Mesencephalic haematoma, successful surgical evacuation Case report V.K. Jain, J.K. Multani,
A.K. Reddy,
B.S. Das*
Introduction Summary Walter Dandy was the first to describe the operative removal of brain stem haematoma’. Since then many cases of brain stem haematomas have been reported, most of them were located in the pans. They usually occur in hypertensive adults. Surgery of brain stem haematomas occurred apparently mainly in cases of pontine haematoma’.‘“. Mesencephalic haematoma is extremely rare”. Among those reported, very few survived and still fewer were operated on. We report a case of mesencephalic haematoma in a child who was successfully treated by surgical removal of the haematoma. Case report A twelve-year-old boy was brought to us on 1.4.83. He had sustained a blow on his forehead with a wooden stick six days earlier. At that moment there was neither impairment of consciousness nor external injury and he remained perfectly well for the next two days. On the third day he complained of moderate headache when he got up from his after-noon nap. At that time he had also developed left hemiplegia and slurring of speech. The intensity of his headache increased so much during the next three days that he would frequently cry due to headache. He involuntarily passed urine and stool in his clothes.
* Department of Neurosurgery,
A case of mesencephalic haematoma is report-
ed. Emergency surgical evacuation of haematoma was done. The patient improved and has done well for five years. Subtemporal and infratentorial supracerebellar approaches have been used earlier to remove mesencephalic haematoma. It is possible to remove caudal midbrain haematoma via a IVth ventricular approach causing minimal damage. Key words: Brain stem, mesencephalon, matoma, surgery.
he-
Examination The child was conscious but irritable and he was crying due to headache most of the time. He could speak a few words and sentences in a slurred speech. Both fundi were normal. There was bilateral ptosis. The right pupil was larger than the left, both reacted sluggishly to light. Eye movements were absent in all directions in the right eye. Upward and medial movements were absent in the left eye. (Thus he had bilateral III nerve palsy which was complete on the right side and partial on the left, right VI nerve palsy and upward gaze palsy). There was left central facial paresis and left hemiplegia (motor power grade 0). Tendon reflexes were exagger-
National Institute of Mental Health & Neurosciences,
Bangalore (India).
Address for correspondence and reprint requests: V. K. Jain, Associate Professor, Dept. of Neurosurgery, Graduate Institute of Medical Sciences, P. B. No. 375, Raebareli Road, Lucknow (India)
Sanjay Gandhi Post
Accepted IO. 4.89 Clin Neural Neurosurg 1990. Vol.92-2.
159
Fig. la,b Large hematoma in the mid brain extending more to the right side.
ated on the left with bilateral extensor plantar response. One hour after admission, he deteriorated and became comatose. Skull films were normal. CT scan showed a large hematoma occupying the midbrain and upper pons extending more towards the right side. There was no hydrocephalus. There was no evidence of blood in the aqueduct, IVth ventricle and subarachnoid space (Fig.1, a,b). Operation
An emergency standard midline suboccipital craniectomy was done. CSF was clear on opening the cisterna magna. On splitting the vermis in midline, a brownish discolouration of the floor of the fourth ventricle was seen in its uppermost part near the opening of the aqueduct. A 0.5 cm long midline incision was made in this discoloured area. The haematoma was found just under the ependyma. About 3.0 cc. haematoma was removed. The opening which we made to remove the haematoma was found to be at the lower pole of the haematoma cavity. The cavity wall was yellowish brown and did not show any evidence of angioma, therefore biopsy was not taken. Microscopic examination of the
haematoma did not reveal any evidence of angioma or tumour. Post operative vertebral angiogram also did not reveal any angioma. Post-operative Course
Patient’s sensorium gradually improved. On 25.0483, the day he was discharged from the hospital, he was alert and oriented. He had complete right third nerve p&y, partial left third nerve palsy, right sixth nerve paresis, left central facial paresis, left hemiparesis (motor power grade III) and signs of left cerebellar dysfunction. He could walk with minimal support. Tendon reflexes were brisk on the left side with bilateral extensor plantar response. He was seen two years and four months later in follow up clinic. He was asymptomatic except that he complained of pain in his extremities after working in the field. He was independent and could perform all activities without any help. Examination showed right internuclear ophthalmoplegia, mild tendency to sway to left side while performing tandem walk and a slight difficulty on suddenly turning to the left side. There was no other neurological deficit. He was again seen five years later in April 1988. Mild internuclear ophthalamoplegia was still persisting. However he had no difficulty in his daytoday work as a farm labourer.
Discussion Several cases of hematoma involving the brain stem have been reported in the literature. Most of them were found in the pontine or medullary areas, only five were located in the midbrain”.14. The greater prevalence in the pontine area seems to be related to the greater incidence of “cryptic” vascular malformations in this region Is. Cause of haemorrhage has not been identified in majority of the reported cases of brain stem haematoma. However, most operated cases have been attributed to cryptic arteriovenous malformations (AVMs). Many pathological reports are available on such lesions,both as incidental findings at autopsy and as causes of Though the pons is the fatal haemorrhage 15-19. commonest site of incidental cryptic AVMs”, the most likely aetiology of mesencephalic haematoma also is a vascular malformation. This was suspected in five previous cases of successfully treated mesencephalic haematomas but it was proved only in two11-14.We believe that the haematoma in our patient was caused by a cryptic AVM. McCormick et aL2’, studied 164 angiomas of the posterior fossa of which 68 were in the brain stem. Of these 68 brain stem angiomas six were mesencephalic. Two of these angiomas were true AVMs, one was cavernous angioma and three were venous angiomas. Of the 68 brain stem angiomas, 12 had bled. Of these 12, nine were AVMs, two were venous angiomas, and one was a varix. Aronson21 has described certain characteristics of mesencephalic AVMs. Most occur in dorsal mid brain, are eccentric but may cross mid saggital line. Ventral extension may occur and hydrocephalus can result from obstruction of the aqueduct of Sylvius. Although the evidence is circumstantial, rupture of cryptic AVMs appears to be the most likely explanation of brain stem haematoma. The lesions are frequently so disrupted by the haemorrhage that identification of blood vessels in the clot may be impossible 15-17 . Failure to identify angioma vessels in the clot may not be due to complete destruction of AVM, but to the difficulty of finding a very small lesion which is often fragmented in a relatively large volume of haematoma’. The alternative aetiology of mesencephalic
haematoma is a vascular disease consequent to although mesencephalon has hypertension, rarely been identified as a site for such haematomas. It was suspected in the case-l of Durward et al. Hypertensive intracerebral hematomas are caused by ruptured arterioles which are the site of fibrinoid necrosis and micro aneurysms (Charcot Bouchard aneurysms)“. The usual site for these microaneurysms within the brain stem of hypertensive individual is the pons, and consequently the pons is the site for most primary brain stem hematoma$. The pattern of branching of the penetrating pontine arteries may predispose these vessels to degenerative changes24. Unfortunately information regarding changes in penetrating mesencephalic vessels is not available”. Due to the compact anatomy of the midbrain, clinical localization can usually be made with great accuracy”. Scoville and Poppen14 described an intrapeduncular mesencephalic haematoma of which the localization and consequent operative removal was planned and executed largely-on the basis of the clinical findings of stupor, paralysis of all conjugate eye movements and a right hemiparesis. Five of six surviving patients with mesencephalic hematoma (including the one case reported here) have had paralysis of upward gaze. This is a reliable sign that localizes the lesion to the central midbrain tegmentum”. There does not seem to be any typical clinical picture of brain stem haematoma due to rupture of a cryptic AVM. The commonest presentations appear to be either progressive deterioration suggesting a pontine glioma5-7~25-27, or relapsing or stepwise deterioration, mimicking demyelination’4~28~29. This entity may also present with the acute onset of a stroke4,5,7.30or of a subarachnoid haemorrhage3,13 or with a subacute onset suggesting brain stem encephalitis’. The natural history of brain stem haemorrhage is not well documented. Before the introduction of effective hypotensive agents and CT scan major brain stem haemorrhage was a common finding in patients dying of malignant hypertension ‘s31.However most of the patients of brain stem haematomas reported to be due AVMs were normotensive and presented with deteriorating neurological condition progressing over days or weeks, months or rarely years 161
until1 surgery1-8~12~13,25”0 or death15~17~18. There does not seem to be any report of spontaneous recovery. The majority of the patients operated on seem to have done we112~8~12~13~25-30. Surgical evacuation of brain stem haematoma has been described earlier. The majority of these haematomas were situated in the pons, therefore evacuation through the floor of the IVth ventricle had been successful. Mesencephalic haematomas have been operated by subtemporal approach to reach anterior and lateral midbrain”~12,14and by supracerebellar infratentorial approach to reach quadrigeminal plate13. Our case is the first reported case which shows that the haematomas extending to caudal midbrain can easily be evacuated via the IVth ventricular approach. We are aware that our decision not to biopsy the wall of hematoma cavity carries some risk of missing a haemorrhagic tumour, but we believe that careful microscopic examination of the clot is adequate and that biopsy of the brain stem tissue would carry an unnecessary risk. The few reported patients in whom biopsy was carried out, deteriorated markedly post operatively, although all recovered eventually’~6~7. Furthermore our patient has been followed for a period of five years without evidence of recurrent disease. The clinical presentation of brain stem haematomas is extremely variable. This probably is true for mesencephalic haematomas also. Therefore it should be considered in the differential diagnosis of any patient with midbrain signs, particularly in children and young adults. Surgical treatment seems safe and effective. Although the evidence is circumstantial, an untreated mesencephalic hematoma is likely to prove fatal.
5
6
7
8
2
3
4
Brain-stem hematoma. A report of six surgically treated cases. J Neurosurg 1982; 56:222-7. ~oc21 T, THOMAS DGT. Successful removal of an intrapontine haematoma. J Neurol Neurosurg Psychiatry 1979; 42:1058-61. KOOS
WT, SUNDER-PLASSMANN
M, SALAH
9
” 11
I*
I3
I4
I5
lb
I’
I8 I9
2a
162
z u 24
S. SUCCeSfUl
removal of a large intrapontine hematoma. Case Report. J Neurosurg 1969; 31:690-4. KO~ADA M, IT~ z, MATSUOKA set al.. Primary pontine haemorrhage revealed by pneumoencephaloroullette tomography, and a report on surgically treated cases.
SUrgiCB~eVXUatiOu Case report.J
Neu-
rosurg 1970; 33:82-4. PAK H, PATEL sc, MALIK GM el al. Successful evacuation of a pontine hematoma secondary to rupture of a venous angioma. Surg Neurol 1981; 15:164-7. PAPO I,PASQUINI u, SALVOLINI u. Subependymal brain stem hematomas: a report of two cases. Neuroradiology 1976; 11:279-82. SCOlT BB, SEEGER JF, SCHNEIDER
RC. SUCCeSSfUleVX-
pathologicallydiagnosed “Cryptic" vascular malforma-
References O'LAOIRESA,CROCKARDHA,THOMASDGT,GORDONDS.
OBRADORS,DIERSSENG,ODORIZB,.
of a pontine medullary hematoma.
uationofapontinehematomasecondarytoruptureofa
”
1
Acta Neurochir 1971; 25:269-76.
z 26
tion.Case
Report. J Neurosurg 1973; 39:104-8. removal of pontine haematoma due to rupture of cryptic arteriovenous malformation. Case report. Acta Neurochir 1983; 69:69-75. UMANSKYF,TOLEDOE,COHENM. etal. Successfulremoval of an acute brain stem hematoma in a young child. Child’s brain 1983; 10:350-4. DURWARD QJ, BARNEY HJM, BARR HWK. Presentation and management of mesencephalic hematoma. Report of two cases. J Neurosurg 1982; 56:123-7. HUMPHREYS RP. Computerized tomographic definition of mesencephalic hematoma with evacuation through pedunculotomy. Case report. J Neurosurg 1978; 49:74952. LATORREE,DEL~TALAA,SORANOV. Hematomaofthe quadrigeminal plate. Case report. J Neurosurg 1978; 49:610-3. SCOVILLE WB, POPPEN JL. Intrapeduncular haemorrhage of the brain. Successful operative approach with evacuation of clot and a seven and one fourth year observation period. Arch Neural Psychiatry 1949; 61:688-94. MCCORMICKWF,NOFZINGERJD. Crypticvascularmalformations of the central nervous system. J Neurosurg 1966; 24:865-75. CRAWFORD JV, RUSSELL DS. Cryptic arteIiOVeIIOUSand venous hamartomas of the brain. J Neural Neurosurg Psychiatry 1956; 19:1-11. MARGOLIS G, ODOM CL, WOODHALL B. etal. The role of small angiomatous malformations in the production of intracerebral hematomas. J Neurosurg 1951; 8564-75. TEILMANN K. Hemangiomas of the pons. Arch Neurol Psychiatry 1953; 69:208-23. WHITE RJ, KERNOHAN JW, WOOD MW. A study Of fifty intracranial vascular tumours found incidentally at autopsy. J Neuropathol Exp Neural 1958; 17:392-8. MCCORMICK WF, HARDMAN JM, BOULTER TR. Vascular malformations (angiomas) of the brain, with special reference to those accurring in the posterior fossa. J Neurosurg 1968; 28:241-251. ARONSON SM. Vascular malformations. In: Minckler J (ed): Pathology of the Nervous system. New York/Toronto/Sydney/London: McGrawHilI, 1971 Vol 2, pp. 1884-96. RUSSELL RWR. Observations on intracerebral aneurysms. Brain 1963; 86:425-442. STEHBENS WE. Pathology of the cerebral blood vessels. St Louis: CV Mosby, 1972,661 pp. DINSDALE HB. Spontaneous hemorrhage in the posterior fossa. A study of primary cerebellar and pontine hemorrhages with observations on their pathogenesis. Arch Neurol 1964; 10:200-17. MATSON DD. Surgery of Posterior fossa tumours in childhood. Clin Neurosurg 1968; 15:247&l. DANDY WE. The Brain. New York: Harper and Row, 1969, pp. 642-3. INOUE Y, SATO o. Successful
MC?.Successful evacuation of acute pontine hematoma. Case report. J Neurosurg 1972; 37:224-25.
MURPHY
z
ABROMS
IF,YESSAYAN
L, SHILLITO I.etd. f$CXltBUeOUS
intracerebral haemorrhage in patients suspected of multiple sclerosis. J Neural Neurosurg Psychiatry 1971; 34:157-62. 29 ARSENI c, STANCIRE M. Primary hematomas of the brain
stem. Acta Neurochir 1973; 28:323-30. KEMPE LG. Surgical removal of an intramedullary hematoma simulating Wallenberg’s syndrome. J Neural Neurosurg Psychiatry 1964; 27:78-80. 3’ SILVERSTEIN A. Primary pontile hemorrhage. A review of 50 cases. Confin Neural 1967; 29:33-46. M
163
A.K. Reddy,
B.S. Das*
Introduction Summary Walter Dandy was the first to describe the operative removal of brain stem haematoma’. Since then many cases of brain stem haematomas have been reported, most of them were located in the pans. They usually occur in hypertensive adults. Surgery of brain stem haematomas occurred apparently mainly in cases of pontine haematoma’.‘“. Mesencephalic haematoma is extremely rare”. Among those reported, very few survived and still fewer were operated on. We report a case of mesencephalic haematoma in a child who was successfully treated by surgical removal of the haematoma. Case report A twelve-year-old boy was brought to us on 1.4.83. He had sustained a blow on his forehead with a wooden stick six days earlier. At that moment there was neither impairment of consciousness nor external injury and he remained perfectly well for the next two days. On the third day he complained of moderate headache when he got up from his after-noon nap. At that time he had also developed left hemiplegia and slurring of speech. The intensity of his headache increased so much during the next three days that he would frequently cry due to headache. He involuntarily passed urine and stool in his clothes.
* Department of Neurosurgery,
A case of mesencephalic haematoma is report-
ed. Emergency surgical evacuation of haematoma was done. The patient improved and has done well for five years. Subtemporal and infratentorial supracerebellar approaches have been used earlier to remove mesencephalic haematoma. It is possible to remove caudal midbrain haematoma via a IVth ventricular approach causing minimal damage. Key words: Brain stem, mesencephalon, matoma, surgery.
he-
Examination The child was conscious but irritable and he was crying due to headache most of the time. He could speak a few words and sentences in a slurred speech. Both fundi were normal. There was bilateral ptosis. The right pupil was larger than the left, both reacted sluggishly to light. Eye movements were absent in all directions in the right eye. Upward and medial movements were absent in the left eye. (Thus he had bilateral III nerve palsy which was complete on the right side and partial on the left, right VI nerve palsy and upward gaze palsy). There was left central facial paresis and left hemiplegia (motor power grade 0). Tendon reflexes were exagger-
National Institute of Mental Health & Neurosciences,
Bangalore (India).
Address for correspondence and reprint requests: V. K. Jain, Associate Professor, Dept. of Neurosurgery, Graduate Institute of Medical Sciences, P. B. No. 375, Raebareli Road, Lucknow (India)
Sanjay Gandhi Post
Accepted IO. 4.89 Clin Neural Neurosurg 1990. Vol.92-2.
159
Fig. la,b Large hematoma in the mid brain extending more to the right side.
ated on the left with bilateral extensor plantar response. One hour after admission, he deteriorated and became comatose. Skull films were normal. CT scan showed a large hematoma occupying the midbrain and upper pons extending more towards the right side. There was no hydrocephalus. There was no evidence of blood in the aqueduct, IVth ventricle and subarachnoid space (Fig.1, a,b). Operation
An emergency standard midline suboccipital craniectomy was done. CSF was clear on opening the cisterna magna. On splitting the vermis in midline, a brownish discolouration of the floor of the fourth ventricle was seen in its uppermost part near the opening of the aqueduct. A 0.5 cm long midline incision was made in this discoloured area. The haematoma was found just under the ependyma. About 3.0 cc. haematoma was removed. The opening which we made to remove the haematoma was found to be at the lower pole of the haematoma cavity. The cavity wall was yellowish brown and did not show any evidence of angioma, therefore biopsy was not taken. Microscopic examination of the
haematoma did not reveal any evidence of angioma or tumour. Post operative vertebral angiogram also did not reveal any angioma. Post-operative Course
Patient’s sensorium gradually improved. On 25.0483, the day he was discharged from the hospital, he was alert and oriented. He had complete right third nerve p&y, partial left third nerve palsy, right sixth nerve paresis, left central facial paresis, left hemiparesis (motor power grade III) and signs of left cerebellar dysfunction. He could walk with minimal support. Tendon reflexes were brisk on the left side with bilateral extensor plantar response. He was seen two years and four months later in follow up clinic. He was asymptomatic except that he complained of pain in his extremities after working in the field. He was independent and could perform all activities without any help. Examination showed right internuclear ophthalmoplegia, mild tendency to sway to left side while performing tandem walk and a slight difficulty on suddenly turning to the left side. There was no other neurological deficit. He was again seen five years later in April 1988. Mild internuclear ophthalamoplegia was still persisting. However he had no difficulty in his daytoday work as a farm labourer.
Discussion Several cases of hematoma involving the brain stem have been reported in the literature. Most of them were found in the pontine or medullary areas, only five were located in the midbrain”.14. The greater prevalence in the pontine area seems to be related to the greater incidence of “cryptic” vascular malformations in this region Is. Cause of haemorrhage has not been identified in majority of the reported cases of brain stem haematoma. However, most operated cases have been attributed to cryptic arteriovenous malformations (AVMs). Many pathological reports are available on such lesions,both as incidental findings at autopsy and as causes of Though the pons is the fatal haemorrhage 15-19. commonest site of incidental cryptic AVMs”, the most likely aetiology of mesencephalic haematoma also is a vascular malformation. This was suspected in five previous cases of successfully treated mesencephalic haematomas but it was proved only in two11-14.We believe that the haematoma in our patient was caused by a cryptic AVM. McCormick et aL2’, studied 164 angiomas of the posterior fossa of which 68 were in the brain stem. Of these 68 brain stem angiomas six were mesencephalic. Two of these angiomas were true AVMs, one was cavernous angioma and three were venous angiomas. Of the 68 brain stem angiomas, 12 had bled. Of these 12, nine were AVMs, two were venous angiomas, and one was a varix. Aronson21 has described certain characteristics of mesencephalic AVMs. Most occur in dorsal mid brain, are eccentric but may cross mid saggital line. Ventral extension may occur and hydrocephalus can result from obstruction of the aqueduct of Sylvius. Although the evidence is circumstantial, rupture of cryptic AVMs appears to be the most likely explanation of brain stem haematoma. The lesions are frequently so disrupted by the haemorrhage that identification of blood vessels in the clot may be impossible 15-17 . Failure to identify angioma vessels in the clot may not be due to complete destruction of AVM, but to the difficulty of finding a very small lesion which is often fragmented in a relatively large volume of haematoma’. The alternative aetiology of mesencephalic
haematoma is a vascular disease consequent to although mesencephalon has hypertension, rarely been identified as a site for such haematomas. It was suspected in the case-l of Durward et al. Hypertensive intracerebral hematomas are caused by ruptured arterioles which are the site of fibrinoid necrosis and micro aneurysms (Charcot Bouchard aneurysms)“. The usual site for these microaneurysms within the brain stem of hypertensive individual is the pons, and consequently the pons is the site for most primary brain stem hematoma$. The pattern of branching of the penetrating pontine arteries may predispose these vessels to degenerative changes24. Unfortunately information regarding changes in penetrating mesencephalic vessels is not available”. Due to the compact anatomy of the midbrain, clinical localization can usually be made with great accuracy”. Scoville and Poppen14 described an intrapeduncular mesencephalic haematoma of which the localization and consequent operative removal was planned and executed largely-on the basis of the clinical findings of stupor, paralysis of all conjugate eye movements and a right hemiparesis. Five of six surviving patients with mesencephalic hematoma (including the one case reported here) have had paralysis of upward gaze. This is a reliable sign that localizes the lesion to the central midbrain tegmentum”. There does not seem to be any typical clinical picture of brain stem haematoma due to rupture of a cryptic AVM. The commonest presentations appear to be either progressive deterioration suggesting a pontine glioma5-7~25-27, or relapsing or stepwise deterioration, mimicking demyelination’4~28~29. This entity may also present with the acute onset of a stroke4,5,7.30or of a subarachnoid haemorrhage3,13 or with a subacute onset suggesting brain stem encephalitis’. The natural history of brain stem haemorrhage is not well documented. Before the introduction of effective hypotensive agents and CT scan major brain stem haemorrhage was a common finding in patients dying of malignant hypertension ‘s31.However most of the patients of brain stem haematomas reported to be due AVMs were normotensive and presented with deteriorating neurological condition progressing over days or weeks, months or rarely years 161
until1 surgery1-8~12~13,25”0 or death15~17~18. There does not seem to be any report of spontaneous recovery. The majority of the patients operated on seem to have done we112~8~12~13~25-30. Surgical evacuation of brain stem haematoma has been described earlier. The majority of these haematomas were situated in the pons, therefore evacuation through the floor of the IVth ventricle had been successful. Mesencephalic haematomas have been operated by subtemporal approach to reach anterior and lateral midbrain”~12,14and by supracerebellar infratentorial approach to reach quadrigeminal plate13. Our case is the first reported case which shows that the haematomas extending to caudal midbrain can easily be evacuated via the IVth ventricular approach. We are aware that our decision not to biopsy the wall of hematoma cavity carries some risk of missing a haemorrhagic tumour, but we believe that careful microscopic examination of the clot is adequate and that biopsy of the brain stem tissue would carry an unnecessary risk. The few reported patients in whom biopsy was carried out, deteriorated markedly post operatively, although all recovered eventually’~6~7. Furthermore our patient has been followed for a period of five years without evidence of recurrent disease. The clinical presentation of brain stem haematomas is extremely variable. This probably is true for mesencephalic haematomas also. Therefore it should be considered in the differential diagnosis of any patient with midbrain signs, particularly in children and young adults. Surgical treatment seems safe and effective. Although the evidence is circumstantial, an untreated mesencephalic hematoma is likely to prove fatal.
5
6
7
8
2
3
4
Brain-stem hematoma. A report of six surgically treated cases. J Neurosurg 1982; 56:222-7. ~oc21 T, THOMAS DGT. Successful removal of an intrapontine haematoma. J Neurol Neurosurg Psychiatry 1979; 42:1058-61. KOOS
WT, SUNDER-PLASSMANN
M, SALAH
9
” 11
I*
I3
I4
I5
lb
I’
I8 I9
2a
162
z u 24
S. SUCCeSfUl
removal of a large intrapontine hematoma. Case Report. J Neurosurg 1969; 31:690-4. KO~ADA M, IT~ z, MATSUOKA set al.. Primary pontine haemorrhage revealed by pneumoencephaloroullette tomography, and a report on surgically treated cases.
SUrgiCB~eVXUatiOu Case report.J
Neu-
rosurg 1970; 33:82-4. PAK H, PATEL sc, MALIK GM el al. Successful evacuation of a pontine hematoma secondary to rupture of a venous angioma. Surg Neurol 1981; 15:164-7. PAPO I,PASQUINI u, SALVOLINI u. Subependymal brain stem hematomas: a report of two cases. Neuroradiology 1976; 11:279-82. SCOlT BB, SEEGER JF, SCHNEIDER
RC. SUCCeSSfUleVX-
pathologicallydiagnosed “Cryptic" vascular malforma-
References O'LAOIRESA,CROCKARDHA,THOMASDGT,GORDONDS.
OBRADORS,DIERSSENG,ODORIZB,.
of a pontine medullary hematoma.
uationofapontinehematomasecondarytoruptureofa
”
1
Acta Neurochir 1971; 25:269-76.
z 26
tion.Case
Report. J Neurosurg 1973; 39:104-8. removal of pontine haematoma due to rupture of cryptic arteriovenous malformation. Case report. Acta Neurochir 1983; 69:69-75. UMANSKYF,TOLEDOE,COHENM. etal. Successfulremoval of an acute brain stem hematoma in a young child. Child’s brain 1983; 10:350-4. DURWARD QJ, BARNEY HJM, BARR HWK. Presentation and management of mesencephalic hematoma. Report of two cases. J Neurosurg 1982; 56:123-7. HUMPHREYS RP. Computerized tomographic definition of mesencephalic hematoma with evacuation through pedunculotomy. Case report. J Neurosurg 1978; 49:74952. LATORREE,DEL~TALAA,SORANOV. Hematomaofthe quadrigeminal plate. Case report. J Neurosurg 1978; 49:610-3. SCOVILLE WB, POPPEN JL. Intrapeduncular haemorrhage of the brain. Successful operative approach with evacuation of clot and a seven and one fourth year observation period. Arch Neural Psychiatry 1949; 61:688-94. MCCORMICKWF,NOFZINGERJD. Crypticvascularmalformations of the central nervous system. J Neurosurg 1966; 24:865-75. CRAWFORD JV, RUSSELL DS. Cryptic arteIiOVeIIOUSand venous hamartomas of the brain. J Neural Neurosurg Psychiatry 1956; 19:1-11. MARGOLIS G, ODOM CL, WOODHALL B. etal. The role of small angiomatous malformations in the production of intracerebral hematomas. J Neurosurg 1951; 8564-75. TEILMANN K. Hemangiomas of the pons. Arch Neurol Psychiatry 1953; 69:208-23. WHITE RJ, KERNOHAN JW, WOOD MW. A study Of fifty intracranial vascular tumours found incidentally at autopsy. J Neuropathol Exp Neural 1958; 17:392-8. MCCORMICK WF, HARDMAN JM, BOULTER TR. Vascular malformations (angiomas) of the brain, with special reference to those accurring in the posterior fossa. J Neurosurg 1968; 28:241-251. ARONSON SM. Vascular malformations. In: Minckler J (ed): Pathology of the Nervous system. New York/Toronto/Sydney/London: McGrawHilI, 1971 Vol 2, pp. 1884-96. RUSSELL RWR. Observations on intracerebral aneurysms. Brain 1963; 86:425-442. STEHBENS WE. Pathology of the cerebral blood vessels. St Louis: CV Mosby, 1972,661 pp. DINSDALE HB. Spontaneous hemorrhage in the posterior fossa. A study of primary cerebellar and pontine hemorrhages with observations on their pathogenesis. Arch Neurol 1964; 10:200-17. MATSON DD. Surgery of Posterior fossa tumours in childhood. Clin Neurosurg 1968; 15:247&l. DANDY WE. The Brain. New York: Harper and Row, 1969, pp. 642-3. INOUE Y, SATO o. Successful
MC?.Successful evacuation of acute pontine hematoma. Case report. J Neurosurg 1972; 37:224-25.
MURPHY
z
ABROMS
IF,YESSAYAN
L, SHILLITO I.etd. f$CXltBUeOUS
intracerebral haemorrhage in patients suspected of multiple sclerosis. J Neural Neurosurg Psychiatry 1971; 34:157-62. 29 ARSENI c, STANCIRE M. Primary hematomas of the brain
stem. Acta Neurochir 1973; 28:323-30. KEMPE LG. Surgical removal of an intramedullary hematoma simulating Wallenberg’s syndrome. J Neural Neurosurg Psychiatry 1964; 27:78-80. 3’ SILVERSTEIN A. Primary pontile hemorrhage. A review of 50 cases. Confin Neural 1967; 29:33-46. M
163
