Postoperative mutism is an infrequent complication of brain surgery. We report a third ventricular astrocytoma in a 16-year-old boy. The tumor was totally removed via anterior transcallosal approach. The operation was uneventful. On the second postoperative day he became mute. He could follow verbal commands, and write and read. Histopathological examination revealed a pilocystic astrocytoma. Four days postoperatively, he began to say simple words, and two weeks later he could talk normally. The possible cause and pathophysiological mechanism of mutism in the lesions of this region are discussed in this paperKey words: Mutism; Third ventricle; Corpus callosum; Transcallosal approac

Akhaddar, A

Belfkih, H

Boucetta, M

Boulahroud, O

El Asri, AC

El Mostarchid, B

Gazzaz, M

Naama, O

English

AJOL - African Journals Online

African Journal of Neurological Sciences 2014 - Vol. 33, No 1CASE REPORT/CAS CLINIQUETRANSIENT MUTISM AFTER ANTERIOR TRANSCALLOSAL APPROACHMUTISME TRANSITOIRE APRÈS UN ABORD ANTÉRIEUR TRANSCALLEUX NAAMA Okacha 1  AKHADDAR Ali 1  BELFKIH Hatim 1  GAZZAZ Miloudi 1  BOULAHROUD Omar 1  EL ASRI Abad Cherif 1  BOUCETTA Mohammed 1  EL MOSTARCHID Brahim 1 1. Services de Neurochirurgie, hôpital militaire Mohammed V, CHU Rabat, Maroc E-Mail Contact - NAAMA Okacha : okacha_naama (at) hotmail (dot) com Mots clés : Abord trans calleux; Corps calleux; Troisième ventricule Key words: Mutism; Third ventricle; Corpus callosum; Transcallosal approach RESUMEPostoperative  mutism  is  an  infrequent  complication  of  brain  surgery.  We  report  a  third  ventricularastrocytoma in a 16-year-old boy. The tumor was totally removed via anterior transcallosal approach. Theoperation was uneventful.  On the second postoperative day he became mute.  He  could  follow verbalcommands, and write and read. Histopathological examination revealed a pilocystic astrocytoma. Four dayspostoperatively, he began to say simple words, and two weeks later he could talk normally. The possiblecause and pathophysiological mechanism of mutism in the lesions of this region are discussed in this paper INTRODUCTIONThe term mutism is usually defined as a clinical state in which a conscious patient is unwilling to or unable tospeak, resulting in the absence or marked paucity of verbal output. The patients may be mute while they arewilling to write, or intact in comprehension (10). Mutism may be a result of division of the corpus callosum.Suppression of the limbic system caused by lesions in the anterior cingulate gyrus, septum pellucidum, andfournix  may  also  have  been  of  importance  in  at  least  two  of  these  three  cases.  Impairments  of  thesupplementary motor cortex, thalamus and basal ganglia may also contribute to reduce speech production(3). The mechanism of such transient mutism seems to be a complex of two or more of these factors, andtheir combination may be different from one case to the other (6). A few authors have contributed their casematerials but the overall number of cases remains small.  We present a patient who developed transientmutism after resection of a third ventricular astrocytoma.CASE REPORTA 16-year right-handed was referred for further management of a third ventricular lesion, which resulted inobstructive  hydrocephalus  that  was  treated  with  a  right  ventriculoperitoneal  shunt.  Three  month  beforeadmission, the patient experienced increasing episodes of vomiting and gait disturbances. His family historywas unremarkable for neurological diseases or phacomatosis syndromes. The general status of the patientwas satisfactory. There was no papilledema or restriction in his extraocular movements. The cranial nerveswere intact, and there were no sensory or motor deficits. The Romberg test was normal. The patient was ableto  heel  and  toe  walk,  but  his  tandem  gait  was  clumsy.  Deep  tendon  reflexes  were  symmetrical,  andBabinski’s  sign  was  absent.  No  stigmata  of  neurofibromatosis  was  noted.  Computed  tomographic  andmagnetic resonance imaging with contrast demonstrated a homogeneously enhancing mass measuring 3 ×2,5 × 3,5 cm in the third ventricle. The patient underwent a right frontoparietal craniotomy with an extension ofthe  bone  flap  across  the  midline  and  two-thirds  of  the  bone  flap  anterior  to  the  coronal  suture.  Theinterhemispheric fissure was identified and retracted down to the edge of the falx. The left and right cingulategyri  were  spread,  and the corpus  callosum was  identified.  A  midline  dissection,  measuring  2  cm,  was65African Journal of Neurological Sciences 2014 - Vol. 33, No 1performed through the corpus callosum. After passing through the corpus callosum, the leaves of the septumpellucidum were separated, and the ependyma of the third ventricle was encountered. The ependyma wasopened, and the tumor was visualized. The right lateral ventricle was then entered, and cerebrospinal fluidwas removed to provide further relaxation. The tumor appeared grayish-white with a firm consistency. Wewere able to find a relatively clean capsule margin  between the tumor and the third ventricle  along theanterior,  superior,  and  lateral  portions  of  the  dissection.  A  gross  total  resection  could  be  achieved.Histopathologic evaluation confirmed the diagnosis of pilocytic astrocytoma. Operation and recovery fromanesthesia were uneventful.  In response to verbal commands the patient could open his mouth.  On thesecond postoperative day, he was alert but totally mute. He suffered fits of crying. He could follow verbalcommands and was able to read and write. A follow-up CT scan on the second postoperative day, showednormal  postoperative changes with no haematoma or significant  oedema. Four days postoperatively, hebegan to say simple words, and two weeks later he could talk normally.DISCUSSIONMutism caused by intracranial surgical intervention has been described in the following areas: (i) Broca’sarea; (ii)  the anterior cingulate area; (iii) the descending tracts bilaterally; (iv) the mesencephalic reticularformation; (v) after callosotomy; (vi) the SMA; and the midline cerebellar structures (5,10).Transient  mutism  is  frequently  observed  following  callosal  operations,  the  nature  of  this  disorder  hasremained elusive (6). Rayport (7) reported mutism in three patient following section of the posterior corpuscallosum. Sass (8) reported that two of 12 patients who underwent complete callosotomy showed a period ofmutism, whereas only one of 20 patients who underwent anterior callosotomy experienced similar transientmutism.  Such  results  seem  to  suggest  an  important  role  of  the  splenium  of  the  corpus  callosum  inprecipitating the transient mutism, and the anterior part of the corpus callosum looks to be relatively innocent(3).  In a series of  three patients with transient  mutism after anterior  transcallosal  approach, all  of  themunderwent a callosal  incision of  2-3 cm and removal of  the septum pellucidum, suggesting that a smallanterior callosal incision behind the genu is not responsible for mutism (6).By contrast, several other report indicate that the surgical section of the anterior body of the corpus callosummay well cause transient mutism (4). Shucart (9) reported that one of 25 cases operated on through ananterior transcallosal approach showed mutism. Geuna (4) reported that a patient with an intraventricularoligodendroglioma became transiently mute after an anterior trancallosal operation. Asgari (2) demonstratedthat postoperative transient mutism was not limited to the anterior callosotomy but also occurred in the frontaltranscortical approach, and all  of  these patients postoperative mutism was due to damage to the septalregion in cases of tumor involvement of the septum pellucidum or damage to both fornices in cases of largesolid third ventricular tumors rather than to the callosal incision itself.It is evident that the surgical section of the corpus callosum is not by itself sufficient to cause the transientmutism, because many subjects who underwent such an operation remain free of mutism after the procedure(3,4). Therefore the mechanism of such transient mutism seems to be a complex of two or more of thesefactors, and their combination may be different from one case to the other (6,10). More likely, this syndromeoccurs in individuals with mixed cerebral dominance for language function. Sass (8) found that right-handedepileptic patients that are right-hemisphere dominant for speech develop permanent speech difficulties aftercallosotomy. It is possible that in some right-handed patients who develop left cerebral dysfunction, languagefunction shifts incompletely to the right hemisphere. Speech and other language functions in these patientsmay depend on interhemispheric communication that is interrupted by a callosal incision.The factors which may contribute to the development of transient mutism following callosal surgery may beclassified into two groups; one is an individual variation in organization of linguistic functions mediated by thecorpus callosum, and the other is a second surgical lesion other than the one in the corpus callosum (6).Factors related to the section of the corpus callosum seem to include the following (3,6): (a) the commissuralfibers may have been acting in a compensatory fashion because of previous brain injury. (b) speech mayrequire some absolute number of relevant brain connections. (c) the callosotomy may produce a diaschisis inthe speaking hemisphere, from which it recovers only slowly. (d) the callosum may carry a corollary dischargefor  speech  output  whose  sudden  loss  results  in  downstream  interhemispheric  conflict.  (e)  temporarycirculatory alterations (particularly of the internal cerebral veins) may transiently derange the more sensitivefunctions of the basal ganglia. (f) damage to one or the other fornix may be contributory. (g) trauma to theanterior third ventricle during division of the anterior commissure or during division of the rostrum from in frontmay be relevant. (h) supplementary motor cortex dysfunction may be contributory. (i) decussating fibers (frommedial frontal cortex to opposite basal ganglia) may be relevant so that their interruption plus medial frontalcortex edema combines to produce mutism when associated with a thalamic or striatal lesion.The outcome for postoperative mutism is favorable (1). Slight disturbance of speech production may resultfrom right-handed patient. But permanent, significant aphasia from such lesions is rare. In addition to deficitsconcerning initiation-related functions, several patients were unable to inhibit certain inappropriate speech66African Journal of Neurological Sciences 2014 - Vol. 33, No 1and  motor  functions  (10).  In  most  reported  cases  postoperative  mutism  is  described  as  a  transientabnormality and it resolves in less than 2 weeks with no treatment (1), as in our case. In rare cases such aswhen dopaminergic pathways are injured, dopamine replacement may be necessary (10).CONCLUSIONThe major  causes in the genesis  of  postoperative mutism would seem to be multi-factorial,  including adisconnection of the callosal fibers and/or impairment of the related neural structures, such as the cingulum,and possibly others.67African Journal of Neurological Sciences 2014 - Vol. 33, No 1FIGURES Figure 1aContrast enhancing axial CT scan (A), and gadolinium enhanced sagittal T1-weighted Figure 1bContrast enhancing axial CT scan (B) MR image showing a homogeneously enhancing mass in the thirdventricle.68African Journal of Neurological Sciences 2014 - Vol. 33, No 1 Figure 2Postoperative CT scan showing normal postoperative changes with no heamatoma or significant oedema.69African Journal of Neurological Sciences 2014 - Vol. 33, No 1REFERENCES1. AKHADDAR A, BELHACHMI A, ELASRI A, BOULAHROUD O, OKACHA N, ELMOUSTARCHID B,BOUCETTA  M.  cerebellar  mutism  after  removal  of  a  vermian  medulloblastoma  in  an  adult.Neurochirurgie 2008;54:548-50.1. ASGARI S,  ENGELHORN T,  BRONDICS A, SANDALCIOGLU IE,  STOLKE D. Transcortical  ortranscallosal  approach to ventricle-associated lesions:  a clinical  study on the prognostic  role  ofsurgical approach. Neurosurg Rev 2003;26:192-97.2. BOGEN JE., . Physiological consequences of complete or partial commissural section. In: ApuzzoMLJ (ed) Surgery of the third ventricle. Williams &Wilkins, Baltimore London Los Angeles Sydney,pp 1987;175-94.3. GEUNA E, REGALIA F, PAPPADA G, et al. Septum pellucidum oligodendroglioma. Case report andreview of literature. J Neurosurg Sci 1981;25 :49-53.4. KAWAL P, KUMAR R. Epidermoid cyst in quadrigeminal cistern presenting with mutism. J pediatricneurosciences 2010; 5:160-63.5. NAKASU Y, ISOZUMI T, HIOKA H, HANDA J. Mechanism of mutism following the transcallosalapproach to the ventricles. Acta Neurochir 1991;110:146-153.6. RAYPORT M, FERGUSON SM, CORRIE WS. Mutism after corpus callosum section for intractableseizure control. Epilepsia 1984;25:665.7. SASS KJ, NOVELTY RA, SPENCER DD, et al. Postcallosotomy language impairments in patientswith crossed cerebral dominance. J Neurosurg 1990;72:85-90.8. SHUCART  WA,  STEIN  BM.  Transcallosal  approach  to  the  anterior  ventricular  system.Neurosurgery 1978; 3:339-343.9. TAHTA K, CIRAK B, PAKDEMIRLI E, SUZER T, TAHTA F. Postoperative mutism after removal ofan anterior falcine meningioma. J Clin Neurosci 2007;14:793-96.70

Transient mutism after anterior transcallosal approach

https://www.ajol.info/index.php/ajns/article/download/122114/111592

Transient mutism after anterior transcallosal approach

Abstract

Similar works

Full text

Available Versions

AJOL - African Journals Online