Dural arteriovenous fistula causing complex visual hallucinations without an anopsia

Back to table of contents Previous article Next article LettersFull AccessComplex Visual Hallucinations, Presumably Due to Subarachnoid Hemorrhage, Treated Successfully With RisperidoneDavid R. Spiegel, M.D., and Tim Petersen, M.D.David R. SpiegelSearch for more papers by this author, M.D., and Tim PetersenSearch for more papers by this author, M.D.Published Online:1 Jul 2011AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Visual hallucinations have several known nonpsychiatric etiologies and may be treated accordingly. We present, with interest, a case of a 56-year-old woman who developed complex visual hallucinations (CVH) status post-cerebrovascular accident (CVA) in her right middle cerebral artery (MCA) distribution. The hallucinations appear to have been successfully treated with risperidone.Case ReportOur patient is a 56-year-old, right-handed woman who presented with a large right-MCA aneurysm and several small left-MCA aneurysms. Her right-MCA aneurysm was successfully surgically repaired; no operative intervention was required for the left aneurysms. In addition to transient sensory and motor deficits, her son noted that after the surgery she would report seeing a woman and a black cat. She had no previous visual dysfunction, although, interestingly, her insight into the CVH improved even before medication treatment. Our patient returned 3 weeks later with new hemorrhages in her right-MCA area, with ischemia. No new surgeries were performed, and her condition stabilized after 1 week with appropriate medical intervention. During this admission, her CVHs persisted, and the authors were consulted because of her “behavioral disturbances.” There was no apparent association between the hallucinations and sleep or time of day. There were no reports of complex partial or generalized seizures. Per her son's report, she had no previous history of psychiatric illness, visual hallucinations, or auditory hallucinations. She had no history of substance abuse. She did not have fluctuating awareness or alertness; she had a Richmond Agitation And Sedation Scale score of 0 and 26/30 on the Mini-Mental State Exam. Risperidone 1.5 mg/day was prescribed in an attempt to treat her CVHs, which resolved within 7 days of initiating treatment.DiscussionAlthough the etiologies for CVHs have been reviewed elsewhere,1 our patient's phenomenology merits a discussion of delineating between Charles-Bonnet syndrome secondary to cortical stroke. With respect to the latter, CVHs may develop secondary to activated occipital cortical regions adjacent to stroke-damaged areas with associated visual field deficits,2 whereas stroke is generally regarded as a condition in which decreased afferent input that yields CVHs of a particular quality (straight ahead, colored, people, insight), although it also occurs in patients with visual-field defects and normal central acuity.3 The theories proposed to explain the etiology of both conditions fall into two categories. The “deafferentation” theory proposes that the lack of visual sensory input into the cortex causes spontaneous neuronal discharge leading to abnormal visual perceptions not unlike the phantom-limb syndrome. The second, “perceptual release” theory, is based on the premise that a normal sensory input inhibits irrelevant impulses from the conscious perception of images. Where there is a reduction in sensory input, the threshold to suppress irrelevant images cannot be achieved, and previously subconscious perceptions are “released” into consciousness, resulting in CVHs.4Risperidone has potent serotonin type-2 receptor antagonism and has been suggested by some authors to have efficacy in treatment of CVH through the blockade of such receptors in the visual cortex.5EVMS Dept. Of Psychiatry Norfolk, VA e-mail: [email protected]edu1. Manford M , Andermann F : Complex visual hallucinations: clinical and neurobiological insights. Brain 1998; 121:1819–1840Crossref, Medline, Google Scholar2. De Haan EH , Nys GM , van Zandvoort MJ , et al.: The physiological basis of visual hallucinations after damage to the primary visual cortex. NeuroReport 2007; 18:1177–1180Crossref, Medline, Google Scholar3. Schadlu AP , Schadlu R , Shepherd JB: Charles Bonnet syndrome: a review. Curr Opin Ophthalmol 2009; 20:219–222Crossref, Medline, Google Scholar4. Ashwin PT , Tsaloumas MD : Complex visual hallucinations (Charles Bonnet syndrome) in the hemianopic visual field following occipital infarction. J Neurol Sci 2007; 263(1–2):184–186Crossref, Medline, Google Scholar5. Howard RJ : Risperidone for visual hallucinations in the elderly. Eur Neuropsychopharmacol 1996; 6:28Crossref, Google Scholar FiguresReferencesCited byDetailsCited ByComplex Visual Hallucinations Associated With Parietal InfarctLokesh Shahani, M.D.1 January 2013 | The Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 25, No. 1 Volume 23Issue 3 Summer 2011Pages E44-E44 Metrics PDF download History Published online 1 July 2011 Published in print 1 July 2011

Cortical venous reflux (CVR) is a high risk factor for aggressive behavior of intracranial dural arteriovenous fistulas (DAVF). The pathological conditions in brain tissue affected by CVR were investigated by diffusion-weighted magnetic resonance imaging. A retrospective review identified 56 patients with DAVFs who underwent diffusion-weighted imaging before treatment. Twenty patients had neurological symptoms corresponding to the brain area affected by CVR (Group I), 21 patients with CVR had no focal brain dysfunctions (Group II), and 15 patients had no CVR (Group III). Apparent diffusion coefficient (ADC) was measured for 11 brain areas predefined based on normal venous drainage patterns in the 56 patients and in 21 normal volunteers. The mean ADC ratio was calculated for each area by dividing the ADC value of patients by that of normal volunteers. Areas affected by CVR in Group I showed a mean ADC-to-control ratio of 0.72, which was significantly lower than that of Group II (0.96, P<0.01). Follow-up studies demonstrated significantly increased ADC ratios in brain areas affected by CVR after the DAVFs were treated successfully. The mean ADC ratio of an affected area remained low, with persistent symptoms in 1 patient who underwent palliative treatment. Decreased ADC was observed in the brain parenchyma affected by CVR and was associated with regional brain dysfunction. Successful treatment of the DAVF increased the ADC toward normal levels. The ADC may be a useful indicator of the severity of CVR.

Neurovascular coupling during nociceptive processing in the primary somatosensory cortex of the rat

The application of gamma knife radiosurgery (GKRS) alone has been expanded for dural arteriovenous fistulas (DAVFs). However, a standardized protocol delineating the appropriate circumstances for GKRS alone in cases of DAVF has yet to be determined. The purpose of this study was to report a single center's treatment algorithm for GKRS alone as a primary treatment for intracranial DAVFs and assess related clinical and radiological data. Among 31 DAVF patients treated according to our institute's treatment algorithm between February 2009 and November 2014, 20 patients underwent GKRS alone. DAVF patients treated with GKRS alone fell in two main subgroups: DAVF patients without cortical venous reflux (CVR) but with symptoms (n = 8) and DAVF patients with CVR but without a high bleeding risk (defined as CVR with aggressive symptoms including hemorrhage or non-hemorrhagic neurological deficit, n = 11). One DAVF patient with a high bleeding risk had GKRS alone because of difficult endovascular access. Mean radiation volume was 4.8cc (range, 0.7-14.2cc), and mean maximal dose was 33.5Gy (range, 28-38Gy). At mean follow-up of 29.1months (range, 8-69 months), radiological findings demonstrated complete cures in 18 patients (90%) and subtotal cures in 2 patients (10%). One patient had a transient complication, but no neurologic sign. All symptomatic patients showed complete resolution. Our treatment algorithm showed GKRS alone may serve as a primary treatment for patients with DAVFs regardless of location and presence of CVR, unless there is a high bleeding risk. However, a multicenter, prospective study is necessary to generalize our treatment algorithm.

The authors report their preliminary experience using a balloon-assisted technique (BAT) in the transarterial embolization of intracranial dural arteriovenous fistulas (DAVFs). The authors reviewed the prospectively collected data obtained in 7 consecutive patients with DAVFs in whom embolization was achieved using transarterially injected Onyx with either the venous or arterial BAT. Procedures were performed at the Division of Interventional Neuroradiology at the University of California at Los Angeles Medical Center between September 2005 and January 2008. Three patients presented with cortical venous reflux and 4 did not. Three patients underwent transarterial Onyx-based embolization combined with transvenous balloon protection; the balloon was inflated in the transverse sinus in 2 of these patients and in the superior sagittal sinus in the third. One of them underwent an additional transarterial Onyx embolization with arterial BAT, whereas 4 other patients were treated with arterial BAT alone. The occipital artery was temporarily occluded with the balloon in 4 of these cases, whereas in the fifth, the authors used temporary balloon occlusion of the middle meningeal artery. Angiograms obtained immediately after embolization demonstrated complete or near-complete obliteration of the fistula in 6 patients and partial occlusion in 1 patient. There were no immediate or postprocedural complications. Two patients who presented with intracranial hemorrhage never suffered a second hemorrhage, and all other patients experienced either complete resolution or significant improvement of their symptoms. The BAT provides a new complementary method in the transarterial embolization of DAVFs that are not amenable to transvenous embolization. The venous BAT protects the patency of critical venous pathways, whereas the arterial BAT provides better control of the Onyx-based embolization.

Dear Editor, We would like to present the case of a patient with a transverse-sigmoid dural arteriovenous fistula (DAVF) associated with a spinal dumbbell schwannoma. Intracranial DAVFs are characterized by an arteriovenous (AV) shunt between the dural arteries and major intracranial dural sinuses [1]. Predisposing causes have been reported to be the presence of an intracranial brain tumor [3], a past history of intracranial surgery [6], head trauma [2], and brain infarction [4]. The most frequent brain tumor in patients with DAVFs is meningioma, which commonly develops adjacent to, and invades into, the dural sinuses [3, 5, 7, 8]. To our knowledge, there have been no case reports of an intracranial DAVF associated with a spinal tumor. A 70-year-old female had become aware of a ‘floating’ gait 10 years prior to admission and later noticed bilateral pulsating tinnitus 2 years prior to admission. On admission, neurological examination revealed slight right spastic hemiparesis, sensory disturbances in the peripheries of the upper and lower extremities, and the Romberg sign. Spinal MR imaging revealed an extramedullary spinal dumbbell tumor, which significantly compressed the spinal cord at the C2 level (Fig. 1). There were many flow voids in the posterior cervical muscle layers around the tumor. Digital subtraction angiography revealed a right transverse-sigmoid DAVF without cortical venous reflux. There were multiple AV connections between the dural arteries and the transverse and sigmoid sinuses mainly at the sinus confluence; these dural branches were fed predominantly by the right vertebral artery as well as the bilateral maxillary and occipital arteries. Contrast-enhanced CT revealed that the right internal carotid vein was severely compressed at the right C2 level between the spinal tumor and anterior deep cervical muscles originating from the right styloid process. As a result, the right internal carotid vein was thrombosed, and the thrombus progressed into the right jugular foramen to the sigmoid sinus (Fig. 1d). Arterial blood flow into the DAVF drained out via the enlarged right condylar emissary vein into the deep cervical vein. We planned to treat the DAVF with endovascular embolization before open surgery because there was massive venous drainage around the tumor and severe bleeding during tumor removal was predicted. First, dural arteries were occluded with NBCA via a transarterial approach. Then, the deep cervical vein was occluded with NBCA via a transvenous approach. Finally, the right transverse and sigmoid sinuses were packed with coils, leading to the occlusion of the DAVF. In the second stage, we performed open surgery via a posterior midline approach. During surgery, bleeding was wellcontrolled because most of the deep cervical veins were occluded with NBCA. The dumbbell tumor, which was mostly located in the epidural space, was extensively removed, piece by piece, leading to successful decompression of the spinal cord. Total blood loss was 312 ml. The pathological diagnosis was schwannoma. * Keisuke Takai takai-nsu@umin.ac.jp

Efficacy of Intraarterial Fluorescence Video Angiography in Surgery for Dural and Perimedullary Arteriovenous Fistula at Craniocervical Junction

Effects of brain stem stimulation on cortical NADH fluorescence, blood flow, and O 2 consumption in the cat

The medical records and arteriograms of 81 patients with spinal arteriovenous malformations (AVM's) were reviewed, and the vascular lesions were classified as dural arteriovenous (AV) fistulas or intradural AVM's. Intradural AVM's were further classified as intramedullary AVM's (juvenile and glomus types) and direct AV fistulas, which were extramedullary or intramedullary in location. Dural AV fistulas were defined as being supplied by a dural artery and draining into spinal veins via an AV shunt in the intervertebral foramen. Intramedullary AVM's were defined as having the AV shunt contained at least partially within the cord or pia and receiving arterial supply by medullary arteries. Of the 81 patients, 27 (33%) had dural AV fistulas and 54 (67%) had intradural AVM's. Several dissimilarities in clinical and radiographic findings of the two subgroups were evident. The patients with intramedullary AVM's were younger; the age at onset of symptoms averaged 27 years compared to 49 years for dural AV fistulas. The most common initial symptom associated with dural AV fistulas was steadily progressive paresis, whereas hemorrhage was the most common presenting symptom in cases of intramedullary lesions. No patients with dural AV fistulas had subarachnoid hemorrhage. Activity exacerbated symptoms more frequently in patients with dural lesions. Associated vascular anomalies occurred only in cases of intradural AVM's. In 96% of the dural lesions the AV nidus was in the low thoracic or lumbar region; in only 15% did the intercostal or lumbar arteries supplying the AVM also provide a medullary artery which supplied the spinal cord. In contrast, most intradural AVM's (84%) were in the cervical or thoracic segments of the spinal cord and all of them were supplied by medullary arteries. Transit of contrast medium through the intradural AVM's was rapid in 80% of cases, suggesting high-flow lesions. Forty-four percent of the patients with AVM's of the spinal cord had associated saccular arterial or venous spinal aneurysms. No dural AV fistulas displayed these characteristics. A good outcome occurred in 88% of patients with dural AV fistulas after nidus obliteration, while 49% of patients with intramedullary AVM's did well after surgery or embolization. These findings suggest that dural and intradural AVM's differ in etiology (acquired vs. congenital) and that they have different pathophysiology, radiographic findings, clinical presentation, and response to treatment.

Retrograde drainage into the cortical veins results in poor outcome in patients with an intracranial dural arteriovenous fistula. However, the pathophysiological features of dural arteriovenous fistulae remain obscure. This study aimed to clarify hemodynamic and metabolic conditions in these patients using positron emission tomography. This study included eight patients with an intracranial dural arteriovenous fistula. All patients had cortical venous reflux, as demonstrated by angiography. Regional cerebral blood flow (rCBF), regional cerebral blood volume (rCBV), regional cerebral metabolic rate for oxygen, and regional oxygen extraction fraction (rOEF) were measured before and after surgical or endovascular treatment using positron emission tomography. Pretreatment positron emission tomographic studies revealed that all patients had abnormal hemodynamic and metabolic parameters in the area that was drained by the involved cortical veins. A severe increase in rCBV was noted in seven of the eight patients. A significant decrease in rCBF also was observed in all eight patients. A negative correlation was observed between rCBF and rCBV. Three patients had an elevated rOEF. Oxygen metabolism was impaired in seven patients. All patients underwent successful treatment. Follow-up studies demonstrated significant improvements in rCBF, rCBV, and regional cerebral metabolic rate for oxygen. The improvement in regional cerebral metabolic rate for oxygen varied among the patients. Normalization of rOEF also was confirmed in three patients who had increased rOEF before the treatment. The present results suggest that hemodynamic and metabolic characteristics vary widely among patients with cortical venous reflux. It is essential to precisely evaluate hemodynamic and metabolic conditions to predict their outcomes and therapeutic effects.

Disruption of local cortical blood flow (CBF) autoregulation and CO2 reactivity, or vasoparalysis, has been documented in humans after aneurysmal subarachnoid hemorrhage (SAH). Generally, the degree of vasoparalysis is related to the patient's clinical grade. Using intraoperative measurement of local CBF, we evaluated pressure autoregulation and CO2 reactivity in patients after SAH. Fourteen patients with SAH and 10 patients with asymptomatic aneurysm underwent craniotomy for clipping of their aneurysms. During operation, local CBF was recorded with thermal conductivity probes placed on the middle frontal gyrus, 4 to 6 cm from the nearest point of retraction. Before retractor placement, CBF was measured with the PCO2 at 25 and 35 mm Hg and the mean arterial blood pressure (MABP) between 70 and 80 mm Hg. After aneurysm clipping, flows were again measured. With the PCO2 at 25 mm Hg, the MABP was raised from 65 to 85 mm Hg. The PCO2 was then allowed to rise to 35 mm Hg, after which the MABP was lowered from 85 to 65 mm Hg. Six patients underwent operation within the 1st week after SAH (Grade I, n = 3; Grade II, n = 3). The remainder (n = 8) were operated on 9 days to 3 months after SAH. After aneurysm clipping, significant CBF changes (P less than 0.001) with PCO2 alteration occurred in control patients and those operated on more than 7 days after SAH. There was no significant change in CBF in patients operated on within 7 days after SAH. Changes in CBF reactivity to alteration of MABP were significantly larger in early operation patients than in other groups (P less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Brain calcification can be either physiological or pathological. Pathological calcification occurs due to a wide spectrum of causes, including congenital disorders, infections, endocrine/metabolic diseases, cerebrovascular diseases, and neoplasms. The patient's age, localization of the calcification, and association with other imaging findings are useful for the correct diagnosis. Dural arteriovenous fistulas with cortical venous reflux should be included in the differential diagnosis of subcortical calcification via CT. MRA should be conducted subsequently. We recently reported the clinical and imaging characteristics of calcified brain metastases in 20 patients. Hemorrhage, necrosis, or degeneration were detected within the lesions in six patients. Both T1WI and T2WI showed a hyperintense mass surrounded by a hypointense rim in one patient. Hemorrhagic brain metastases can mimic cerebral cavernous malformations. Cancer metastasis should be considered as a differential diagnosis when calcified or hemorrhagic masses are detected in middle-aged and elderly patients. We recommend conducting MRI with Gd enhancement.

Dural arteriovenous fistulas (dAVFs) represent 10% to 15% of all intracranial arteriovenous malformations. Most often, embolization is accomplished with transfemoral catheter techniques. We present a case in which embolization of a cavernous sinus dAVF was made possible through transcranial cannulation of a cortical draining vein. An 82-year-old woman presented with diplopia, left sixth cranial nerve palsy, intraocular hypertension, and bilateral chemosis. Angiography revealed a complex cavernous dAVF with cortical venous reflux, supplied by both external carotid arteries and the left meningohypophyseal trunk. Percutaneous transvenous access failed, and only partial occlusion was achieved by transarterial embolization. A frontotemporal craniotomy was performed to access the superficial middle cerebral vein in the left sylvian fissure. Under fluoroscopic guidance, a microcatheter was advanced through this vein to the floor of the middle cranial fossa and into the dAVF, permitting coil occlusion. This transcranial vein technique may be a useful adjunct in dAVF therapy when percutaneous transarterial or transvenous approaches fail or are not possible.

This study aimed to evaluate the feasibility of non-contrast-enhanced 4D magnetic resonance angiography (NCE 4D MRA) with signal targeting with alternative radiofrequency (STAR) spin labeling and variable flip angle (VFA) sampling in the assessment of dural arteriovenous fistula (DAVF) in the transverse sinus. Nine patients underwent NCE 4D MRA for the evaluation of DAVF in the transverse sinus at 3T. One patient was examined twice, once before and once after the interventional treatment. All patients also underwent digital subtraction angiography (DSA) and/or contrast-enhanced magnetic resonance angiography (CEMRA). For the acquisition of NCE 4D MRA, a STAR spin tagging method was used, and a VFA sampling was applied in the data readout module instead of a constant flip angle. Two readers evaluated the NCE 4D MRA data for the diagnosis of DAVF and its type with consensus. The results were compared with those from DSA and/or CEMRA. All patients underwent NCE 4D MRA without any difficulty. Among seven patients with patent DAVFs, all cases showed an early visualization of the transverse sinus on NCE 4D MRA. Except for one case, the type of DAVF of NCE 4D MRA was agreed with that of reference standard study. Cortical venous reflux (CVR) was demonstrated in two cases out of three patients with CVR. NCE 4D MRA with STAR tagging and VFA sampling is technically and clinically feasible and represents a promising technique for assessment of DAVF in the transverse sinus. Further technical developments should aim at improvements of spatial and temporal coverage.

Hypointensity of draining veins on susceptibility-weighted magnetic resonance images might indicate normal venous flow and a lower risk of intracerebral hemorrhage in patients with intracranial arteriovenous shunt(s)