Brainstem cavernous malformations: anatomical, clinical, and surgical considerations

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Symptomatic brainstem cavernous malformations carry a high risk of permanent neurological deficit related to recurrent hemorrhage, which justifies aggressive management. Detailed knowledge of the microscopic and surface anatomy is important for understanding the clinical presentation, predicting possible surgical complications, and formulating an adequate surgical plan. In this article the authors review and illustrate the surgical and microscopic anatomy of the brainstem, provide anatomoclinical correlations, and illustrate a few clinical cases of cavernous malformations in the most common brainstem areas.

Abbreviations used in this paper:BA = basilar artery; CM = cavernous malformation; CN = cranial nerve; DVA = developmental venous anomaly; FOZ = frontoorbitozygomatic; MLF = medial longitudinal fasciculus; PCA = posterior cerebral artery; PICA = posterior inferior cerebellar artery; SCA = superior cerebellar artery; UMN = upper motor neuron.

Symptomatic brainstem cavernous malformations carry a high risk of permanent neurological deficit related to recurrent hemorrhage, which justifies aggressive management. Detailed knowledge of the microscopic and surface anatomy is important for understanding the clinical presentation, predicting possible surgical complications, and formulating an adequate surgical plan. In this article the authors review and illustrate the surgical and microscopic anatomy of the brainstem, provide anatomoclinical correlations, and illustrate a few clinical cases of cavernous malformations in the most common brainstem areas.

Abbreviations used in this paper:BA = basilar artery; CM = cavernous malformation; CN = cranial nerve; DVA = developmental venous anomaly; FOZ = frontoorbitozygomatic; MLF = medial longitudinal fasciculus; PCA = posterior cerebral artery; PICA = posterior inferior cerebellar artery; SCA = superior cerebellar artery; UMN = upper motor neuron.

With recent advances in imaging, surgical techniques and electrophysiological monitoring, CMs of the brainstem can be treated safely with resection. To maximize the chances of effective and safe removal, a thorough knowledge of the surface and intrinsic brainstem anatomy, as well as of the clinical and surgical correlates, is critical. In this article, we review and illustrate the anatomy of the brainstem and correlate it with clinical considerations in relation to the most common locations of CMs in this area. Moreover, we provide clinical examples and summarize some general technical principles to guide surgery in this challenging area.

General Clinical and Surgical Considerations

Various surgical approaches are available to gain access to the different sections of the brainstem (Fig. 1). A comprehensive description of these well-established approaches is beyond the scope of this review. For each location, we will describe and illustrate the specific surface anatomy encountered by the surgeon after exposure of the particular area and briefly discuss the pros and cons of the various routes. Various approaches can be used to remove a given lesion, and multiple considerations play a role in choosing the correct approach. These include the following: clinical presentation, lesion location, area to which the lesion comes closest to the surface, clinical functions of specific areas, pattern and distribution of associated hemorrhage, relationships to the adjacent DVA, and last but not least the degree of comfort of the individual surgeon with a specific approach. For educative and logistical purposes we will try to schematize the surgical considerations as they relate to a specific area. It is important, however, to understand that no dogma exists and the approach as well as the surgical strategy must be tailored to the particular characteristics of the individual patient.

Fig. 1.
Fig. 1.

Schematic drawing illustrating the most common surgical approaches used for different areas of the brainstem.

There is lack of agreement about the indications for surgery in patients with brainstem CMs. We usually recommend resection for symptomatic CMs after a recent first hemorrhage for superficial lesions. We tend to be more aggressive in patients with hemorrhagic lesions if the hemorrhage extends beyond the boundaries of the CM. It has been our anecdotal experience that these patients have a higher risk of bleeding.

Surgery for brainstem CMs requires careful preoperative planning. Cavernous malformations compress and displace the surrounding parenchyma rather than infiltrating it. If the malformation abuts the pial or ependymal surface, it provides a direct and safe entry route5 (Fig. 2). When the lesion is deep and separated from the surface by a thin parenchymal layer, surgery can still be performed safely by following a “safe entry zone;”5,15,28,46,49,52 these are relatively safe but narrow surgical corridors into the brainstem parenchyma where “critical neural structures are sparse and no perforating arteries are encountered.”49

Fig. 2.
Fig. 2.

Intraoperative photograph showing a posterolateral CM of the left medulla abutting the pial surface. The CM was exposed through a posterior suboccipital approach after elevation of the ipsilateral tonsil. The PICA loop and the vertebral artery (deeper in the left corner) are visible. The superficial portion of the CM in this case provided a natural and atraumatic entry route.

Intraoperative monitoring is helpful in identifying safe entry zones especially in the presence of large underlying lesions that distort normal anatomy. With intraoperative monitoring, structures such as the corticospinal tract in the cerebral peduncle, CN nuclei (CNs VII, IX, X, and XII), the facial colliculus, and hypoglossal and vagal trigones on the floor of the fourth ventricle can be identified.51 Frameless stereotaxy registered to the focus of the surgical microscope is also very helpful, especially when the CM is hidden under a very thin layer of normal-appearing parenchyma.

The goal of surgery for brainstem CMs is radical removal of the lesion. Partial removal is associated with a persistent and probably higher risk of recurrent hemorrhage from the residual lesion. We recommend delaying surgery after a symptomatic hemorrhage if possible for 2–3 weeks. This delay allows for partial liquefaction of the hematoma, providing a natural buffer that diminishes surgery-related trauma. We also try to avoid operating months after a symptomatic bleed when hematoma retraction and organization lead to tight adherence between the CM and the surrounding parenchyma, which increases the likelihood of mechanical trauma from surgical manipulation.

Brainstem CMs are usually removed through an incision smaller than the lesion itself. This makes internal decompression and piecemeal removal necessary30 (Fig. 3). “En bloc” resection is usually neither safe nor feasible in this location. In contrast to the situation with supratentorial CMs, after resection of a brainstem CM the hemosiderin-stained parenchyma is not disturbed and is left in situ. Every attempt must be made to preserve any associated DVA30,43,46,48 (Fig. 4); the presence of a DVA should be suspected even when the preoperative MR imaging does not show one. Sacrifice of the DVA will invariably lead to a venous infarct with disastrous clinical sequelae.32,46,50,53 Developmental venous anomalies are usually absent in patients with familial CMs.44

Fig. 3.
Fig. 3.

Artist's illustration showing internal emptying of the same CM as in Fig. 2 and piecemeal removal with a pituitary forceps through a small opening.

Fig. 4.
Fig. 4.

Intraoperative photograph obtained after resection of the CM shown in Figs. 2 and 3. A typical DVA is visible along the inferior wall of the surgical cavity although no clear-cut evidence of a DVA was visible on the preoperative MR images.

Anatomical, Clinical, and Surgical Considerations in Relation to Common Brainstem Locations

Midbrain: Internal and Functional Anatomy

The anterior midbrain contains the crus cerebri, which are composed of cortical projections to the brainstem and spinal cord (Fig. 5). Projections to the pontine nuclei from the parietal, occipital, and temporal lobes are found laterally, whereas frontal projections are found medially. At the center of the crus cerebri is the corticospinal tract and medial to that the corticobulbar tract.

Fig. 5.
Fig. 5.

Schematic 3D illustration (left) and axial view at the level of the superior colliculus (right) of the nuclei and fascicles in the midbrain. CB = corticobulbar tract; CS = corticospinal tract; CTT = central tegmental tract; EW = Edinger-Westphal nucleus; FP = frontopontine fibers; III = CN III; ML = medial lemniscus; MLF = medial longitudinal fasciculus; Nc III = CN III (oculomotor nerve) nuclei; PAG = periaqueductal gray matter; PTOP = parietotemporooccipitopontine tract; RN = red nucleus; SC = superior colliculus; SN = substantia nigra; ST = spinothalamic tract.

Dorsal to the crus, the substantia nigra extends the width of the crus and separates it from the midbrain tegmentum. Containing dopaminergic and GABAergic cells, the substantia nigra contains reciprocal projections with the striatum, as well as efferents to the brainstem and thalamus.

Progressing dorsally, the red nucleus lies medially and the medial lemniscus lies laterally in the cross-section. The red nucleus is facilitatory to upper extremity flexors and is thought to be responsible for the upper extremity flexor pattern that occurs in classic decorticate posturing. The red nucleus exerts its influence on the musculoskeletal system through the rubrospinal tract, which descends to the contralateral spinal cord. The medial lemniscus carries proprioception, vibration, and discriminative touch information from the contralateral spinal cord to the ventral posterior lateral nucleus of the thalamus.

In more caudal sections, the decussation of the superior cerebellar peduncle lies centrally and medially instead of the more rostrally located red nucleus.

Continuing dorsally, CN nuclei are located medially and the spinothalamic tract (anterolateral system) laterally. The CN nuclei found in the midbrain are the oculomotor nuclear complex and Edinger-Westphal nucleus rostrally and the trochlear nucleus caudally.

The nuclei of CN III, the oculomotor nuclei and Edinger-Westphal nucleus, are found primarily at the level of the superior colliculus. The oculomotor nuclei supply the somatic innervation to the superior, inferior, and medial rectus; the inferior oblique; and the levator palpebrae muscles. The Edinger-Westphal nucleus supplies the parasympathetic innervation to the intraocular muscles for the accommodation reflex (pupillary constriction and ciliary muscle activation to change the shape of the lens allowing for near vision).

The trochlear nucleus (motor to the contralateral superior oblique muscle) is located caudal to the nuclei of CN III and at the level of the inferior colliculus.

The CNs III and IV nuclei are connected by the medial longitudinal fasciculus (MLF). It is positioned lateral to those nuclei, and within its most rostral portion is found the vertical gaze center, the rostral interstitial nucleus of the MLF. Deficits of upward gaze result from lesions of the uppermost portion of this nucleus, whereas deficits of downward gaze occur when the caudal part of the nucleus is damaged.

Central and dorsal in location to the CN nuclei is the cerebral aqueduct, connecting the third and fourth ventricles. Impingement of the aqueduct will result in hydrocephalus. The cerebral aqueduct is surrounded by the periaqueductal gray matter, which manufactures various neurotransmitters and projects to the spinal cord to inhibit ascending pain transmission. The locus ceruleus is found laterally in this region and contains norepinephrine.

The corpora quadrigemina rounds out the dorsal aspect of the midbrain. Rostrally, the superior colliculus serves as the “orientation center.” All sensory input projects to the superior colliculus, which in turn projects efferents to extraocular motor nuclei and gaze centers, as well as the upper cervical and thoracic spinal cord (via the tectospinal tract) to orient the eyes and head to sensory stimuli.

The inferior colliculus receives auditory sensory input through a series of relay nuclei that convey this information from bilateral dorsal and ventral cochlear nuclei. Unilateral damage usually results in no deficits, since auditory information ascends through the CNS in a bilateral fashion.

The various nuclei and fascicles in the midbrain are illustrated in Fig. 5.

Midbrain: Clinical Correlations

The clinical correlates of the midbrain structures are summarized in Table 1.

TABLE 1:

Midbrain nuclei and structures listed by anatomical location, function, and dysfunction*

StructureLocation (ventral to dorsal, medial to lat)FunctionDysfunction
crus cerebriventral, lattransmits descending corticopontines, corticospinals, corticobulbarscontralat UMN signs, weakness
substantia nigraventral, latdopaminergic input to striatum, GABAergic input to thalamus & brainstemparkinsonism38,40
red nucleuscentral, medial, rostralfacilitatory to UE flexorscontralat ataxia, rubral tremor54
superior cerebellar peduncle & decussationcentral, medial, caudaltransmits ascending rostral & anterior spinocerebellar input to bilat cerebellar hemispheres, dentatothalamic tract from cerebellum to contralat thalamuscontralat cerebellar ataxia & tremor
medial lemniscuscentral, lattransmits incoming proprioceptive, vibratory, & discrim touch info from contralat spinal cordcontralat hemianesthesia of trunk & extremities
spinothalamic tract (anterolat system)dorsal, lattransmits incoming pain & temp info from contralat spinal cordcontralat loss of pain & temp sensation in trunk & extremities
ventral trigeminothalamic tractdorsal, lat (along mediodorsal edge of medial lemniscus)transmits sensory input from contralat face to the ventral pst medial nucleus of thalamushemianesthesia of contralat face
medial longitudinal fasciculusdorsal, medialpathway btwn extraocular motor nuclei & gaze centersinternuclear ophthalmoplegia
oculomotor nucleusdorsal, medial, rostralinnervates ipsilat superior, medial, inferior rectus muscles, inferior oblique & levator palpebrae musclesipsilat oculomotor ophthalmoplegia
Edinger-Westphal nucleusdorsal, medial, rostralparasymp innervation to eyeipsilat loss of pupillary constriction, difficulty focusing
trochlear nucleusdorsal, medial, caudalinnervates contralat superior obliquedifficulty moving contralat eye down & inward
rostral interstitial nucleus of MLFdorsal, medialvertical gaze centerproblems w/ vertical gaze, contralesional torsional nystagmus7
periaqueductal graydorsal, medialproduces multiple neurotransmitters, role in micturition23none reported
cerebral aqueductdorsal, medialtransmits CSFhydrocephalus
superior colliculusdorsal, rostralreflex movements of eyes & headpupillary disturbances, vertical gaze deficits, gaze palsy
inferior colliculusdorsal, caudalauditory relay nucleusdifficulty localizing sounds in space17, hypoacusia59
* discrim = discriminative; info = information; LE = lower extremity; parasymp = parasympathetic; pst = posterior; symp = sympathetic; temp = temperature; UE = upper extremity.

Midbrain: Surface Surgical Anatomy, Clinical-Anatomical Correlations, and Illustrative Cases

Ventral and Ventrolateral Midbrain CMs

Surface Surgical Anatomy of the Ventral and Ventrolateral Midbrain. The surface anatomy of the ventral midbrain is illustrated in Fig. 6. Grossly, the midbrain is composed of the cerebral peduncles, the tegmentum, and the tectum. Its superior limit is the optic tract, while its inferior limit is the pontomesencephalic sulcus, which runs posteriorly to meet the lateral mesencephalic sulcus. The lateral mesencephalic sulcus extends from the medial geniculate body superiorly to the pontomesencephalic sulcus inferiorly. This sulcus is considered the posterior limit of the ventrolateral mesencephalon,49 separating the cerebral peduncle surface from the tegmentum surface.35 The depression between the cerebral peduncles and the root of CN III, containing the posterior perforated substance, is the interpeduncular fossa.

Fig. 6.
Fig. 6.

A: Schematic illustration of the surface anatomy of the ventral brainstem. B: Schematic illustration of the arterial (left) and venous (right) anatomy

The BA divides into the 2 PCAs in the interpeduncular cistern. Blood supply to the midbrain comes from penetrating branches of the BA, the PCA, and the SCA. The peduncular vein of each side arises from the interpeduncular fossa and anastomoses with the contralateral vein, forming the posterior communicating vein, which crosses the interpeduncular fossa. The peduncular vein drains into the basal vein of Rosenthal together with the lateral mesencephalic vein after curving around the cerebral peduncle below the optic tract.35 The anterior pontomesencephalic vein, running on the ventral midline surface of the pons as a single trunk, is usually a paired vein in its mesencephalic course. The vein of the pontomesencephalic sulcus runs on the homonymous sulcus.

Surgical Approaches to the Ventral and Ventrolateral Midbrain. The more central CMs of the midbrain (anterior and interpeduncular) can be reached through a transsylvian route with the classic pterional58 or the frontoorbitozygomatic (FOZ) craniotomy20,25,42 (Fig. 7) with one of its numerous modifications. The FOZ approach offers the surgeon a flatter view of the midbrain and of the interpeduncular fossa by the transsylvian approach than the pterional approach.45 A fairly safe entry zone has been described by Bricolo and Turazzi6 as a narrow corridor lateral to the emergence of CN III between the SCA and the PCA, and medial to the pyramidal tract (Fig. 6).

Fig. 7.
Fig. 7.

Illustrations of the FOZ approach. Schematic 3D view of the skull after craniotomy, showing the region of the brainstem that can be approached (left), and axial view of the skull (right) showing the area of the craniotomy (dotted lines). Arrow indicates the surgical trajectory.

Ventrolateral CMs of the midbrain can be reached either through the transsylvian route or though the subtemporal transtentorial approach.12,13 Placement of a lumbar drain preoperatively in such cases decreases the amount of temporal lobe retraction required for the exposure with the subtemporal approach. Known complications of the subtemporal route include ophthalmoparesis secondary to mechanical manipulation of CNs III and IV and the risk of retraction injury and/or venous infarct from damage to the vein of Labbé complex. These complications are a major drawback especially when the dominant hemisphere is considered. Ventrolateral midbrain CMs, especially those extending caudally (see Illustrative Case 2) can also be approached via more complex skull base transpetrosal approaches that afford a wider and more lateral exposure for the lower midbrain, pons, and higher medulla. These approaches, though, carry the risk of complications such as hearing loss, CN VII deficit, or CFS leakage.19

It can be difficult to achieve complete resection of lesions centered in the ventral and ventrolateral midbrain, as extension of the CM into other compartments (primarily the thalamus) is not uncommon (Fig. 8). In a recent systematic review of 745 patients from 56 surgical series of brainstem CMs, the subgroup with ventral and ventrolateral midbrain lesions displayed the highest percentage of incomplete resections with subsequent persistent risk of rebleeding at follow-up.19

Fig. 8.
Fig. 8.

Sagittal (left) and coronal (right) MR images obtained in a 24-year-old woman with sudden onset of facial numbness and left hand weakness showing a hemorrhagic CM extending from the upper midbrain to the ipsilateral thalamus.

Clinical Correlates of a Ventral Midbrain CM. For a CM located in the central midbrain–cerebral peduncle as shown in Fig. 9, the more likely clinical presentations/possible sequelae from surgery include contralateral facial weakness from the compression of the corticobulbar tract, contralateral ataxia or tremor from compression of the red nucleus, and ipsilateral oculomotor ophthalmoplegia from compression of CN III. Larger lesions may also cause contralateral weakness and upper motor neuron (UMN) signs due to compression of the corticospinal tract.

Fig. 9.
Fig. 9.

Schematic 3D illustration of the anatomy of the midbrain (left) and axial view of a ventral midbrain CM displacing internal structures (right).

Illustrative Case 1: CM of the Ventral Midbrain. This 49-year-old man developed transient right ptosis. Magnetic resonance imaging (Fig. 10) showed a central brainstem CM, likely involving the fibers and nuclei of the right CN III. Because the CM did not come to the pial surface but was separated by a thin layer of parenchyma and the symptoms completely resolved, surgery was not considered.

Fig. 10.
Fig. 10.

Illustrative Case 1: CM in the central midbrain. Sagittal T1-weighted (A), axial T2-weighted (B), and Gd-enhanced axial T1-weighted (C) MR images demonstrating a CM in the central midbrain. The lesion is hyperintense on T1-weighted images (A), heterogeneous on T2-weighted images with a fluid-fluid/debris level (B), and nonenhancing (C).

Clinical Correlates of a Ventrolateral Midbrain CM. For a CM located in the ventrolateral midbrain as shown in Fig. 11, the more likely clinical presentations or possible sequelae from surgery include contralateral weakness and UMN signs due to compression of the corticospinal tract, and contralateral facial weakness due to compression of corticobulbar tract. Larger lesions can cause contralateral loss of tactile sensation from trunk and extremities due to medial lemniscus compression and/or contralateral ataxia due to compression of the red nucleus.

Fig. 11.
Fig. 11.

Schematic 3D illustration of the anatomy of the midbrain (left) and axial view of a ventrolateral midbrain CM displacing internal structures (right).

Illustrative Case 2: CM of the Ventrolateral Midbrain. This 39-year-old woman experienced acute right-sided hearing loss that led to the diagnosis of a CM of the right ventrolateral midbrain and upper pons (Fig. 12). Resection was performed through a subtemporal/presigmoid approach with partial petrosectomy.

Fig. 12.
Fig. 12.

Illustrative Case 2: CM in the right ventrolateral midbrain and upper pons. A–E: Preoperative sagittal T1-weighted (A), axial T1-weighted (B), axial T2-weighted (C), axial gradient echo (GRE) (D), and axial T1-weighted Gd-enhanced (E) MR images demonstrating a CM involving the right anterolateral midbrain and upper pons, extending to the surface. Note the precontrast T1 hyperintensity (A and B); speckled, “popcorn” morphology (A and B); extensive blooming on GRE sequence due to magnetic susceptibility artifact (D); and minimal enhancement (E). F: Postoperative axial T1-weighted Gd-enhanced image demonstrating resection of the CM, with a resection cavity at the operative site and no residual enhancement.

Posterior Midbrain CMs

Surface Surgical Anatomy of the Posterior Midbrain. The lateral mesencephalic sulcus is considered the limit between the so-called anterolateral midbrain and the posterior midbrain (Figs. 13 and 14). The sulcus, as explained above, is located in the posterior aspect of the midbrain; it runs from the medial geniculate body above to the pontomesencephalic sulcus. The quadrigeminal plate, with the paired superior and inferior colliculi is posteromedial to the lateral mesencephalic sulcus. The CN IV decussates into the medullary velum and exits just below the inferior colliculus running anteriorly between the PCA and SCA.

Fig. 13.
Fig. 13.

A: Schematic illustration of the surface anatomy of the dorsal brainstem. B: Schematic illustration of the arterial (left) and venous (right) brainstem anatomy.

Fig. 14.
Fig. 14.

Axial view of the midbrain showing the surgical route through the lateral mesencephalic sulcus, covered by the lateral mesencephalic vein (blue circle). This safe entry zone allows a trajectory (arrow) of approach between the substantia nigra (SN) and the medial lemniscus (ML) posterior to the cerebral peduncle.

Surgical Approaches to the Posterior Midbrain. Cavernous malformations involving the posterior midbrain are approached through a supracerebellar infratentorial route, which allows an adequate view of the posterior and posterolateral surface of the midbrain and quadrigeminal plate, as well as the posterolateral surface of the upper pons. This approach includes median, paramedian, and extreme lateral variants,10 which provide access to different parts of the posterior midbrain. Moreover, their convergent trajectory to similar regions allows the surgeon to choose the most convenient trajectory to CMs in analogous sites but approach the pial or ependymal surface in different points.10 We prefer the sitting position because it maximizes the effects of gravity by allowing the superior aspect of the cerebellum to “fall down,” obviating the need for retraction. The occipital transtentorial approach is an alternative for patients with a steep tentorial slope.19

The median supracerebellar infratentorial approach2,33,55,56 requires a craniotomy exposing the entire width of the transverse sinus as well as the confluence of sinuses to increase the angle of view by upward retraction of the sinus. In doing so, care must be taken to avoid excessive retraction of the sinus to prevent sinus thrombosis. Small veins running from the superior aspect of the cerebellum to the tentorium can be coagulated and divided close to the cerebellar surface.10 After opening the posterior wall of the quadrigeminal cistern, the precentral cerebellar veins draining to the vein of Galen are visible. Whenever possible we prefer to avoid coagulation and division of the precentral cerebellar vein, and we try work around it. Sharp opening of the cerebellomesencephalic fissure under high magnification leads to exposure of the corpora quadrigemina.

The lateral supracerebellar infratentorial approach requires a paramedian craniotomy, again exposing the entire width of the transverse sinus. This provides access to the posterior portion of the ambient cistern, including the proximal portion of the trochlear nerve, the SCA, and the posterolateral aspect of the midbrain, with the lateral mesencephalic vein running in the lateral mesencephalic sulcus. The lateral mesencephalic vein, as discussed later, is an important landmark for identifying a safe entry zone in this area2 (Figs. 14 and 15).

Fig. 15.
Fig. 15.

Posterior view of the brainstem showing the various safe entry zones.

The extreme-lateral supracerebellar infratentorial approach is performed through a classical retrosigmoid craniectomy, with full exposure of the transverse/sigmoid sinus junction. It allows for a more lateral view of the posterolateral midbrain than the lateral approach.10

In the posterior midbrain, the lateral mesencephalic sulcus is a relatively safe entry zone (Figs. 1315). This sulcus represents the anatomical surface separation between the colliculi and the cerebral peduncle and runs from the medial geniculate body superiorly to cross inferiorly, almost at a right angle, the pontomesencephalic sulcus. The lateral mesencephalic vein runs into the lateral mesencephalic sulcus, thus representing an easily identifiable surface landmark for this structure. Entry into the posterolateral midbrain through the lateral mesencephalic sulcus minimizes the risk of damaging the cerebral peduncles. A vertical incision in this sulcus provides a narrow corridor between the substantia nigra ventrally and the medial lemniscus dorsally49 (Fig. 14). This area can be reached also through a subtemporal route with the limitations and possible risks of this approach as previously discussed.49

In the more medial posterior midbrain, Bricolo5 described 2 safe entry zones at the level of the supracollicular and infracollicular areas (Fig. 15). These are 2 narrow horizontal lines immediately above and below the lamina quadrigemina.

Usually CMs of the posterior midbrain can be resected with good results, the most common complication being a CN III paresis.19

Clinical Correlates of a Posterior Midbrain CM. For a CM located in the posterior midbrain as shown in Fig. 16, the more likely clinical presentations or possible sequelae of surgery include difficulty tracking and contralateral neglect due to compression of the superior colliculus; hydrocephalus due to impingement of the aqueductus; pupillary changes (large, irregular) and accommodation impairment due to compression of the Edinger-Westphal nucleus; and, in patients with larger lesions, ipsilateral oculomotor ophthalmoplegia due to compression of the CN III nuclei, vertical gaze palsy from compression of MLF, and torsional nystagmus (rostral interstitial nucleus).

Fig. 16.
Fig. 16.

Schematic 3D illustration of the midbrain (left) and axial view of a posterior midbrain CM displacing internal structures (right).

Pons: Internal and Functional Anatomy

The ventral (basilar) pons contains pontine nuclei throughout its structure. Within this region the corticospinal tract is found ventromedially in each hemisection. The corticobulbar tracts are closely associated with the most dorsal corticospinal fibers.

The medial lemniscus runs medially to laterally in the pons, in effect separating the basilar region from the dorsally located tegmentum.

Lateral and in the same plane as the medial lemniscus is the spinothalamic tract (anterolateral system).

Moving dorsally in the section and in a midline position is the tectospinal tract and posterior to that the medial longitudinal fasciculus (MLF). The MLF connects the nuclei of CNs III, IV, and VI to coordinate extraocular movements. Lateral to these axonal pathways is the central tegmental tract. Multiple connections involving the reticular formation and brainstem nuclei occur through the central tegmental tract.

The branchial arch motor nuclei (trigeminal and facial motor nuclei) can be seen lateral to the central tegmental tract. The trigeminal motor nucleus innervates the muscles of mastication and is located rostrally. The facial motor nucleus innervates the muscles of facial expression and is found caudally.

Most dorsal in the pons and medially located is the abducent nucleus, which innervates the ipsilateral lateral rectus. The paramedian pontine reticular formation, responsible for initiating horizontal gaze, is found just lateral to the abducent nucleus.

The trigeminal sensory nuclei (spinal trigeminal nucleus, mesencephalic nucleus, and chief sensory nucleus) are found far laterally in the cross-section at the level of the rostral pons. The vestibular nuclei are also far lateral and dorsal to the trigeminal nuclei.

Laterally, the pons is bordered by the middle cerebellar peduncle, which carries fibers into the cerebellar hemisphere from the contralateral pontine nuclei. The inferior border of the middle cerebellar peduncle shares an intimate relationship with the inferior cerebellar peduncle.

The various nuclei and fascicles in the pons are illustrated in Fig. 17.

Fig. 17.
Fig. 17.

Schematic 3D illustration (left) and axial view of the pontine nuclei and fascicles in a section at the level of the facial colliculus (right). CN VI = abducent nerve fibers; CN VII = facial nerve fibers; DN = dentate nucleus; GE = globose end emboliform nuclei; ICP = inferior cerebellar peduncle; LVN = lateral vestibular nucleus; MCP = middle cerebellar peduncle; MVN = medial vestibular nucleus; NcV = spinal nucleus of trigeminal nerve; NcVI = abducent nerve nucleus; NcVII = facial nerve nucleus; SCP = superior cerebellar peduncle; SVN = superior vestibular nucleus; TSp = tectospinal tract; TV = spinal tract of trigeminal nerve.

Pons: Clinical Correlations

Clinical correlates of pontine nuclei and tracts are summarized in Table 2.

TABLE 2:

Pontine nuclei and structures listed by anatomical location, function, and dysfunction

StructureLocation (ventral to dorsal, medial to lat)FunctionDysfunction
pontine nucleiscattered throughout ventral half of cross-sectionrelay input from ipsilat cerebral cortex to contralat cerebellumcontralat hemiataxia, but may be masked by UMN weakness if corticospinal tract is also involved
corticospinal tractventral, medialUMN from cortex to contralat spinal cordcontralat UMN signs, weakness
medial lemniscuscentral, medialtransmits incoming proprioceptive, vibratory, & discrim touch info from contralat spinal cordcontralat hemianesthesia of trunk & extremities
ventral trigeminothalamic tractcentral, medial (along dorsal edge of medial lemniscus)transmits sensory input from contralat face to ventral pst medial nucleus of thalamushemianesthesia of contralat face
spinothalamic tract (anterolat system)central, lattransmits incoming pain & temp info from contralat spinal cordcontralat loss of pain & temp sensation in trunk & extremities
hypothalamospinal tract (not shown)central, lat near spinothalamic tractcarries symp projections from hypothalamus to spinal cordHorner syndrome
tectospinal tractcentral-dorsal, medialreflex movement of head & neckunappreciable
medial longitudinal fasciculusdorsal, medialpathway btwn extraocular motor nuclei, vestibular nuclei, & gaze centersinternuclear ophthalmoplegia
central tegmental tractcentralconnects multiple reticular formation & brainstem nucleinystagmus,34 intention tremor16
trigeminal motor nucleuscentral, lat, rostralinnervation of muscles of masticationparalysis of ipsilat muscles of mastication
facial motor nucleuscentral, lat, caudalinnervation of ipsilat muscles of facial expressionlower motor neuron facial weakness
abducent nucleusdorsal, medial, caudalinnervates ipsilat lat rectusloss of ipsilat eye abduction, possible ipsilat gaze palsy
spinal trigeminal nucleus & tractdorsal, lattransmits pain & temp info from face, sensory input from around external auditory meatus, & pharynxipsilat loss of pain & temp sensation in areas around ear, decreased sensation in ipsilat oropharynx
chief (principal) sensory nucleusdorsal, latreceives sensory input from faceloss of tactile sensation in ipsilat face
vestibular nucleidorsal, latvestibular relay nuclei, integrates sensory inputdizziness/vertigo, postural instability, eye movement disorders
middle cerebellar pedunclelatcarries projections from contralat pontine nuclei to ipsilat cerebellar hemisphereipsilat hemiataxia

Pons: Surface Surgical Anatomy, Clinical-Anatomical Correlations, and Illustrative Cases

Ventral and Ventrolateral Pons CMs

Surface Surgical Anatomy of the Ventral and Ventrolateral Pons. The ventral pons is convex and is indented along the midline by the basilar sulcus (Fig. 6). The emergence of the trigeminal nerve defines the limit between the pons proper medially and the middle cerebellar peduncle laterally. Inferiorly, the pontomedullary sulcus separates the pons from the medulla. Cranial nerves VII and VIII emerge from the pontomedullary sulcus at the level of the supraolivary fossette. During its course in the basilar sulcus, the BA sends several perforating branches to the ventral pons.35

On the ventral surface of the pons, the pontine portion of the median anterior pontomesencephalic vein anastomoses with a transverse pontine vein before continuing on the medulla as the median anterior medullary vein. The vein of the pontomedullary sulcus courses along the pontomedullary sulcus.35

Surgical Approaches to the Ventral and Ventrolateral Pons. Truly ventral pontine lesions pose a significant surgical challenge and usually require invasive skull base approaches. However, exclusively ventral pontine CMs are rare, and more often the CM has a more lateral extension. For ventrolateral and lateral pontine lesions we prefer a classical retrosigmoid approach and usually enter the brainstem between CNs V and VII. For more ventral lesions, this approach can be extended by anterior mobilization of the skeletonized sigmoid sinus.47 Alternatives to the retrosigmoid approach for lateral and ventrolateral pontine lesions include the subtemporal transtentorial route (for lesions with more rostral extension) or the presigmoid route, which provides a more lateral and direct view to the lesion.21 Combination of various approaches is rarely necessary and useful only in a few exceptional cases of giant lesions spanning multiple compartments.

Transpetrosal approaches1,26,36 are also useful for lesions in these locations, but in our opinion their application is limited by their invasive nature and potential complications. A detailed review of the pros and cons of the various transpetrosal skull base approaches to this region is beyond the scope of this review, and the reader is referred to various publications on the topic.4,9,18,24,26,31

A well-established safe entry zone into the lateral pons is the so-called “peritrigeminal area” (Fig. 18) between the emergence of CNs V and VII. This is an area located medially to the CN V and laterally to the pyramidal tract.49 This area is adequately exposed with any of the aforementioned approaches.

Fig. 18.
Fig. 18.

Peritrigeminal safe entry zone in the ventrolateral pons.

Clinical Correlations of a CM of the Ventral Pons. For a CM located in the ventral pons as shown in Fig. 19, the more likely clinical presentations/possible sequelae of surgery include contralateral weakness and UMN signs due to compression of the corticospinal tract; ipsilateral CN VI palsy due to compression of the nerve fibers; and contralateral loss of tactile sensation from the trunk and extremities due to compression of the medial lemniscus. In larger lesions, ipsilateral hemifacial weakness due to compression of the CN VII nucleus is possible and central tegmental tract compression may result in nystagmus and intention tremor.

Fig. 19.
Fig. 19.

Schematic 3D illustration of the pons (left) and axial view at the level of the facial colliculus of a ventral pontine CM displacing internal structures (right).

Illustrative Case 3: CM of the Ventrolateral Pons. This 27-year-old woman developed intractable nausea, vomiting, ataxia, bilateral (right greater than left) weakness and loss of sensitivity, left eye-abduction weakness, and a complete left facial palsy. Magnetic resonance imaging (Fig. 20) showed a large CM extensively involving the ventrolateral pons. Using a classic retrosigmoid approach, the brainstem was entered between CNs V and VII at a point where the hemorrhage had reached the surface. The CM was completely removed.

Fig. 20.
Fig. 20.

Illustrative Case 3: CM in the pons. A–C: Sagittal T1-weighted (A), axial T2-weighted (B), and Gd-enhanced coronal T1-weighted (C) MR images demonstrating a large CM centered in the left ventrolateral aspect of the pons. The lesion is hyperintense on T1-weighted imaging (A), heterogeneous on T2-weighted imaging with surrounding vasogenic edema (B), and nonenhancing (C). D–F: Postoperative correlative images demonstrating complete resection of the lesion.

Dorsal Pons CMs

Surface Surgical Anatomy of the Dorsal Pons and Dorsal Medulla (Floor of the Fourth Ventricle). The floor of the fourth ventricle (Fig. 13) is also known as the rhomboid fossa because of its shape. The rhomboid fossa is divided into a larger upper triangle (pontine) and a smaller inferior triangle (medullary) by a line connecting the 2 foramina of Luschka.35 The junctional part with the striae medullares lies between the 2 triangles. The intraventricular portion of the cerebellar peduncles forms the lateral boundaries of the upper triangle with the apex of the upper triangle located at the sylvian aqueduct. The teniae of the fourth ventricle form the lateral limit of the inferior triangle, and the obex forms its most inferior and medial limit.39 The median sulcus runs in the midline along the extent of the rhomboid fossa. On each side of the median sulcus are the paired vertically oriented sulci limitans. The median eminence is situated on either side of the median sulcus and is medial to the sulcus limitans. The pontine (upper) portion of the median eminence includes the facial colliculus (an eminence formed by the genu of the facial nerve curving around the abducent nucleus). The medullary (lower) portion of the median eminence includes 3 triangular areas: the hypoglossal and vagal trigones and the area postrema. These areas are often included in a region that is called the “calamus scriptorius” because of its shape. In the pontine triangle, lateral to the sulcus limitans, there are 2 anatomical structures: the locus coeruleus rostrally and the vestibular area (a prominence corresponding to the vestibular nuclei) caudally. Lateral to the vestibular area, closer to the lateral recess, the acoustic tubercle overlies the dorsal cochlear nucleus.39

The most important vascular structures of this region (Fig. 13) are the PICA and veins of the cerebellomedullary fissure.

Surgical Approaches to the Floor of the Fourth Ventricle. Dorsally located lesions involving the pons and upper medulla can be reached through the floor of the fourth ventricle. This area can be exposed through the telovelar transcerebellar-medullary fissure or the transvermian approaches after a suboccipital midline craniectomy or craniotomy. We prefer the sitting position although the prone position is a good alternative. Both in the semisitting and prone positions a maximal flexion is required to allow for ideal exposure of the floor of the fourth ventricle. In many instances, resection of the vermis (with the underlying risk of postoperative truncal ataxia) is not necessary. Instead the surgical corridor can be maximized by enlarging the opening into the fourth ventricle by dividing the tela chorioidea. If access to the superior half of the floor of the fourth ventricle is necessary, then division of the inferior medullary velum provides access to the entire floor of the fourth ventricle up to the aqueduct.

The median suboccipital vermis–splitting approach is an alternative route to this region. This approach affords better exposure and a more direct view of the uppermost part of the fourth ventricle as compared with the telovelar approach.11

However, due to the risk of trunk ataxia with the transvermian approach,22,57 the telovelar approach is preferred.3,19,39 It is not unusual that a minimal division of the inferior vermis is needed in conjunction with the telovelar approach for more cranial lesions. Removal of the posterior arch of C-1 maximizes the exposure obtained with the telovelar approach.11

Although safe entry zones through the floor of the fourth ventricle have been described,28 because of the potential for morbidity we approach CMs of the dorsal pons through the floor of the fourth ventricle only if the lesion comes to the surface or the hemorrhage has created a natural corridor (see Illustrative Case 4). For completeness, we describe these safe entry zones that are located in the upper half of the floor of the fourth ventricle: the median sulcus above the facial colliculus, the suprafacial triangle, and the infrafacial triangles (Fig. 15). In those exceptional cases of lesions not approaching the surface of the rhomboid fossa, intraoperative electrophysiological monitoring and mapping of the floor are indispensable tools for identifying the best area to enter.

The median sulcus above the facial colliculus is a virtual passage between the 2 parallel medial longitudinal fascicles. Sharp dissection along the median sulcus (similar to the dissection used to reach intramedullary spinal cord lesions) is possible as there are no crossing fibers above the facial colliculus.5 Damage of the MLF results in internuclear ophthalmoplegia.

On the lateral surface of the floor of the fourth ventricle there are 2 relatively safe entry zones. One, the suprafacial triangle, is located immediately above the facial colliculus between the MLF (medially) and the cerebellar peduncles (laterally).28 The second one, the infrafacial triangle, is immediately below the facial colliculus, lateral to the MLF, and is bordered inferiorly by the striae medullares and superolaterally by the facial nerve.28

The region of the calamus scriptorius must be avoided to prevent dysphagia and cardiorespiratory disturbances related to damage of the vagal and hypoglossal triangles. Damage to the slightly more lateral nucleus ambiguus (which sends fibers to CNs IX, X, and XI) will cause palatal, pharyngeal and laryngeal palsy.

Lesions of this portion of the pons can be resected completely in 95% of patients and the overall results are generally good.19 However, there is a significant transient morbidity related to the numerous vital structures present in this area. The most common reported deficits are internuclear ophthalmoplegia and CN VI and VII deficits. Up to 20% of patients with CMs in this location may need a tracheostomy and/or a feeding tube.19

Clinical Correlates of a Dorsal Pons CM. For a CM located in the dorsal pons, as shown in Fig. 21, the more likely clinical presentations or possible sequelae of surgery include: ipsilateral hemifacial weakness from compression of the intraaxial CN VII fibers; ipsilateral CN VI palsy from compression of CN VI nucleus; ipsilateral loss of horizontal gaze from involvement of the paramedian pontine reticular formation; possible weakness of right face due to impingement of the intraaxial CN VII fibers on the right.

Fig. 21.
Fig. 21.

Schematic 3D illustration of the pons (left) and axial view at the level of the facial colliculus showing a dorsal pontine CM displacing internal structures (right).

Illustrative Case 4: CM of the Dorsal Pons. This 52-year-old man was initially conservatively followed up after bleeding of an upper pons–lower midbrain CM (Fig. 22), which was diagnosed after the patient noted hemibody numbness (medial lemniscus), inability to look up (MLF), and ataxia (red nucleus).

Fig. 22.
Fig. 22.

Illustrative Case 4: CM in the midbrain–upper pons and right middle cerebellar peduncle. Sagittal T1-weighted (A), axial T1-weighted (B and C), axial T2-weighted (D and E), and axial T1-weighted Gd-enhanced (F and G) MR images demonstrating a large CM in the left midbrain–upper pons (A, B, D, and F), with predominantly T1 and T2 hyperintensity, subacute blood products, and a hypointense hemosiderin ring. A smaller focal area of hemosiderin related to prior hemorrhage is seen in the left middle cerebellar peduncle (C and E). Both areas of hemorrhage are in the drainage field of a moderately sized DVA (F and G).

A subsequent bleed resulted in significant neurological deterioration. A new MR imaging study (Fig. 23) surprisingly showed that the second bleed occurred from a separate CM in the pons. The patient's new symptoms included bilateral CN VI palsy (bilateral abducent nuclei), bilateral pain/temperature and fine touch sensory deficits (spinothalamic tract and medial lemniscus), and facial numbness (chief sensory nucleus of CN V).

Fig. 23.
Fig. 23.

Illustrative Case 4: new CM in the central pons. Sagittal T1-weighted (A), axial T1-weighted (B, C, and F), and axial T2-weighted (D, E, and G) MR images obtained 16 months after the images in Fig. 22, demonstrating a new large CM in the left central pons (A, C, and E), with predominantly T1-hyperintense, subacute blood products. Moderate vasogenic edema with mild effacement of the fourth ventricle is associated (E). The previously seen midbrain–upper pontine CM has undergone temporal evolution of blood products, and is now predominantly T1 and T2 hypointense, compatible with hemosiderin. A stable smaller focal area of hemosiderin related to prior hemorrhage is seen in the left middle cerebellar peduncle (C and E). All 3 areas of hemorrhage are in the drainage field of the previously seen DVA.

The CM was abutting the floor of the fourth ventricle at the level of the pontomesencephalic junction and was resected through a left-sided telovelotonsillar approach to the floor of the fourth ventricle (Fig. 24). A very small inferior vermian incision was required to obtain optimal exposure of the uppermost portion of the floor of the fourth ventricle.

Fig. 24.
Fig. 24.

Illustrative Case 4: intraoperative photographs. Left: Initial steps of the telovelar approach to the floor of the fourth ventricle. After opening the cisterna magna, the cerebellar hemispheres, the tonsils and the uvula of the vermis are visible. Right: After sharp opening of the telovelotonsillar cleft, the tela choroidea is exposed (black asterisk). The floor of the fourth ventricle is visible in the depth of the operative field. Division of the tela choroidea (not shown) further opens the field of view into the fourth ventricle.

The CM was entered at the point where it was abutting the ependyma without violating any normal nerve structures in the rhomboid fossa.

Medulla: Internal and Functional Anatomy

Approaching the medulla's ventral surface, the prominent medially placed pyramid extends rostrally to caudally, containing the corticospinal tract. The lateral corticospinal tract crosses at the pyramidal decussation at the most caudal section of the medulla.

Just dorsal to the pyramid and running in a ventral-dorsal orientation is the medial lemniscus. Sensory projections from the uppermost cervical spine lie most dorsal, whereas those from the sacral cord are most ventral.

Two other white matter tracts can be found just dorsal to the medial lemniscus: the tectospinal tract (from the superior colliculus) and the MLF. At this level, the MLF contains descending projections from the medial vestibular nucleus, forming the medial vestibulospinal tract. This is important in coordinating eye and neck movement.

Lateral to the medial lemniscus and dorsolateral to the pyramid is the inferior olivary nucleus, which receives input from the ipsilateral red nucleus (as well as other areas) and projects fibers to the contralateral cerebellar hemisphere.

Dorsal to the inferior olivary nucleus is the nucleus ambiguus. This nucleus houses efferent neuronal cell bodies that innervate laryngeal, pharyngeal, and palatal muscles, primarily by way of the vagus nerve (the glossopharyngeal nerve innervates only the stylopharyngeus).

A cluster of white matter tracts are found lateral in the medulla. They are the spinothalamic tract (anterolateral system), the rubrospinal tract (from the red nucleus), and the anterior spinocerebellar tract, carrying unconscious proprioceptive input to the ipsilateral cerebellar hemisphere. The spinal trigeminal tract lies dorsal to this cluster and carries nociceptive input from CNs VII, IX, and X from various structures around the external auditory canal and oropharynx.

Various nuclei fill most of the dorsal region of the cross-section. Beginning most medially is the hypoglossal nucleus, containing efferent motor neurons whose projections run in CN XII. A lesion here will result in ipsilateral tongue weakness. This nucleus is responsible for the formation of the hypoglossal trigone found medially in the caudal rhomboid fossa.

Laterally, the next nucleus is the dorsal motor nucleus of the vagus, accounting for most of the body's parasympathetic nervous system innervation. This nucleus is responsible for the formation of the vagal trigone found laterally in the caudal rhomboid fossa.

Continuing laterally, the solitary nucleus can be found. Rostral functioning involves the transmission of taste sensation. Caudal function concerns the afferent processing from CNs IX and X regarding chemo- and baroreception.

Most lateral are the vestibular nuclei, which extend rostrally into the dorsolateral pons, and the inferior cerebellar peduncle. The inferior cerebellar peduncle contains reciprocal connections to and from the ipsilateral cerebellum. Although it is associated with the medulla, it borders the inferior margin of the middle cerebellar peduncle as it connects to the cerebellum. The dorsal and ventral cochlear nuclei are adjacent to the inferior cerebellar peduncle at this rostral-most level.

The various nuclei and fascicles in the upper and lower medulla are illustrated in Figs. 25 and 26.

Fig. 25.
Fig. 25.

Schematic 3D illustration (left) and axial orientation (right) of nuclei and fascicles in the upper medulla. CN X = vagus nerve fibers; CN XII = hypoglossal nerve fibers; DAO = dorsal accessory olivary nucleus; ECN = external cuneate nucleus; IO = inferior olivary nucleus; MAO = medial accessory olivary nucleus; NA nucleus ambiguus; NC = nucleus cuneatus; Nc X = dorsal motor nucleus of vagal nerve; Nc XII = hypoglossal nerve nucleus; NS = nucleus solitarius; P = pyramid; SN V = spinal nucleus of trigeminal nerve; STh = spinothalamic tract; ST V = spinal tract of trigeminal nerve; TSo = tractus solitarius.

Fig. 26.
Fig. 26.

Schematic 3D illustration (left) and axial view (right) of nuclei and fascicles in the lower medulla. ECu = external cuneate nucleus; IAF = internal arcuate fibers; NCu = nucleus cuneatus; NG = nucleus gracilis.

Medulla: Clinical Correlations

The clinical correlations of the nuclei and tracts of the medulla are summarized in Table 3.

TABLE 3:

Medullary nuclei and structures listed by anatomical location, function, and dysfunction

StructureLocation (ventral to dorsal, medial to lat)FunctionDysfunction
pyramidventral, medialupper motor neuron from cortex to contralat spinal cordcontralat UMN signs, weakness
inferior olivary nucleusventral, latrelay nucleus to the contralat cerebellumtremor27 & possible cerebellar signs
medial lemniscusventral, medialtransmits incoming proprioceptive, vibratory, & discrim touch info from contralat spinal cordcontralat hemianesthesia of trunk & extremities
tectospinal tractcentral, medialreflex movement of head & neckunappreciable
medial longitudinal fasciculuscentral, medialpathway btwn extraocular motor nuclei & gaze centersunappreciable
nucleus ambiguuscentral, latinnervates the muscles of palate, pharynx, larynxipsilat paralysis of palate, pharynx, larynx (dysphagia, vocal changes)
spinothalamic tract (anterolat system)central, lattransmits incoming pain & temp info from contralat spinal cordcontralat loss of pain & temp sensation in trunk & extremities
hypothalamospinal tract (not shown)central, lat near the spinothalamic tractcarries symp projections from hypothalamus to spinal cordHorner syndrome
spinal trigeminal nucleus/tractdorsal, lattransmits pain & temp info from face, sensory input from around external auditory meatus & orophayrnxipsilat loss of pain & temp sensation in areas around ear, decreased sensation in ipsilat oropharynx
hypoglossal nucleusdorsal, medialinnervation of most intrinsic & extrinsic muscles of tongueipsilat tongue weakness, tongue deviates ipsilaterally
dorsal motor nucleus of the vagus nervedorsal, centralparasymp innervation to level of the transverse colonipsilat loss of taste & increased heart rate
solitary nucleus tract (tract ascends throughout lat brainstem, though not shown)dorsal, latreceives incoming taste, chemo/baroreceptor sensationloss of taste sensation,14 intractable hiccup & nausea,37 sleep apnea41
vestibular nucleidorsal, latvestibular relay, integrates sensory inputdizziness/vertigo, postural instability, eye movement disorders
inferior cerebellar peduncledorsal, lattransmits vestibular & proprioceptive input to ipsilat cerebellum, inferior olivary nucleus input to contralat cerebellumipsilat ataxia, hearing loss
nucleus gracilisdorsal, medial, caudaltransmits ipsilat LE proprioceptive, vibratory, discrim touch sensory inputipsilat loss of tactile & vibratory input from LE (below T-6 level)
nucleus cuneatusdorsal, centra, caudaltransmits ipsilat UE proprioceptive, vibratory, discrim touch sensory inputipsilat loss of tactile & vibratory input from UE (above T-6 level)

Medulla: Surface Surgical Anatomy, Clinical-Anatomical Correlations, and Illustrative Cases

Upper (Ventricular) Dorsal Medulla CMs

Surface Surgical Anatomy and Surgical Approaches to the Upper (Ventricular) Dorsal Medulla. The surface surgical anatomy and the surgical approaches to the upper part (intraventricular) of the dorsal medulla have been described above (floor of the fourth ventricle).

Clinical Correlates of a CM of the Posterior Upper (Ventricular) Dorsal Medulla. For a CM located in the upper dorsal medulla, as shown in Fig. 27, the more likely clinical presentations or possible sequelae of surgery include: ipsilateral tongue weakness or CN XII palsy due to compression of the CN XII nucleus; cardiac and respiratory irregularities or instability due to compression of the CN X nucleus; and possible problems coordinating eye and head movement due to MLF or medial vestibulospinal tract involvement.

Fig. 27.
Fig. 27.

Schematic 3D illustration of the medulla (left) and axial view of an upper dorsal medullary CM displacing internal structures (right).

Lower Dorsal Medulla CMs

Surface Surgical Anatomy of the Lower Dorsal Medulla. The inferior part of the dorsal medulla is divided in 2 lateral parts by the posterior median sulcus, which is continuous with the median sulcus separating the posterior columns in the spinal cord (Fig. 13). The gracile fasciculus underlying the homonymous tubercle is lateral to the median sulcus on either side. The posterior intermediate sulcus separates the gracile fasciculus (medially) from the lateral cuneate fasciculus (laterally), which underlies the homonymous tubercle. The more lateral posterolateral sulcus delineates the cuneate fasciculus.

Surgical Approaches to the Lower Dorsal Medulla. The posterior medulla is usually approached by a median suboccipital craniotomy.

Bricolo5 describes 3 safe entry zones for the posterior medulla (Fig. 15): the posterior median fissure below the obex, the posterior intermediate sulcus between the gracile and cuneate fascicles, and the posterior lateral sulcus between the cuneate fascicle medially and the spinal trigeminal tract and nucleus laterally.

Clinical Correlates of a CM of the Lower Dorsal Medulla. For a CM located in the lower dorsal medulla, as shown in Fig. 28, the more likely clinical presentations or possible sequelae of surgery include the following: ipsilateral loss of tactile sensation from the mid-trunk and below due to compression of the nucleus gracilis; ipsilateral loss of tactile sensation from the mid-trunk and above due to compression of the nucleus cuneatus; possible cardiac/respiratory instability due to compression of the solitary nucleus and dorsal motor nucleus of the vagus; and possible ipsilateral tongue weakness due to compression of the CN XII nucleus.

Fig. 28.
Fig. 28.

Schematic 3D illustration of the medulla (left) and axial view of a lower dorsal medulla CM displacing internal structures (right).

Illustrative Case 5: CM of the Lower Dorsal Medulla. This 34-year-old woman developed sudden nausea with severe headache and numbness in her left arm and leg and dysmetria involving the left arm with gait ataxia (involvement of the inferior cerebellar peduncle). Imaging studies (Fig. 29) showed a CM of the left posterior medulla with evidence of recent and recurrent hemorrhage. She underwent a suboccipital craniotomy in the semisitting position and complete resection of the lesion. Intraoperative photographs are shown in Figs. 2 and 4 and an artistic representation in Fig. 3.

Fig. 29.
Fig. 29.

Illustrative Case 5: CM of the dorsal medulla. A–D: Initial imaging studies. Axial noncontrast CT (A) and T1-weighted (B), GRE (C), and T2-weighted (D) MR images demonstrating an exophytic CM at the left-posterior aspect of the medulla. The lesion is hyperdense on CT (A). There is mild T1 hyperintensity (B), significant “blooming” (C), and T2 heterogeneity (D). E: Axial T2-weighted image obtained 4 weeks later showing that the lesion has slightly increased size and developed a peripheral hypointense hemosiderin rim. F: Postoperative axial T2-weighted MR image demonstrating that the cavernoma has been resected, with a small amount of residual T2 hypointense hemosiderin at the operative site.

Cavernous Malformations of the Ventrolateral Medulla

Surface Surgical Anatomy of the Ventrolateral Medulla. The ventral aspect of the medulla (Fig. 6) presents a median longitudinal sulcus, the anterior median fissure, which divides the 2 pyramids. An additional sulcus lateral to the main anterior median fissure is the anterolateral sulcus. The anterolateral sulcus contains the origin of CN XII and separates the medial pyramid from the lateral olive. Dorsolaterally to the olive, CNs IX and X arise from the posterolateral sulcus.

Surgical Approaches to the Ventrolateral Medulla. Cavernous malformations located in the ventrolateral medulla can be resected through a far-lateral approach, which offers an anterolateral trajectory to the lower brainstem. This approach requires a lateral suboccipital craniectomy, resection of the posterior arch of the atlas, and partial drilling of the posterior third of the occipital condyle. For more ventral lesions, additional drilling of the occipital condyle may be required to achieve optimal exposure.19 This approach offers a lateral view of the medulla, the vertebral artery and the origin and proximal portion of the PICA and CNs IX, X, and XI emerging from the retro-olivary area, the origin of the fascicles of CN XII, and the C-1 spinal nerve.8,29

A safe entry zone has been described in this region at the level of the retro-olivary sulcus49 or between CN XII and C-1 in the anterolateral sulcus.8 However, because of the small diameter of the medulla, most symptomatic CMs come to the surface and provide a direct route of attack without the need to violate normal parenchyma.

Clinical Correlates of a CM of the Ventrolateral Medulla. For a CM located in the ventrolateral medulla, as shown in Fig. 30, the more likely clinical presentations/possible sequelae of surgery include: ipsilateral tongue weakness or CN XII nerve palsy due to compression of the CN XII nucleus; loss or weakness of the gag reflex due to compression of the nucleus ambiguus; change in voice quality due to nucleus ambiguus compression; possible loss of pain/temperature sensation in the contralateral trunk and extremities due to compression of the spinothalamic tract; and contralateral loss of tactile sensation in the trunk and extremities due to compression of the medial lemniscus.

Fig. 30.
Fig. 30.

Schematic 3D illustration of the medulla (left) and axial view of a ventrolateral medulla CM displacing internal structures (right).

Illustrative Case 6: CM of the Ventrolateral Medulla. This 27-year-old woman experienced sudden hemiparesis and decreased sensation. The MR imaging study (Fig. 31) demonstrated a left CM of the ventrolateral medulla. The CM appeared to be compressing the left pyramid (causing right hemiparesis) and the medial lemniscus (causing right hemianesthesia).

Fig. 31.
Fig. 31.

Illustrative Case 6: CM of the ventrolateral medulla. A–E: Axial noncontrast CT (A) and T1-weighted (B), GRE (C), and T2-weighted (D and E) MR images demonstrating an exophytic CM at the left-ventral aspect of the medulla. The lesion is hyperdense on CT (A). There is mild T1 hyperintensity (B), significant “blooming” (C), and T2 heterogeneity (D). The lesion extends into the lower pons (E). F: Axial T1-weighted Gd-enhanced MR image demonstrating an associated DVA.

Conclusions

The increasingly widespread availability of noninvasive imaging and the known morbidity of brainstem CMs, together with modern technologies such as intraoperative monitoring and frameless stereotaxy, have led to an aggressive management of symptomatic brainstem CMs. Thorough knowledge of the surgical and functional anatomy of the brainstem is an indispensible prerequisite to establish proper indications and minimize the surgical morbidity related to such a challenging procedure.

Disclosure

Dr. Lanzino reports that he is a consultant for Edge Therapeutics and Actelion, Inc. He also reports receiving clinical or research report for this study from ev3, Inc., and Synthes.

Author contributions to the study and manuscript preparation include the following. Conception and design: G Lanzino, Giliberto. Acquisition of data: Giliberto. Analysis and interpretation of data: Giliberto, DJ Lanzino, Diehn. Drafting the article: Giliberto. Critically revising the article: Giliberto, DJ Lanzino, Flemming. Reviewed final version of the manuscript and approved it for submission: G Lanzino. Study supervision: G Lanzino. Illustrations: Factor.

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    Hakuba ALiu SNishimura S: The orbitozygomatic infratemporal approach: a new surgical technique. Surg Neurol 26:2712761986

  • 21

    Hauck EFBarnett SLWhite JASamson D: Symptomatic brainstem cavernomas. Neurosurgery 64:61712009

  • 22

    Heffez DSZinreich SJLong DM: Surgical resection of intrinsic brain stem lesions: an overview. Neurosurgery 27:7897981990

  • 23

    Holstege G: The emotional motor system and micturition control. Neurourol Urodyn 29:42482010

  • 24

    Horgan MADelashaw JBSchwartz MSKellogg JXSpektor SMcMenomey SO: Transcrusal approach to the petroclival region with hearing preservation. Technical note and illustrative cases. J Neurosurg 94:6606662001

    • Search Google Scholar
    • Export Citation
  • 25

    Jane JAPark TSPobereskin LHWinn HRButler AB: The supraorbital approach: technical note. Neurosurgery 11:5375421982

  • 26

    Kawase TToya SShiobara RMine T: Transpetrosal approach for aneurysms of the lower basilar artery. J Neurosurg 63:8578611985

  • 27

    Kim JSPark JWKim YIHan SJKim HTLee KS: Tremors associated with an inferior olivary lesion that developed after a pontine hemorrhage. Mov Disord 21:153915402006

    • Search Google Scholar
    • Export Citation
  • 28

    Kyoshima KKobayashi SGibo HKuroyanagi T: A study of safe entry zones via the floor of the fourth ventricle for brainstem lesions. Report of three cases. J Neurosurg 78:9879931993

    • Search Google Scholar
    • Export Citation
  • 29

    Lanzino GPaolini SSpetzler RF: Far-lateral approach to the craniocervical junction. Neurosurgery 57:4 Suppl3673712005

  • 30

    Lanzino GSpetzler RF: Cavernous Malformations of the Brain and Spinal Cord New YorkThieme2008. 11

  • 31

    Lawton MTDaspit CPSpetzler RF: Transpetrosal and combination approaches to skull base lesions. Clin Neurosurg 43:911121996

  • 32

    Lekovic GPGonzalez LFKhurana VGSpetzler RF: Intraoperative rupture of brainstem cavernous malformation. Case report. Neurosurg Focus 21:1e142006

    • Search Google Scholar
    • Export Citation
  • 33

    Little KMFriedman AHFukushima T: Surgical approaches to pineal region tumors. J Neurooncol 54:2872992001

  • 34

    Lopez LIBronstein AMGresty MADu Boulay EPRudge P: Clinical and MRI correlates in 27 patients with acquired pendular nystagmus. Brain 119:4654721996

    • Search Google Scholar
    • Export Citation
  • 35

    Martinez JAGde Oliveira ETedeschi HWen HTRhoton AL Jr: Microsurgical anatomy of the brain stem. Op Tech Neurosurg 3:80862000

    • Search Google Scholar
    • Export Citation
  • 36

    Miller CGvan Loveren HRKeller JTPensak Mel-Kalliny MTew JM Jr: Transpetrosal approach: surgical anatomy and technique. Neurosurgery 33:4614691993

    • Search Google Scholar
    • Export Citation
  • 37

    Misu TFujihara KNakashima ISato SItoyama Y: Intractable hiccup and nausea with periaqueductal lesions in neuromyelitis optica. Neurology 65:147914822005

    • Search Google Scholar
    • Export Citation
  • 38

    Morgan JCSethi KD: Midbrain infarct with parkinsonism. Neurology 60:E102003

  • 39

    Mussi ACRhoton AL Jr: Telovelar approach to the fourth ventricle: microsurgical anatomy. J Neurosurg 92:8128232000

  • 40

    Orta Daniel SJUlises RO: Stroke of the substance nigra and parkinsonism as first manifestation of systemic lupus erythematosus. Parkinsonism Relat Disord 14:3673692008

    • Search Google Scholar
    • Export Citation
  • 41

    Parenti AMacchi VSnenghi RPorzionato AScaravilli TFerrara SD: Selective stroke of the solitary tract nuclei in two cases of central sleep apnoea. Clin Neuropathol 24:2392462005

    • Search Google Scholar
    • Export Citation
  • 42

    Pellerin PLesoin FDhellemmes PDonazzan MJomin M: Usefulness of the orbitofrontomalar approach associated with bone reconstruction for frontotemporosphenoid meningiomas. Neurosurgery 15:7157181984

    • Search Google Scholar
    • Export Citation
  • 43

    Perrini PLanzino G: The association of venous developmental anomalies and cavernous malformations: pathophysiological, diagnostic, and surgical considerations. Neurosurg Focus 21:1e52006

    • Search Google Scholar
    • Export Citation
  • 44

    Petersen TAMorrison LASchrader RMHart BL: Familial versus sporadic cavernous malformations: differences in developmental venous anomaly association and lesion phenotype. AJNR Am J Neuroradiol 31:3773822010

    • Search Google Scholar
    • Export Citation
  • 45

    Porter RWDetwiler PWSpetzler RF: Surgical approaches to the brain stem. Op Tech Neurosurg 3:1141232000

  • 46

    Porter RWDetwiler PWSpetzler RFLawton MTBaskin JJDerksen PT: Cavernous malformations of the brainstem: experience with 100 patients. J Neurosurg 90:50581999

    • Search Google Scholar
    • Export Citation
  • 47

    Quinones-Hinojosa AChang EFLawton MT: The extended retrosigmoid approach: an alternative to radical cranial base approaches for posterior fossa lesions. Neurosurgery 58:4 Suppl 2ONS-208ONS-2142006

    • Search Google Scholar
    • Export Citation
  • 48

    Rammos SKMaina RLanzino G: Developmental venous anomalies: current concepts and implications for management. Neurosurgery 65:20302009

    • Search Google Scholar
    • Export Citation
  • 49

    Recalde RJFigueiredo EGde Oliveira E: Microsurgical anatomy of the safe entry zones on the anterolateral brainstem related to surgical approaches to cavernous malformations. Neurosurgery 62:3 Suppl 19172008

    • Search Google Scholar
    • Export Citation
  • 50

    Rigamonti DSpetzler RF: The association of venous and cavernous malformations. Report of four cases and discussion of the pathophysiological, diagnostic, and therapeutic implications. Acta Neurochir (Wien) 92:1001051988

    • Search Google Scholar
    • Export Citation
  • 51

    Sala FManganotti PTramontano VBricolo AGerosa M: Monitoring of motor pathways during brain stem surgery: what we have achieved and what we still miss?. Neurophysiol Clin 37:3994062007

    • Search Google Scholar
    • Export Citation
  • 52

    Samii MEghbal RCarvalho GAMatthies C: Surgical management of brainstem cavernomas. J Neurosurg 95:8258322001

  • 53

    Sasaki OTanaka RKoike TKoide AKoizumi TOgawa H: Excision of cavernous angioma with preservation of coexisting venous angioma. Case report. J Neurosurg 75:4614641991

    • Search Google Scholar
    • Export Citation
  • 54

    Shen YC: Unilateral rubral tremor following treatment with risperidone. World J Biol Psychiatry 10:6296312009

  • 55

    Stein BM: The infratentorial supracerebellar approach to pineal lesions. J Neurosurg 35:1972021971

  • 56

    Stein BM: Supracerebellar-infratentorial approach to pineal tumors. Surg Neurol 11:3313371979

  • 57

    Weil SMTew JM Jr: Surgical management of brain stem vascular malformations. Acta Neurochir (Wien) 105:14231990

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    Yaşargil MGFox JL: The microsurgical approach to intracranial aneurysms. Surg Neurol 3:7141975

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Article Information

Contributor Notes

Address correspondence to: Giuseppe Lanzino, M.D., 200 First Street SW, Rochester, Minnesota 55905. email: Lanzino.giuseppe@mayo.edu.
Headings
Figures
  • View in gallery

    Schematic drawing illustrating the most common surgical approaches used for different areas of the brainstem.

  • View in gallery

    Intraoperative photograph showing a posterolateral CM of the left medulla abutting the pial surface. The CM was exposed through a posterior suboccipital approach after elevation of the ipsilateral tonsil. The PICA loop and the vertebral artery (deeper in the left corner) are visible. The superficial portion of the CM in this case provided a natural and atraumatic entry route.

  • View in gallery

    Artist's illustration showing internal emptying of the same CM as in Fig. 2 and piecemeal removal with a pituitary forceps through a small opening.

  • View in gallery

    Intraoperative photograph obtained after resection of the CM shown in Figs. 2 and 3. A typical DVA is visible along the inferior wall of the surgical cavity although no clear-cut evidence of a DVA was visible on the preoperative MR images.

  • View in gallery

    Schematic 3D illustration (left) and axial view at the level of the superior colliculus (right) of the nuclei and fascicles in the midbrain. CB = corticobulbar tract; CS = corticospinal tract; CTT = central tegmental tract; EW = Edinger-Westphal nucleus; FP = frontopontine fibers; III = CN III; ML = medial lemniscus; MLF = medial longitudinal fasciculus; Nc III = CN III (oculomotor nerve) nuclei; PAG = periaqueductal gray matter; PTOP = parietotemporooccipitopontine tract; RN = red nucleus; SC = superior colliculus; SN = substantia nigra; ST = spinothalamic tract.

  • View in gallery

    A: Schematic illustration of the surface anatomy of the ventral brainstem. B: Schematic illustration of the arterial (left) and venous (right) anatomy

  • View in gallery

    Illustrations of the FOZ approach. Schematic 3D view of the skull after craniotomy, showing the region of the brainstem that can be approached (left), and axial view of the skull (right) showing the area of the craniotomy (dotted lines). Arrow indicates the surgical trajectory.

  • View in gallery

    Sagittal (left) and coronal (right) MR images obtained in a 24-year-old woman with sudden onset of facial numbness and left hand weakness showing a hemorrhagic CM extending from the upper midbrain to the ipsilateral thalamus.

  • View in gallery

    Schematic 3D illustration of the anatomy of the midbrain (left) and axial view of a ventral midbrain CM displacing internal structures (right).

  • View in gallery

    Illustrative Case 1: CM in the central midbrain. Sagittal T1-weighted (A), axial T2-weighted (B), and Gd-enhanced axial T1-weighted (C) MR images demonstrating a CM in the central midbrain. The lesion is hyperintense on T1-weighted images (A), heterogeneous on T2-weighted images with a fluid-fluid/debris level (B), and nonenhancing (C).

  • View in gallery

    Schematic 3D illustration of the anatomy of the midbrain (left) and axial view of a ventrolateral midbrain CM displacing internal structures (right).

  • View in gallery

    Illustrative Case 2: CM in the right ventrolateral midbrain and upper pons. A–E: Preoperative sagittal T1-weighted (A), axial T1-weighted (B), axial T2-weighted (C), axial gradient echo (GRE) (D), and axial T1-weighted Gd-enhanced (E) MR images demonstrating a CM involving the right anterolateral midbrain and upper pons, extending to the surface. Note the precontrast T1 hyperintensity (A and B); speckled, “popcorn” morphology (A and B); extensive blooming on GRE sequence due to magnetic susceptibility artifact (D); and minimal enhancement (E). F: Postoperative axial T1-weighted Gd-enhanced image demonstrating resection of the CM, with a resection cavity at the operative site and no residual enhancement.

  • View in gallery

    A: Schematic illustration of the surface anatomy of the dorsal brainstem. B: Schematic illustration of the arterial (left) and venous (right) brainstem anatomy.

  • View in gallery

    Axial view of the midbrain showing the surgical route through the lateral mesencephalic sulcus, covered by the lateral mesencephalic vein (blue circle). This safe entry zone allows a trajectory (arrow) of approach between the substantia nigra (SN) and the medial lemniscus (ML) posterior to the cerebral peduncle.

  • View in gallery

    Posterior view of the brainstem showing the various safe entry zones.

  • View in gallery

    Schematic 3D illustration of the midbrain (left) and axial view of a posterior midbrain CM displacing internal structures (right).

  • View in gallery

    Schematic 3D illustration (left) and axial view of the pontine nuclei and fascicles in a section at the level of the facial colliculus (right). CN VI = abducent nerve fibers; CN VII = facial nerve fibers; DN = dentate nucleus; GE = globose end emboliform nuclei; ICP = inferior cerebellar peduncle; LVN = lateral vestibular nucleus; MCP = middle cerebellar peduncle; MVN = medial vestibular nucleus; NcV = spinal nucleus of trigeminal nerve; NcVI = abducent nerve nucleus; NcVII = facial nerve nucleus; SCP = superior cerebellar peduncle; SVN = superior vestibular nucleus; TSp = tectospinal tract; TV = spinal tract of trigeminal nerve.

  • View in gallery

    Peritrigeminal safe entry zone in the ventrolateral pons.

  • View in gallery

    Schematic 3D illustration of the pons (left) and axial view at the level of the facial colliculus of a ventral pontine CM displacing internal structures (right).

  • View in gallery

    Illustrative Case 3: CM in the pons. A–C: Sagittal T1-weighted (A), axial T2-weighted (B), and Gd-enhanced coronal T1-weighted (C) MR images demonstrating a large CM centered in the left ventrolateral aspect of the pons. The lesion is hyperintense on T1-weighted imaging (A), heterogeneous on T2-weighted imaging with surrounding vasogenic edema (B), and nonenhancing (C). D–F: Postoperative correlative images demonstrating complete resection of the lesion.

  • View in gallery

    Schematic 3D illustration of the pons (left) and axial view at the level of the facial colliculus showing a dorsal pontine CM displacing internal structures (right).

  • View in gallery

    Illustrative Case 4: CM in the midbrain–upper pons and right middle cerebellar peduncle. Sagittal T1-weighted (A), axial T1-weighted (B and C), axial T2-weighted (D and E), and axial T1-weighted Gd-enhanced (F and G) MR images demonstrating a large CM in the left midbrain–upper pons (A, B, D, and F), with predominantly T1 and T2 hyperintensity, subacute blood products, and a hypointense hemosiderin ring. A smaller focal area of hemosiderin related to prior hemorrhage is seen in the left middle cerebellar peduncle (C and E). Both areas of hemorrhage are in the drainage field of a moderately sized DVA (F and G).

  • View in gallery

    Illustrative Case 4: new CM in the central pons. Sagittal T1-weighted (A), axial T1-weighted (B, C, and F), and axial T2-weighted (D, E, and G) MR images obtained 16 months after the images in Fig. 22, demonstrating a new large CM in the left central pons (A, C, and E), with predominantly T1-hyperintense, subacute blood products. Moderate vasogenic edema with mild effacement of the fourth ventricle is associated (E). The previously seen midbrain–upper pontine CM has undergone temporal evolution of blood products, and is now predominantly T1 and T2 hypointense, compatible with hemosiderin. A stable smaller focal area of hemosiderin related to prior hemorrhage is seen in the left middle cerebellar peduncle (C and E). All 3 areas of hemorrhage are in the drainage field of the previously seen DVA.

  • View in gallery

    Illustrative Case 4: intraoperative photographs. Left: Initial steps of the telovelar approach to the floor of the fourth ventricle. After opening the cisterna magna, the cerebellar hemispheres, the tonsils and the uvula of the vermis are visible. Right: After sharp opening of the telovelotonsillar cleft, the tela choroidea is exposed (black asterisk). The floor of the fourth ventricle is visible in the depth of the operative field. Division of the tela choroidea (not shown) further opens the field of view into the fourth ventricle.

  • View in gallery

    Schematic 3D illustration (left) and axial orientation (right) of nuclei and fascicles in the upper medulla. CN X = vagus nerve fibers; CN XII = hypoglossal nerve fibers; DAO = dorsal accessory olivary nucleus; ECN = external cuneate nucleus; IO = inferior olivary nucleus; MAO = medial accessory olivary nucleus; NA nucleus ambiguus; NC = nucleus cuneatus; Nc X = dorsal motor nucleus of vagal nerve; Nc XII = hypoglossal nerve nucleus; NS = nucleus solitarius; P = pyramid; SN V = spinal nucleus of trigeminal nerve; STh = spinothalamic tract; ST V = spinal tract of trigeminal nerve; TSo = tractus solitarius.

  • View in gallery

    Schematic 3D illustration (left) and axial view (right) of nuclei and fascicles in the lower medulla. ECu = external cuneate nucleus; IAF = internal arcuate fibers; NCu = nucleus cuneatus; NG = nucleus gracilis.

  • View in gallery

    Schematic 3D illustration of the medulla (left) and axial view of an upper dorsal medullary CM displacing internal structures (right).

  • View in gallery

    Schematic 3D illustration of the medulla (left) and axial view of a lower dorsal medulla CM displacing internal structures (right).

  • View in gallery

    Illustrative Case 5: CM of the dorsal medulla. A–D: Initial imaging studies. Axial noncontrast CT (A) and T1-weighted (B), GRE (C), and T2-weighted (D) MR images demonstrating an exophytic CM at the left-posterior aspect of the medulla. The lesion is hyperdense on CT (A). There is mild T1 hyperintensity (B), significant “blooming” (C), and T2 heterogeneity (D). E: Axial T2-weighted image obtained 4 weeks later showing that the lesion has slightly increased size and developed a peripheral hypointense hemosiderin rim. F: Postoperative axial T2-weighted MR image demonstrating that the cavernoma has been resected, with a small amount of residual T2 hypointense hemosiderin at the operative site.

  • View in gallery

    Schematic 3D illustration of the medulla (left) and axial view of a ventrolateral medulla CM displacing internal structures (right).

  • View in gallery

    Illustrative Case 6: CM of the ventrolateral medulla. A–E: Axial noncontrast CT (A) and T1-weighted (B), GRE (C), and T2-weighted (D and E) MR images demonstrating an exophytic CM at the left-ventral aspect of the medulla. The lesion is hyperdense on CT (A). There is mild T1 hyperintensity (B), significant “blooming” (C), and T2 heterogeneity (D). The lesion extends into the lower pons (E). F: Axial T1-weighted Gd-enhanced MR image demonstrating an associated DVA.

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    Horgan MADelashaw JBSchwartz MSKellogg JXSpektor SMcMenomey SO: Transcrusal approach to the petroclival region with hearing preservation. Technical note and illustrative cases. J Neurosurg 94:6606662001

    • Search Google Scholar
    • Export Citation
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    Jane JAPark TSPobereskin LHWinn HRButler AB: The supraorbital approach: technical note. Neurosurgery 11:5375421982

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    • Search Google Scholar
    • Export Citation
  • 28

    Kyoshima KKobayashi SGibo HKuroyanagi T: A study of safe entry zones via the floor of the fourth ventricle for brainstem lesions. Report of three cases. J Neurosurg 78:9879931993

    • Search Google Scholar
    • Export Citation
  • 29

    Lanzino GPaolini SSpetzler RF: Far-lateral approach to the craniocervical junction. Neurosurgery 57:4 Suppl3673712005

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    Lanzino GSpetzler RF: Cavernous Malformations of the Brain and Spinal Cord New YorkThieme2008. 11

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    Lawton MTDaspit CPSpetzler RF: Transpetrosal and combination approaches to skull base lesions. Clin Neurosurg 43:911121996

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    Lekovic GPGonzalez LFKhurana VGSpetzler RF: Intraoperative rupture of brainstem cavernous malformation. Case report. Neurosurg Focus 21:1e142006

    • Search Google Scholar
    • Export Citation
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    Little KMFriedman AHFukushima T: Surgical approaches to pineal region tumors. J Neurooncol 54:2872992001

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    Lopez LIBronstein AMGresty MADu Boulay EPRudge P: Clinical and MRI correlates in 27 patients with acquired pendular nystagmus. Brain 119:4654721996

    • Search Google Scholar
    • Export Citation
  • 35

    Martinez JAGde Oliveira ETedeschi HWen HTRhoton AL Jr: Microsurgical anatomy of the brain stem. Op Tech Neurosurg 3:80862000

    • Search Google Scholar
    • Export Citation
  • 36

    Miller CGvan Loveren HRKeller JTPensak Mel-Kalliny MTew JM Jr: Transpetrosal approach: surgical anatomy and technique. Neurosurgery 33:4614691993

    • Search Google Scholar
    • Export Citation
  • 37

    Misu TFujihara KNakashima ISato SItoyama Y: Intractable hiccup and nausea with periaqueductal lesions in neuromyelitis optica. Neurology 65:147914822005

    • Search Google Scholar
    • Export Citation
  • 38

    Morgan JCSethi KD: Midbrain infarct with parkinsonism. Neurology 60:E102003

  • 39

    Mussi ACRhoton AL Jr: Telovelar approach to the fourth ventricle: microsurgical anatomy. J Neurosurg 92:8128232000

  • 40

    Orta Daniel SJUlises RO: Stroke of the substance nigra and parkinsonism as first manifestation of systemic lupus erythematosus. Parkinsonism Relat Disord 14:3673692008

    • Search Google Scholar
    • Export Citation
  • 41

    Parenti AMacchi VSnenghi RPorzionato AScaravilli TFerrara SD: Selective stroke of the solitary tract nuclei in two cases of central sleep apnoea. Clin Neuropathol 24:2392462005

    • Search Google Scholar
    • Export Citation
  • 42

    Pellerin PLesoin FDhellemmes PDonazzan MJomin M: Usefulness of the orbitofrontomalar approach associated with bone reconstruction for frontotemporosphenoid meningiomas. Neurosurgery 15:7157181984

    • Search Google Scholar
    • Export Citation
  • 43

    Perrini PLanzino G: The association of venous developmental anomalies and cavernous malformations: pathophysiological, diagnostic, and surgical considerations. Neurosurg Focus 21:1e52006

    • Search Google Scholar
    • Export Citation
  • 44

    Petersen TAMorrison LASchrader RMHart BL: Familial versus sporadic cavernous malformations: differences in developmental venous anomaly association and lesion phenotype. AJNR Am J Neuroradiol 31:3773822010

    • Search Google Scholar
    • Export Citation
  • 45

    Porter RWDetwiler PWSpetzler RF: Surgical approaches to the brain stem. Op Tech Neurosurg 3:1141232000

  • 46

    Porter RWDetwiler PWSpetzler RFLawton MTBaskin JJDerksen PT: Cavernous malformations of the brainstem: experience with 100 patients. J Neurosurg 90:50581999

    • Search Google Scholar
    • Export Citation
  • 47

    Quinones-Hinojosa AChang EFLawton MT: The extended retrosigmoid approach: an alternative to radical cranial base approaches for posterior fossa lesions. Neurosurgery 58:4 Suppl 2ONS-208ONS-2142006

    • Search Google Scholar
    • Export Citation
  • 48

    Rammos SKMaina RLanzino G: Developmental venous anomalies: current concepts and implications for management. Neurosurgery 65:20302009

    • Search Google Scholar
    • Export Citation
  • 49

    Recalde RJFigueiredo EGde Oliveira E: Microsurgical anatomy of the safe entry zones on the anterolateral brainstem related to surgical approaches to cavernous malformations. Neurosurgery 62:3 Suppl 19172008

    • Search Google Scholar
    • Export Citation
  • 50

    Rigamonti DSpetzler RF: The association of venous and cavernous malformations. Report of four cases and discussion of the pathophysiological, diagnostic, and therapeutic implications. Acta Neurochir (Wien) 92:1001051988

    • Search Google Scholar
    • Export Citation
  • 51

    Sala FManganotti PTramontano VBricolo AGerosa M: Monitoring of motor pathways during brain stem surgery: what we have achieved and what we still miss?. Neurophysiol Clin 37:3994062007

    • Search Google Scholar
    • Export Citation
  • 52

    Samii MEghbal RCarvalho GAMatthies C: Surgical management of brainstem cavernomas. J Neurosurg 95:8258322001

  • 53

    Sasaki OTanaka RKoike TKoide AKoizumi TOgawa H: Excision of cavernous angioma with preservation of coexisting venous angioma. Case report. J Neurosurg 75:4614641991

    • Search Google Scholar
    • Export Citation
  • 54

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