144
Mutism After Cerebellar Medulloblastoma Surgery By E. Herb] and U. Thyen2 lKlinik für Neurochirurgie der Medizinischen Universität Lübeck and 2Klinik für Pädiatrie der Medizinischen Universität Lübeck, Germany
Case report
The case of a 9-year-old boy is presented, who developed transient mutism after removal of a medulloblastoma in the region of the cerebellar vermis. The mutism disappeared within 6 months. Neither reduction of consciousness nor disturbances of caudal cranial nerves or phonation ever appeared. The case is discussed with regard to its phenomenology, pathogenesis, and etiology, corresponding case reports are also taken into consideration.
Keywords Dysarthria - Cerebellar tumor - Medulloblastoma - Mutism
Zusammenfassung Es kommt der Fall eines 9jährigen. Jungen zur Darstellung, bei dem nach der Operation eines Medulloblastoms im Bereich des Kleinhirnwurms vorübergehend ein völliger Sprachverlust aufgetreten war, der sich innerhalb von 6 Monaten wieder zurückbildete. Eine eigentliche Bewußtseinstrübung bzw. Störungen der kaudalen Hirnnerven oder der Phonationsorgane waren nicht vorhanden. Der Fall wird zusammen mit weiteren entsprechenden Kasuistiken aus der Literatur diskutiert im Hinblick auf die Phänomenologie, Pathogenese und Ätiologie dieser Störung.
Schlüsselwörter Dysarthrie - Kleinhirntumor - Medulloblastom - Mutismus
Received February 29,1991; accepted August 9,1991 Neuropediatrics 23 (1992) 144-146 © Hippokrates Verlag Stuttgart
H.M.,m,9y
Since the age of 6, H. complained of recurrent headaches and later on occasional nausea. At the age of 8 3/4 years, vomiting and headaches coincided for the first time. Neither dizziness nor visual disturbances had appeared so far, but the parents had repeatedly noted depressive moods lately. H. often wept and refused to attend school. His mother attributed this behaviour to a high stress of performance at school. Once she came upon H. just fixing a rope at his bed to hang himself. Eventually H. turned more and more aggressive. An ophthalmological examination revealed bilateral papilledema. The following neurological examination disclosed a horizontal nystagmus to both sides and a slight paresis of the facial nerve on the left. Moreover, there was a mild rightsided hemiparesis. Tendon reflexes were normal. No pathological pyramidal tract signs nor disturbances of sensory functions were apparent. Coordination was impaired in terms of a mild ataxia with accentuation on the right side. Cranial computed tomography disclosed a primarily hyperdense, contrast-enhancing tumor with small calcifications in the region of the cerebellar vermis and compression of the fourth ventricle with consecutive internal hydrocephalus. The localisation of the tumor suggested a medulloblastoma. But the 3-year-history and the calcifications, which are not common in medulloblastoma, made a benign tumor most likely. Three days after CT examination surgery was performed without consent of the timid child, pretending false informations. After insertion of an external ventricular drainage the tumor was removed subtotally. The biopsy specimen was classified as a medulloblastoma. The diagnosis was affirmed by profound histological examination with a dignity of grade IV according to WHO. The tumor infiltrated the right wall of the fourth ventricle and the adjacent caudal section of the rhomboid fossa. It was removed to the level of the rhomboid fossa, the rest of the tumor was evaporated by CO 2 -laser. After 12 hours in pediatric intensive care H. was extubated. He was awake, but did not speak - apart from answering "yes" and "no", what he also ceased to do after a few days. He was slightly apathetic in the beginning, but non-verbal reactions to requests were adequate. Compared to the preoperative situation, there were no additional neurological deficits. Repeat CT-scan four days after surgery showed hyperdense structures in the area of the fourth ventricle, which enhanced following intravenous contrast medium. Differentiation between residual tumor and disturbances of the bloodbrain-barrier was impossible. Ventricle width had remarkably diminished, with ventricular drainage in function.
Downloaded by: Scott Memorial Library, AISR. Copyrighted material.
Abstract
Neuropediatrics 23 (1992)
Five days after surgery, chemotherapy was started according to the Brain-Tumor-Pilot-Protocol of the Wo~ki~g Group for Brain Tumors HIT 89 of the Society for Pedlatrlc Oncology. (The medication included procarbazine ifosfamide, VP 16, MTX, cisplatinum, cytarabine.) ,
give evidence to an occlusion of a perforating branch of this artery, identified as the posterior thalamo-subthalamic paramedian artery. The tissue loss caused by the vessel occlusion produces a deafferentation of thalamic nuclei from ascending mesencephalic reticular impulses.
Magnetic resonance tomography did not show spinal metastasis. CT-scan two months postoperatively could not reliably demonstrate residual tumor tissue, but showed edema in the region of surgery and pronounced cerebral and cerebellar sulci. . After four and a half months of chemotherapy MRT dlsclosed a small high intensity lesion, which could be interpreted as a zone of gliosis. CT-scanning with contrast after a period of eight months did not display any residual tumor.
In a wider sense the organic mutism also means a complete Broca's aphasia or a loss of speech due to alesion of the supplementary motor cortex of the dominant hemisphere or abilateral pharyngeal or vocal cord paralysis.
Irradiation of the cranio-spinal axis was started five months after surgery in accordance with the protocol. Primarily, the neurocranium and at the same time the spinal cord were irradiated with a single dose of 1.6 Gy up to a dose of 35.2 Gy for both of the two sections. Then, radiotherapy was completed in the cerebellar region up to a total dose of 55 Gy by administering single doses of 1.8 Gy. Strikingly a complete loss of speech occurred postoperatively. In addition, slight apathy was apparent initially. After a few weeks the boy was fully alert, but did not speak anything, only whimpered and groaned. The reception of speech was not impaired. After ten weeks the boy showed accurate, but very slow movements of articulation, that were ap?oneti~. At this time he had - under great effort - asounding ~olce, WhlCh he could not modulate. There was no synchronizabon of phonation and articulation. ENT-examination did not S?OW any organic lesion of the larynx. Nor were there any leSlons of the caudal cranial nerves. Six months after surgery the boy had regained full speech.
Discussion
Disturbances of speech occurring subsequently to posterior fossa surgery are a rather common event. Mostly they are typical dysarthric disturbances like smearing syllables, slow rhythm with monotone modulation or the characteristic cerebellar "scanning" speech, i. e. an explosive thrusting of syllables in the ductus of speech. Mutism, however, i. e. a complete loss of speech, is a quite unusual finding. On the one hand, mutism can be of a purely functional origin in the course of certain psychiatric diseases like autism of a child or some forms of psychosis in adults. In its strict sense, however, organic mutism is represented in the syndrome of akinetic mutism, which can be of frontal or mesencephalic origin. With mutism caused by a frontallesion, called the hyperpathetic form, the patients are awake and do not have any oculomotor disturbances. The lesion is located in the septal region or in the septohypothalamic junction area with or without involvement of the orbitomedial walls of the frontal lobes. Alesion in the region of the dimesencephalic junction of the median zone of the midbrain tegmentum and pretectal area with the median zone of the dorsal thalamus and subthalamus causes the apathetic form of mutism, also called somnolent mutism, which mostly is combined with oculomotor and pupillary paralysis. Segarra (8) described the clinical feature of apathetic akinetic mutism as the "syndrome of the mesencephalic artery". The autoptic findings
The loss of speech described in this case report cannot be assigned to any of the etiologies listed above. There is some evidence that we deal with a form of mutism of a mere cerebellar origin. In their report about survival and functional results of medulloblastoma surgery in childhood, Hirsch et al (3) mention postoperative mutism, but do not go into detail about frequency or pathogenesis. Rekate et al (7) followed up six children with large tumors of the cerebellar vermis and acute postoperative lesions of both cerebellar hemispheres, who consecutively suffered from mutism lasting three weeks to three months. In aseries of 152 posterior fossa surgeries, H umphreys (5) observed five children with postoperative mutism, occurring with a delay of 18 to 72 hours. Humphreys also mentions four cases of Yonemasu (9) with large fourth ventricular tumors, who also suffered a complete loss of speech postoperatively, after a short interval of normal speech. Three corresponding case reports by Ferrante et al (1) can be added. Their common feature are large midline tumors of the posterior fossa, which extend to one or both lateral recessus of the fourth ventricle. An involvement of the cerebellar hemispheres is found inconstantly. Reduction of consciousness or additional neurological deficits are missing. Often there is a short interval of normal speech, so that there must be an additional pathogenetic factor like swelling or ischemia. Where can the originallesion be located? The study of the literature discloses a controversy between advocates of the hemispheral and those of the vermal origin of the cerebellar dysarthria. For a long time the thesis of Holmes (4) was not questioned. In World War I he examined patients with bullet wounds of the posterior fossa and attributed the observed disturbances of speech to alesion of the cerebellar vermis. Fraioli and Guidetti (2) described the effects of stereotactic lesions to the nucleus dentatus in 47 patients with dyskinesia and three patients with epilepsy. In 44 patients these lesions were set bilateraIIy. The authors observed a complete loss of speech in two cases lasting one and three months, respectively. Lechtenberg and Gilman (6) provided a well-founded study including autoptic findings about speech disorders in cerebellar diseases. They observed, that cerebellar dysarthria is most often associated with alesion of the upper part of the left cerebellar hemisphere. They concluded that the lateralization of speech function is also present in the cerebellum, because the cerebrocerebellar tracts predominantly are crossing tracts. The non-dominant right cerebral hemisphere plays an important role in the reception of non-verbal acoustic stimuli as weIl as in the appreciation of melody of speech. As the main components of cerebellar dysarthria relate to prosody, it seems reasonable, that the left cerebellar hemisphere, which is connected to the subdominant right hemisphere, chiefly is responsible for these harmonic components of speech.
145
Downloaded by: Scott Memorial Library, AISR. Copyrighted material.
M utism After Cerebellar M edulloblastoma Surgery
N europediatrics 23 (1992)
E. Herb and U. Thyen
Psychogenesis of this form of mutism has always been discussed as in our case, too. For different reasons our patient was not informed about the extent of surgery, so that the postoperative mutism could be explained as total refusal after having been betrayed. Humphreys (5) described a dramatical and rapid recurrence of speech after demission, giving rise to the assumption of a psychological component in this disturbance. From our point of view, there is no doubt about the organic nature of mutism in our patient. It must be considered as the extreme form of cerebellar dysarthria, namely as a complete anarthria. Ferrante (1) uses the expressions "phonetic disintegration" and "apraxia of speech" in the sense of inability to coordinate the movements of the organs of phonation (vocal cord, tongue, facial and respiratory muscles). The dysarthria which we saw during the process of recovery supports the supposition of its organic origin. Gf course, there can be a functional superposition, as in every organic disease. This superposition can prolong the time of recovery, especially in long-time hospitalized children. It still remains open, whether this sort of mutism is due to alesion of the midline or of the hemisphere of the cerebellum.
References Ferrante, L., et al: Mutism after posterior fossa surgery in children. J. Neurosurg.72(1990)959-963 2 Fraioli, B., B. Guidetti: Effects of stereotactic lesions ofthe dentate nucleus ofthe cerebellum in man. Appl. Neurophysiol. 38 (1975) 81-90 3 Hirsch,]. F., et al: Medulloblastoma in childhood. Survival and functional results. Acta Neurochir. 48 (1979) 1-15 4 Holmes G: The symptoms of acute cerebellar injuries due to gunshot injuries. Brain 40 (1917) 461-535 5 Humphreys, R. P.: Mutism after posterior fossa tumor surgery. Concepts Pediatr. Neurosurg. (Basel, Karger) 9 (1989) 57-64 6 Lechtenberg, R., S. Gilman: Speech disorders in cerebellar disease. Ann. Neurol. 3 (1978) 285-290 7 Rekate, H. L., et al: Muteness of cerebellar origin. Arch. Neurol. 42 (1985) 697-698 8 Segarra,]. M.: Cerebral vascular disease and behavior. Arch. Neurol. 22 (1970) 408-418 9 Yonemasu, Y.: "Cerebellar mutism" and speech disturbance as a complication of posterior fossa surgery in children. 13th Annual Meeting of the Japanese Society for Pediatric Neurosurgery, Tsukuba 1985 (cited by: Humphreys RP: Mutism after posterior fossa tumor surgery, Concepts Pediatr. Neurosurg. 9 [1989] 57)
- - - - - Covers - - - - -
Within Easy Reach ... ... a thorough grasp of One Year's information ... ... just by geuing your subscribed journals bound. Any article or subject can be found at a glance via the author and subject index preceding each volume. If you wish, we can send you the covers (black cloth, gilt-Ieuered). Your bookbinders will take care of the rest. That's how your subscription grows into a broadspectrum reference book that will prove invaluable to you in years to come.
0" alternatively, send us the complete issues for each volume and we will ask our bookbinders to do the job for you for DM 44.60 inclusive of the originalcover.
1
Dr. E. Herb Klinik für Neurochirurgie der Medizinische Universität zu Lübeck Ratzeburger Allee 160 D-2400 Lübeck
- @) Hippokrates _ Hippokrates Verlag Stuttgart Coupon - p~ease c~t Covers Neuropediatrics out and mail to Hlp. pokrates Verlag, Scien- I Wish supply tific Journals Oepart- D Price for volume 1991 DM 26 ment, Rüdigerstr. 14, . 0-7000 Stuttgart 30. D other volumes - - - - - - - - - - D I send under separate cover the issues to Buchbinderei Mende, Klingenstr. 123, 0-7000 Stuttgart 1 to bind the volume in the original cover. Price DM 44.60. All prices plus postage and delivery charges.
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146
Mutism After Cerebellar Medulloblastoma Surgery By E. Herb] and U. Thyen2 lKlinik für Neurochirurgie der Medizinischen Universität Lübeck and 2Klinik für Pädiatrie der Medizinischen Universität Lübeck, Germany
Case report
The case of a 9-year-old boy is presented, who developed transient mutism after removal of a medulloblastoma in the region of the cerebellar vermis. The mutism disappeared within 6 months. Neither reduction of consciousness nor disturbances of caudal cranial nerves or phonation ever appeared. The case is discussed with regard to its phenomenology, pathogenesis, and etiology, corresponding case reports are also taken into consideration.
Keywords Dysarthria - Cerebellar tumor - Medulloblastoma - Mutism
Zusammenfassung Es kommt der Fall eines 9jährigen. Jungen zur Darstellung, bei dem nach der Operation eines Medulloblastoms im Bereich des Kleinhirnwurms vorübergehend ein völliger Sprachverlust aufgetreten war, der sich innerhalb von 6 Monaten wieder zurückbildete. Eine eigentliche Bewußtseinstrübung bzw. Störungen der kaudalen Hirnnerven oder der Phonationsorgane waren nicht vorhanden. Der Fall wird zusammen mit weiteren entsprechenden Kasuistiken aus der Literatur diskutiert im Hinblick auf die Phänomenologie, Pathogenese und Ätiologie dieser Störung.
Schlüsselwörter Dysarthrie - Kleinhirntumor - Medulloblastom - Mutismus
Received February 29,1991; accepted August 9,1991 Neuropediatrics 23 (1992) 144-146 © Hippokrates Verlag Stuttgart
H.M.,m,9y
Since the age of 6, H. complained of recurrent headaches and later on occasional nausea. At the age of 8 3/4 years, vomiting and headaches coincided for the first time. Neither dizziness nor visual disturbances had appeared so far, but the parents had repeatedly noted depressive moods lately. H. often wept and refused to attend school. His mother attributed this behaviour to a high stress of performance at school. Once she came upon H. just fixing a rope at his bed to hang himself. Eventually H. turned more and more aggressive. An ophthalmological examination revealed bilateral papilledema. The following neurological examination disclosed a horizontal nystagmus to both sides and a slight paresis of the facial nerve on the left. Moreover, there was a mild rightsided hemiparesis. Tendon reflexes were normal. No pathological pyramidal tract signs nor disturbances of sensory functions were apparent. Coordination was impaired in terms of a mild ataxia with accentuation on the right side. Cranial computed tomography disclosed a primarily hyperdense, contrast-enhancing tumor with small calcifications in the region of the cerebellar vermis and compression of the fourth ventricle with consecutive internal hydrocephalus. The localisation of the tumor suggested a medulloblastoma. But the 3-year-history and the calcifications, which are not common in medulloblastoma, made a benign tumor most likely. Three days after CT examination surgery was performed without consent of the timid child, pretending false informations. After insertion of an external ventricular drainage the tumor was removed subtotally. The biopsy specimen was classified as a medulloblastoma. The diagnosis was affirmed by profound histological examination with a dignity of grade IV according to WHO. The tumor infiltrated the right wall of the fourth ventricle and the adjacent caudal section of the rhomboid fossa. It was removed to the level of the rhomboid fossa, the rest of the tumor was evaporated by CO 2 -laser. After 12 hours in pediatric intensive care H. was extubated. He was awake, but did not speak - apart from answering "yes" and "no", what he also ceased to do after a few days. He was slightly apathetic in the beginning, but non-verbal reactions to requests were adequate. Compared to the preoperative situation, there were no additional neurological deficits. Repeat CT-scan four days after surgery showed hyperdense structures in the area of the fourth ventricle, which enhanced following intravenous contrast medium. Differentiation between residual tumor and disturbances of the bloodbrain-barrier was impossible. Ventricle width had remarkably diminished, with ventricular drainage in function.
Downloaded by: Scott Memorial Library, AISR. Copyrighted material.
Abstract
Neuropediatrics 23 (1992)
Five days after surgery, chemotherapy was started according to the Brain-Tumor-Pilot-Protocol of the Wo~ki~g Group for Brain Tumors HIT 89 of the Society for Pedlatrlc Oncology. (The medication included procarbazine ifosfamide, VP 16, MTX, cisplatinum, cytarabine.) ,
give evidence to an occlusion of a perforating branch of this artery, identified as the posterior thalamo-subthalamic paramedian artery. The tissue loss caused by the vessel occlusion produces a deafferentation of thalamic nuclei from ascending mesencephalic reticular impulses.
Magnetic resonance tomography did not show spinal metastasis. CT-scan two months postoperatively could not reliably demonstrate residual tumor tissue, but showed edema in the region of surgery and pronounced cerebral and cerebellar sulci. . After four and a half months of chemotherapy MRT dlsclosed a small high intensity lesion, which could be interpreted as a zone of gliosis. CT-scanning with contrast after a period of eight months did not display any residual tumor.
In a wider sense the organic mutism also means a complete Broca's aphasia or a loss of speech due to alesion of the supplementary motor cortex of the dominant hemisphere or abilateral pharyngeal or vocal cord paralysis.
Irradiation of the cranio-spinal axis was started five months after surgery in accordance with the protocol. Primarily, the neurocranium and at the same time the spinal cord were irradiated with a single dose of 1.6 Gy up to a dose of 35.2 Gy for both of the two sections. Then, radiotherapy was completed in the cerebellar region up to a total dose of 55 Gy by administering single doses of 1.8 Gy. Strikingly a complete loss of speech occurred postoperatively. In addition, slight apathy was apparent initially. After a few weeks the boy was fully alert, but did not speak anything, only whimpered and groaned. The reception of speech was not impaired. After ten weeks the boy showed accurate, but very slow movements of articulation, that were ap?oneti~. At this time he had - under great effort - asounding ~olce, WhlCh he could not modulate. There was no synchronizabon of phonation and articulation. ENT-examination did not S?OW any organic lesion of the larynx. Nor were there any leSlons of the caudal cranial nerves. Six months after surgery the boy had regained full speech.
Discussion
Disturbances of speech occurring subsequently to posterior fossa surgery are a rather common event. Mostly they are typical dysarthric disturbances like smearing syllables, slow rhythm with monotone modulation or the characteristic cerebellar "scanning" speech, i. e. an explosive thrusting of syllables in the ductus of speech. Mutism, however, i. e. a complete loss of speech, is a quite unusual finding. On the one hand, mutism can be of a purely functional origin in the course of certain psychiatric diseases like autism of a child or some forms of psychosis in adults. In its strict sense, however, organic mutism is represented in the syndrome of akinetic mutism, which can be of frontal or mesencephalic origin. With mutism caused by a frontallesion, called the hyperpathetic form, the patients are awake and do not have any oculomotor disturbances. The lesion is located in the septal region or in the septohypothalamic junction area with or without involvement of the orbitomedial walls of the frontal lobes. Alesion in the region of the dimesencephalic junction of the median zone of the midbrain tegmentum and pretectal area with the median zone of the dorsal thalamus and subthalamus causes the apathetic form of mutism, also called somnolent mutism, which mostly is combined with oculomotor and pupillary paralysis. Segarra (8) described the clinical feature of apathetic akinetic mutism as the "syndrome of the mesencephalic artery". The autoptic findings
The loss of speech described in this case report cannot be assigned to any of the etiologies listed above. There is some evidence that we deal with a form of mutism of a mere cerebellar origin. In their report about survival and functional results of medulloblastoma surgery in childhood, Hirsch et al (3) mention postoperative mutism, but do not go into detail about frequency or pathogenesis. Rekate et al (7) followed up six children with large tumors of the cerebellar vermis and acute postoperative lesions of both cerebellar hemispheres, who consecutively suffered from mutism lasting three weeks to three months. In aseries of 152 posterior fossa surgeries, H umphreys (5) observed five children with postoperative mutism, occurring with a delay of 18 to 72 hours. Humphreys also mentions four cases of Yonemasu (9) with large fourth ventricular tumors, who also suffered a complete loss of speech postoperatively, after a short interval of normal speech. Three corresponding case reports by Ferrante et al (1) can be added. Their common feature are large midline tumors of the posterior fossa, which extend to one or both lateral recessus of the fourth ventricle. An involvement of the cerebellar hemispheres is found inconstantly. Reduction of consciousness or additional neurological deficits are missing. Often there is a short interval of normal speech, so that there must be an additional pathogenetic factor like swelling or ischemia. Where can the originallesion be located? The study of the literature discloses a controversy between advocates of the hemispheral and those of the vermal origin of the cerebellar dysarthria. For a long time the thesis of Holmes (4) was not questioned. In World War I he examined patients with bullet wounds of the posterior fossa and attributed the observed disturbances of speech to alesion of the cerebellar vermis. Fraioli and Guidetti (2) described the effects of stereotactic lesions to the nucleus dentatus in 47 patients with dyskinesia and three patients with epilepsy. In 44 patients these lesions were set bilateraIIy. The authors observed a complete loss of speech in two cases lasting one and three months, respectively. Lechtenberg and Gilman (6) provided a well-founded study including autoptic findings about speech disorders in cerebellar diseases. They observed, that cerebellar dysarthria is most often associated with alesion of the upper part of the left cerebellar hemisphere. They concluded that the lateralization of speech function is also present in the cerebellum, because the cerebrocerebellar tracts predominantly are crossing tracts. The non-dominant right cerebral hemisphere plays an important role in the reception of non-verbal acoustic stimuli as weIl as in the appreciation of melody of speech. As the main components of cerebellar dysarthria relate to prosody, it seems reasonable, that the left cerebellar hemisphere, which is connected to the subdominant right hemisphere, chiefly is responsible for these harmonic components of speech.
145
Downloaded by: Scott Memorial Library, AISR. Copyrighted material.
M utism After Cerebellar M edulloblastoma Surgery
N europediatrics 23 (1992)
E. Herb and U. Thyen
Psychogenesis of this form of mutism has always been discussed as in our case, too. For different reasons our patient was not informed about the extent of surgery, so that the postoperative mutism could be explained as total refusal after having been betrayed. Humphreys (5) described a dramatical and rapid recurrence of speech after demission, giving rise to the assumption of a psychological component in this disturbance. From our point of view, there is no doubt about the organic nature of mutism in our patient. It must be considered as the extreme form of cerebellar dysarthria, namely as a complete anarthria. Ferrante (1) uses the expressions "phonetic disintegration" and "apraxia of speech" in the sense of inability to coordinate the movements of the organs of phonation (vocal cord, tongue, facial and respiratory muscles). The dysarthria which we saw during the process of recovery supports the supposition of its organic origin. Gf course, there can be a functional superposition, as in every organic disease. This superposition can prolong the time of recovery, especially in long-time hospitalized children. It still remains open, whether this sort of mutism is due to alesion of the midline or of the hemisphere of the cerebellum.
References Ferrante, L., et al: Mutism after posterior fossa surgery in children. J. Neurosurg.72(1990)959-963 2 Fraioli, B., B. Guidetti: Effects of stereotactic lesions ofthe dentate nucleus ofthe cerebellum in man. Appl. Neurophysiol. 38 (1975) 81-90 3 Hirsch,]. F., et al: Medulloblastoma in childhood. Survival and functional results. Acta Neurochir. 48 (1979) 1-15 4 Holmes G: The symptoms of acute cerebellar injuries due to gunshot injuries. Brain 40 (1917) 461-535 5 Humphreys, R. P.: Mutism after posterior fossa tumor surgery. Concepts Pediatr. Neurosurg. (Basel, Karger) 9 (1989) 57-64 6 Lechtenberg, R., S. Gilman: Speech disorders in cerebellar disease. Ann. Neurol. 3 (1978) 285-290 7 Rekate, H. L., et al: Muteness of cerebellar origin. Arch. Neurol. 42 (1985) 697-698 8 Segarra,]. M.: Cerebral vascular disease and behavior. Arch. Neurol. 22 (1970) 408-418 9 Yonemasu, Y.: "Cerebellar mutism" and speech disturbance as a complication of posterior fossa surgery in children. 13th Annual Meeting of the Japanese Society for Pediatric Neurosurgery, Tsukuba 1985 (cited by: Humphreys RP: Mutism after posterior fossa tumor surgery, Concepts Pediatr. Neurosurg. 9 [1989] 57)
- - - - - Covers - - - - -
Within Easy Reach ... ... a thorough grasp of One Year's information ... ... just by geuing your subscribed journals bound. Any article or subject can be found at a glance via the author and subject index preceding each volume. If you wish, we can send you the covers (black cloth, gilt-Ieuered). Your bookbinders will take care of the rest. That's how your subscription grows into a broadspectrum reference book that will prove invaluable to you in years to come.
0" alternatively, send us the complete issues for each volume and we will ask our bookbinders to do the job for you for DM 44.60 inclusive of the originalcover.
1
Dr. E. Herb Klinik für Neurochirurgie der Medizinische Universität zu Lübeck Ratzeburger Allee 160 D-2400 Lübeck
- @) Hippokrates _ Hippokrates Verlag Stuttgart Coupon - p~ease c~t Covers Neuropediatrics out and mail to Hlp. pokrates Verlag, Scien- I Wish supply tific Journals Oepart- D Price for volume 1991 DM 26 ment, Rüdigerstr. 14, . 0-7000 Stuttgart 30. D other volumes - - - - - - - - - - D I send under separate cover the issues to Buchbinderei Mende, Klingenstr. 123, 0-7000 Stuttgart 1 to bind the volume in the original cover. Price DM 44.60. All prices plus postage and delivery charges.
Date Name & address
EK3F
Signature _
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146
