M1 cortex at the paracentral lobule. If facial weakness is noted, it is likely that the recurrent artery of Heubner was also occluded. Sensory loss will be minimal, usually impaired two-point discrimination if present, and in the same distribution as the motor impairment.
Patients with ACA infarcts will often have limb apraxia that is limited to the left side when a verbal command is given. This is because the ACA supplies the anterior corpus callosum, which disconnects the right premotor and M1 cortex from the left language network. Motor performance of the right upper limb is not involved because the left motor cortex is adjacent to the Broca area.
When the eye fields of the dorsomedial frontal cortex are damaged, the head and eyes deviate away from the hemiplegia Associated findings include the grasp reflex of the affected hand, paratonia (a force-dependent limb rigidity that becomes more prominent with an increase in effort by the examiner during muscle stretches), and other “frontal release” signs, such as the palmomental or snout reflexes.
Injury to the supplementary motor area and cingulate gyrus can also result in reduced initiation and, if severe, psychomotor bradykinesia. Psychomotor bradykinesia can be severe enough to cause reduced verbal expression or even mutism that may be difficult to differentiate from aphasia. Injury to the prefrontal cortex can also have a negative effect on executive cognitive functioning.
Patients with strokes involving the left recurrent artery of Heubner can have symptoms including a transcortical motor aphasia with reduced fluency, some apraxic errors of speech, and intact repetition. This is as a result of damage of the white-matter portions of the language network in the region between the supplementary motor area and the Broca area.
Middle Cerebral Artery Syndromes
Mainstem Middle Cerebral Artery (M1 Segment)
Occlusion of the M1 segment can cause injury to most of the lateral convexity of the cerebral hemisphere, as well as subcortical structures—including the internal capsule, visual radiations, and thalamocortical white matter—resulting from hypoperfusion of the lenticulostriate arterial branches. Those who survive M1 infarcts will usually have significant neurologic impairment.
A patient with an M1 infarct will usually exhibit complete contralateral hemiplegia from injury to the M1 cortex and the entire internal capsule. Contralateral hemisensory loss or hemianesthesia results from injury to the subcortical sensory tracts and the S1 cortex, although the thalamus itself may be spared. Infarcts of the ipsilateral frontal eye fields in the lateral prefrontal area will cause head and eye deviation away from the hemiplegia. Infarction to the geniculocalcarine tract causes homonymous hemianopsia in the contralateral visual field.
If the infarct is in the dominant MCA distribution, the patient may have global aphasia with reduced fluency, severely impaired comprehension, and an inability to repeat, read, or write resulting from damage of the Broca area, Wernicke area, the angular gyrus, and the arcuate fasciculus. A nondominant MCA stroke will cause severe visual and perceptual deficits with disrupted spatial body orientation, dressing apraxia, constructional apraxia, and a severe left hemineglect syndrome contributed in part by reduced left attention (from parietal injury) and reduced exploration (from frontal injury) of the left body and hemispace. Patients may deny that they even have any stroke-related impairments (anosognosia).
Superior-Division Middle Cerebral Artery
Occlusion of the superior division of the MCA results in a cortical infarct of the frontal lobe convexity, sparing the medial frontal lobe and subcortical tissue. Symptoms include contralateral hemiplegia affecting the arm and hand more than the leg, and loss only of two-point discrimination in the same distribution as the weakness. Patients may have transient head and eye deviation away from the hemiplegia, but visual fields are usually spared.
When the dominant hemisphere is affected, patients have Broca aphasia with decreased fluency of speech, apraxic errors, inability to repeat, and minimally impaired comprehension. Patients have bilateral limb apraxia from injury of the frontal-lobe language network, but often also struggle to follow nonverbal motor command cues.
Patients with superior-division MCA strokes in the nondominant hemisphere usually have a hemineglect syndrome with reduced exploration of left hemispace and mildly reduced attention to left-sided stimuli. They often have deficits in visual spatial perception. The normal inflections that emphasize the meaning, importance, or emotional content of speech (prosody) may be reduced or absent.
Inferior-Division Middle Cerebral Artery
Occlusion in the inferior division of the MCA results in a primarily cortical infarct of the lateral convexity of the parietal, occipital, and temporal lobes. Patients with infarctions in this region have no motor or somatosensory deficits, but may have a partial contralateral hemianopsia because of partial injury to the visual radiations in the temporal lobe.
Injury to the dominant hemisphere from an inferior-division MCA stroke usually causes a Wernicke aphasia with fluent speech characterized by paraphasic errors and poor comprehension of spoken and written language. Patients with nondominant injuries have a hemineglect syndrome with reduced attention to the left hemispace and perceptual deficits. They may also have a sensory aprosodia , or affective agnosia, in which the individual has a difficult time comprehending the prosody in another’s speech.
Posterior Cerebral Artery Syndromes
If an occlusion occurs in the P1 segment, hypoperfusion occurs in the distal PCA and the thalamoperforating arteries supplying the thalamus. This infarct will result in a contralateral sensory syndrome with hypoesthesia, a feeling of heaviness in the limbs, and in some cases dysesthesia (called Déjerine-Roussy syndrome ). Patients may also have a contralateral homonymous hemianopsia from direct injury to the primary visual cortex in the medial occipital lobe.
On rare occasions, a PCA infarct in the left occipital lobe can result in alexia without agraphia , in which patients are not able to read but can write. The infarct includes the left primary visual cortex, causing a right homonymous hemianopsia. An infarct of the posterior corpus callosum disconnects the right primary visual cortex from the language network, thus preventing the patient from transferring words seen in the left hemispace to the language centers. Writing is not affected because there is no disconnection between the language network and motor cortex. Patients may also have a left hemineglect syndrome. Thromboembolism to both PCAs is uncommon but can result in Anton syndrome, characterized by blindness and visual anosognosia.
Lacunar Stroke Syndromes
By definition, lacunar infarcts are 1.5 cm or less in the largest diameter. Lacunar strokes are associated with hypertension and are caused by small-vessel occlusion from lipohyalinosis of the vascular intima. C. Miller Fischer reintroduced the term lacunar stroke into clinical stroke neurology when he described the lacunar syndromes. Although as many as 100 lacunar syndromes have been described, 5 stand out as the most common seen in clinical practice.
The pure sensory stroke is characterized by numbness in the face, arm, and leg on one side of the body. There are no associated motor or cognitive deficits. The infarct is usually located in the thalamus. Patients with sensory strokes can develop late or chronic pain syndromes as a result of disruptions of normal sensory tracts. Lesions in other regions of the central nervous system along sensory pathways may also cause central poststroke pain syndrome.
Pure motor hemiparesis is also common and often results in functional limitations that require rehabilitation. The patient may have symptoms of only motor loss in the face, arm, and leg, with or without spastic dystonia on one side of the body. The stroke usually occurs in the posterior limb of the internal capsule, cerebral peduncle, or in the base of the pons. Prognosis for functional recovery is good because patients lack other symptoms, such as language, visual deficits, or apraxia. Spastic dystonia may complicate the rehabilitation process.
Dysarthria-clumsy hand syndrome , along with ataxic hemiparesis , are lacunar syndromes that occur commonly from lesions in the base of the pons caused by occlusions of the paramedian pontine perforating vessels from the basilar artery. However, dysarthria-clumsy hand syndrome can also present following infarcts of the genu of the internal capsule in the somatotopic regions for face and hand, as well as other areas of subcortical white matter. These patients have dysarthria and unilateral facial weakness without language deficits, and a mild hemiparesis of the upper limb on one side of the body. The prognosis for recovery is usually very good. Patients with ataxic hemiparesis often have a considerable challenge regaining independence in mobility because of problems with dynamic balance. The prognosis is still very good, because the ataxic component often recovers more rapidly than the hemiparesis.
Sensorimotor strokes most likely occur at the junction of the ventrolateral thalamus and the internal capsule, resulting in sensory and motor loss on the contralateral side of the body. Because the vascular supplies to thalamus and internal capsule are distinct, the likely explanation is that edema from a thalamic stroke compresses adjacent motor fibers in the internal capsule.
Infratentorial Neuroanatomy
The infratentorial region, comprising the brainstem and cerebellum, spans between the diencephalon and the spinal cord. Despite its size, the brainstem has the potential to cause neurologic devastation if damaged. It carries fibers that affect motor and sensory function, as well as arousal and survival. The brainstem carries fibers that have important modulatory effects on both the cerebral cortex and the spinal cord. Although the cerebellum does not carry direct pathways from the cerebrum to the spinal cord, it also has the potential to cause neurologic devastation because it also modulates movement and tone.
Anatomy of the Brainstem ( Figure 44-4 )
The brainstem is the lower extension of the brain where it connects to the spinal cord. Neurologic functions located in the brainstem include those necessary for survival (breathing, gastrointestinal function, heart rate, blood pressure) and for arousal and wakefulness. The brainstem also surrounds a narrow passage for the circulation of cerebrospinal fluid. The occlusion of the passage, the aqueduct of Sylvius, is often accompanied by the neurologic complications of hydrocephalus.
Structures of the Brainstem
Midbrain
The midbrain ( Figure 44-5 ) connects the pons and cerebellum with the thalamus and cerebral hemispheres. It consists of the cerebral peduncles, the corpora quadrigemina, and the cerebral aqueduct, a passage representing the original cavity of the midbrain that connects the third and fourth ventricles. Each cerebral peduncle is divided by the substantia nigra into a dorsal (tegmentum) and ventral (base or crusta) part. The major gray matter structures of the tegmentum are the red nucleus and the interpeduncular ganglion. The major tracts include superior cerebellar peduncle, the medial longitudinal fasciculus, and the medial lemniscus.
The red nucleus appears circular in shape and receives fibers from the superior cerebellar peduncle and medial lemniscus. Axons cross the midline and project into the rubrospinal tract, an important part of the pathway from the cerebellum to the lower motor centers.
The superior cerebellar peduncles (brachia conjunctiva) arise from the dentate nucleus of the cerebellum, pass rostrally through the dorsal pons to the level of the inferior colliculus, decussate, ascend farther, and terminate either in the red nucleus or within the motor, ventral lateral, or ventral anterior nuclei of the thalamus. The majority of fibers in these tracts convey signals from the cerebellum to the brainstem.
The medial longitudinal fasciculus (MLF) arises from the vestibular nucleus and is thought to mediate conjugate gaze. The MLF carries electrical signals from the abducens (cranial nerve VI) nuclei, across the midline, and then ascends to the oculomotor (cranial nerve III) and trochlear (cranial nerve IV) nuclei. The MLF also descends into the cervical spinal cord, where it innervates some muscles of the neck.
The vertical gaze center is located in the rostral interstitial nucleus of the MLF, just posterior to the red nucleus. Signals from each vertical gaze center are conducted to the subnuclei of the ocular muscles that control vertical gaze in both eyes. Cells mediating downward eye movements are intermingled in the vertical gaze center, but ischemia of this region usually results in selective paralysis of upgaze.
Pons
The pons ( Figure 44-6 ) links different parts of the brain and relays information from the medulla oblongata to the higher cortical structures of the cerebrum. It contains the ventilatory and horizontal gaze centers. The pons is connected to the cerebellum through the middle cerebellar peduncle. The ventral surface of the pons (pars basilaris pontis) consists of superficial and deep transverse fibers, longitudinal fasciculi, and some small nuclei of gray substance (nuclei pontis). Cortical axons travel through the internal capsule and cerebral peduncle form synapses with transverse fibers in the nuclei pontis, decussate, and pass through the middle peduncle into the cerebellum. The dorsal surface of the pons (pars dorsalis pontis) largely consists of ascending projections of the reticular formation and gray matter from the medulla oblongata. Other significant structures in the pons include the superior olivary nucleus and the paramedian pontine reticular formation.
