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De Novo Cerebral Arteriovenous Malformation: Pink Floyd's Song “Brick in the Wall” as a Warning Sign
The Journal of Emergency Medicine, Vol. 43, No. 1, pp. e17– e20, 2012 Copyright © 2012 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$–see front matter
http://dx.doi.org/10.1016/j.jemermed.2009.05.035
Clinical Communications: Adults
DE NOVO CEREBRAL ARTERIOVENOUS MALFORMATION: PINK FLOYD’S SONG “BRICK IN THE WALL” AS A WARNING SIGN Murat Ozsarac,
MD,*
Ersin Aksay,
MD,*
Selahattin Kiyan,
MD,*
Orkun Unek,
MD,*
and F. Feray Gulec,
MD†
*Department of Emergency Medicine and †Department of Neurology, Ege University Hospital, Izmir, Turkey Reprint Address: Murat Ozsarac, MD, Department of Emergency Medicine, Ege University, Bornova, Izmir 35100, Turkey
e Abstract—Background: Arteriovenous malformations are shunts between an artery and the venous system that lie within a nidus without an intervening capillary bed. These lesions are thought to be congenital, but recent reports have challenged this assumption. Case Report: A 50-year-old man presented to the emergency department with a generalized tonic-clonic seizure. Before the onset of his seizure, he experienced a vivid auditory hallucination of his favorite song by the band Pink Floyd, “A Brick in the Wall.” He had been diagnosed with epilepsy 25 years previously. On presentation, his neurological examination was normal, but a computed tomography scan of the brain revealed a large arteriovenous malformation (AVM) occupying the left temporal lobe. Upon more detailed questioning, he recalled that a brain angiogram had been performed 25 years before and was reported to be normal. Neurosurgery was not performed in view of the size of the malformation. The patient is being followed-up as an outpatient. Conclusion: AVMs may arise de novo and then spontaneously become symptomatic. Cerebral de novo AVM should be considered in the differential diagnosis in patients with complex auditory musical hallucinations or any new neuropsychiatric symptoms. © 2012 Elsevier Inc.
lesions that can cause serious neurological symptoms or death. Although AVMs can present with hemorrhage or seizure, since the advent of contemporary brain imaging techniques, an increasing number are detected before rupture (1). Usually, AVMs are clinically silent and become symptomatic in only the second, third, or fourth decade of life. The annual risk for bleeding from an unruptured AVM is 2– 4%. Each episode has a 15% rate of mortality and a 30% rate of permanent neurologic deficit (2). We describe a rare case of a de novo cerebral AVM in a 50-year-old man.
CASE REPORT A 50-year-old man presented to the emergency department (ED) after a generalized tonic-clonic seizure. He had been diagnosed with epilepsy 25 years previously, for which he was taking phenytoin. His medical history was non-contributory and he denied recreational or illicit drug use. On presentation, he was alert and cooperative with normal vital signs and neurological examination. All cranial nerves were intact. A sensory examination revealed nothing abnormal. Routine blood analyses (complete blood count, liver function tests, cardiac enzymes, blood urea nitrogen, and electrolytes) were all within normal limits. A non-contrast (Figure 1) and contrast (Figure 2) computed tomography (CT) scan of the brain revealed a large AVM occupying the left temporal lobe and a portion of the left parietal lobe. Upon
e Keywords— de novo arteriovenous malformation; cerebrovascular malformation; seizure; musical hallucinations; auditory aura; auditory hallucinations; epilepsy
INTRODUCTION Intracranial arteriovenous malformations (AVMs) are relatively uncommon but are increasingly recognized as
RECEIVED: 19 November 2008; FINAL ACCEPTED: 30 May 2009
SUBMISSION RECEIVED:
13 May 2009;
e17
e18
M. Ozsarac et al.
Figure 1. Non-contrast computed tomography scan of the head demonstrates an isodense-to-hyperdense hemispheric mass in the temporal lobe and in a portion of the parietal lobe.
thought to be congenital, but recent reports have challenged this assumption. A few rare cases have been reported of de novo acquired cerebral AVM development later in life (3–9). Three of these case reports are of patients with pre-existing vascular pathology who developed AVMs in or near pathologically altered brain (3– 6). Only two previous reports document a cerebral AVM arising in brain parenchyma shown to be without vascular pathology on prior magnetic resonance imaging. Although some vascular abnormalities may be present at birth, the compact nidus or band heterotopia may enlarge at a later age for unknown reasons (3,7,8). Environmental factors, increasing hemodynamic stress, vascular remodeling, disorders of neuronal migration, and abnormalities of endothelial proliferation may play a role in their development (3,8). Intracranial AVMs are occasionally seen in the elderly but are typically diagnosed before the patient has reached the age of 40 years. More than 50% of patients with AVMs present with intracranial hemorrhage (9). Of these, intraparenchymal hemorrhage occurs most commonly, although subarachnoid hemorrhage and intraventricular hemorrhage can occur. The next most common presentation is seizure (1). Seizures can be either focal or generalized and may correspond to the location of the lesion. Other presentations include headaches, a focal
more detailed questioning, the patient recalled that he had had brain angiography 25 years previously and the results were normal. Cranial CT scan was not performed at that time. Although the phenytoin level was in the normal therapeutic range, he stated that he usually had generalized convulsions once every month or two. For the past 10 years he had auras before most of his seizures; these would consist of vivid auditory hallucinations of conversations with friends, dialogues from movies he had watched, or songs of his favorite groups. The song by Pink Floyd, “Brick in the Wall,” was a frequent auditory hallucination that occurred before his epileptic seizures. In view of the size of the malformation, along with the relatively infrequent seizures, surgery to remove or ablate the AVM was not undertaken. The patient is being followed-up as an outpatient. DISCUSSION AVMs typically involve the brain but occasionally are associated with the spinal cord and its dura mater. They may be microscopic or large enough to involve an entire hemisphere of the brain (2). The pathogenesis of AVMs is not well understood. AVMs are shunts between an artery and the venous system that lie within a nidus without an intervening capillary bed. These lesions are
Figure 2. Contrast computed tomography scan of the head demonstrates an arteriovenous malformation in the temporal lobe and in a portion of the parietal lobe, with multiple calcified phleboliths and serpiginous vascular enhancement.
De Novo Cerebral Arteriovenous Malformation
neurological deficit, weakness, numbness, visual problems, and loss of consciousness. The coexistence of migraine and seizures is particularly suggestive of a vascular malformation. Dural AVMs of the sigmoid or cavernous sinus also may produce migraine-like episodic headaches or pulsatile tinnitus (2,10). Insular cortex involvement is associated with more pronounced autonomic imbalance, leading to life-threatening cardiac dysrhythmia, sudden death, and electrocardiographic abnormalities (11,12). In children younger than 2 years of age, presentation can include congestive heart failure, large head due to hydrocephalus, and seizures (1). Musical auditory hallucination (in this case, Pink Floyd’s “Brick in the Wall”) before seizure in the setting of the patient’s AVM is a unique finding in this case. Auditory hallucinations are perceptions of external speech in the absence of a stimulus and are associated with activation in the inferior frontal/insular, temporal cortex bilaterally, the right thalamus, and the left hippocampus and parahippocampal cortex (13). Musical hallucination is a subset of complex auditory hallucinations and is a poorly understood clinical phenomenon (14). These hallucinations have been associated with stroke, epilepsy, brain tumors, alcohol withdrawal, psychotropic medications, and Parkinson’s disease, and they have been linked to cortical and midbrain infections, including neurosyphilis and Lyme (15). Auditory aura is considered a symptom of temporal lobe epilepsy and is rare in a general population of patients with epilepsy (1.9%) (16). In our case, auditory hallucinations may have resulted from left temporoparietal AVM involvement in the cortical and subcortical areas that are connected to auditory centers. Intracranial AVMs may be diagnosed with a variety of imaging studies. CT scan without contrast has a low sensitivity, but calcification and hypodensity may be noted; after contrast administration, enhancement is seen (1). CT imaging of a brain AVM can show an isodenseto-hyperdense hemispheric mass, and CT scans also can detect an accompanying abnormal vascular supply. Other possible findings include cystic cavities representing previous hemorrhage and hypoattenuation of surrounding parenchyma representing encephalomalacia, cerebral atrophy, or gliosis. Serpiginous vascular enhancement is a finding typical of an AVM on a contrast CT scan. Occasionally, non-contrast CT scan can demonstrate edema, mass effect, or ischemic changes associated with an AVM. The addition of contrast in performing a head CT scan may help to identify small AVMs missed by a non-contrast CT scan (2). The most common classification of AVMs is the Spetzler-Martin classification. This grading system attempts to predict the risk of surgical morbidity and mortality by assigning points to an AVM on the basis of
e19
its size, the eloquence of the adjacent brain, and the pattern of venous drainage (deep or superficial). The grading system includes five possible points. For a small AVM (⬍ 3 cm), 1 point is assigned; for a medium AVM (3– 6 cm), 2 points; for a large AVM (⬎ 6 cm), 3 points (17). The goal of treatment is to reduce the risk of bleeding. This can be accomplished only when the AVM is obliterated completely. Partial obliteration is not known to reduce the risk of hemorrhage. Other treatment goals can be seizure reduction or reduction in mass effect (18). CONCLUSION AVMs may arise de novo and then spontaneously become symptomatic. Cerebral de novo AVM should be considered in the differential diagnosis of patients with complex auditory musical hallucinations or any new neuropsychiatric symptoms. Acknowledgment—The authors thank John Fowler, viewing the manuscript.
MD
for re-
REFERENCES 1. Ogilvy CS, Stieg PE, Awad I, et al. Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association. Circulation 2001;103:2644 –57. 2. Koenigsberg RA, Wasserman JR, Diegnan BR. Brain, arteriovenous malformation. Available at: http://www.emedicine.com/ radio/topic93.htm. Accessed November 10, 2008. 3. Stevens J, Leach JL, Abruzzo T, Jones BV. De novo cerebral arteriovenous malformation: case report and literature review. AJNR Am J Neuroradiol 2009;30:111–2. 4. Schmit BP, Burrows PE, Kuban K, Goumnerova L, Scott RM. Acquired cerebral arteriovenous malformation in a child with moyamoya disease. Case report. J Neurosurg 1996;84:677– 80. 5. Rodriquez-Arias C, Martinez R, Rey G, Bravo G. Recurrence in a different location of a cerebral arteriovenous malformation in a child after radiosurgery. Childs Nerv Syst 2000;16:363–5. 6. Song JK, Niimi Y, Kupersmith MJ, Berenstein A. Postnatal growth and development of a cerebral arteriovenous malformation on serial magnetic resonance imaging in a child with hemangiomatosis. J Neurosurg 2007;106:384 –7. 7. Gonzalez LF, Bristol RE, Porter RW, Spetzler RF. De novo presentation of an arteriovenous malformation. Case report and review of the literature. J Neurosurg 2005;102:726 –9. 8. Bulsara KR, Alexander MJ, Villavicencio AT, Graffagnino C. De novo cerebral arteriovenous malformation: case report. Neurosurgery 2002;50:1137– 41. 9. Brown RD, Wiebers DO, Torner JC, O’Fallon WM. Frequency of intracranial hemorrhage as a presenting symptom and subtype analysis: a population-based study of intracranial vascular malformations in Olmsted County, Minnesota. J Neurosurg 1996;85:29 –32. 10. Jayaraman MV, Marcellus ML, Do HM, et al. Hemorrhage rate in patients with Spetzler-Martin grades IV and V arteriovenous malformations: is treatment justified? Stroke 2007;38:325–9. 11. Oppenheimer S. Cerebrogenic cardiac arrhythmias: cortical lateralization and clinical significance. Clin Auton Res 2006;16: 6 –11.
e20 12. Noordally O, Mircev D, Luabeya MK. Cerebral arteriovenous malformation mimicking acute coronary syndrome. Acta Neurol Belg 2002;102:36 – 8. 13. Shergill SS, Brammer MJ, Williams SC, Murray RM, McGuire PK. Mapping auditory hallucinations in schizophrenia using functional magnetic resonance imaging. Arch Gen Psychiatry 2000;57: 1033– 8. 14. Fischer C, Marchie A, Norris M. Musical and auditory hallucinations: a spectrum. Psychiatry Clin Neurosci 2004;58:96 – 8.
M. Ozsarac et al. 15. Stricker RB, Winger EE. Musical hallucinations in patients with Lyme disease. South Med J 2003;96:711–5. 16. Florindo I, Bisulli F, Pittau F, et al. Lateralizing value of the auditory aura in partial seizures. Epilepsia 2006;47:68 –72. 17. Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. J Neurosurg 1986;65:476 – 83. 18. Mattle HP, Schroth G, Seiler RW. Dilemmas in the management of patients with arteriovenous malformations. J Neurol 2000;247: 917–28.
http://dx.doi.org/10.1016/j.jemermed.2009.05.035
Clinical Communications: Adults
DE NOVO CEREBRAL ARTERIOVENOUS MALFORMATION: PINK FLOYD’S SONG “BRICK IN THE WALL” AS A WARNING SIGN Murat Ozsarac,
MD,*
Ersin Aksay,
MD,*
Selahattin Kiyan,
MD,*
Orkun Unek,
MD,*
and F. Feray Gulec,
MD†
*Department of Emergency Medicine and †Department of Neurology, Ege University Hospital, Izmir, Turkey Reprint Address: Murat Ozsarac, MD, Department of Emergency Medicine, Ege University, Bornova, Izmir 35100, Turkey
e Abstract—Background: Arteriovenous malformations are shunts between an artery and the venous system that lie within a nidus without an intervening capillary bed. These lesions are thought to be congenital, but recent reports have challenged this assumption. Case Report: A 50-year-old man presented to the emergency department with a generalized tonic-clonic seizure. Before the onset of his seizure, he experienced a vivid auditory hallucination of his favorite song by the band Pink Floyd, “A Brick in the Wall.” He had been diagnosed with epilepsy 25 years previously. On presentation, his neurological examination was normal, but a computed tomography scan of the brain revealed a large arteriovenous malformation (AVM) occupying the left temporal lobe. Upon more detailed questioning, he recalled that a brain angiogram had been performed 25 years before and was reported to be normal. Neurosurgery was not performed in view of the size of the malformation. The patient is being followed-up as an outpatient. Conclusion: AVMs may arise de novo and then spontaneously become symptomatic. Cerebral de novo AVM should be considered in the differential diagnosis in patients with complex auditory musical hallucinations or any new neuropsychiatric symptoms. © 2012 Elsevier Inc.
lesions that can cause serious neurological symptoms or death. Although AVMs can present with hemorrhage or seizure, since the advent of contemporary brain imaging techniques, an increasing number are detected before rupture (1). Usually, AVMs are clinically silent and become symptomatic in only the second, third, or fourth decade of life. The annual risk for bleeding from an unruptured AVM is 2– 4%. Each episode has a 15% rate of mortality and a 30% rate of permanent neurologic deficit (2). We describe a rare case of a de novo cerebral AVM in a 50-year-old man.
CASE REPORT A 50-year-old man presented to the emergency department (ED) after a generalized tonic-clonic seizure. He had been diagnosed with epilepsy 25 years previously, for which he was taking phenytoin. His medical history was non-contributory and he denied recreational or illicit drug use. On presentation, he was alert and cooperative with normal vital signs and neurological examination. All cranial nerves were intact. A sensory examination revealed nothing abnormal. Routine blood analyses (complete blood count, liver function tests, cardiac enzymes, blood urea nitrogen, and electrolytes) were all within normal limits. A non-contrast (Figure 1) and contrast (Figure 2) computed tomography (CT) scan of the brain revealed a large AVM occupying the left temporal lobe and a portion of the left parietal lobe. Upon
e Keywords— de novo arteriovenous malformation; cerebrovascular malformation; seizure; musical hallucinations; auditory aura; auditory hallucinations; epilepsy
INTRODUCTION Intracranial arteriovenous malformations (AVMs) are relatively uncommon but are increasingly recognized as
RECEIVED: 19 November 2008; FINAL ACCEPTED: 30 May 2009
SUBMISSION RECEIVED:
13 May 2009;
e17
e18
M. Ozsarac et al.
Figure 1. Non-contrast computed tomography scan of the head demonstrates an isodense-to-hyperdense hemispheric mass in the temporal lobe and in a portion of the parietal lobe.
thought to be congenital, but recent reports have challenged this assumption. A few rare cases have been reported of de novo acquired cerebral AVM development later in life (3–9). Three of these case reports are of patients with pre-existing vascular pathology who developed AVMs in or near pathologically altered brain (3– 6). Only two previous reports document a cerebral AVM arising in brain parenchyma shown to be without vascular pathology on prior magnetic resonance imaging. Although some vascular abnormalities may be present at birth, the compact nidus or band heterotopia may enlarge at a later age for unknown reasons (3,7,8). Environmental factors, increasing hemodynamic stress, vascular remodeling, disorders of neuronal migration, and abnormalities of endothelial proliferation may play a role in their development (3,8). Intracranial AVMs are occasionally seen in the elderly but are typically diagnosed before the patient has reached the age of 40 years. More than 50% of patients with AVMs present with intracranial hemorrhage (9). Of these, intraparenchymal hemorrhage occurs most commonly, although subarachnoid hemorrhage and intraventricular hemorrhage can occur. The next most common presentation is seizure (1). Seizures can be either focal or generalized and may correspond to the location of the lesion. Other presentations include headaches, a focal
more detailed questioning, the patient recalled that he had had brain angiography 25 years previously and the results were normal. Cranial CT scan was not performed at that time. Although the phenytoin level was in the normal therapeutic range, he stated that he usually had generalized convulsions once every month or two. For the past 10 years he had auras before most of his seizures; these would consist of vivid auditory hallucinations of conversations with friends, dialogues from movies he had watched, or songs of his favorite groups. The song by Pink Floyd, “Brick in the Wall,” was a frequent auditory hallucination that occurred before his epileptic seizures. In view of the size of the malformation, along with the relatively infrequent seizures, surgery to remove or ablate the AVM was not undertaken. The patient is being followed-up as an outpatient. DISCUSSION AVMs typically involve the brain but occasionally are associated with the spinal cord and its dura mater. They may be microscopic or large enough to involve an entire hemisphere of the brain (2). The pathogenesis of AVMs is not well understood. AVMs are shunts between an artery and the venous system that lie within a nidus without an intervening capillary bed. These lesions are
Figure 2. Contrast computed tomography scan of the head demonstrates an arteriovenous malformation in the temporal lobe and in a portion of the parietal lobe, with multiple calcified phleboliths and serpiginous vascular enhancement.
De Novo Cerebral Arteriovenous Malformation
neurological deficit, weakness, numbness, visual problems, and loss of consciousness. The coexistence of migraine and seizures is particularly suggestive of a vascular malformation. Dural AVMs of the sigmoid or cavernous sinus also may produce migraine-like episodic headaches or pulsatile tinnitus (2,10). Insular cortex involvement is associated with more pronounced autonomic imbalance, leading to life-threatening cardiac dysrhythmia, sudden death, and electrocardiographic abnormalities (11,12). In children younger than 2 years of age, presentation can include congestive heart failure, large head due to hydrocephalus, and seizures (1). Musical auditory hallucination (in this case, Pink Floyd’s “Brick in the Wall”) before seizure in the setting of the patient’s AVM is a unique finding in this case. Auditory hallucinations are perceptions of external speech in the absence of a stimulus and are associated with activation in the inferior frontal/insular, temporal cortex bilaterally, the right thalamus, and the left hippocampus and parahippocampal cortex (13). Musical hallucination is a subset of complex auditory hallucinations and is a poorly understood clinical phenomenon (14). These hallucinations have been associated with stroke, epilepsy, brain tumors, alcohol withdrawal, psychotropic medications, and Parkinson’s disease, and they have been linked to cortical and midbrain infections, including neurosyphilis and Lyme (15). Auditory aura is considered a symptom of temporal lobe epilepsy and is rare in a general population of patients with epilepsy (1.9%) (16). In our case, auditory hallucinations may have resulted from left temporoparietal AVM involvement in the cortical and subcortical areas that are connected to auditory centers. Intracranial AVMs may be diagnosed with a variety of imaging studies. CT scan without contrast has a low sensitivity, but calcification and hypodensity may be noted; after contrast administration, enhancement is seen (1). CT imaging of a brain AVM can show an isodenseto-hyperdense hemispheric mass, and CT scans also can detect an accompanying abnormal vascular supply. Other possible findings include cystic cavities representing previous hemorrhage and hypoattenuation of surrounding parenchyma representing encephalomalacia, cerebral atrophy, or gliosis. Serpiginous vascular enhancement is a finding typical of an AVM on a contrast CT scan. Occasionally, non-contrast CT scan can demonstrate edema, mass effect, or ischemic changes associated with an AVM. The addition of contrast in performing a head CT scan may help to identify small AVMs missed by a non-contrast CT scan (2). The most common classification of AVMs is the Spetzler-Martin classification. This grading system attempts to predict the risk of surgical morbidity and mortality by assigning points to an AVM on the basis of
e19
its size, the eloquence of the adjacent brain, and the pattern of venous drainage (deep or superficial). The grading system includes five possible points. For a small AVM (⬍ 3 cm), 1 point is assigned; for a medium AVM (3– 6 cm), 2 points; for a large AVM (⬎ 6 cm), 3 points (17). The goal of treatment is to reduce the risk of bleeding. This can be accomplished only when the AVM is obliterated completely. Partial obliteration is not known to reduce the risk of hemorrhage. Other treatment goals can be seizure reduction or reduction in mass effect (18). CONCLUSION AVMs may arise de novo and then spontaneously become symptomatic. Cerebral de novo AVM should be considered in the differential diagnosis of patients with complex auditory musical hallucinations or any new neuropsychiatric symptoms. Acknowledgment—The authors thank John Fowler, viewing the manuscript.
MD
for re-
REFERENCES 1. Ogilvy CS, Stieg PE, Awad I, et al. Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association. Circulation 2001;103:2644 –57. 2. Koenigsberg RA, Wasserman JR, Diegnan BR. Brain, arteriovenous malformation. Available at: http://www.emedicine.com/ radio/topic93.htm. Accessed November 10, 2008. 3. Stevens J, Leach JL, Abruzzo T, Jones BV. De novo cerebral arteriovenous malformation: case report and literature review. AJNR Am J Neuroradiol 2009;30:111–2. 4. Schmit BP, Burrows PE, Kuban K, Goumnerova L, Scott RM. Acquired cerebral arteriovenous malformation in a child with moyamoya disease. Case report. J Neurosurg 1996;84:677– 80. 5. Rodriquez-Arias C, Martinez R, Rey G, Bravo G. Recurrence in a different location of a cerebral arteriovenous malformation in a child after radiosurgery. Childs Nerv Syst 2000;16:363–5. 6. Song JK, Niimi Y, Kupersmith MJ, Berenstein A. Postnatal growth and development of a cerebral arteriovenous malformation on serial magnetic resonance imaging in a child with hemangiomatosis. J Neurosurg 2007;106:384 –7. 7. Gonzalez LF, Bristol RE, Porter RW, Spetzler RF. De novo presentation of an arteriovenous malformation. Case report and review of the literature. J Neurosurg 2005;102:726 –9. 8. Bulsara KR, Alexander MJ, Villavicencio AT, Graffagnino C. De novo cerebral arteriovenous malformation: case report. Neurosurgery 2002;50:1137– 41. 9. Brown RD, Wiebers DO, Torner JC, O’Fallon WM. Frequency of intracranial hemorrhage as a presenting symptom and subtype analysis: a population-based study of intracranial vascular malformations in Olmsted County, Minnesota. J Neurosurg 1996;85:29 –32. 10. Jayaraman MV, Marcellus ML, Do HM, et al. Hemorrhage rate in patients with Spetzler-Martin grades IV and V arteriovenous malformations: is treatment justified? Stroke 2007;38:325–9. 11. Oppenheimer S. Cerebrogenic cardiac arrhythmias: cortical lateralization and clinical significance. Clin Auton Res 2006;16: 6 –11.
e20 12. Noordally O, Mircev D, Luabeya MK. Cerebral arteriovenous malformation mimicking acute coronary syndrome. Acta Neurol Belg 2002;102:36 – 8. 13. Shergill SS, Brammer MJ, Williams SC, Murray RM, McGuire PK. Mapping auditory hallucinations in schizophrenia using functional magnetic resonance imaging. Arch Gen Psychiatry 2000;57: 1033– 8. 14. Fischer C, Marchie A, Norris M. Musical and auditory hallucinations: a spectrum. Psychiatry Clin Neurosci 2004;58:96 – 8.
M. Ozsarac et al. 15. Stricker RB, Winger EE. Musical hallucinations in patients with Lyme disease. South Med J 2003;96:711–5. 16. Florindo I, Bisulli F, Pittau F, et al. Lateralizing value of the auditory aura in partial seizures. Epilepsia 2006;47:68 –72. 17. Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. J Neurosurg 1986;65:476 – 83. 18. Mattle HP, Schroth G, Seiler RW. Dilemmas in the management of patients with arteriovenous malformations. J Neurol 2000;247: 917–28.