Cavernous angiomas are being increasingly diagnosed with better imaging techniques. Management of these lesions, however, remains controversial. Decision making for deep seated lesions is more difficult because of their greater tendency for frequent bleeds and debilitating deficits they may cause, coupled with the greater morbidity their surgical excision might produce. 

Diffusion tensor imaging (DTI) and functional magnetic resonance imaging (fMRI), along with image guidance (neuro-navigation) and intraoperative monitoring have helped in reducing the complications associated with surgery. Brainstem as well as deep cerebral and basal ganglia lesions, especially following hemorrhage, can be safely tackled now with use of safe corridors. We recommend surgery for those deep-seated lesions which are accessible through a sulcus or fissure or have come up to either the ependymal or pial surface.

 

Keywords

Cavernous angioma, Cavernous malformation, Cavernoma, Deep-seated, Thalamic, Brainstem, Infratentorial, Hemorrhage, Surgical approach

INTRODUCTION

 

Cavernous malformations constitute 5-15% of all cerebrovascular malformations, and are the second most common intracranial vascular formation responsible for hemorrhage [1-3]. They consist of a heterogeneous series of lesions with ‘mulberry-like’ dark red-purple coloration on gross examination. Histologically, they are defined by clusters of dilated (‘cavernous’), sinusoid-like capillary vessels of varying size (Figure 1.). Pathognomic of this lesion, capillaries are directly adjacent to one another, separated by a collagenous stroma with little or no intervening neural parenchyma [4]. Though it contains arteries and veins with normal structure, the capillaries have a single endothelial layer devoid of elastin or smooth muscle.

 

As a result of their weak endothelial structure and absence of astrocytic foot process these lesions are predisposed to spontaneous and recurrent hemorrhage [4,5]. Single lesions are typical of the sporadic form of the disease while multiple lesions often indicate the autosomal dominant disease type [6]. These are known to occur anywhere along the neuro-axis, including on cranial and spinal nerves [7,8]. Those located in the deep-seated areas (brainstem, thalamus, and basal ganglia) present a considerable problem for neurosurgical treatment due to the sheer density of the surrounding eloquent parenchyma.

 

Incidence

Estimates of incidence based on large radiological and cadaveric studies place total cavernous malformation prevalence in the general public around 0.4-0.5% [9-11]. This may underestimate true incidence, as up to 25% of all cavernous malformations remain completely asymptomatic [4]. Deep-seated cavernomas compose 15-30% of all such lesions [2, 12, 13].

 

These figures may overestimate the relative frequency of cavernomas in eloquent areas as they are reported more readily being symptomatic than those in the non-eloquent subcortical region. [2, 14, 15]. The majority of infratentorial lesions reside within the pons, with significantly fewer reported in other brainstem areas or deep-supratentorial locations [7,16,17].

Clinical Features

Cavernous malformations are diagnosed most commonly in adults of both genders. Symptoms typically arise in the second and third decades, with a relapsing and remitting course corresponding to periods of hemorrhage and resolution. Compared to those in the superficial areas, deep-seated cavernomas show a greater propensity for recurrent hemorrhage [13, 19] and are more likely to result in severe neurological deficits [1, 15, 20].

Hemorrhage

Hemorrhage may be intralesional or extralesional. Intralesional hemorrhage exerts a typical mass effect on surrounding parenchyma, whereas extralesional blood exerts mass effect compounded by the reaction of surrounding parenchyma to blood degradation products [21]. Cavernomas are low pressure, low flow systems vascular malformations [7, 14], and as such initial hemorrhages tend to be smaller and less symptomatic, though recurrent, worsening episodes may occur in increasing shorter intervals following initial bleed [13]. Hemorrhage rates vary significantly between studies, and are further confused by the difficulty of identifying asymptomatic lesions, disagreement in the literature as to what constitutes a hemorrhagic event, and a paucity of natural history studies without selection bias for observational and surgical groups.

With this in mind, hemorrhage rates per patient-year in natural history studies of brainstem cavernomas range from 2.3-4.1% [3, 7, 19, 22], though 0.6% per patient year is

reported for un-ruptured lesions [2]. Surgical studies likely represent more aggressive forms of cavernous malformation, with reported initial hemorrhage rates from 2.68-6.8% per patient-year [22]. The risk of recurrent hemorrhage is reported as between 5-21.5% in natural history studies [7, 23], and between 1-3.8% per patient year pre-operatively in surgical series [13, 19, 22].

The natural history of thalamic lesions is even less clear, with little available literature. Some studies, however, have indicated an increased tendency of thalamic cavernomas to bleed compared to brainstem lesions [2, 22]. Conversely, Barker et al. [24] identified a tendency for spontaneous resolution in untreated cavernous malformations, noting a decrease in monthly bleeding rates from 2.1% down to 0.8% across 28 months.

Focal Neurological Deficits

Whilst seizure remains a common presenting complaint for supratentorial cavernous malformations, including those of the thalamus and basal ganglia, less than 18% of patients with infratentorial lesions present with seizure [11, 25, 26]. Instead, presence of cranial nerve disturbance with relapsing and remitting course is indicative of brainstem cavernous malformation. Specific deficits are dependent on location and recurrence, with multiple hemorrhagic events associated with increased likelihood of refractory neurological deficits [13], particularly if hemorrhage directly damages neural tissue rather than simply exerting mass effect [27]. Somatic motor, sensory, and cranial nerve deficits predominate due to presence of these fibers along length of brainstem [28, 29].

Thalamic malformations are accompanied by a diversity of clinical features due to the varied and integrative nature of thalamic nuclei. Relatively nondescript symptoms such as hemiparesis, paresthesia, headache, and dysesthesia predominate [30, 31], with diplopia, language and visual disturbances also occassionally reported [30, 32].

Mesencephalic lesions may be associated with oculomotor and trochlear nerve palsy with ipsilateral opthalmoplegia [33]. Corticobulbar, corticospinal, cerebellar and red nuclei symptoms may also be evident, resulting in worsening hemiparesis, facial paresis,paresthesia, dysphagia, dysarthria and gait ataxia [1, 13, 34].

Clinical findings indicative of pontine lesions include ipsilateral trochlear nerve palsy, ipsilateral facial weakness due to compression of the facial nucleus, ipsilateral loss of horizontal gaze due to damage of paramedian pontine reticular formation, and trigeminal nerve palsy [35]. Vertigo and nausea have also been reported as a common presentation of pontine lesions [34].

Medullary cavernomas are most commonly associated with paresthesia, resulting from gracile and cuneate nuclei compression, vocal cord paralysis and cardiac and respiratory distress due to involvement of solitary nucleus and vagal dorsal motor nucleus, ipsilateral tongue paresis with compression of hypoglossal nucleus, and difficulty in swallowing [35]. Whilst the cerebellar peduncles are present at all brainstem levels, ataxia is more commonly associated with lesions of the medulla [34].

Imaging

Magnetic resonance imaging remains the gold standard for diagnostic imaging of cavernous malformations, with excellent sensitivity and specificity [36-38], especially withT2 weighted and gradient echo sequences [19, 37, 38] and at higher resolutions [39]. These show as well-defined, lobulated masses with mixed signal density at their core and a hypointense rim [36]. It is worth noting that this characteristic MRI appearance is the result of hemosiderin deposition following hemorrhage, and as such these lesions may not be particularly apparent prior to bleeding unless susceptibility-weighting is used [3, 38].

Computerized tomography (CT) demonstrates slightly hyperdense, well circumscribed, ‘popcorn’ like lesions. This modality is highly sensitive with poor specificity [11]. Cavernomas are capillary malformations, and as such angiography is rarely abnormal. It may, however, play a role in distinguishing cavernous malformations from arteriovenous malformations and other vascular lesions.

Diffusor tension imaging (DTI) provides an accurate method for identification of position of lesions relative to white matter pathways, and along with fMRI imaging of cranial nuclei often proves useful in guiding surgical decision making [40]. When combined with neuro-navigation, these adjuncts somewhat compensate for distortion of overlying anatomy by intrinsic cavernomas, particularly when operating in the nuclei rich areas of the dorsal pons. Their usefulness in deep-seated lesions is limited by the available resolution of images in these white-matter rich areas and susceptibility artefacts related to hemosiderin deposition [41]. Similarly, T1-weighted images are recommended for surgical planning of edematous cavernous malformations as T2-weighted MRI images may overestimate the size and relation of the lesion to the surface, again due to the ferromagnetic effects of hemosiderin [12, 29].

Neuronavigation itself is highly useful in choice of cortex entry zone, particularly as cavernous malformations tend to distort the overlying and surrounding tissue, reducing the accuracy of sighted anatomy alone [42]. In the highly delicate deep brain areas there is the obvious concern of increased navigation error with shifts in brain tissue previously related to pressure changes [42, 43]. The use of intra-operative CT, MRI, or ultrasound reduces this error, though the brainstem, being tethered to the skull base in the midline, appears to undergo minimal following cerebrospinal fluid drainage [29, 42].  

Management

Choice of management strategy is dependent upon the presence of current or previous neurological deficit, evidence of hemorrhage related to the lesion, and the location relative to appropriate surgical corridors [39]. There is a general agreement that incidental finding of an asymptomatic lesion, particularly without evidence of hemorrhage, is not an indication for intervention [7, 14, 19, 22, 32, 44-47]. There is no role of vascular interventional procedures for cavernous angiomas because they are not in communication with major arterial or venous system. Therefore, we can either observe or consider surgery or, rarely, focused radiation. Out of 157 patients referred to our unit for cavernoma management, 85 underwent surgery initially, 4 patients had surgery after a period of observation and nobody received radiosurgery. Deep seated lesions were seen in 36 of these patients, 24 of them in the brainstem.

Observation

Surgical intervention is curative, but may carry a significant risk of transient or permanent morbidity. Indication for observation is based on a benign history of the lesion, particularly if the patient is asymptomatic and lesion is discovered incidentally. Conservative management is useful for small, non-aggressive lesions that demonstrate rapid clinical improvement following hemorrhage [48], particularly as the natural history of minimally symptomatic cavernomas is regression in bleeding rates [24]. In a study of patients with brainstem cavernoma selected for observation, Li et al. [49] found 95% had completely recovered at follow up (m=6.5yr). Patients without a history of hemorrhage demonstrated an 8.7% annual risk of bleeding, whilst those with prior bleeding and neurological deficits had a much higher annual risk of 15.9%. Comparing the risk of hemorrhage with time compared to the risks of transient and permanent morbidity following surgery, observation is warranted only for poorly accessible and asymptomatic deep-seated cavernomas [7, 13, 15, 22, 29, 35, 49-51].

Radiosurgery

The principle underlying radiosurgery of cavernous malformations is thrombo-obliteration of the lesion, with thrombosis occurring slowly during a two-year latency period following irradiation, if at all [22, 52, 53]. Due to angiographically occult nature of these lesions it is difficult to confirm the success of radiosurgical treatment [37]. Whilst some proponents have demonstrated cure and complication rates improving on the natural risk of recurrent hemorrhage, efficacy of treatment is difficult to assess [2, 27, 37, 45-47, 52-54]. Outcomes occur over a timeframe of years, and reductions may in part reflect the tendency of some of these lesions to resolve [24].

The annual risk of hemorrhage in cavernomas following stereotactic radiosurgery varies from 9-44%, with 7-27% long term morbidity, though larger scale studies report post-radiosurgery hemorrhage rates ranging from 10.8-17.3% per year in the first two years, followed by a reduction to 1-2.4%in later years [2, 22, 33, 37, 45-47, 53]. Concern also exists over the risk of radiation-associated sequelae, which vary from 7.3% to 15% [37, 47, 53]. In the absence of a standardized treatment protocol regarding dosage, differences in inter-study intensity of radiation therapy likely contributes to this confusion.

Whilst reduction of the risk of hemorrhage occurs more slowly, this method lacks any immediate risk of operation-related morbidity and mortality. Minimization of radiation sequelae may be achieved using low dose radiotherapy [27]. It is recommended that radiosurgical management be included when considering alternative to observation of cavernous malformations otherwise inaccessible to experienced neurosurgical teams, but not a replacement for surgical resection [37, 47-48, 55].

Surgery

General agreement over the specific radiological and symptomatic criteria for surgical resection of cavernous malformations of the brainstem and deep supratentorial locations is lacking. Due to the high morbidity of symptomatic lesions, however, surgery is generally indicated if the lesion is located near the pial or ependymal surface, there is hemorrhage associated with significant neurological deterioration or if there is severe cardiac or respiratory instability [6, 13, 22, 50]. After two symptomatic hemorrhages, the risk of significant permanent morbidity following a third bleed significantly diminishes the relative risks of surgical intervention [22]. An even more aggressive stance is recommended for thalamic lesions, due to the vital nature of this structure [55].

Morbidity and mortality rates vary between surgical series and are related to the experience and skill of the attending neurosurgical team [34]. Up to 84% of surgical patients with deep brain lesions demonstrated the same or improved function following microsurgical excision in large scale reviews [22, 33, 50, 55]. Specific publications with respect to thalamic and basal ganglia lesions are few and have a paucity of patients due to the relative rarity of this lesion. However Li et al. [30] and Gross et al. [22] report good functional outcomes at follow up in 77.8% of patients treated by excision. In surgical series immediate post-operative morbidity ranges from 29-67% [22, 50] though this is often transient. It is likely related to the effects of manipulation and intra-operative hemorrhage on the parenchyma, and the patient’s pre-operative condition [51]. Ameta-analysis by Qiao et al. [56] on surgical resection of deep-seated cavernomas places transient neural deficits at 33.1%, but found lasting morbidity at follow up reduced to 8.8%. Post-operative mortality is typically quite low, with a combined rate of approximately 1.9% through the literature [22]. Transient deficits may mimic a hemorrhagic event, and patients should be warned accordingly [50].

The timing of surgery relevant to recent hemorrhage is important. Studies by Mathieson et al. [33] and Pandey et al. [29] found intervention less than four weeks from last hemorrhage resulted in less immediate morbidity and a faster improvement in neurological outcomes than in those operated on after this time. Attempting surgical resection during the sub-acute stage is widely recommended, as it allows time for hematoma to liquefy and partially resolve [35]. This increases the accuracy of pre-op imaging, allows greater intra-operative visualization, as well as providing a cleaner dissection plane [57]. Attempted resection following resolution and organization of hematoma increases the risk of manipulation and damage of normal tissue.

Complete lesion resection is key to patient outcomes, as partially resected lesions are prone to hemorrhage and can worsen patient condition [58, 59]. Surgical studies typically report complete resection rates up to 95% [7, 22, 27]. Associated venous malformations should be preserved as these often drain the normal surrounding tissue, resulting in ischemia or infarct following their obliteration [14].

As previously stated, intra-operative Neuronavigation with pre-operative identification of fiber tracts and nuclei provides a significant advantage in accurate dissection, most perceptibly when the characteristic hemosiderin staining at a pial surface is absent. Some authors advocate the use of intra-operative electrophysiological monitoring of motor evoked potentials for identification of white matter tracts and cranial nerves in cavernoma surgery [7, 42, 60]. Careful interpretation of intra-operative monitoring and reliance on a variety of modalities is suggested, as Shiban et al. [61] have found good specificity but poor sensitivity through an inconstant literature in their own study of electrophysiological monitoring of infratentorial cavernous malformations.

Approaches

Choice of craniotomy varies according to the location and lateralization of lesions, but can be broadly classified into five categories – Interhemispheric, supracerebellar, cerebello-pontine angle, fourth ventricle, and lateral supracerebellar. Abla et al. [7] promote the almost exclusive use of the retrosigmoid, sub-occipital (with or without telovelar), and lateral Supracerebellar craniotomy. Their reasoning follows that these, in conjunction with occasional use of far-lateral and modified orbitozygomatic craniotomy, allow access to the entirety of the brainstem with the least invasiveness.

In determining approach, the size and location of cavernous malformations relative to neurovascular structures and the closest surface, and the surgeons’ skill and experience are key. Whilst the ‘Two-point’ method [62] is useful in identifying the shortest path to the closest pial or ependymal surface, a longer but more elegant route is sometimes advisable to avoid unnecessary damage of eloquent parenchyma. The intra-operative approach selected ideally should align the surgeon’s perspective with the pial incision and surgical target, maximizing visibility whilst minimizing the need for surgical retraction [14]. In addition to this, excision should generally be done piecemeal from within the lesion itself to reduce the need for retraction of delicate structures.

Thalamic and Basal Ganglia Cavernous Malformations

Similar approaches are recommended for lesions of the thalamus and basal ganglia [29]. No safe entry zones are described for the thalamus, and resection is cautioned against unless the lesion abuts a pial or ependymal wall. Some surgical groups have demonstrated intrinsic lesions may sometimes be resected with relatively little risk of morbidity [29, 33], though this remains controversial.

The most common of approaches include the sub-occipital trans-tentorial, anterior ipsilateral or contralateral trans choroidal transcallosal, and trans-ventricular parieto-occipital [29-30, 33, 55, 63]. In contrast to previous studies, Rangel-Castiella et al. [32] describe a series of different approaches to thalamic cavernomas with reference to a thalamic anatomical classification system. In addition to those described above, an orbitozygomatic transsylvian supracarotid-infrafrontal approach was indicated for antero-inferior thalamic lesions, mitigating the need for excessive distention of parenchyma required by other methods.

Supracerebellar approaches via the ambient and quadrigeminal cisterns allow access to the posterior-medial lesions and brainstem cavernomas extending into thalamus and basal ganglia [7, 30, 64]. Anterior transcallosal approaches provide visualization of superomedial lesions without excessive disturbance of parenchyma required by trans-cortex approaches [30, 32]. Posterior interhemispheric transplenial approaches have been recommended for posterior lateral lesions [30], as the posterior limb of the internal capsule shields the posterior thalamus from lateral approach via transsylvian or parieto-occipital methods [55]. These, however, carry risk of retraction injury to occipital lobe and poor visualization due to obstruction by the Galenic system [63]. Transsylvian and parieto-occipital approaches allow excellent access to the lateral ventricles, though care should be taken with parieto-occipital approaches that the incision should be sufficiently superior and posterior to avoid the optic radiations and language centers, respectively [65].

Anterior and Anterolateral Mesencephalic Cavernous Malformations

In the approach to anterior and interpeduncular lesions, the transsylvian approach is most commonly used [35, 42], with either a classic anterior petrosal or frontal orbitozygomatic craniotomy. Whilst some surgical series endorse petrosal approaches in anterior brainstem lesions [66] this has lately fallen out of fashion due to unnecessarily increased risk of morbidity, specifically loss of hearing and facial nerve paresis [22, 63, 67]. Anterolateral lesions may be accessed with either transsylvian or sub-temporal transtentorial approach. The latter also provides excellent visualization of the posterior brainstem features without significant retraction [22, 67]. Sub-temporal approaches should be performed with caution, however, as it carries risks of mechanical or ischemic injury to the vein of Labbé or the temporal lobe that it drains [63], as well as oculomotor and trochlear nerve damage during tentorial manipulation [28].

The key structures within the anterior mesencephalon include the crux cerebri, lined posteriorly by the substantia niagra, and the medial lemniscus postero-laterally again. An anterior safe entry zone is described by Briccolo et al. [68], demarcated by the posterior cerebral artery superiorly, the superior cerebellar artery posteriorly, the basilar artery and emergence of the oculomotor nerve medially, and the pyramidal tract laterally. Alternatively, the lateral mesencephalic sulcus indicates a much more lateral corridor between the substantia niagra and medial lemniscus allowing a potential working distance of greater than a centimeter [44]. The medial accessibility for both approaches is limited by oculomotor fibers traversing the substantia niagra. The medial longitudinal fasciculus in the midline is a second critical consideration as bilateral internuclear opthalmoplegia that results from its dissection is devastating[29].

Posterior and Postero-Medial Mesencephalic Cavernomas

Whilst a variety of approaches are possible to visualize posterior mesencephalic lesions, the supracerebellar infratentorial route (including median, para-median, and extreme lateral variants) with retro or presigmoid craniotomy is the most highly recommended [7, 22, 35, 42, 55]. This corridor provides excellent exposure of the posterolateral surface of midbrain and upper pons, transverse sinus, and confluence, but carries risk of sinus thrombosis with the use of excessive traction [64]. Sub-temporal and petrosal approaches may also be used, either individually or combined, but carry the same risks previously mentioned.

The lateral mesencephalic sulcus demarks the posterior segment of the mesencephalon, with the quadrigeminal plate (and corpora quadrigemina) lying posteromedial to this. Vertical incision in the lateral mesencephalic sulcus allows access to more lateralized lesions, though horizontal approach via the supra- and infra-collicular areas may be required to reach more posterior and medial aspects [35]. As the mesencephalon contains the highest density of auditory sensory and oculomotion fibers [66], discretion is advisable in considering entry, particularly with peri-quadreminal incisions.

Anterior and Anterolateral Cavernous Malformations Of The Pons

Purely anterior pontine lesions are difficult to excise due to clustering of cranial nerve nuclei, but are a relatively rare occurrence [35]. Usage of the retrosigmoid approach for anterolateral lesions is highly endorsed [35, 55, 67]. The pre-sigmoid approach allows a more direct and lateral view of the pons [35]. A combined sub-temporal trans-petrosal approach provides excellent visualization more rostrally, which minimizes mechanical trauma to the facial and vestibulocochlear nerve complexes [66, 67]. For anterior pontine lesions, Chen et al. [67] propose a petrosal ridge extension to sub-temporal craniotomy as an alternative in order to provide a wide anterior and significant caudal exposure with comparatively little risk of facial and vestibulocochlear palsy.

The trigeminal, trochlear, facial, and vestibulocochlear nuclei are all located in the anterior section of the pons. Instead of risking significant morbidity by violating these structures, Recalde RJ et al. [44] nominate the peritrigeminal area, defined as a triangle bordered medially by the pyramidal tract, laterally by the line between midline and the trigeminal nerve, and basally by the pontomedullary sulcus. This area contains transverse fibers of the middle cerebellar peduncle, which tolerates horizontal incision well [12, 55], though care should be made to avoid proceeding too far medially. The corticospinal and corticopontine fasciculi descend through the anteromedial portion, risking motor deficit if severed [66].

Posterior Cavernous Malformations of the Pons

Trans-cerebellar-medullary fissure or trans-Vermian approaches using a sub occipital midline Craniectomy are recommended here [7, 28, 67]. The inferior vermis may be split for better access to lesions of the upper pons, however this carries a significant risk of truncal ataxia [67].

The telachorioidea may instead be divided to widen the surgical corridor [22, 34, 35]. The telovelar approach provides an alternative that minimizes damaging the vermis but may require removal of the posterior arch of C1 to maximize exposure [28, 35].

Approaches through the floor of the fourth ventricle are generally accompanied by greater morbidity than those performed laterally or anteriorly [12, 22], though this applies largely to resections of intrinsic cavernomas rather than those abutting the floor of the ventricle. The common agreement is that the floor of the fourth ventricle should be used only if the lesion is immediately accessible without resecting the important structures immediately therein [7, 12, 13, 22, 35, 44]. Violation of the caudal segment of the floor particularly may result in cardiopulmonary arrest and increased risk of morbidity [12, 13]. Here particularly electrophysiological monitoring has an important role in localizing cranial nerve nuclei, particularly of the sixth and seventh nerves.

If an intrinsic cavernoma must be excised, Kyoshima et al. [69] recommend the suprafacial and infrafacial triangles, and medial sulcus superior to the facial colliculus as reasonably safe entry zones. Mechanical damage to the superior medial sulcus is cautioned against as this designates the parallel fibers of the median longitudinal fasciculus [35], resulting in disabling internuclear opthalmoplegia as stated before.

Anterior and Anterolateral Cavernous Malformations of the Medulla

A low retrosigmoid approach provides the greatest exposure for rostral medullary lesions, and is reportedly better tolerated than the far lateral craniotomy [55]. The far lateral partial trans condylar with removal of part of ipsilateral posterior arch of C1 is still the approach of choice for anterolateral lesions. Entry may be made via the retro-olivary sulci [44], or in the anterolateral sulcus between the hypoglossal nerve and C-1 [66].

Posterior Cavernous Malformations of the Medulla

Approaches to the rostral section of the posterior medulla are largely the same as for dorsal pontine lesions (i.e. via the floor of fourth ventricle). Lesions sitting within the midline or more caudally may be exposed using a medial sub-occipital craniotomy [55]. Entry in the dorsal medulla may be made by the posterior median fissure below the obex, the posterior intermediate sulcus between the gracile and cuneate fascicles, and the posterior lateral sulcus between cuneate and spinal trigeminal tract and nucleus [70].

 

CONCLUSION

Cavernous malformations are a rare vascular lesion of redundant, disorganized, and dilated capillary clusters. Hemorrhage typically results in recurrent bleeding events accompanied by progressive neurological deficit. Infratentorial and deep-seated cavernomas show an increased risk of bleeding compared to those in supratentorial regions, though this may reflect the greater symptomatic presentation due to the volume of eloquent tissue in these areas. Given the risk of transient and permanent morbidity following surgical resection, those in eloquent brain regions are surrounded by controversy regarding the relative risks and merits of management options.

 

Despite being essentially curative, surgical management within deep structures was initially advised against due to the risks of operating in tissue crowded with essential nuclei and white matter tracts. Observation is indicated for small, asymptomatic lesions Refinement of surgical technique and evolving understanding of the risks and benefits of approaches has significantly reduced surgical morbidity and mortality. With unfavorable outcomes now reported in only a small proportion of cases, surgical excision of lesions that are directly accessible through a pial or ependymal surface or that are symptomatic is recommended by experienced surgeons, accompanied by the use of neuro-navigation and electrophysiological monitoring to reduce the risk to eloquent tissue.

 

ACKNOWLEDGEMENT

The Authors would like to acknowledge the help of Dr. Salman Shaikh (Senior Resident in Department of Neurosurgery) for his help with the manuscript and pictures.

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