The insula is a functionally and anatomically complex cortical structure that can be affected by both low-grade and high-grade gliomas. This complexity often prevents many neurosurgeons from attempting to surgically manage insular gliomas. This article reviews the anatomic and functional uniqueness of the insula and the surgical outcomes and lessons learned from previously reported surgical series. Successful management of insular gliomas, defined as maximal resection of the tumor without postoperative neurologic morbidity, can be achieved through a sophisticated understanding of the neurovascular structure of the insular region and an intraoperative functional mapping using cortico-subcortical electrical stimulation.
In 1809, Johann Christian Reil (1759–1813), the German anatomist, physiologist, and psychiatrist, first described the island (or insula) of Reil. This anatomically and functionally complex structure is located in the depth of the sylvian fissure, overlies the basal ganglia block, and is hidden by the opercula of the frontal, parietal, and temporal lobes. It is thought to play roles in autonomic sensation, gustatory function, olfaction, memory, drive, auditory–vestibular function, and the motor integration and motor planning of speech in the dominant hemisphere. The insula is also associated with cardioregulatory and vasomotor functions, pain perception, and bio-behavioral dysfunction characteristics of schizophrenia. Moreover, the insula is adjacent to essential peri-sylvian language areas (ie, Broca areas and Wernicke areas and their association fibers, the primary auditory area, and both the primary motor and sensory areas).
Therefore, intrinsic tumors located in the insular and peri-insular areas present with a variety of ill-defined symptoms and neurologic signs dominated by a single entity, such as motor dysphasia with or without lower facial paresis. The anatomic complexity of the insula and its functionally critical nature have caused radical insula operations to be taboo among neurosurgeons for a long time, and they have often recommended a conservative strategy for the treatment of intrinsic insular tumors. However, since the seminal 1992 study by Yasargil and colleagues, which demonstrated that it was possible to extirpate intrinsic insular tumors with less risk than initially thought, some experienced neurosurgeons have reported favorable outcomes of insular tumor surgery based on a detailed understanding of the pertinent anatomy and the application of modern microneurosurgical techniques.
Nonetheless, achieving both maximal resection and a favorable functional outcome in intrinsic insular tumor surgery has been challenging for most neurosurgeons. This article reviews the anatomic and surgical characteristics of insular gliomas (which are the most frequent intrinsic tumor in the insula) and evaluates the reported oncological and functional outcomes after insular glioma surgery.
Anatomy of insular glioma and surgical approaches
A detailed understanding of the complex anatomy of the insula and its surrounding structures is required for the removal of insular gliomas with minimal morbidity. The insula, a well-defined cerebral cortical surface, is a pyramidal structure whose 3 sides meet at a peak called the insular apex, the most lateral projection of the insula. The central sulcus separates the larger anterior portion from the smaller posterior portion. The anterior portion is composed of 3 short gyri (ie, the anterior, middle, and posterior short insular gyri) as well as the transverse gyrus and the accessory gyrus. The posterior portion is composed of the anterior and posterior long insular gyri. The limen insulae, a white matter structure in the anterobasal portion of the insula, parallels the course of the lateral olfactory stria, extending from the anterior perforated substance medially to the insular pole along what is known as the sylvian stem.
In the central portion of the insula, the extreme capsule, claustrum, external capsule, putamen, and globus pallidus lie in a lateral-to-medial direction. The perimeter of the insula is provided by the anterior, superior, and inferior peri-insular sulci, which separate the insula from the fronto–orbital, fronto–parietal, and temporal opercula, respectively. These are critical internal landmarks that define the internal extent of the insula for the neurosurgeon. Superior to the central portion of the insula, at the level of the superior peri-insular sulcus, is the corticospinal tract in the corona radiata; the uncinate fasciculus is located anteroinferiorly, and the arcuate fasciculus is located posteriorly along the same sulcus. The anterior and posterior limits of the insula are defined as the meeting point of the anterior with the superior peri-insular sulcus and that of the superior with the inferior peri-insular sulcus, respectively.
The course and supply of the middle cerebral artery (MCA) and its perforating vessels are most important for insular glioma surgery. The blood supply of insular gliomas is largely derived from the M2 segment of the MCA through its short- and medium-sized perforating vessels. Devascularization of an insular glioma can be achieved by advertent coagulation and cutting each of the M2 perforators after subpial dissection. Long perforating vessels of the M2 overlying the posterior portion of the insula supply the corona radiate, particularly the corticospinal and thalamocortical fibers, and they therefore must be preserved during surgery. The M1 segment of the MCA lies at the anteroinferior portion of the insula, extending laterally from the carotid bifurcation under the anterior perforated substance, and it supplies the basal ganglia and internal capsule via lateral lenticulostriate perforating vessels. The mean distance from the insular apex to the most lateral lenticulostriate artery is less than 1.5 cm, and the neurosurgeon must preserve the first lenticulostriate artery encountered, which is usually located in the medial side of the tumor, without creating a dense hemiplegia.
Yasargil and colleagues reported an extensive surgical series of limbic and paralimbic intrinsic tumors (including insular gliomas), and they demonstrated for the first time that microsurgery is possible for tumors occupying that region without critical neurologic deterioration. They proposed a classification scheme for tumors in paralimbic regions. In this scheme, type 3a tumors (purely insular tumors), type 3b tumors (those infiltrating the peri-sylvian opercula), and type 5 tumors (those extending to other paralimbic areas) were included in the broad category of insular gliomas.
Tables 1 and 2 present the summarized data of the patients with insular gliomas in the previously reported surgical series. The traditional approach for insular gliomas had been the trans-sylvian approach because of the seminal work of Yasargil and colleagues. The advantages of the trans-sylvian approach include a direct corridor to the insular region, the possibility of a wide surgical view by widely opening the sylvian fissure, and the great familiarity of this approach to neurosurgeons. However, the risk of vascular damage, in particular to the perforating vessels, by means of the trans-sylvian approach to the insular region, is never negligible. Therefore, in recently reported papers, a transcortical approach (ie, a transopercular approach) has been used as an alternative or adjunctive method to the traditional trans-sylvian approach. A transcortical approach by means of subpial dissection prevents injuries to and iatrogenic spasms of the MCA and its branches. In addition, intraoperative monitoring, such as of somatosensory-evoked potentials and motor-evoked potentials, is necessary to preserve the integrity of the peri-insular regions. Likewise, awake craniotomy enables the neurosurgeon to monitor the language function of the patient, which is especially important for tumors in the dominant hemisphere.
| Author, Year | Total Number | Age (Range) | Sex | Description of Seizure | Presenting Symptoms and Signs | Histology | F/U Duration (Range) |
|---|---|---|---|---|---|---|---|
| Yasargil et al, 1992 | 80 | Peak age 41–50 y | NA | SPS (5%) CPS (28%) 2nd GTCS (13%) GTCS (10%) Absence (15%) Others (4%) | Seizure (78%) Sensorimotor hemideficit (26%) Speech impairment (26%) Neuropsychological defect (35%) Visual acuity decrease (10%) Visual field defect (10%) | LGG (44%) HGG (56%) | NA |
| Vanaclocha et al, 1997 | 23 | Median 40 y (12–64 y) | Male (65%) Female (35%) | NA | NA | LGG (70%) HGG (30%) | Median 2.5 y (1–6.5 y) |
| Lang et al, 2001 | 22 | Median 36 y (2–78 y) | Male (32%) Female (68%) | Total (64%) | Seizure (64%) Weakness/hemiparesis (32%) Dysphasia/dysnomia (18%) | LGG (50%) HGG (50%) | Median 1.2 y (0.2–4 y) |
| Moshel et al, 2008 | 38 | Mean 38 y (15–59 y) | Male (61%) Female (39%) | SPS (8%) CPS (34%) GTCS (29%) | Seizure (71%) Hemiparesis (8%) Hemianesthesia (8%) Dysphasia (16%) Headache (29%) Memory deficits (8%) Visual problems (3%) | LGG (74%) HGG (26%) | NA |
| Duffau, 2009 | 51 | Mean 36 y (19–57 y) | Male (59%) Female (41%) | SPS (69%) GTCS (29%) Intractable (35%) | Seizure (98%) Intracerebral hemorrhage (2%) Hemiparesis (2%) | LGG (100%) HGG (0%) | Median 4 y (0.3–10.1 y) |
| Simon et al, 2010 | 94 | Median 41 y (9–77) | Male (61%) Female (39%) | Total (82%) Intractable (13%) | Seizure (82%) Hemiparesis or dysphasia (24%) | LGG (36%) HGG (64%) | Median 3.1 y (0–17.1 y) |
| Sanai et al, 2010 | 104 | Median 40 y (18–75) | Male (40%) Female (60%) | Total (72%) | Seizure (72%) Sensory impairments (13%) Headache (7%) Languade deficits (5%) Incidental (4%) | LGG (60%) HGG (40%) | Median 4.2 y (1.4–10.2 y) |
| Author, Year | Total Number | Approach | Extent of Resection | Immediate N/D | Permanent N/D | Survival Data | F/U Duration (Range) |
|---|---|---|---|---|---|---|---|
| Yasargil et al, 1992 | 80 | Trans-sylvian | NA | NA | Total (11%) | NA | NA |
| Vanaclocha, et al, 1997 | 23 | Trans-sylvian | GTR (87%) STR (13%) |
| Total (0%) | Alive at last F/U (87%) | Median 2.5 y (1–6.5 y) |
| Lang et al, 2001 | 22 | Trans-sylvian (36%) + ATL (36%) + transopercular (28%) | >90% (45%) 75%–90% (27%) <75% (28%) |
| Total (9%) Weakness (9%) | Alive at last F/U (68%) | Median 1.2 y (0.2–4 y) |
| Moshel et al, 2008 | 38 | Trans-sylvian | GTR (55%) NTR (18%) STR (26%) |
| Total (13%) Hemiparesis (13%) Dysphasia (5%) | NA | NA |
| Duffau, 2009 | 51 | Transopercular (94%) Transsylvian (6%) | GTR (16%) STR (61%) PR (24%) |
|
| Alive at last F/U (82%) | Median 4 y (0.3–10.1 y) |
| Simon et al, 2010 | 94 | Trans-sylvian (25%) Transopercular (50%) Combined (25%) | >90% (42%) 70%–90% (51%) <70% (7%) | NA |
| a | Median 3.1 y (0–17.1 y) |
| Sanai et al, 2010 | 104 | Transcortical | >90% (23%) 80%–90% (39%) 60%–80% (28%) <60% (11%) |
|
| Alive at last F/U (91%) | Median 4.2 y (1.4–10.2 y) |
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