Biomedical subjects
Publications and source records attributed to G Rodesch.
CASE REPORT: We report the case of a nine-year-old child with a cervical medullary arteriovenous malformation (AVM), revealed by total paraplegia, whose regression started during steroid therapy, before embolization. CONCLUSION: The frequency of AVM's spontaneous favorable outcome is unknown but should not be underestimated. It might be improved by steroids.
OBJECTIVE: The standard categorization of arteriovenous malformations (AVMs) involves the Spetzler-Martin grading system, which uses a simple analysis of size, location (superficial or deep), and the presence of deep or superficial drainage. Hemodynamic risk factors are also thought to play important roles in the pathogenesis of these lesions and to be associated with the intracranial hemorrhage (ICH) rate. The actual hemodynamic factors for AVMs cannot be easily measured, but angioarchitectural features can be assessed and used as surrogate parameters. METHODS: The AVM angioarchitectural features for 662 patients were analyzed, and their associations with ICH as a presenting sign were studied. A cross-sectional analysis was used to qualify the strength of associations among clinical features, angioarchitectural characteristics, and ICH before treatment. RESULTS: The multivariate analysis indicated that arterial stenosis and arterial ectasia were associated with lower ICH rates, whereas venous stenosis increased the rate of ICH. The presence of angiogenesis modified the effects of arterial and venous stenosis. Furthermore, the effect of venous stenosis depended on the location of the nidus. The presented data do not support a direct positive association between associated aneurysms and ICH. CONCLUSION: Certain angiographic features seem to have prognostic potential with respect to the occurrence of ICH among patients with AVMs. A discriminatory prognostic index is proposed; its relevance must be proven in a future prospective study.
OBJECTIVE: Spontaneous intracranial hemorrhage is the primary danger for patients with cerebral arteriovenous malformations (AVMs). Associated aneurysms are considered weak points that increase the risk of intracranial hemorrhage. Aneurysms are classified as proximal aneurysms (PROXs) or intranidal aneurysms (INs). METHODS: The present study was based on a series of 662 patients who presented with AVMs between 1985 and 1995. Its purpose was to evaluate prestated hypotheses using prospectively collected data. In 305 of these 662 patients, 372 INs and 313 PROXs were observed and analyzed with respect to their shapes, locations, and sizes. Partial targeted endovascular treatment with n-butylcyanoacrylate was performed for 450 of the 662 patients (68%) in this series, using a standard protocol. Of 450 treated patients, 181 (40%) had at least one IN and 138 (30.7%) had at least one PROX. Analysis of changes in the sizes of PROXs was based on the follow-up data for 83 treated patients, with a total of 149 PROXs. Changes in the sizes of PROXs in treated patients were analyzed with respect to PROX shapes, PROX locations, and treated AVM occlusion rates. Univariate and multivariate event data analyses were used to study factors influencing aneurysm shrinkage. False aneurysms were excluded from the series. RESULTS: Presentation with intracranial hemorrhage was not correlated with any type of aneurysm. However, INs demonstrated a higher rebleeding rate (P < 0.002) before treatment. Among 181 patients, 92.2% of INs were occluded, together with the related portions of the AVM nidi. In cases of PROXs, embolization of the cerebral AVM compartment fed by the artery with the aneurysm was a priority. During follow-up monitoring of 83 treated patients with 149 PROXs, 100% shrinkage was observed for 12 PROXs and more than 50% shrinkage was observed for 33 PROXs. The median time required for more than 50% shrinkage was 3.5 years. The shrinkage of PROXs was influenced by the degree of AVM occlusion (P = 0.027) and occurred faster for PROXs on midline structures, such as the anterior cerebral artery and the circle of Willis, compared with arteries distal to the circle of Willis (P = 0.004). No rupture of untreated PROXs was observed after partial targeted treatment of AVMs. CONCLUSION: PROXs are not primary treatment targets, compared with AVMs themselves. INs should be primary targets of endovascular therapy, because of their increased risk of rebleeding.
PURPOSE: To assess the clinical utility and accuracy of contrast material-enhanced dynamic three-dimensional (3D) T1-weighted magnetic resonance (MR) angiography in the detection of unruptured intracranial aneurysms. MATERIALS AND METHODS: A prospective blinded comparison of 3D contrast-enhanced T1-weighted MR angiography with 3D inflow magnetization transfer and tilted optimized nonsaturating excitation (MT TONE) imaging, phase-contrast MR angiography, and conventional digital subtraction angiography (DSA) was performed in 32 consecutive patients. The first dynamic 3D contrast-enhanced T1-weighted acquisition was individually timed after injection of a bolus of gadolinium-based contrast agent to obtain an arterial phase image followed by two sequential venous phase images (three 18-second acquisitions). Two readers independently interpreted and graded the MR images for diagnostic confidence and depiction of aneurysms and subsequently compared them with DSA images. RESULTS: Three-dimensional contrast-enhanced T1-weighted MR angiograms depicted all 23 aneurysms detected in 17 patients at DSA (mean size, 6 mm; range, 2-21 mm) with one false-positive result by one reader (sensitivity, 100%; specificity, 94%). MT TONE and phase-contrast images failed to depict one and seven aneurysms, respectively (MT TONE sensitivity of 96% and specificity of 100%, phase-contrast sensitivity of 70% and specificity of 100%). Aneurysm depiction at 3D contrast-enhanced T1-weighted MR angiography was significantly better than that at MT TONE imaging (P <.012), and that with both was significantly superior to that of phase-contrast imaging (P <. 001). Differences in diagnostic confidence in the presence of an aneurysm were not significant between 3D contrast-enhanced T1-weighted and MT TONE imaging (P =.076). CONCLUSION: Dynamic 3D contrast-enhanced T1-weighted MR angiography is a fast, efficient, and minimally invasive imaging method with which to diagnose intracranial aneurysms.
We report an unusual case of ophthalmoplegia after maxillofacial surgery. A thirteen year old girl with unilateral left cleft lip and palate underwent maxillary advancement by distraction osteogenesis. Postoperatively she developed diplopia. The diplopia was not due to orbital lesions, most often seen after maxillofacial surgery, but to a haemorrhage posterior to the cavernous sinus.
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PURPOSE: To analyze arteriovenous malformations (AVMs) of maxillo-mandibular arcades seen in our department since 1977, and to determine adequate treatment. MATERIAL AND METHODS: Fourteen AVMs were reviewed to determine their revelation, their semiology, the treatment applied and the results that could be obtained. All these lesions were true AV shunts involving bone with or without soft tissue extension. RESULTS: Eight patients belonged to the pediatric population. Six lesions were maxillary and 8 mandibular. All lesions were revealed during or after puberty by local swelling, pain, mass effect or bruit. Hemorrhage was the most frequent (71%) symptom. Teeth instability was detected in all these patients and was origin of the bleeding. The lesions were suspected clinically and confirmed radiologically. Angiography analyzed properly the architecture of the lesion (4 arteriovenous fistulas). Embolization was the clinical treatment in all patients: particles helped to stabilize the acute situations but failed to offer stable results, necessitating complementary embolizations and/or surgery (hemimandibulectomy in 2 patients). The use of acrylic glue (Histoacryl), injected percutaneously (5 patients), or transarterially in the AVM (4 patients)) provided cure in 6 of these lesions (43%) and long term stabilization for all the other AVMs. Teeth extraction could be performed thereafter in good conditions. Antibiotics and anti-inflammatory treatment helped to stabilize the evolutive risk of these lesions. CONCLUSION: Embolization is the therapy of choice in these lesions. Appropriate use of glue offers a high rate of cure and/or clinical stabilizations and avoids unneeded surgery.
We studied three patients with aneurysmal malformations of the vein of Galen: all underwent embolisation followed by MRI and conventional angiography; two also underwent postembolisation magnetic resonance angiography (MRA). MRI was performed before treatment in two patients, MRA in only one, diagnosed prenatally. Two patients had normal appearances on follow-up MR studies and were completely cured by embolisation. However, the last patient, after two embolisations, despite the stabilisation of the clinical condition, underwent surgery and died. We think MRI is mandatory before endoarterial treatment, to assess the conditions of the brain. Angiography is mandatory only at the time of endovascular treatment, while MRA and MRI have a role in follow-up. Endoarterial embolisation remains the treatment of choice, and surgery is not advisable.
Twelve arteriovenous malformations of the dental arcades (AVMDAs) (seven mandibular and five maxillary) were seen in our institution between 1977 and 1997. All these lesions consisted of true arteriovenous shunts (of either nidus or fistulous type) involving the bone, with or without soft tissue extension. Haemorrhage was present in eight patients (67%); either torrential, necessitating emergency embolization, or recurrent and progressive. Teeth instability was detected in all patients and was the origin of the bleeding. All lesions were embolized. Lesions in nine patients were embolized with Polyvinyl Alcohol Particles (PVA): this helped to stabilize the situation but could not avoid recurrences in all patients, necessitating complementary embolizations and or surgery. The use of acrylic glue (N-Butyl-Cyano-Acrylate [NBCA] Histoacryl) as the embolic agent has changed the results obtained tremendously. Eight patients have been treated with NBCA (five as complementary therapy to PVA during later sessions and three at the first attempt); injection either via the transarterial route or direct transcutaneous puncture (four patients) achieved a cure in four of these lesions (34%) with stability at long-term follow-up of all the other AVMs. Embolization with glue represents the therapy of choice in these sometimes life-threatening lesions, achieving a cure if directed towards the osseous venous lakes. Surgery, often leading to facial mutilation and necessitating massive reconstruction should be avoided nowadays, at least as the initial therapy.
Repeated clinical evaluation and cerebral arteriography during the evolution of ischemic strokes of idiopathic origin allowed us to characterize a transient cerebral arteriopathy. We retrospectively studied the clinical characteristics, course, and neuroimaging features of this disorder in nine children. Of 34 children with ischemic strokes seen consecutively between 1984 and 1995, 9 (26%) were diagnosed as having transient attack of the cerebral arterial wall, termed transient cerebral arteriopathy. All of these patients had previously been in good health. The mean age at the time of the first stroke was 6 years (range, 2 9/12 years to 13 4/12 years). All children presented with acute hemiplegia. A recurrence of the stroke took place 3 months at the latest after the initial infarct in three children (mean clinical follow-up 2 7/12 years). Cerebral imaging in all the patients showed small subcortical infarcts located in basal ganglia or internal capsule. Arteriography revealed multifocal lesions of the arterial wall (focal stenosis or segmental narrowing), mostly located in the initial parts of basal arteries of the carotid system. Longitudinal arteriographic follow-up showed initial worsening of these arterial lesions (n = 5) for a maximum duration of 7 months followed by complete regression (n = 2), improvement (n = 5), or stabilization of the lesions (n = 2). Five patients had a complete clinical recovery. Further studies are necessary to confirm a presumed inflammatory cause of this arteriopathy.
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We report a case of giant single-hole direct arteriovenous fistula (AVF) located in the posterior fossa of a child with Rendu-Osler-Weber disease (ROW). There is neither a clinical nor an angioarchitectural difference between AVFs associated with ROW and sporadic AVFs, but ROW should be suspected in children with multifocal pial AVFs. Transarterial embolization was performed to obliterate the AVF in a unique procedure using simultaneous bifemoral catheterization. At follow up 4 years later, the clinical examination was normal. Control MR scans and angiography showed the total occlusion of the fistula, permanent thrombosis of the venous pouch, and disappearance of the abnormal venous drainage. In this case, the endovascular procedure was available and we estimated that it represented a lesser risk than the surgical approach (risk of hemorrhage and risk of thrombosis involving the feeding arteries and the brain stem venous drainage). Furthermore, it avoids craniotomy and reduces the duration of hospitalization.
We report 28 patients with nonsurgical intracranial aneurysms referred by neurosurgeons for endovascular treatment using platinum detachable coils (GDC, Target Therapeutics, Fremont, Calif., USA). Because of unfavourable anatomical features or failed hyperselective catheterisation, 4 patients were not treated. In the other 24 patients (26 aneurysms) embolisation was successful. No manufacturing defect was detected in the coils used. Complete occlusion of the sac was obtained in 22 of the 26 aneurysms (85%) regardless of their size. The glasgow outcome score was good on discharge in 20 of the 24 patients (83%). The Karnovski score at 3 months after embolisation revealed that 20 patients (83%) lead a normal life, with minor neurological signs. Morbidity related directly to treatment occurred in 2 cases (8%): a superior hemianopia due to mass effect on the optic nerve from a carotid-ophthalmic aneurysm, and hemiparesis due to an embolus. Five transient deficits lasting hours to a few days were related to proven or suspected emboli. No death occurred. Anatomical, technical and clinical data are reported; the mean cost of materials (catheters and coils) per patient and aneurysm was FF 13,500. The mean hospitalisation time was 6.5 days in the neurosurgical department with 2.8 days of intensive care.
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We present 26 consecutive cases of nongalenic pial arteriovenous malformations (PAVMs) diagnosed in the neonatal period or in infancy. No diagnosis was made antenatally. Presenting symptoms in neonates were systemic cardiac manifestations (54%), seizures (31%), and hemorrhages (15%). In infants, hemorrhagic strokes and hydrodynamic disorders (external or internal hydrocephaly, macrocephaly, atrophy) both occurred in 38% of cases. Systemic cardiac manifestations and seizures were rare at that age (respectively 16% and 8%). Sixty-two percent of neonates and 31% of infants already had neurocognitive disorders (assessed by pediatric neurocognitive testing: Brunet-Leizine and Denver tests) when referred. The venous drainage and its anomalies (ectasias, stenoses, thromboses) were the main causes of symptoms. Atrophy and leukomalacic lesions occurred rapidly; they express local hydrovenous disorders and are specific to this population group. Untreated neonates and infants have a poor prognosis. Endovascular treatment, although partial and challenging in all instances, represents the treatment of choice in our series. Of the eight neonates treated, one improved to normal (12.5%), while four remained stable (50%): two neurologically normal, two with mild neurological deficit. Three (37%) died despite embolization (heart failure, multiorgan failure, postoperative death). Transient neurological complications occurred in two cases (25%): hemiparesis in one patient with a rolandic and in one with a thalamic AVM. Of the eight infants successfully embolized, one was significantly improved (12.5%) and is now neurologically normal, while five remained stable (62.5%): four neurologically normal, one with mild neurological deficit. One died between two sessions of embolization from intracerebral hemorrhage (12.5%). Hemianopsy occurred in one case (12.5%) after embolization of an occipital AVM. In one additional case in a normal child we failed to embolize the last small pial AVM of four after the three others had spontaneously thrombosed. With a minimal follow-up of 18 months and a maximum of 7 years, the review of our series shows 53% of the initial group of neonates and infants growing neurologically normal after therapeutic management in our institution; 23.5% died despite treatment, and the remaining 23.5% present minor neurological deficit. When targeted at the points of angioarchitectural weakness, embolization contributes to stabilizing a lesion. It should be undertaken rapidly to avoid loss of brain substance secondary to hemorrhage, atrophy, or leukomalacia, and to allow neurocognitive recovery and normal brain maturation. In our experience, these lesions are the most aggressive ones for the maturing brain, and the most difficult to approach technically. They represent a new therapeutic field and have their own specific anatomy and physiology.
Over the past 10 years (1982-1992), we have been actively involved in the management of 179 cerebral arteriovenous malformations (CAVMs) in children and infants. Seventy-seven were true vein of Galen malformations (VGAMs) and 102 were pial AVMs (PAVMs), i.e., developed in the subpial space. Hemorrhage occurred as the first symptom in 50% of the children with pial AVMs, but was present in none of the VGAM cases. Only 31 children were found to be unsuitable for endovascular treatment, and in 124 cases embolization was indicated as the primary treatment (104 embolization performed). Only 21 children underwent a direct surgical approach (none in the VGAM group). In the embolized group in whom treatment has been completed (n = 56), 8 children died, 39 have an anatomical cure, and 34 are clinically normal. In the group under treatment (n = 48), 16 are not normal. The problems are timing and the aims (total or partial treatment) of the therapeutic procedures. In the nonembolized group (n = 31), 8/13 of the pial lesions were operated on (no mortality, 2 patients with moderate neurological deficits). In the VGAM group 13/18 died and 4 had spontaneous thrombosis (only 1 is neurologically normal). In the nonembolized group 13 lesions have been completely excluded, but only 5 patients are neurologically normal. This fact again stresses the need for prognostic evaluation before treatment and a clear definition of the treatment aims. Analysis of a large number of published series on the management of children with AVMs (1017 cases) reveals inconsistencies that hamper proper evaluation and comparison. In our experience, endovascular treatment always seems to be the best primary treatment in both VGAMs and PAVMs. However, management of children with these lesions requires a large multidisciplinary team, which is the only way of offering the most suitable and effective treatment, the sole guarantee of a good result.
We present four cases of pial arteriovenous fistula (AVF) in children as the presenting manifestation of Rendu-Osler-Weber disease (ROW). The common clinical manifestations of ROW in adults, such as skin telangiectasia and mucosal haemorrhagic complications, seldom occur in children, since telangiectases develop with age. Pial AVF in ROW also conform to the usual age incidence and are therefore present in childhood. Of the four children in this series, three had multiple AVF. Two presented with central nervous system haemorrhage, one with seizures and the other with progressive neurological deficit. There were no clinical or angioarchitectural differences between the AVF associated with ROW and sporadic AVF. The diagnosis was based in all cases on the family history. Transarterial embolisation to obliterate the AVF was carried out in all patients. One patient had early rebleeding after partial embolisation of the AVF, with a fatal outcome. Three patients were cured and one asymptomatic in long-term follow up. No exhaustive search was conducted for multiorgan telangiectases, since there is no indication for treatment of asymptomatic telangiectasia in ROW. No pulmonary fistulae were found. ROW should be suspected in children with multiple pial AVF; they may be the only manifestation of the disease, since epistaxis and telangiectasia are unusual in early life.
The authors present three cases of vein of Galen aneurysmal malformations (VGAMs) diagnosed in infancy and submitted by the referring teams for stereotactic radiosurgery as the initial therapy (therapeutic doses ranging between 20-25 Gy and 40-50 Gy to the peak dose). After the conventional follow-up of 18-24 months, no change could be detected in the angioarchitecture of the lesions. All three cases were then referred for endovascular treatment and underwent embolization by the transarterial route using liquid adhesives (N-butyl cyanoacrylate). This resulted in complete anatomical exclusion of the lesion. Regardless of the theoretical efficiency of radiosurgery in the management of brain arteriovenous malformations, the present authors believe that transarterial embolization remains the treatment of choice in VGAMs. It offers a high rate of morphological cure and the best chances for normal neurocognitive development. The time required by radiosurgery to achieve a significant result is too long for developing and maturing brain and may not prevent the negative effects of the lesion, mainly in regard to hemo- and hydrodynamic disorders (atrophy, subcortical calcifications, etc.) created by the VGAM, thus leading to irreversible mental retardation.