Transient cerebellar mutism after posterior cranial fossa surgery in an adult. Case report and review of the literature. M. Salvati, P. Missori, P. Lunardi, and E. Ramundo
Orlando*
Introduction Summary The onset of mutism after operations on the posterior cranial fossa unaccompanied by clouding of consciousness or cranial nerve deficits (CEREBELLAR MUTISM SYNDROME, CMS) is a rare occurrence that has been recognized only quite recently’-‘. The first descriptions appeared barely 4 years ago (1985) in reports by Rekate et ak5 and Yonemasu et al.‘. And CMS is still a matter of much debate, even its status as a nosographic entity being questioned. We report the case of a young adult who developed a clinical syndrome that fits the description of CMS after an operation for the removal of a tumor of the cerebellar vermis. This is the first report of the sydrome in an adult. Case report A 20-year-old man came to observation with a one-month history of subcontinuous frontonuchal headache, nausea, vomiting, ataxia and reduced visual acuity. Craniocerebral CT and MRI scans (Figs. la and lb), performed elsewhere, revealed a space-occupying lesion in the posterior cranial fossa at the level of the vermis and occupying the fourth ventricle. Marked triventricular hydrocephalus was also present. Neurological examination on admission re* University of Rome “La Supienza”, Address for correspondence Accepted
Transient mutism, without disorders of consciousness or cranial nerve deficits, arising after surgical operations on the posterior cranial fossa is a recently described entity. To date 22 cases have been reported, to which we add the present case (the first report of the syndrome in an adult). We review the salient features of the syndrome in the light of the published cases and speculate on the underlying physiopathology. Key words: Mutism, surgery, mours, speech disorders.
cerebellar
tu-
vealed a mild sixth cranial nerve deficit bilaterally, static and dynamic ataxia, slight dysmetria and asynergy on the right side. The symbolic functions were unimpaired but there was medium grade mental slowing. The fundus oculi examination revealed florid papilledema. At surgery a red, friable mass that filled the fourth ventricle and extended laterally as far as the lateral recesses was grossly totally removed with the aid of an operating microscope and Cavitron ultrasound surgical aspirator. No particular problems arose during the operation. The histological diagnosis was: a densely cellular tumor with the characteristics of medulloblastoma. The patients recovered normally from anes-
Department of Neurological Sciences-Neurosurgery,
and reprint requests: Maurizio Salvati, M.D.,
Rome, Italy.
Via Cardinal Agliardi 15, 00165 Rome, Italy.
19.3.91
Gin Neural Neurosurg 1991. Voi. 93-4.
313
Figure 1. Cerebral MRI. sagittal (a) and axial (b) sections. The examination at the level of the cerebellar vermis occupying the fourth ventricle.
thesia and fully regained consciousness with normal speech. About 46 hours after the end of the operation he became incapable of speech, uttering only a few rudimentary sounds; 2 hours later he became totally mute. The patient was clear-headed with intact cranial nerves. He understood what was said to him and made himself understood, with the aid of gestures. A CT scan of the head, performed immediately and again 48 hours later showed no pathological density changes. A speech-pathologist could find no changes in the peripheral organs or in the symbolic functions. An EEG examination and auditory evoked potential study showed no significant pathological changes. Intensive speech reabilitation was instituted. After about 4 weeks the patient began to utter rudimentary sounds and then more organized sounds until at last he was able to express himself, although with great difficulty due to evident articulatory disturbances. About 3 weeks later the patient was able to speak without undue difficulty and with only faint hints of dysarthria. At clinical and instrumental follow-up (MRI, auditory evoked potentials, EEG and neurological examination) 6 months after the operation the patient was in good general health and on neurological examination presented only traces of dysmetria and dysarthria, which were steadily 314
shows a posterior
fossa tumour
(medulloblastorna
J
receding. The speech disorder had practically cleared up. Unfortunately, after having resumed a normal relational and social life, the patient died of severe virus bronchopneumonia 7 months later. Discussion
Muteness in awake neurological patients is unfrequent. This symptom is described for lesions localized at Broca’s area, dominant hemisphere’s supplementary motor area, reticular formation of the mesencephalon, in pseudobulbar palsy, in peripheric bilateral paralysis of the phonatory system and rarely in bilateral thalamotomy for Parkinson’s diseases. Speech disorders due to a cerebellar lesion are usually marked by disturbed articulation slow, jerky, drawling, monotonous and slurred speech8 - covered by the term cerebellar dysarthria exemplarily described by Gordon Holmes in his class paper of 1922”. Cerebellar mutism after surgery on the posterior cranial fossa is something different, a rare occurrence (though probably more frequent than has so far been reported) that has only recently come to light’-‘. The following features are prerequisites of the diagnosis of CMS: - unimpaired consciousness; - unimpaired symbolic functions;
‘fable 1. Mutism after posterior cranial fossa surgery. Cases reported in literature
Case n.
1st author/ year
1 2 3 4 5 6 7 8 9 10 11 12 13 14 1.5 16 17 18 19 20 21 22 23
Rekate, 1985 Rekate, 1985 Rekate, 1985 Rekate, 1985 Rekate, 1985 Rekate, 198.5 Yonemasu, 1985 Yonemasu, 1985 Yonemasu, 1985 Yonemasu, 1985 Volcan, 1986 Ammirati, 1989 Humphreys, 1989 Humphreys, 1989 Humphreys, 1989 Humphreys, 1989 Humphreys, 1989 Ferrante, 1990 Ferrante, 1990 Ferrante, 1990 Dietze, 1990 Dietze, 1990 Our case
Agelsex (years) 8 6 2 10 9 11
F M M -
8 14 7 3 7 4.5 10 9 5.5 6
F M M M M M M M F M
20
M
Histology
Latency* (hours)
Duration of CMS
MeduliobIastoma Cystic Astrocytoma Ependymoma Meduiloblastoma Medulioblastoma Medulloblastoma Ependymoma Ependymoma Medulloblastoma Medulloblastoma Medulloblastoma Pilocytic Astrocytoma Medulloblastoma Medulloblastoma Medulloblastoma Fibrillar Astrocytoma Ependymoma Pilocytic Astrocytoma Pilocytic Astrocytoma Piiocytic Astrocytoma Medulloblastoma Arteriovenous Malformation Medulloblastoma
48 72 _ -
6 weeks 4 weeks 8 weeks 8 weeks 12 weeks 3 weeks 4-12 weeks 3 weeks 4-12 weeks 4-12 weeks 2 weeks 6 weeks 16 weeks 7 weeks 10 weeks 7 weeks 10 weeks 4 weeks 8 weeks 8 weeks 12 weeks 12 weeks 4 weeks
18-72 18-72 18-72 18-72 Immediately 48 24
72 24 48 48 36 46
* Latency between the end of surgery and the begin of Cerebellar Mutism Syndrome (CMS).
no detectable deficit of the cranial nerves or the peripheral organs of speech; - no lesions of the long pathways in their course at the level of the brainstern. This syndrome must therefore be distinguished separate from the one described in 1984 by Wisoff and Epstein’, classificable among the pseudobulbar syndromes and marked by paralysis of cranial nerves, inability to speak and psychic lability following the removal of midline cerebellar tumors. CMS is, moreover, a transient disorder with recovery of speech in 2 to 16 weeks (mean 7.4 weeks -.l-7). It arises after a period of latency ranging from 12 to 72 hours (mean 43.2 hours, for cases in which the datum is specified) during which the patient is able to speak’-‘%‘. Only in the case described by Volcan et a1.6 was mutism practically complete immediately after the operation. In our patient, in line with other cases, CMS developed after 46 hours, becoming complete 2 hours later. To date 22 cases of CMS have been reported (Table l), to which we add our case. The age range is 2 to 20 years with a mean age of 6.6 -
years for the cases in which age is specified. In the 13 cases in which sex is stated (including our case) males predominate 8 to 5 (male: female ratio is 1.61). The case reported here is, as far as we know, the first to be described in adult. The underlying lesion, neoplastic in almost every case (except in one arteriovenous malformation -2-), is usually large and located in the midline with or without spread toward the cerebellar hemispheres. Involvement of the roof of the fourth ventricle appears to be decisive, as is penetration into the peduncles and/or development towards the lateral recesses and floor of the fourth ventricle’,“. In our case the tumor involved the cerebellar vermis and occupied the entire fourth ventricle, reaching the lateral recesses and floor of the ventricle. The predominant histotype was medulloblastoma (in 11 out of 21 cases or 52.4%), followed by astrocytoma (6 cases, of which 5 were pilocytic and 1 fibrillary, 28.6%) and ependymoma (4 cases, 19%). Only in one case, Dietze and Mick315
le2 described a non-neoplastic lesion (a vermal and para-vermal arteriovenous malformation). Probably damage, especially edematous or ischemic, to the dentate nuclei and related circuits plays a part in the triggering of CMSL*5. In this connexion, Fraioh and Guidetti”‘*“’ reported the onset of mutism, which lasted 3 months, in 2 cases of bilateral stereotactic lesions of the dentate nuclei performed to relieve spasticity. Siegfried” described a similar condition following an accidental lesion to the nucleus interpositus. Stark13, and Lechtenbergh and Gilman14 reported noting that damage to the lateral portions of the cerebellar hemispheres, especially the left, plays some part in the onset of articulatory speech disorders. As all the subjects who have had CMS gained their speech after passing through a stage of dysarthria, the predominant role of the cerebellum in the development of CMS looks plausible’,3-5 Brown et ~1.” recently noted a tendency in young people to reduced verba~ation and a regression of personality and of emotional content after surgery on the posterior cranial fossa. It is, however, unlikely that a psychic factor is wholly responsible for the syndrome. The emotional stress, the “betrayer” figure of the parents and medical staff and then the prolonged hospital~ation of the child could be an important role in arising and maintenance of the CMS3,4. These findings are partly recognizable in hypothetical adult patients. The presence of hydro~phalus or the onset of a meningeal syndrome in the postoperative period would not be devoid of effect, probably acting as a facilitatory or precipitating factor. In conclusion, major factors in the genesis of CMS would seem, in the present state of knowledge, to be extensive involvement of the median and/or par~edian structures of the cerebellum, lateral recesses, roof and floor of the fourth ventricle combined with psychic factors.
316
The underlying lesion is usually a large vermian tumor developing in varying degree towards the cerebellar hemispheres, frequently a medulloblastoma. References AMMIRATI M, MIR~AI s, s.4Mr1h4.Transient mutism following removai of a cerebellar tumor. A case report and review of the literature. Child’s Nervous Syst 1989; .5:12-4. DIETZE DD, MILCKLE JP.Cerebellar mutism as a result of posterior fossa surgery. (Abstract) Forty-second Annud Meeting of the Southern Neur~~r~~I Society. Key West, Florida, March 30-April 1, 1990. Neurosurgery 1990; 261077. FERRANTE
L, MASTRONARDI
L, ACQUI M, FoRTUNA
A.
Mutism after posterior cranial fossa surgery in children. Report of three cases. J. Neurosurg 1990; 72:959-63. HUMPHREYS RP. Mutism after posterior fossa tumor surgery. In: Marlin AE, ed. Concepts Pediat Neurosurg. Base]: Karger, 1989; 9:57-64. REKA~LH,GRUBBRL,ARAM~,~AHNJF,RATCHESONA.
Muteness of cerebellar origin. Arch Neurot 1985; 42; 697-8. VOLCAN I,COLEGP,J~HNSTON K. Acaseofmutenessof cerebellar origin (Letter). Arch Neural 1986; 43:313-4. YONEMASU Y. “Cerebellar mutism” and speech disturbance as a complication of posterior fossa surgery in chitdren. 13th Annual Meeting of the Japanese Society for Pediatric Neurosurgery. Tsukuba, 1985. HOLMES G. The Croonian lectures on the clinical symptoms of cerebellar disease and their inte~retation. Lancet 1922; 259-65. WISOFFJH, EPSTEIN FJ. Pseudobulbar palsy after posterior fossa operation in children. Neurosurgery 1984; 15:707-9. FRAIOLI B, GU~DETTI 8. Effects of stereotactic IeSiOnSOf the dentate nucleus of the cerebellum in man. AppI Neurophysiol 1975; 38:81-90. GUIDETTI B, FRAIOLI B. Neurosurgical treatment of Spasticity and dyskinesias. Acta Neurochir (Suppl), 1977; 24:27-39. SIEGFRIEDJ,ESSLENE,GRETENERU. Functional 23natOItIy of the dentate nucleus in the light of stereotaxic operations. Confin Neural 1970; 32:1-10. STARK RE. Dysarthrya in children. In: Darby ed. Speech and language evaluation in neurology: childhood disorders. New York: Prune & Stratton, 1985; l-190. LECHTENBERG R. GILMAN s. Speech disorders in cerebellar disease. Ann Neural 1987; 3:285-90. BROWN E.SLOBOGINP.E~TEINF~. Pe~o~tyand~havioural changes associated with tumors of the IV ventricle and brainstem. 15th Annual Meeting of the Intemational Society for Pediatric Neurosurgery. New York, 1987.
Orlando*
Introduction Summary The onset of mutism after operations on the posterior cranial fossa unaccompanied by clouding of consciousness or cranial nerve deficits (CEREBELLAR MUTISM SYNDROME, CMS) is a rare occurrence that has been recognized only quite recently’-‘. The first descriptions appeared barely 4 years ago (1985) in reports by Rekate et ak5 and Yonemasu et al.‘. And CMS is still a matter of much debate, even its status as a nosographic entity being questioned. We report the case of a young adult who developed a clinical syndrome that fits the description of CMS after an operation for the removal of a tumor of the cerebellar vermis. This is the first report of the sydrome in an adult. Case report A 20-year-old man came to observation with a one-month history of subcontinuous frontonuchal headache, nausea, vomiting, ataxia and reduced visual acuity. Craniocerebral CT and MRI scans (Figs. la and lb), performed elsewhere, revealed a space-occupying lesion in the posterior cranial fossa at the level of the vermis and occupying the fourth ventricle. Marked triventricular hydrocephalus was also present. Neurological examination on admission re* University of Rome “La Supienza”, Address for correspondence Accepted
Transient mutism, without disorders of consciousness or cranial nerve deficits, arising after surgical operations on the posterior cranial fossa is a recently described entity. To date 22 cases have been reported, to which we add the present case (the first report of the syndrome in an adult). We review the salient features of the syndrome in the light of the published cases and speculate on the underlying physiopathology. Key words: Mutism, surgery, mours, speech disorders.
cerebellar
tu-
vealed a mild sixth cranial nerve deficit bilaterally, static and dynamic ataxia, slight dysmetria and asynergy on the right side. The symbolic functions were unimpaired but there was medium grade mental slowing. The fundus oculi examination revealed florid papilledema. At surgery a red, friable mass that filled the fourth ventricle and extended laterally as far as the lateral recesses was grossly totally removed with the aid of an operating microscope and Cavitron ultrasound surgical aspirator. No particular problems arose during the operation. The histological diagnosis was: a densely cellular tumor with the characteristics of medulloblastoma. The patients recovered normally from anes-
Department of Neurological Sciences-Neurosurgery,
and reprint requests: Maurizio Salvati, M.D.,
Rome, Italy.
Via Cardinal Agliardi 15, 00165 Rome, Italy.
19.3.91
Gin Neural Neurosurg 1991. Voi. 93-4.
313
Figure 1. Cerebral MRI. sagittal (a) and axial (b) sections. The examination at the level of the cerebellar vermis occupying the fourth ventricle.
thesia and fully regained consciousness with normal speech. About 46 hours after the end of the operation he became incapable of speech, uttering only a few rudimentary sounds; 2 hours later he became totally mute. The patient was clear-headed with intact cranial nerves. He understood what was said to him and made himself understood, with the aid of gestures. A CT scan of the head, performed immediately and again 48 hours later showed no pathological density changes. A speech-pathologist could find no changes in the peripheral organs or in the symbolic functions. An EEG examination and auditory evoked potential study showed no significant pathological changes. Intensive speech reabilitation was instituted. After about 4 weeks the patient began to utter rudimentary sounds and then more organized sounds until at last he was able to express himself, although with great difficulty due to evident articulatory disturbances. About 3 weeks later the patient was able to speak without undue difficulty and with only faint hints of dysarthria. At clinical and instrumental follow-up (MRI, auditory evoked potentials, EEG and neurological examination) 6 months after the operation the patient was in good general health and on neurological examination presented only traces of dysmetria and dysarthria, which were steadily 314
shows a posterior
fossa tumour
(medulloblastorna
J
receding. The speech disorder had practically cleared up. Unfortunately, after having resumed a normal relational and social life, the patient died of severe virus bronchopneumonia 7 months later. Discussion
Muteness in awake neurological patients is unfrequent. This symptom is described for lesions localized at Broca’s area, dominant hemisphere’s supplementary motor area, reticular formation of the mesencephalon, in pseudobulbar palsy, in peripheric bilateral paralysis of the phonatory system and rarely in bilateral thalamotomy for Parkinson’s diseases. Speech disorders due to a cerebellar lesion are usually marked by disturbed articulation slow, jerky, drawling, monotonous and slurred speech8 - covered by the term cerebellar dysarthria exemplarily described by Gordon Holmes in his class paper of 1922”. Cerebellar mutism after surgery on the posterior cranial fossa is something different, a rare occurrence (though probably more frequent than has so far been reported) that has only recently come to light’-‘. The following features are prerequisites of the diagnosis of CMS: - unimpaired consciousness; - unimpaired symbolic functions;
‘fable 1. Mutism after posterior cranial fossa surgery. Cases reported in literature
Case n.
1st author/ year
1 2 3 4 5 6 7 8 9 10 11 12 13 14 1.5 16 17 18 19 20 21 22 23
Rekate, 1985 Rekate, 1985 Rekate, 1985 Rekate, 1985 Rekate, 1985 Rekate, 198.5 Yonemasu, 1985 Yonemasu, 1985 Yonemasu, 1985 Yonemasu, 1985 Volcan, 1986 Ammirati, 1989 Humphreys, 1989 Humphreys, 1989 Humphreys, 1989 Humphreys, 1989 Humphreys, 1989 Ferrante, 1990 Ferrante, 1990 Ferrante, 1990 Dietze, 1990 Dietze, 1990 Our case
Agelsex (years) 8 6 2 10 9 11
F M M -
8 14 7 3 7 4.5 10 9 5.5 6
F M M M M M M M F M
20
M
Histology
Latency* (hours)
Duration of CMS
MeduliobIastoma Cystic Astrocytoma Ependymoma Meduiloblastoma Medulioblastoma Medulloblastoma Ependymoma Ependymoma Medulloblastoma Medulloblastoma Medulloblastoma Pilocytic Astrocytoma Medulloblastoma Medulloblastoma Medulloblastoma Fibrillar Astrocytoma Ependymoma Pilocytic Astrocytoma Pilocytic Astrocytoma Piiocytic Astrocytoma Medulloblastoma Arteriovenous Malformation Medulloblastoma
48 72 _ -
6 weeks 4 weeks 8 weeks 8 weeks 12 weeks 3 weeks 4-12 weeks 3 weeks 4-12 weeks 4-12 weeks 2 weeks 6 weeks 16 weeks 7 weeks 10 weeks 7 weeks 10 weeks 4 weeks 8 weeks 8 weeks 12 weeks 12 weeks 4 weeks
18-72 18-72 18-72 18-72 Immediately 48 24
72 24 48 48 36 46
* Latency between the end of surgery and the begin of Cerebellar Mutism Syndrome (CMS).
no detectable deficit of the cranial nerves or the peripheral organs of speech; - no lesions of the long pathways in their course at the level of the brainstern. This syndrome must therefore be distinguished separate from the one described in 1984 by Wisoff and Epstein’, classificable among the pseudobulbar syndromes and marked by paralysis of cranial nerves, inability to speak and psychic lability following the removal of midline cerebellar tumors. CMS is, moreover, a transient disorder with recovery of speech in 2 to 16 weeks (mean 7.4 weeks -.l-7). It arises after a period of latency ranging from 12 to 72 hours (mean 43.2 hours, for cases in which the datum is specified) during which the patient is able to speak’-‘%‘. Only in the case described by Volcan et a1.6 was mutism practically complete immediately after the operation. In our patient, in line with other cases, CMS developed after 46 hours, becoming complete 2 hours later. To date 22 cases of CMS have been reported (Table l), to which we add our case. The age range is 2 to 20 years with a mean age of 6.6 -
years for the cases in which age is specified. In the 13 cases in which sex is stated (including our case) males predominate 8 to 5 (male: female ratio is 1.61). The case reported here is, as far as we know, the first to be described in adult. The underlying lesion, neoplastic in almost every case (except in one arteriovenous malformation -2-), is usually large and located in the midline with or without spread toward the cerebellar hemispheres. Involvement of the roof of the fourth ventricle appears to be decisive, as is penetration into the peduncles and/or development towards the lateral recesses and floor of the fourth ventricle’,“. In our case the tumor involved the cerebellar vermis and occupied the entire fourth ventricle, reaching the lateral recesses and floor of the ventricle. The predominant histotype was medulloblastoma (in 11 out of 21 cases or 52.4%), followed by astrocytoma (6 cases, of which 5 were pilocytic and 1 fibrillary, 28.6%) and ependymoma (4 cases, 19%). Only in one case, Dietze and Mick315
le2 described a non-neoplastic lesion (a vermal and para-vermal arteriovenous malformation). Probably damage, especially edematous or ischemic, to the dentate nuclei and related circuits plays a part in the triggering of CMSL*5. In this connexion, Fraioh and Guidetti”‘*“’ reported the onset of mutism, which lasted 3 months, in 2 cases of bilateral stereotactic lesions of the dentate nuclei performed to relieve spasticity. Siegfried” described a similar condition following an accidental lesion to the nucleus interpositus. Stark13, and Lechtenbergh and Gilman14 reported noting that damage to the lateral portions of the cerebellar hemispheres, especially the left, plays some part in the onset of articulatory speech disorders. As all the subjects who have had CMS gained their speech after passing through a stage of dysarthria, the predominant role of the cerebellum in the development of CMS looks plausible’,3-5 Brown et ~1.” recently noted a tendency in young people to reduced verba~ation and a regression of personality and of emotional content after surgery on the posterior cranial fossa. It is, however, unlikely that a psychic factor is wholly responsible for the syndrome. The emotional stress, the “betrayer” figure of the parents and medical staff and then the prolonged hospital~ation of the child could be an important role in arising and maintenance of the CMS3,4. These findings are partly recognizable in hypothetical adult patients. The presence of hydro~phalus or the onset of a meningeal syndrome in the postoperative period would not be devoid of effect, probably acting as a facilitatory or precipitating factor. In conclusion, major factors in the genesis of CMS would seem, in the present state of knowledge, to be extensive involvement of the median and/or par~edian structures of the cerebellum, lateral recesses, roof and floor of the fourth ventricle combined with psychic factors.
316
The underlying lesion is usually a large vermian tumor developing in varying degree towards the cerebellar hemispheres, frequently a medulloblastoma. References AMMIRATI M, MIR~AI s, s.4Mr1h4.Transient mutism following removai of a cerebellar tumor. A case report and review of the literature. Child’s Nervous Syst 1989; .5:12-4. DIETZE DD, MILCKLE JP.Cerebellar mutism as a result of posterior fossa surgery. (Abstract) Forty-second Annud Meeting of the Southern Neur~~r~~I Society. Key West, Florida, March 30-April 1, 1990. Neurosurgery 1990; 261077. FERRANTE
L, MASTRONARDI
L, ACQUI M, FoRTUNA
A.
Mutism after posterior cranial fossa surgery in children. Report of three cases. J. Neurosurg 1990; 72:959-63. HUMPHREYS RP. Mutism after posterior fossa tumor surgery. In: Marlin AE, ed. Concepts Pediat Neurosurg. Base]: Karger, 1989; 9:57-64. REKA~LH,GRUBBRL,ARAM~,~AHNJF,RATCHESONA.
Muteness of cerebellar origin. Arch Neurot 1985; 42; 697-8. VOLCAN I,COLEGP,J~HNSTON K. Acaseofmutenessof cerebellar origin (Letter). Arch Neural 1986; 43:313-4. YONEMASU Y. “Cerebellar mutism” and speech disturbance as a complication of posterior fossa surgery in chitdren. 13th Annual Meeting of the Japanese Society for Pediatric Neurosurgery. Tsukuba, 1985. HOLMES G. The Croonian lectures on the clinical symptoms of cerebellar disease and their inte~retation. Lancet 1922; 259-65. WISOFFJH, EPSTEIN FJ. Pseudobulbar palsy after posterior fossa operation in children. Neurosurgery 1984; 15:707-9. FRAIOLI B, GU~DETTI 8. Effects of stereotactic IeSiOnSOf the dentate nucleus of the cerebellum in man. AppI Neurophysiol 1975; 38:81-90. GUIDETTI B, FRAIOLI B. Neurosurgical treatment of Spasticity and dyskinesias. Acta Neurochir (Suppl), 1977; 24:27-39. SIEGFRIEDJ,ESSLENE,GRETENERU. Functional 23natOItIy of the dentate nucleus in the light of stereotaxic operations. Confin Neural 1970; 32:1-10. STARK RE. Dysarthrya in children. In: Darby ed. Speech and language evaluation in neurology: childhood disorders. New York: Prune & Stratton, 1985; l-190. LECHTENBERG R. GILMAN s. Speech disorders in cerebellar disease. Ann Neural 1987; 3:285-90. BROWN E.SLOBOGINP.E~TEINF~. Pe~o~tyand~havioural changes associated with tumors of the IV ventricle and brainstem. 15th Annual Meeting of the Intemational Society for Pediatric Neurosurgery. New York, 1987.
