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Joseph M. Zabramski, Thomas M. Wascher, Robert F. Spetzler, Blake Johnson, John Golfinos, Burton P. Drayer, Ben Brown, Daniel Rigamonti and Geraldine Brown

✓ Cavernous malformations are congenital abnormalities of the cerebral vessels that affect 0.5% to 0.7% of the population. They occur in two forms: a sporadic form characterized by isolated lesions, and a familial form characterized by multiple lesions with an autosomal dominant mode of inheritance. The management of patients with cavernous malformations, particularly those with the familial form of the disease, remains a challenge because little is known regarding the natural history.

The authors report the results of an ongoing study in which six families afflicted by familial cavernous malformations have been prospectively followed with serial interviews, physical examinations, and magnetic resonance (MR) imaging at 6- to 12-month intervals. A total of 59 members of these six families were screened for protocol enrollment; 31 (53%) had MR evidence of familial cavernous malformations. Nineteen (61%) of these 31 patients were symptomatic, with seizures in 12 (39%), recurrent headaches in 16 (52%), focal sensory/motor deficits in three (10%), and visual field deficits in two (6%). Twenty-one of these 31 patients underwent at least two serial clinical and MR imaging examinations. A total of 128 individual cavernous malformations (mean 6.5 ± 3.8 lesions/patient) were identified and followed radiographically. During a mean follow-up period of 2.2 years (range 1 to 5.5 years), serial MR images demonstrated 17 new lesions in six (29%) of the 21 patients; 13 lesions (10%) showed changes in signal characteristics, and five lesions (3.9%) changed significantly in size. The incidence of symptomatic hemorrhage was 1.1% per lesion per year.

The results of this study demonstrate that the familial form of cavernous malformations is a dynamic disease; serial MR images revealed changes in the number, size, and imaging characteristics of lesions consistent with acute or resolving hemorrhage. It is believed that the de novo development of new lesions in this disease has not been previously reported. These findings suggest that patients with familial cavernous malformations require careful follow-up monitoring, and that significant changes in neurological symptoms warrant repeat MR imaging. Surgery should be considered only for lesions that produce repetitive or progressive symptoms. Prophylactic resection of asymptomatic lesions does not appear to be indicated.

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Berndt P. Schmit, Patricia E. Burrows, Karl Kuban, Liliana Goumnerova and R. Michael Scott

supplying an arteriovenous malformation in the left parietal lobe. Right: Left vertebral arteriogram, lateral projection, early-venous phase, demonstrating early opacification of the vein of Trolard, which was not visible on the angiograms obtained when the patient was 3 years old. Discussion This remarkable case documents the de novo development of a cerebral AVM in the exact location of a previous infarct in a child with moyamoya disease. No other published case of an acquired cerebral AVM is known to these authors. As cerebral infarction is common

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J. Nozipo Maraire, Saleem I. Abdulrauf, Scott Berger, Jonathan Knisely and Issam A. Awad

✓ Analysis of recent reports has suggested that cavernous malformations (CMs) of the brain may have an acquired pathogenesis and a dynamic pathophysiological composition, with documented appearance of new lesions in familial cases and following radiotherapy. The authors report the first case of demonstrated de novo formation of an intramedullary CM following spinal radiation therapy.

A 17 year-old boy presented with diabetes insipidus and delayed puberty. Evaluation of endocrine levels revealed hypopituitarism, and magnetic resonance (MR) imaging demonstrated an infundibular mass. The patient underwent a pterional craniotomy and removal of an infundibular germinoma. The MR image of the spine demonstrated normal results. The patient received craniospinal radiation therapy and did well. He presented 5 years later with acute onset of back pain, lower-extremity weakness and numbness, and difficulty with urination. An MR image obtained of the spine revealed an intramedullary T-7 lesion; its signal characteristics were consistent with a CM.

The patient was initially managed conservatively but developed progressive myelopathy and partial Brown—Séquard syndrome. Although he received high-dose steroids and bed rest, his symptoms worsened. He underwent a costotransversectomy and excision of a hemorrhagic vascular lesion via an anterolateral myelotomy. Pathological examination confirmed features of a CM. The patient has done well and was walking without assistance within 4 weeks of surgery.

De novo genesis of CMs may be associated with prior radiation therapy to the spinal cord.

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child with neurofibromatosis Type 2 Paul D. Sawin Nicholas Theodore Harold L. Rekate April 1999 90 2 231 233 10.3171/spi.1999.90.2.0231 De novo development of a cavernous malformation of the spinal cord following spinal axis radiation J. Nozipo Maraire Saleem I. Abdulrauf Scott Berger Jonathan Knisely Issam A. Awad April 1999 90 2 234 238 10.3171/spi.1999.90.2.0234 Lobular capillary hemangioma of the cauda equina Robert N. N. Holtzman Paul M. Brisson Richard E. Pearl Michael L. Gruber

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Carlos A. David, A. Giancarlo Vishteh, Robert F. Spetzler, Michael Lemole, Michael T. Lawton and Shahram Partovi

novo development of an aneurysm: case report. Neurosurgery 29 : 756 – 759 , 1991 Koeleveld RF, Heilman CB, Klucznik RP, et al: De novo development of an aneurysm: case report. Neurosurgery 29: 756–759, 1991 9. Lin T , Fox AJ , Drake CG : Regrowth of aneurysm sacs from residual neck following aneurysm clipping. J Neurosurg 70 : 556 – 560 , 1989 Lin T, Fox AJ, Drake CG: Regrowth of aneurysm sacs from residual neck following aneurysm clipping. J Neurosurg 70: 556–560, 1989 10. Macdonald RL , Wallace MC , Kestle JRW : Role of angiography

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Wolfgang Dietrich, Andrea Reinprecht, Andreas Gruber and Thomas Czech

7782 CA angiograms, Huber and colleagues 6 observed only 17 cases (0.2%) of a large unpaired pericallosal trunk dividing into two vessels close to the genu corporis callosi. The anomaly of a large unpaired pericallosal trunk is closely associated with saccular aneurysms. Some authors postulate that, in spite of the low incidence of the anomaly, aneurysms of the bifurcation of an APCA represent a large number of all pericallosal artery aneurysms, varying between 13.6% and 25.9%, according to different investigators. 6, 11 De novo development of saccular aneurysms of

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Jonathan A. Friedman, Bruce E. Pollock and Douglas A. Nichols

novo development of the AVM in this case is local venous hypertension secondary to the adjacent DAVF. 18 In addition to the possible role of local angiogenic factors, chronic venous hypertension may have dilated the venous end of parenchymal capillaries, ultimately causing ectatic dilation of the entire capillary network and precipitating direct arteriovenous connections. This is analogous to the formation of mucosal AVMs in the gastrointestinal tract, which are thought to occur by a similar mechanism. 6 It has been suggested previously that both cerebral AVMs and

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Siviero Agazzi, Luca Regli, Antoine Uske, Philippe Maeder and Nicolas de Tribolet

DVAs. The role of thrombosis in a DVA would be to induce fistulization, as occurs in dural sinus thrombosis and development of dural fistulae. Although fistulized DVAs are not always explicitly called AVMs, several authors 1, 2, 9, 11, 22 believe that such lesions are at greater risk to develop complications than classic DVAs, and that their natural history resembles that of classic AVMs. The implication of DVAs in the development of AVMs has also been indicated by Nussbaum and associates, 22 based on an observation of de novo development of several AVMs close to

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Aatif M. Husain, Melissa Mendez and Allan H. Friedman

histological obliteration of her AVM would also be the same. 11 The cause of this patient's seizures remains uncertain. The possibilities include de novo development of intractable epilepsy or a delayed effect of GKS. Although de novo development of intractable temporal lobe epilepsy is possible, it would be very unusual for it to arise during the fourth decade of life. It is possible that delayed effects of GKS could result in such a syndrome. Delayed injury and destruction to areas near the radiosurgical target site have been demonstrated. Sheline, et al., 12 showed

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Takao Yasuhara, Takashi Tamiya, Kenji Sugiu, Satoshi Inoue and Takashi Ohmoto

– 475 , 1997 Kanemoto Y, Hisanaga M, Bessho H: De novo vertebral artery-posterior inferior cerebellar artery aneurysm: a case report. Surg Neurol 47: 473–475, 1997 11. Koeleveld RF , Heilman CB , Klucznik RP , et al : De novo development of an aneurysm: case report. Neurosurgery 29 : 756 – 759 , 1991 Koeleveld RF, Heilman CB, Klucznik RP, et al: De novo development of an aneurysm: case report. Neurosurgery 29: 756–759, 1991 12. Lebland R : De novo formation of familial cerebral aneurysms