|Spinal arteriovenous shunts presenting as intracranial subarachnoid haemorrhage.|
|Jump to Full Text|
|PMID: 17401739 Owner: NLM Status: MEDLINE|
|BACKGROUND: In approximately 5% of patients with intracranial subarachnoid haemorrhage (SAH), the cause is another than a ruptured aneurysm or perimesencephalic haemorrhage. One of these causes is a spinal arteriovenous shunt (SAVS). The aim of this study was to investigate the characteristics of patients with SAVS who present with intracranial SAH without symptoms and signs suggesting a spinal cause.
METHODS: We systematically reviewed the literature and searched the SAH database of the University Medical Center Utrecht, The Netherlands, for patients with SAVS presenting with intracranial SAH and studied the characteristics of patients with SAVS whose clinical presentation mimicked intracranial SAH caused by rupture of a saccular aneurysm.
RESULTS: Thirty-five patients were identified after a review of the literature. In our SAH database, comprising 2142 patients included in the period 1985-2004, we found one patient (0.05%, 95 % CI 0.006- 0.3%). SAH due to SAVS occurred at any age (4-72 years). The SAVS was located at the craniocervical junction in 14 patients, at the cervical level in 11, and at the thoracolumbar level in the remaining 11 patients. The majority of patients (n = 26, 72%) had no disabling deficits at discharge or follow-up.
CONCLUSION: Rupture of a SAVS presenting as intracranial SAH is rare and can occur at any age. The SAVS can be located not only at the craniocervical junction or cervical level but also in the thoracolumbar region. Most patients with SAVS presenting as intracranial SAH have a good recovery.
|J van Beijnum; D C G Straver; G J E Rinkel; C J M Klijn|
Related Documents :
|25326049 - Long-term outcome of epilepsy in patients with prader-willi syndrome.
25336239 - Hba1c levels as predictors of ablation outcome in type 2 diabetes mellitus and paroxysm...
25170669 - Increased rate of positive penicillin skin tests among patients with glioma: insights i...
25245039 - Type x collagen levels are elevated in serum from human osteoarthritis patients and ass...
25458779 - Usefulness of low- and high-volume multiple rapid swallowing during high-resolution man...
25169789 - Ivacaftor and sinonasal pathology in a cystic fibrosis patient with genotype deltaf508/...
11940969 - Seizure elicitation blocked by pretreatment with lidocaine.
12218309 - Experience with the use of an iron polymaltose (dextrin) complex given by single total ...
6607329 - Dosing implications of rapid elimination of trimethoprim-sulfamethoxazole in patients w...
|Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-04-02|
|Title: Journal of neurology Volume: 254 ISSN: 0340-5354 ISO Abbreviation: J. Neurol. Publication Date: 2007 Aug|
|Created Date: 2007-08-31 Completed Date: 2008-02-01 Revised Date: 2013-06-06|
Medline Journal Info:
|Nlm Unique ID: 0423161 Medline TA: J Neurol Country: Germany|
|Languages: eng Pagination: 1044-51 Citation Subset: IM|
|Department of Neurology and Neurosurgery, University Medical Center Utrecht, Utrecht, The Netherlands. email@example.com|
|APA/MLA Format Download EndNote Download BibTex|
Arteriovenous Malformations / complications*
Databases, Factual / statistics & numerical data
Magnetic Resonance Imaging / methods
Spinal Cord Vascular Diseases / complications*
Subarachnoid Hemorrhage / diagnosis, etiology*
Journal ID (nlm-ta): J Neurol
Publisher: Steinkopff-Verlag, Darmstadt
? Steinkopff-Verlag 2007
Received Day: 1 Month: 9 Year: 2006
Accepted Day: 1 Month: 11 Year: 2006
Electronic publication date: Day: 2 Month: 4 Year: 2007
Print publication date: Month: 8 Year: 2007
Volume: 254 Issue: 8
First Page: 1044 Last Page: 1051
PubMed Id: 17401739
Publisher Id: 485
issue-copyright-statement: ? Steinkopff-Verlag 2007
|Spinal arteriovenous shunts presenting as intracranial subarachnoid haemorrhage|
|J. van Beijnum12||
Address: +31-30/2507969 +31-30/2542100 firstname.lastname@example.org
|D. C. G. Straver1|
|G. J. E. Rinkel1|
|C. J. M. Klijn1|
1Dept. of Neurology and Neurosurgery, University Medical Center Utrecht, Utrecht, The Netherlands
2Dept. of Neurology and Neurosurgery, G03.124, University Medical Center Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands
In approximately 15% of patients with intracranial subarachnoid haemorrhage (SAH), the cause of the haemorrhage is another than a ruptured intracranial saccular aneurysm. Two-thirds of these patients, thus comprising 10% of all patients with intracranial SAH, have a non-aneurysmal perimesencephalic haemorrhage. The remaining 5% of intracranial SAH is caused by a variety of rare conditions such as a (transmural) arterial dissection, a cerebral arteriovenous malformation, a cranial dural arteriovenous fistula, a mycotic/septic aneurysm, pituitary apoplexy, cocaine abuse, sickle cell disease, a coagulation disorder or trauma [1, 2]. In addition, spinal arteriovenous shunts (SAVS), in particular if localized in the cervical region, have been reported to present with symptoms and signs suggesting an intracranial cause of the SAH [1, 2].
Most commonly, SAVS present with gradually worsening sensory disturbances, diffuse back and muscle pain, weakness and sphincter disturbances. Acute onset of symptoms is mostly attributed to spinal haemorrhage either into the subarachnoid space or intramedullary and rarely to venous thrombosis [3, 4]. SAVS can be divided into arteriovenous fistulas (AVF) and arteriovenous malformations (AVM). Spinal AVF commonly presents with signs and symptoms of progressive myelopathy. Spinal AVM may also present with pain, acute myelopathy, or radiculopathy . Spinal SAH is reported in approximately half of symptomatic spinal cord AVM [6, 7] and is frequently accompanied by intracranial signs and symptoms .
The aim of this study was to investigate the clinical characteristics and type and location of the SAVS of patients with SAVS who present with symptoms and signs suggesting an intracranial and not a spinal cause of the SAH. We also aimed to assess the proportion of patients with intracranial SAH in whom the cause is a SAVS.
To identify patients with intracranial SAH caused by SAVS we performed a literature search using PubMed (up to December 2005) with the following keywords: spinal arteriovenous malformation(s), spinal arteriovenous shunt(s), spinal vascular malformation(s) and subarachnoid haemorrhage. Additional articles were found by searching the reference lists of relevant articles.
We included all articles reporting patients diagnosed with intracranial SAH caused by a SAVS with extracranial arterial supply, without signs and symptoms directly suggestive of spinal pathology. Patients were included when a diagnosis of intracranial SAH was reported. Preferably the diagnosis was confirmed on CT but patients with confirmation of SAH by cerebrospinal fluid investigation only or patients, in whom the details on how the diagnosis of intracranial SAH was reached were lacking, were not excluded. Articles in languages other than English were excluded.
Two authors (J.v.B, D.C.G.S) independently reviewed and extracted the following data on eligible patients: demographic characteristics, method of diagnosis of SAH, medical history, presenting symptoms, findings at neurological examination on admission, neuro-imaging, angio-architectural features of SAVS, classification of SAVS (according to Spetzler et al. ), treatment, clinical and radiological follow-up (including obliteration after treatment), and clinical outcome, which we aimed to classify according to the Glasgow Outcome Scale (GOS) . In case of disagreement between these two authors, extracted items were reviewed together to reach consensus. If necessary, a third author (C.J.M.K.) resolved the disagreement between the first two authors. The included cases were subdivided into three subgroups: craniocervical junction SAVS (CCJ, between the foramen magnum and C2), cervical SAVS (C3?C8), and thoracolumbar SAVS.
The records of all patients registered in the SAH database of the University Medical Center Utrecht from January 1985 to January 2005 were reviewed to find additional cases. The same inclusion and exclusion criteria as for inclusion of cases reported in the literature were applied. The method of data-extraction was identical to that for the patients reported in the literature.
The data were analyzed using SPSS for Windows, version 12.0.1 (SPSS Inc.). We used the Students T-test to compare mean ages between the different subgroups of patients. We used proportions with corresponding 95% confidence intervals (CI) to assess the estimated prevalence of SAVS among patients registered in our SAH database and to compare clinical and radiological characteristics of the patient subgroups.
The literature search yielded 35 patients reported in 28 articles. In the SAH database, consisting of 2142 patients with SAH in the studied period, we found one patient (0.05%, 95% CI 0.006?0.3%). Of the 2142 patients, 1740 (81.2%) patients were diagnosed with an aneurysmal SAH, 149 (7.0%) with a perimesencephalic haemorrhage, and 130 (6.1%) with another cause, including the one SAVS. In 123 (5.7%) patients no definite cause was identified. All patients underwent four-vessel angiography if CT angiography demonstrated no abnormalities but we have not systematically searched for SAVS by MRI screening in every patient with a negative angiogram.
A summary of the 36 patients with intracranial SAH caused by SAVS is presented in Table 1. In 14 of the 36 patients (39%), the SAVS was located at the CCJ, in 11 patients (30.5%) at the cervical level, and in another 11 (30.5%) at the thoracolumbar level. In only one of the 11 patients with a thoracolumbar SAVS, the malformation was located at the midthoracic level.
Twenty-two patients (61%) were men. Mean age of patients at presentation was 36 years (range 4?72 years). Patients with a SAVS at the CCJ presented at older age than patients with a SAVS in the cervical or thoracolumbar region (mean difference, 33 years; 95% CI 21?44 years; p-value < 0.0001). The delay between the (first) SAH and the diagnosis of a SAVS varied from 0 to 15 years. A delayed diagnosis had occurred mostly in cervical (n = 5; delay of 2?15 years) and thoracolumbar SAVS (n = 4; delay of 2?5 years). Twenty-six patients (72%) had only one episode of SAH, the remaining ten patients had two or more episodes (range 2?12 SAH). In all ten patients with two or more episodes, the diagnosis was made only after a repeated episode. The presenting symptoms, findings on examination, CT findings, and treatment results of all 36 patients are listed in Table 2.
Most patients (n = 27, 75%) presented with headache. In two of the remaining nine patients, no clinical details about the first SAH were reported but these two patients did present with headache after subsequent SAH [19, 22]. In the other seven patients, primarily patients with cervical or thoracolumbar SAVS, there was no information on whether or not patients also had headache at the time of presentation. Two of these seven patients presented with impaired consciousness [28, 32]. In one of them, generalized tonic seizures, abnormal breathing pattern, and bilateral papiledema with retinal haemorrhages were reported . In one other patient, who presented with a mild hemiparesis, CT of the brain showed SAH [27, 29]. The reported signs and symptoms that may have added to the diagnosis of intracranial SAH in another two patients for whom there was no information on the presence or absence of headache, were vomiting and dizziness in one patient  and nuchal rigidity in another . In two patients no further information was available .
A period of unresponsiveness was found in eight patients (22%), three of whom had a thoracolumbar SAVS. Back pain associated with the symptoms and signs suggesting an intracranial cause was found only in patients with a thoracolumbar SAVS; it occurred in four (36%) of the patients with thoracolumbar SAVS. Neck pain was reported in nine patients (25%), four of whom had thoracolumbar SAVS. In eight of these nine patients, the neck pain was associated with headache. In the ninth patient, a 13-year-old boy, acute pain in the neck was the only symptom during the first episode of SAH. At the second episode he also had headache and vomited. At this second episode, a cervical vascular malformation was diagnosed after vertebral angiography . Only one of the 11 patients with a cervical SAVS complained of pain between the shoulder blades after this patient had a second SAH . Two patients (6%) had a history of transient spinal cord signs before the SAH; one of these patients had a transient paraplegia 6 years before SAH, and the other had a history of quadriparesis 11 years before the SAH (diagnosed as Pertussis and Poliomyelitis) [26, 37]. One patient mentioned, after further questioning, difficulty with urination in the year before presentation with a SAH .
Six patients had neurological deficits at the time of the first episode of SAH. A hemiparesis was present in three patients [14, 24, 27]. One patient presented with a weakness of all extremities, but more pronounced on one side . Two patients presented with a mild weakness in one leg only [34, 37]. The sixth patient had a peripheral facial nerve palsy . Papiledema [20, 28] and retinal haemorrhages  were found in three patients (9%). Presence of nuchal rigidity was reported in two patients (18%) with cervical SAVS, in five patients (36%) with CCJ SAVS, and in six patients (55%) with a thoracolumbar SAVS from a total of 15 patients in whom information on the presence or absence of nuchal rigidity was reported.
Seven patients developed neurological deficits after their first SAH but before diagnosis [19, 27, 36]. In four patients, this was after additional episodes of SAH [19, 22]. The signs and symptoms included quadriparesis [19, 27], paraparesis with weakness of one arm , hemiparesis , paresis of one leg , sphincter [22, 27] and sensory [19, 36] disturbances, and decreased unilateral abdominal reflexes .
A brain CT was done in 25 (69%) of the 36 patients, and showed SAH in 17 (47%). Details about the delay between initial symptoms and timing of CT were not mentioned. In 12 patients (34%), the diagnosis of SAH was based upon a positive lumbar puncture. In seven (20%) patients, the diagnostic method was not mentioned. In four of them there was headache or pain in the neck, and in three patients details on the clinical presentation were not given. Six of these seven patients presented with a first episode of SAH in the fifties , sixties  or early seventies  of the last century, when CT scanning was not available. The seventh patient presented with severe headache from SAH, but a four-vessel cerebral angiography showed no abnormalities, and subsequent cervical spinal MRI scan revealed a vascular malformation .
The distribution of blood on the brain CT is summarized in Table 2. Intracranial SAH on CT was frequently seen in CCJ SAVS (in nine of 11 patients in whom a CT was performed), but also in the majority (six of ten patients in whom a CT was performed) of patients with thoracolumbar SAVS and in half of patients with a cervical SAVS (in two of four patients in whom a CT was performed).
In 13 of the 14 patients with a CCJ SAVS cerebral angiography revealed the diagnosis, in the remaining patient after spinal angiography. The diagnosis of a cervical SAVS was made after cerebral angiogram in five of the 11 patients, on a diagnostic laminectomy [19, 27] in three, on spinal MRI in two [20, 21], and after myelography in one patient . Three CCJ SAVS [10, 11, 18] and three cervical SAVS [19, 24, 25] were not diagnosed directly after the first cerebral angiogram because initially not all four cerebropetal vessels were catheterized selectively. Of the 11 patients with thoracolumbar SAVS, seven patients were diagnosed with MRI, two after spinal angiography, and two with myelography.
Patients with a SAVS at the CCJ were treated surgically (86%) or received no treatment to obliterate the SAVS (14%). Embolization was performed only in cervical and thoracolumbar SAVS. Three patients were reported to await treatment and two patients [18, 26] did not receive treatment of the SAVS. Five of the 36 patients (14%) were treated because they developed hydrocephalus. Three patients needed temporary drainage by means of an external ventricular drain [10, 28]. A ventriculoperitoneal drain was placed in one patient . Another patient was treated with acetazolamide to reduce intracranial pressure .
Information on outcome was available for 33 patients. Twenty-six patients (79%; 95% CI 61?91%) made a good recovery (GOS 5), four patients remained moderately disabled (GOS 4), and two patients were severely disabled (GOS 3). One patient died of shuntrelated complications .
This study of 36 patients with SAVS presenting with signs and symptoms suggesting an intracranial cause of SAH showed that intracranial SAH from a SAVS can occur at any age and that the SAVS can be located at any level: at the craniocervical junction, the cervical level and at the thoracolumbar level. Most patients with intracranial SAH from a SAVS have a good recovery.
SAVS have been reported as a rare cause of intracranial SAH. However, mainly patients with cervical SAVS have been described as being indistinguishable from patients with an intracranial source of bleeding [1, 2, 44]. Our search retrieved 11 patients with a thoracolumbar SAVS, emphasizing that SAVS localized at any level of the spinal cord can present with signs and symptoms of intracranial SAH.
We found no SAVS located between the thoracic levels two and eight. Because of the small number of patients included in this study this is most likely due to chance. In general, SAVS frequently occur in the midthoracic region [7, 45]. Dorsal intradural spinal AVF are found mainly in the low thoracic and lumbar regions in contrast to other types of SAVS that are spread more equally along the cord [7, 46, 47]. In this study, two dorsal intradural spinal AVF were located in the thoracolumbar region [28, 30], but in two other patients dorsal intradural spinal AVF were situated in the cervical region [13, 27].
The pathological mechanism of intracranial SAH from a SAVS remains unclarified. The most straightforward mechanism is migration or extension of subarachnoid blood from the spinal to the intracranial level [26, 28, 31]. Haemorrhage may be caused by venous hypertension when arterialized blood flows via the medullary vein to the valveless coronal venous plexus and radial vein [11, 25]. Another hypothesis suggests that the vein around the midbrain is compressed or stretched by the tentorial incisura when, eg., physical exercise elevates the ICP, which then leads to aggravation of venous hypertension with subsequent rupture of the vein . In patients with intracranial drainage of their SAVS, the relatively fast venous flow may cause formation of a varix on the draining vessel, which may result in intracranial SAH after rupture . Ascending venous drainage was associated with an increased risk of SAH in six patients with CCJ perimedullary and dural AVF . In this light, it is not surprising that in patients with SAVS also other cranial symptoms and signs than those suggestive of intracranial SAH caused by rupture of a saccular aneurysm have been reported, such as intermittent double vision, slurred speech, and nystagmus .
A limitation of this study is that in only about half of the reported patients with SAVS presenting with intracranial SAH the diagnosis was confirmed on brain CT. However, in all 36 patients the authors were convinced of the diagnosis of intracranial SAH and at first instance searched for a saccular aneurysm.
It remains questionable whether in patients with SAH without an intracranial source of the haemorrhage SAVS should be searched for, since intracranial SAH caused by SAVS is very rare. Four-vessel angiography can detect a CCJ or cervical SAVS and should always be performed before investigating the spinal cord. MRI screening of the spine in all patients with (repeated) negative angiograms will probably have a low yield and be very expensive. In a cohort of 15 patients with an aneurysmal pattern of SAH and three negative four-vessel angiograms, but no imaging of the spine, no episodes of new episodes of SAH occurred during an average follow-up of 65 months . We suggest that in patients with an intracranial SAH without identifiable cause, close attention should be given to sometimes subtle clues in the history and examination (such as back pain, pain between shoulder blades, and difficulty with urination) that may point to a spinal cause of the SAH. A delayed diagnosis can have negative implications for patients, because they may develop new or progressive neurological deficits that may or may not be related to new episodes of SAH. In patients with multiple episodes of SAH and repeated negative cerebral fourvessel angiograms, further investigations (e.g., MRI) should probably be considered to exclude a SAVS as a rare but possible cause, even in the absence of symptoms or signs of medullary or spinal root involvement. In those rare cases the full length of the spinal cord should be investigated.
C.J.M. Klijn is supported by a clinical fellowship from The Netherlands Organization for Health Research and Development (grant number 907-00-103) and by a grant from the Netherlands Heart Association (grant number 2003B263).
|1..||Rinkel. Stroke 1993;24:1403.|
|1..||Rinkel GJ, van Gijn J, Wijdicks EF (1993) Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. Stroke 24:1403?409 [pmid: 8362440]|
|2..||van Gijn. Brain 2001;124:249. [doi: 10.1093/brain/124.2.249]|
|2..||van Gijn J, Rinkel GJ (2001) Subarachnoid haemorrhage: diagnosis, causes and management. Brain 124:249?78 [pmid: 11157554]|
|3..||Ferch. J Clin Neurosci 2001;8:299. [doi: 10.1054/jocn.2000.0914]|
|3..||Ferch RD, Morgan MK, Sears WR (2001) Spinal arteriovenous malformations: a review with case illustrations. J Clin Neurosci 8:299?04 [pmid: 11437566]|
|4..||Krings. Eur Radiol 2005;15:267. [doi: 10.1007/s00330-004-2510-2]|
|4..||Krings T, Mull M, Gilsbach JM, Thron A (2005) Spinal vascular malformations. Eur Radiol 15:267?78 [pmid: 15538580]|
|5..||Spetzler. J Neurosurg Spine 2002;96:145. [doi: 10.3171/spi.2002.96.2.0145]|
|5..||Spetzler RF, Detwiler PW, Riina HA, Porter RW (2002) Modified classification of spinal cord vascular lesions. J Neurosurg Spine 96:145?56|
|6..||Niimi. Intervent Neuroradiol 2000;6:199.|
|6..||Niimi Y, Berenstein A, Setton A, Pryor J (2000) Symptoms, vascular anatomy and endovascular treatment of spinal cord arteriovenous malformations. Intervent Neuroradiol 6:199?02|
|7..||Rosenblum. J Neurosurg 1987;67:795. [doi: 10.3171/jns.1987.67.6.0795]|
|7..||Rosenblum B, Oldfield EH, Doppman JL, Di Chiro G (1987) Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVM?s in 81 patients. J Neurosurg 67:795?02 [pmid: 3681418]|
|8..||Caroscio. Arch Neurol 1980;37:101.|
|8..||Caroscio JT, Brannan T, Budabin M, Huang YP, Yahr MD (1980) Subarachnoid hemorrhage secondary to spinal arteriovenous malformation and aneurysm. Report of a case and review of the literature. Arch Neurol 37:101?03 [pmid: 7356401]|
|9..||Jennett. Lancet 1975;1:480. [doi: 10.1016/S0140-6736(75)92830-5]|
|9..||Jennett B, Bond M (1975) Assessment of outcome after severe brain damage. Lancet 1:480?84 [pmid: 46957]|
|10..||Aviv. AJNR Am J Neuroradiol 2004;25:854.|
|10..||Aviv RI, Shad A, Tomlinson G, Niemann D, Teddy PJ, Molyneux AJ, Byrne JV (2004) Cervical dural arteriovenous fistulae manifesting as subarachnoid hemorrhage: report of two cases and literature review. AJNR Am J Neuroradiol 25:854?58 [pmid: 15140735]|
|11..||Do. AJNR Am J Neuroradiol 1999;20:348.|
|11..||Do HM, Jensen ME, Cloft HJ, Kallmes DF, Dion JE (1999) Dural arteriovenous fistula of the cervical spine presenting with subarachnoid hemorrhage. AJNR Am J Neuroradiol 20:348?50 [pmid: 10094368]|
|12..||Endo. J Neurosurg Anesthesiol 2001;13:310. [doi: 10.1097/00008506-200110000-00005]|
|12..||Endo T, Sato K, Takahashi T, Kato M (2001) Acute hypotension and bradycardia by medulla oblongata compression in spinal surgery. J Neurosurg Anesthesiol 13:310?13 [pmid: 11733662]|
|13..||Hashimoto. J Clin Neurosci 2000;7:64. [doi: 10.1054/jocn.1998.0145]|
|13..||Hashimoto H, Iida J, Shin Y, Hironaka Y, Sakaki T (2000) Spinal dural arteriovenous fistula with perimesencephalic subarachnoid haemorrhage. J Clin Neurosci 7:64?6 [pmid: 10847656]|
|14..||Hosoda. Neurosurgery 1994;34:748. [doi: 10.1097/00006123-199404000-00029]|
|14..||Hosoda K, Fujita S, Kawaguchi T, Yamada H (1994) A transcondylar approach to the arteriovenous malformation at the ventral cervicomedullary junction: report of three cases. Neurosurgery 34:748?52 [pmid: 8008179]|
|15..||Kai. AJNR Am J Neuroradiol 2005;26:1949.|
|15..||Kai Y, Hamada J, Morioka M, Yano S, Mizuno T, Kuratsu J (2005) Arteriovenous fistulas at the cervicomedullary junction presenting with subarachnoid hemorrhage: six case reports with special reference to the angiographic pattern of venous drainage. AJNR Am J Neuroradiol 26:1949?954 [pmid: 16155140]|
|16..||Kinouchi. J Neurosurg 1998;89:755. [doi: 10.3171/jns.1998.89.5.0755]|
|16..||Kinouchi H, Mizoi K, Takahashi A, Nagamine Y, Koshu K, Yoshimoto T (1998) Dural arteriovenous shunts at the craniocervical junction. J Neurosurg 89:755?61 [pmid: 9817413]|
|17..||Markert. Neurosurgery 1996;38:412. [doi: 10.1097/00006123-199602000-00038]|
|17..||Markert JM, Chandler WF, Deveikis JP, Ross DA (1996) Use of the extreme lateral approach in the surgical treatment of an intradural ventral cervical spinal cord vascular malformation: technical case report. Neurosurgery 38:412?15 [pmid: 8869075]|
|18..||Morris. Radiology 1960;75:785.|
|18..||Morris L (1960) Angioma of the cervical spinal cord. Radiology 75:785?87 [pmid: 13772851]|
|19..||Ya?argil. Surg Neurol 1975;4:211.|
|19..||Ya?argil MG, DeLong WB, Guarnaschelli JJ (1975) Complete microsurgical excision of cervical extramedullary and intramedullary vascular malformations. Surg Neurol 4:211?24 [pmid: 1162593]|
|20..||Bassuk. Neurology 2003;60:1724.|
|20..||Bassuk AG, Burrowes DM, Velimirovic B, Grant J, Keating GF (2003) A child with spinal cord AVM presenting with raised intracranial pressure. Neurology 60:1724?725 [pmid: 12771285]|
|21..||Halbach. Neurosurgery 1993;33:972. [doi: 10.1097/00006123-199312000-00003]|
|21..||Halbach VV, Higashida RT, Dowd CF, Fraser KW, Edwards MS, Barnwell SL (1993) Treatment of giant intradural (perimedullary) arteriovenous fistulas. Neurosurgery 33:972?79 [pmid: 8134010]|
|22..||Henson. Q J Med 1956;25:53.|
|22..||Henson RA, Croft PB (1956) Spontaneous spinal subarachnoid haemorrhage. Q J Med 25:53?6 [pmid: 13323242]|
|23..||Hida. J Neurosurg 2002;96:157.|
|23..||Hida K, Iwasaki Y, Ushikoshi S, Fujimoto S, Seki T, Miyasaka K (2002) Corpectomy: a direct approach to perimedullary arteriovenous fistulas of the anterior cervical spinal cord. J Neurosurg 96:157?61 [pmid: 12450277]|
|24..||H??k. J Neurosurg 1958;15:84. [doi: 10.3171/jns.1958.15.1.0084]|
|24..||H??k O, Lidvall H (1958) Arteriovenous aneurysms of the spinal cord; a report of two cases investigated by vertebral angiography. J Neurosurg 15:84?1 [pmid: 13492078]|
|25..||Morimoto. Neurosurgery 1992;31:118. [doi: 10.1097/00006123-199207000-00017]|
|25..||Morimoto T, Yoshida S, Basugi N (1992) Dural arteriovenous malformation in the cervical spine presenting with subarachnoid hemorrhage: case report. Neurosurgery 31:118?20 [pmid: 1641089]|
|26..||Odom. Clin Neurosurg 1962;8:196.|
|26..||Odom GL (1962) Vascular lesions of the spinal cord: malformations, spinal subarachnoid and extradural hemorrhage. Clin Neurosurg 8:196?36 [pmid: 14481116]|
|27..||Willinsky. Surg Neurol 1990;34:118. [doi: 10.1016/0090-3019(90)90107-Z]|
|27..||Willinsky R, Terbrugge K, Lasjaunias P, Montanera W (1990) The variable presentations of craniocervical and cervical dural arteriovenous malformations. Surg Neurol 34:118?23 [pmid: 2367931]|
|28..||Clark. Clin Pediatr (Phila) 1995;34:281. [doi: 10.1177/000992289503400512]|
|28..||Clark RS, Orr RA, Atkinson CS, Towbin RB, Pang D (1995) Retinal hemorrhages associated with spinal cord arteriovenous malformation. Clin Pediatr (Phila) 34:281?83 [pmid: 7628174]|
|29..||Cogen. J Neurosurg 1983;59:471. [doi: 10.3171/jns.1983.59.3.0471]|
|29..||Cogen P, Stein BM (1983) Spinal cord arteriovenous malformations with significant intramedullary components. J Neurosurg 59:471?78 [pmid: 6886760]|
|30..||Koch. J Neurosurg 2004;100:385.|
|30..||Koch C, Gottschalk S, Giese A (2004) Dural arteriovenous fistula of the lumbar spine presenting with subarachnoid hemorrhage. Case report and review of the literature. J Neurosurg 100:385?91 [pmid: 15070151]|
|31..||Maggioni. Cephalalgia 1995;15:237. [doi: 10.1046/j.1468-2982.1995.015003237.x]|
|31..||Maggioni F, Rossi P, Casson S, Fiore D, Zanchin G (1995) Initially migrainelike manifestation of a ruptured spinal arteriovenous malformation. Cephalalgia 15:237?40 [pmid: 7553815]|
|32..||Mandzia. Childs Nerv Syst 1999;15:80. [doi: 10.1007/s003810050336]|
|32..||Mandzia JL, terBrugge KG, Faughnan ME, Hyland RH (1999) Spinal cord arteriovenous malformations in two patients with hereditary hemorrhagic telangiectasia. Childs Nerv Syst 15:80?3 [pmid: 10230660]|
|33..||Parkinson. J Neurosurg 1977;47:965. [doi: 10.3171/jns.1977.47.6.0965]|
|33..||Parkinson D, West M (1977) Spontaneous subarachnoid hemorrhage first from an intracranial and then from a spinal arteriovenous malformation. Case report. J Neurosurg 47:965?68 [pmid: 925754]|
|34..||Rosenow. Neurosurgery 2000;46:1240. [doi: 10.1097/00006123-200005000-00043]|
|34..||Rosenow J, Rawanduzy A, Weitzner I Jr., Couldwell WT (2000) Type IV spinal arteriovenous malformation in association with familial pulmonary vascular malformations: case report. Neurosurgery 46:1240?244 [pmid: 10807258]|
|35..||van Santbrink. Lancet 2003;361:1766. [doi: 10.1016/S0140-6736(03)13411-3]|
|35..||van Santbrink H, de Witt Hamer PC (2003) Spinal AV malformation. Lancet 361:1766 [pmid: 12781534]|
|36..||Wakai. Childs Nerv Syst 1992;8:347. [doi: 10.1007/BF00296567]|
|36..||Wakai S, Inoh S, Iwanaga H, Nagai M, Sato T, Izumi J (1992) Successful surgical obliteration of a huge intradural arteriovenous fistula of the spinal cord in a child. Childs Nerv Syst 8:347?50 [pmid: 1394283]|
|37..||Williams. J Neurosurg 1991;74:1004. [doi: 10.3171/jns.1922.214.171.1244]|
|37..||Williams FC, Zabramski JM, Spetzler RF, Rekate HL (1991) Anterolateral transthoracic transvertebral resection of an intramedullary spinal arteriovenous malformation. Case report. J Neurosurg 74:1004?008 [pmid: 2033435]|
|38..||Meisel. Neuroradiology 1996;38:490. [doi: 10.1007/BF00607286]|
|38..||Meisel HJ, Lasjaunias P, Brock M (1996) Multiple arteriovenous malformations of the spinal cord in an adolescent: case report. Neuroradiology 38:490?93 [pmid: 8837101]|
|39..||Vates. Neurosurgery 2001;49:457. [doi: 10.1097/00006123-200108000-00038]|
|39..||Vates GE, Quinones-Hinojosa A, Halbach VV, Lawton MT (2001) Conus perimedullary arteriovenous fistula with intracranial drainage: case report. Neurosurgery 49:457?61 [pmid: 11504125]|
|40..||Defreyne. Eur Radiol 1999;9:734. [doi: 10.1007/s003300050745]|
|40..||Defreyne L, Achten E, Vandekerckhove T, Kunnen M (1999) Rupture of a cervical spinal cord arteriovenous malformation: a rare complication of endovascular embolization. Eur Radiol 9:734?37 [pmid: 10354897]|
|41..||Hash. J Neurosurg 1975;43:104. [doi: 10.3171/jns.1975.43.1.0104]|
|41..||Hash CJ, Grossman CB, Shenkin HA (1975) Concurrent intracranial and spinal cord arteriovenous malformations. Case report. J Neurosurg 43:104?07 [pmid: 1141976]|
|42..||Sugiu. Neurosurgery 2001;49:1257. [doi: 10.1097/00006123-200111000-00046]|
|42..||Sugiu K, Meguro T, Nakashiama H, Ohmoto T (2001) Successful embolization of a spinal perimedullary arteriovenous fistula with cellulose acetate polymer solution: technical case report. Neurosurgery 49:1257?260 [pmid: 11846922]|
|43..||Hoffman. Childs Brain 1976;2:317.|
|43..||Hoffman HJ, Mohr G, Kusunoki T (1976) Multiple arteriovenous malformations of spinal cord and brain in a child. Case report. Childs Brain 2:317?24 [pmid: 1022423]|
|44..||Warlow CP, Dennis MS, van Gijn J, Hankey GJ, Sandercock PAG, Bamford JM, Wardlaw JM (2001) What caused this subarachnoid haemorrhage? Stroke: a practical guide to management. Blackwell Science Ltd, Oxford|
|45..||Jellema. J Neurol Neurosurg Psychiatry 2003;74:1438. [doi: 10.1136/jnnp.74.10.1438]|
|45..||Jellema K, Canta LR, Tijssen CC, van Rooij WJ, Koudstaal PJ, van Gijn J (2003) Spinal dural arteriovenous fistulas: clinical features in 80 patients. J Neurol Neurosurg Psychiatry 74:1438?440 [pmid: 14570843]|
|46..||Symon. J Neurosurg 1984;60:238. [doi: 10.3171/jns.1984.60.2.0238]|
|46..||Symon L, Kuyama H, Kendall B (1984) Dural arteriovenous malformations of the spine. Clinical features and surgical results in 55 cases. J Neurosurg 60:238?47 [pmid: 6693950]|
|47..||Ya?argil. Adv Tech Stand Neurosurg 1984;11:61.|
|47..||Ya?argil MG, Symon L, Teddy PJ (1984) Arteriovenous malformations of the spinal cord. Adv Tech Stand Neurosurg 11:61?02 [pmid: 6536268]|
|48..||Ruigrok. Cerebrovasc Dis 2002;14:221. [doi: 10.1159/000065668]|
|48..||Ruigrok YM, Rinkel GJ, van Gijn J (2002) CT patterns and long-term outcome in patients with an aneurysmal type of subarachnoid hemorrhage and repeatedly negative angiograms. Cerebrovasc Dis 14:221?27 [pmid: 12403955]|
|GOS:||Glasgow Outcome Scale|
|SAVS:||Spinal arteriovenous shunt|
Summary of characteristics of 36 patients with intracranial SAH caused by SAVS
|First author (year of publication)||Gender||Age*||n of SAH||Delaya||Location SAVS||Classification SAVS|
|Craniocervical SAVS (n = 14)|
|Aviv (2004) ||M||57||1||No delay||C1||Unknown|
|Do (1999) ||M||50||1||No delay||C1||Unknown|
|Endo (2001) ||M||70||1||No delay||C1||Unknown|
|Hashimoto (2000) ||F||66||1||No delay||C1||Dorsal intradural AVF|
|Hosoda (1994) ||M||69||1||No delay||CCJ||Intramedullary AVM|
|M||59||1||No delay||CCJ||Intramedullary AVM|
|M||70||1||No delay||CCJ||Intramedullary AVM|
|Kai (2005) ||M||54||1||No delay||CCJ||Ventral intradural AVF|
|Kinouchi (1998) ||M||68||1||No delay||C1||Unknown|
|Markert (1996) ||F||72||1||No delay||C1?C2||Ventral intradural AVF|
|Morris (1960) ||M||34||2||No delay||C1?C2||Unknown|
|Ya?argil (1975) ||M||37||1||No delay||C1?C2||Unknown|
|Mean (SD)||56 (14)|
|Cervical SAVS (n = 11)|
|Bassuk (2003) ||F||13||1||No delay||C4||Extra-intradural AVM|
|Halbach (1993) ||F||11||1||No delay||Midcervical||Ventral intradural AVF|
|Henson (1956) ||M||13||2||2||C1?4||Unknown|
|Hida (2002) ||F||62||1||No delay||C5||Ventral intradural AVF|
|H??k (1958) ||F||25||2||9||C4?6||Unknown|
|Morimoto (1992) ||M||61||1||No delay||C5||Unknown|
|Odom(1962) ||F||11||1||No delay||C3?7||Unknown|
|Willinksy (1990) ||M||36||1||No delay||C8||Dorsal intradural AVM|
|Ya?argil (1975) ||M||20||9||15||C3||Unknown|
|Mean (SD)||26 (19)|
|Thoracolumbar SAVS (n = 11)|
|Clark (1995) ||M||4||1||No delay||T9?L2||Dorsal intradural AVF|
|Cogen (1983) ||M||7||3||2||T9?12||Intramedullary AVM|
|Koch (2004) b||F||46||1||No delay||L4||Dorsal intradural AVF|
|Maggioni (1995) ||F||23||1||No delay||T10?12||Intramedullary AVM|
|Mandzia (1999) ||M||9||1||No delay||T12||Conus medullaris AVM|
|Parkinson (1977) c||M||47||2||5||T12||Unknown|
|Rosenow (2000) ||M||27||1||No delay||T10?11||Ventral intradural AVF|
|van Santbrink (2003) ||M||38||1||No delay||L1||Conus medullaris AVM|
|Wakai (1992) ||M||6||2||2||C7?T2||Ventral intradural AVM|
|Williams (1991) ||F||16||4||3||T8||Intramedullary AVM|
|This study (2006)||F||6||1||No delay||T12?L3||Extra-intradural AVM|
|Mean (SD)||21 (17)|
AVF Arteriovenous fistula, AVM Arteriovenous malformation, CCJ Craniocervical junction, F Female, M Male, n Number, SAH Subarachnoid haemorrhage, SAVS Spinal arteriovenous malformation. *With first symptoms of SAH; a Delay between first SAH and diagnosis of SAVS (in years); b In this patient, a posterior communicating artery aneurysm was initially thought to be the cause of her SAH. During the operation, the surgeon was not convinced that the aneurysm had ruptured and caused the symptoms. A subsequent MRI showed a lumbar SAVS surrounded by a subarachnoid blood clot and was confirmed after spinal angiography ; c In this patient, intracranial SAH was first attributed to a temporal AVM. After angiographically confirmed total excision of the AVM, the patient presented with another intracranial SAH 4 years later. Four-vessel angiography revealed no intracranial vascular malformation but a subsequent myelogram demonstrated a thoracolumbar SAVS . Eight patients presenting with SAH due to a SAVS were not included in this table because of symptoms that at first presentation immediately indicated a cause with spinal location: presentation with a paraparesis [38, 39], quadriparesis, and sensory disturbances below the midcervical level within a few hours after sudden severe headache [19, 40], and back pain as predominant clinical symptom [41, 42]. An additional patient was diagnosed with a spinal AVM in 1967 when he presented with a bilateral foot drop, increased lower extremity deep tendon reflexes with extensor plantar responses, and a sensory impairment below T8 level. Five years later, a cerebral AVM and a large cervical AVM were diagnosed on angiography after he presented with a two-month history of headaches and right leg pain. After another two years, he presented with an acute SAH that could be attributed to either AVM 
Clinical characteristics, diagnostic tests, and treatment in 36 patients presenting with SAH due to SAVS
|All patients||CCJ SAVS||Cervical SAVS||Thoracolumber SAVS|
|n = 36||%||n = 14 Present||Absent||Unknown||n = 11 Present||Absent||Unknown||n = 11 Present||Absent||Unknown|
|Focal neurological deficit||6a||17a||1||8||5a||3||3||5a||2||5||4|
|Performed||25||69%||11||3 NA||?||4||6 NA||1||10||1 NA||?|
|Blood distribution (CT)|
|SAH, not specified||6||17||3||1||2|
|Embolization and surgery||3||8||?||1||2|
|Results treatment SAVS||n = 31|
*CCJ Craniocervical junction, NA, Not available, SAH Subarachnoid haemorrhage, SAVS Spinal arteriovenous malformation, *At first presentation, aFor three patients details of their first SAH were not described but information about subsequent SAH were documented [19, 22]
Keywords: Key words subarachnoid haemorrhage, spinal arteriovenous shunt.
Previous Document: Does freezing in Parkinson's disease change limb coordination? A kinematic analysis.
Next Document: Spread of primary dystonia in relation to initially affected region.