Cavernous malformations of the brain stem

1991 ◽  
Vol 75 (1) ◽  
pp. 32-39 ◽  
Author(s):  
Richard S. Zimmerman ◽  
Robert F. Spetzler ◽  
K. Stuart Lee ◽  
Joseph M. Zabramski ◽  
Ronald W. Hargraves

✓ Once they become symptomatic, cavernous malformations of the brain stem appear to cause progressive morbidity from repetitive hemorrhage, and can even be fatal. Twenty-four patients with long-tract and/or cranial nerve findings from their cavernous malformations of the brain stem were seen for initial evaluation or surgical consultation and thereafter received either surgical or continued conservative treatment. The decision to operate was based on the proximity of the cavernous malformation to the pial surface of the brain stem, the patient's neurological status, and the number of symptomatic episodes. Sixteen patients were treated by definitive surgery directed at excision of their malformation. In four patients, associated venous malformations influenced the surgical approach and their recognition avoided the risk of inappropriate excision of the venous malformation. Although some of the 16 patients had transient, immediate, postoperative worsening of their neurological deficits, the outcome of all except one was the same or improved. Only one patient developed recurrent symptoms: a new deficit 2½ years after surgery required reoperation after regrowth of the cavernous malformation. She has been neurologically stable since the second surgery. One patient died 6 months postoperatively from a shunt infection and sepsis. The eight conservatively treated patients are followed with annual magnetic resonance imaging studies. One has a dramatic associated venous malformation. Seven patients have either minor intermittent or no symptoms, and the eighth died from a hemorrhage 1 year after his initial presentation. Based on these results, surgical extirpation of symptomatic cavernous malformations of the brain stem appears to be the treatment of choice when a patient is symptomatic, the lesion is located superficially, and an operative approach can spare eloquent tissue. When cavernous malformations of the brain stem are completely excised, cure appears permanent.

1996 ◽  
Vol 85 (6) ◽  
pp. 1135-1142 ◽  
Author(s):  
Richard Leblanc ◽  
Denis Melanson ◽  
Ralph D. Wilkinson

✓ The authors report the coexistence of vascular nevi (hemangiomas and arteriovenous malformations (AVMs) of the skin) with AVMs and venous malformations of the brain in male siblings from two related but nonconsanguineous families of three generations. The proband, his siblings, parents, aunts, uncles, and cousins were examined, underwent magnetic resonance (MR) imaging and MR angiography, and when appropriate, cerebral angiography. A father had vascular nevi and a mother, his sister, had an azygos anterior cerebral artery. No other cutaneous or cerebrovascular malformations were present in the parents. Each of the two families had two boys and one girl, 9 to 18 years of age. All the children had vascular nevi and all of the boys had coexisting cerebrovascular malformations: AVMs in three, and a venous malformation in another. One boy had three cerebral AVMs. Two boys had a cerebral hemorrhage, and one also had focal motor seizures. The skin lesions were not those of the Sturge-Weber-Dimitri, Rendu-Osler-Weber, or Wyburn—Mason syndromes. The association of cutaneous and cerebrovascular malformations was seen only in males in these families, but females have also been reported in the literature. The results obtained in these families and three other families reported from Western and Central Europe indicate that the association of cerebral and cutaneous vascular hamartomas constitutes a distinct, hereditary clinicopathological entity with autosomal dominant inheritance and variable penetrance. The clinical manifestations of this syndrome are visible, painful vascular nevi, epilepsy, cerebral hemorrhage, and focal neurological deficits. The preponderance of male patients with the full expression of the syndrome suggests a possible hormonal influence on the expression of the gene.


1971 ◽  
Vol 35 (4) ◽  
pp. 477-482 ◽  
Author(s):  
Nitya R. Ghatak ◽  
Grace J. Mushrush

✓ The clinical and pathological features of a primary supratentorial arachnoid cyst are described. Expansion of the cyst led to progressive neurological deficits that terminated fatally. There was severe compression and marked distortion of the brain with secondary brain stem hemorrhage. It is suggested that intra-arachnoid cysts may represent a distinct pathological entity among the heterogeneous cysts overlying the cerebral hemisphere.


1975 ◽  
Vol 43 (6) ◽  
pp. 661-670 ◽  
Author(s):  
Charles G. Drake

✓ The author reports his surgical experience with five cases of arteriovenous malformation of the brain stem and cerebellopontine angle causing multiple hemorrhages and severe neurological deficits. Surgical removal of the lesions had good results in four cases; there was one death.


1977 ◽  
Vol 47 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Hiroshi Matsumura ◽  
Yasumasa Makita ◽  
Kuniyuki Someda ◽  
Akinori Kondo

✓ We have operated on 12 of 14 cases of arteriovenous malformation (AVM) in the posterior fossa since 1968, with one death. The lesions were in the cerebellum in 10 cases (three anteromedial, one central, three lateral, and three posteromedial), and in the cerebellopontine angle in two; in two cases the lesions were directly related to the brain stem. The AVM's in the anterior part of the cerebellum were operated on through a transtentorial occipital approach.


1973 ◽  
Vol 39 (1) ◽  
pp. 104-108 ◽  
Author(s):  
Ben B. Scott ◽  
Joachim F. Seeger ◽  
Richard C. Schneider

✓ A posterior fossa exploration was performed on a child thought initially to have an inoperable brain stem lesion. A pontine hematoma was discovered and evacuated. The pathological specimen was designated as a “cryptic” arteriovenous malformation. All preoperative neurological deficits disappeared except for a minimal left seventh nerve palsy.


1972 ◽  
Vol 37 (5) ◽  
pp. 538-542 ◽  
Author(s):  
George J. Dohrmann

✓ Adult dogs were rendered hydrocephalic by the injection of kaolin into the cisterna magna. One group of dogs was sacrificed 1 month after kaolin administration, and ventriculojugular shunts were performed on the other group. Hydrocephalic dogs with shunts were sacrificed 1 day or 1 week after the shunting procedure. All dogs were perfused with formalin at physiological pressure, and the brain stem and cervical spinal cord were examined by light microscopy. Subarachnoid granulomata encompassed the superior cervical spinal cord and dependent surface of the brain stem. Rarefaction of the posterior white columns and clefts or cavities involving the gray matter posterior to the central canal and/or posterior white columns were present in the spinal cords of both hydrocephalic and shunted hydrocephalic dogs. Predominantly in the dogs with shunts, hemorrhages were noted in the spinal cord in association with the clefts or cavities. A mechanism of ischemia followed by reflow of blood is postulated to explain the hemorrhages in the spinal cords of hydrocephalic dogs with shunts.


1980 ◽  
Vol 53 (2) ◽  
pp. 252-255 ◽  
Author(s):  
Tung Pui Poon ◽  
Edward J. Arida ◽  
Wolodymyr P. Tyschenko

✓ The authors report a case of cerebral cysticercosis which presented with generalized nonspecific neurological signs and symptoms attributed to acute aqueductal obstruction, with concomitant intracranial hypertension. These were characteristic intracranial calcifications along with angiographically demonstrated signs of hydrocephalus. Contrast encephalography clearly demonstrated aqueductal obstruction. Pathologically, the aqueductal obstruction was shown to be due to parasitic invasion of the brain stem with compression of the aqueduct. The presence of typical intracranial calcification in conjunction with either obstructive or normal-pressure hydrocephalus should alert the observer to the possibility of cerebral cysticercosis.


1990 ◽  
Vol 73 (4) ◽  
pp. 560-564 ◽  
Author(s):  
Daniele Rigamonti ◽  
Robert F. Spetzler ◽  
Marjorie Medina ◽  
Karen Rigamonti ◽  
David S. Geckle ◽  
...  

✓ Although cerebral venous malformations have been reported to cause epilepsy, progressive neurological deficits, and hemorrhage, their clinical significance remains controversial. In an attempt to clarify the natural history of the lesion and suggest an appropriate management strategy, the authors review their experience with 30 patients. In four patients with cerebellar venous angioma, an acute episode of ataxia was documented. The coexistence of a cavernous malformation was pathologically confirmed in the two patients who underwent surgery for bleeding presumed caused by the venous angioma. Infarction was shown in two patients and a tumor in two others. Follow-up periods ranged between 18 and 104 months, with only five patients symptomatic at the time of this report. Rebleeding had not occurred, nor had acute episodes of neurological dysfunction been documented. This clinical experience suggests that a venous malformation is frequently associated with other, more symptomatic conditions and is often erroneously identified as the source of the symptoms. Because the nature of the relationship between the venous malformation and the allied conditions remains ambiguous, it is recommended that patients harboring a “symptomatic” venous malformation undergo high-field magnetic resonance imaging to rule out underlying pathology, and that any such pathology be treated independently of the venous malformation.


1980 ◽  
Vol 53 (6) ◽  
pp. 841-845 ◽  
Author(s):  
Harold P. Smith ◽  
Venkata R. Challa ◽  
Eben Alexander

✓ Cervical spine involvement by rheumatoid arthritis is common; brain-stem compression secondary to vertical subluxation of the odontoid in patients with rheumatoid arthritis is rare. Vertical subluxation results from 1) destruction of the transverse atlantal, apical, and alar ligaments of the atlas and odontoid, and 2) bone resorption in the occipital condyles, lateral masses of the atlas, and basilar processes of the skull. Neurological symptoms result from direct compression of the brain stem or from ischemia secondary to compression of vertebral arteries, anterior spinal arteries, or small perforating arteries of the brain stem and spinal cord. A case is reported in which a slowly progressive neurological deficit developed in a woman with rheumatoid arthritis following a fall from a stretcher. Neurological symptoms represented direct compression of the medulla by the dens, a mechanism confirmed at operation and autopsy. Recognition of progressive neurological deficit is often difficult in patients with rheumatoid arthritis because of their inactivity and their atrophic and immobile joints, but is essential if appropriate decompressive or stabilizing procedures are to be done. In patients with vertical subluxation of the dens, the transoral approach with removal of the odontoid is recommended. Decompression should be extensive, including the fibrous capsule around the odontoid and overlying synovial tissue as well as the odontoid itself.


1989 ◽  
Vol 70 (6) ◽  
pp. 847-852 ◽  
Author(s):  
Douglas Chyatte

✓ Vascular malformations of the brain stem are unusual lesions that may pose a diagnostic and therapeutic challenge. Seven patients with vascular malformations involving the brain stem were evaluated; six were treated surgically, with complete obliteration of the lesion in five patients. In five patients symptoms developed only after a hemorrhage had occurred, and three of these suffered a rebleed before appropriate treatment was given. Angiography failed to demonstrate lesions in three cases, which did not appear to protect from repeat hemorrhage since two of the three rebled. There were no operative deaths, and no patients were made permanently worse after surgery. Useful recovery occurred commonly after appropriate treatment and appeared to be possible even in patients who had suffered a catastrophic neurological deficit at the time of presentation. These data indicate that surgical removal of the lesion may be warranted in some patients with symptomatic brain-stem vascular malformation.


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