Symptomatic cerebral vasospasm after intraventricular hemorrhage from ruptured arteriovenous malformation

Surg Neurol 1992 ;38 :63-7

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Symptomatic Cerebral Vasospasm After Intraventricular Hemorrhage from Ruptured Arteriovenous Malformation Kiyoyuki Yanaka, M.D ., Akio Hyodo, M.D ., Yukihiro Tsuchida, M .D ., Yoshihiko Yoshii, M .D ., and Tadao Nose, M .D . Department of Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan

Yanaka K, Hyodo A, Tsuchida Y, Yoshii Y, Nose T . Symptomatic cerebral vasospasm after intraventricular hemorrhage from ruptured arteriovenous malformation. Surg Neurol 1992 ;38 :63-7 . We present a rare case showing symptomatic vasospasm after intraventricular hemorrhage from a ruptured arteriovenous malformation . No significant subarachnoid hemorrhage in the basal cisterns was observed on computed tomography in the entire course of illness . Although most cases showing vasospasm are associated with the deposition of blood in the basal cisterns, this case suggests the possibility of some other important factor in causing the subsequent development of vasospasm . KEY WORDS : Arteriovenous malformation ; Cerebral infarction ; Intraventricular hemorrhage ; Subarachnoid hemorrhage ; Vasospasm

Although vasospasm is commonly observed in subarachnoid hemorrhage (SAH) from ruptured aneurysm with the deposition of blood in the basal subarachnoid cisterns, reports of vasospasm in ruptured arteriovenous malformation (AVM) are rare, and only 12 cases have been reported to our knowledge . We report a rare case showing vasospasm after intraventricular hemorrhage from ruptured AVM without significant SAH in the basal cisterns .

Case Report An 11-year-old girl developed a sudden severe headache and vomiting on February 8, 1991 . She was admitted to a local hospital . Computed tomography (CT) revealed intracranial hemorrhage . On February 9 she was transferred to Tsukuba University Hospital . A neurological examination on admission revealed that she was alert and had a slight stiffness of the neck . There was neither Addreu reprint requests to .' Kiyoyuki Yanaka, M .D ., Department of Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Tsukuba,lbaraki 305,Japan . Received September 30, 1991 ; accepted December 31, 1991 .

F. 1992 by Elsevicr Science Publishing Co ., Inc

motor paresis nor speech disturbance . CT showed intraventricular hemorrhage in the lateral, third, and fourth ventricles . No low-density area in the brain parenchyma or significant subarachnoid hemorrhage in the basal cisterns was observed (Figure 1) . Contrast-enhanced CT revealed a left parieto-occipital AVM . Cerebral angiography was carried out on February 10, demonstrating a left parieto-occipital AVM . The AVM was fed by branches of the left anterior and middle cerebral artery without vasospasm (Figure 2) .The posterior cerebral artery fed a posterior segment of this AVM (not illustrated) . Venous drainage was through the superior sagittal sinus . No aneurysmal formation was seen . In spite of osmotherapy with glycerol and corticosteroid, the patient developed a right hemiparesis, speech disturbance, and right hemianopsia, followed by disturbance of consciousness on February 11 . CT revealed a low-density area around the AVM without fresh intracerebral hemorrhage . No significant subarachnoid hemorrhage in the basal cisterns was seen (Figure 3) . Magnetic resonance imaging (MR1) revealed hypointensity on the axial TI-weighted image and hyperintensity on T2weighted image of the corresponding area around the AVM (Figure 4) . It was diagnosed as cerebral infarction . Cerebral angiography showed severe vasospasm ; Al and M 1 segments of both anterior and middle cerebral arteries exhibited vasospasm (Figure 5) . Circulation time was delayed and the nidus was decreased in size . The cerebral infarction seemed to be due to vasospasm, causing a neurological deficit . Osmotherapy was maintained, but a new low-density area in the left frontal lobe and a spotty low-density area in the right internal capsule were detected on CT on February 26 . Repeated cerebral angiography revealed continuation of vasospasm . On March 8 disappearance of vasospasm was observed angiographically. After the disappearance ofvasospasm, staged superselective embolization to the feeding arteries was performed four times from April 10 to May 15 . The size of the nidus was decreased after embolization, and a left parieto-occipital craniotomy was carried out on May 21 ; 0090-3019,921$5 .00



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Surg Neurol 1992 ;38 :63-?

Figure 1 . Computed tomography on admission revealed entravertoricul

hemorrhage . No .vubarachnoid hemorrhage in the basal cistenu was detected.

Table 1 . Summary of Crises Showing Vasosparm Due to Ruptured AVMs Location Authorlyear

No .

Age/sex

1

Nishimura and Hawkins (19?5)

2

22 M

3

50 M

6 Sasaki et al (19811

8

56 F 65 F 10 M 16 F 28 M

Matsumori ct al ( 1983)

9

45 M

Present case ( 1991)

IVH

AVM

VasosPasm

Onset (day)

r

Stornelli and French (1964]

10 11 12 13

ICH

44 47 9 11

F F F F

(-)

Rt. temporal Rt. thalamic Lt . occipital

,-) (+) (+) (-) I-)

(-)

Rt . parieral Lt . temporal Lt. basal ganglia Rt . parietal Rt . frontal

(+)

Lt. frontal

( +)

Rt . frontal Lt, parietal Lt . frontal Lt . parieto-occipital

+

(-)

25 .09/ (1/4) 11 .5% (6/52)

Rt . Cl Rt . Cl, At Lt . Cl, Al Rt. Cl, MI Lt, C I .r. C Lt. IC, BA Rr. CI, At, MI Lt. Cl, Al, MI Rt . A, M, P Rt . MI Rr . MI Rr. CI Rt. A1, Ml Lc Al, MI

Incidence (cases)

8 U) 8 .39/ (1/12) 30 .8% (4/13) 26

Note. Abbreviations : ICH, mtracerebral hemorrhage : IVH, intraven[ricular licit orrhage ; AVM, arreriovenous malfnrmatiun ; BA, basilar artery ; A, anterior cerebral artery : AI, middle cerebral artery ; P . posterior cerebral artery ; C, internal carotid artery .



Vasospasm After Intraventricular Hemorrhage

Figure 2 . Left carotid argiogrant on admission reaealed left parieto-occipital AVM fed by branches of anterior and middle cerebral arteries without i asospasm,

the AVM was successfully removed . Cerebral angiography was performed on June 19, showing total excision of the AVM . After surgery and rehabilitation the patient was discharged with slight right hemiparesis on September 19 .

Discussion Cerebral vasospasm may be caused by a pathological constriction of major intracranial arteries at the base of the brain that results from exposure to blood deposited within the basal cisterns through rupture of an intracranial aneurysm (demonstrable by cerebral angiography), followed by cerebral ischemia or infarction [11] . Cases of vasospasm with SAH from ruptured AVM have been reported (Table 1) [5-7,9,10] . There is no relation between location of AVM and of vasospasm . The incidence of vasospasm is lower (8 .3%-30 .8%) than that of ruptured aneurysm . The occurrence of vaso-

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spasm has no relation to age, sex, or combined intracerebral hemorrhage . Vasospasm usually appears about 10 days after rupturing of the AVM . The reason for the lower incidence of vasospasm due to ruptured AVM can be explained : The formation of subarachnoid blood around the arteries of the circle of Willis is relatively rare because the majority of AVMs are peripherally or deeply situated and bleeding from an AVM is commonly less severe than from the rupture of an aneurysm . In all 12 cases that have shown vasospasm, SAH was detected by lumbar puncture or CT and it played an important role in producing vasospasm [10} . It is our opinion that the lower incidence of vasospasm due to AVM may be related to a large quantity of blood flow through the nidus . AVM may play a role in irrigating blood to peripheral areas . Therefore even if the conditions causing vasospasm occur, vasospasm may be slight and not demonstrable by angiography . On the other hand the mechanism of vasospasm in this case is not clear . In general patients who sustain bleeding into the brain parenchyma, ventricles, or subarachnoid space over the cerebral convexities without significant bleeding into the basal cisterns do not develop angiographically demonstrable cerebral vasospasm [11} . However, cerebral vasospasm occurs in patients with conditions other than a ruptured intracranial aneurysm, for example, following head trauma and after surgery in the hypothalamic-pituitary area [11] . Vasospasm in a patient who had a traumatic lumbar puncture for myelography has been reported [8] . A case of pheochromocytoma with elevated circulating catecholamines with vasospasm has been reported [1] . Vasospasm with an unruptured and unoperated aneurysm has also been reported [3] . These cases offer evidence that a small amount of subarachnoid blood from a spinal source or abnormal amounts of serum catecholamines or vasoconstrictive prostaglandins can narrow the cerebral arteries [1,3,8] . Furthermore, there are several reports that endothelia may play an important role in the pathogenesis of cerebral vasospasm [4], although its mechanism has not been clear . Vasospasm in our case may have been due to these causes . If a small amount of subarachnoid blood from a spinal source can lead to cerebral vasospasm, blood from a ventricle may be capable of narrowing cerebral arteries . In spite of many cases with intraventricular hemorrhage, no symptomatic vasospasm cases have been reported to our knowledge . However, in a particular condition such as neonatal asphyxia, the intraventricular hemorrhage itself induces vasospasm, as demonstrated by Doppler ultrasound detection of pulsations in the cerebral artery [2] . The possibility remains that vasospasm after intraventricular hemorrhage may be overlooked because the patients with usual intraventricular hemorrhage are not



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Surg Neurol 1992 ;38 : 6 3 -7

Figure

3 . Computed tomography revealed a nest low-density area around the AVM without intracerebral hemorrhage .

routinely examined by cerebral angiography . This rare condition raises the possibility that some other factors than the deposition of blood around the arteries are

Yanaka et al

important in causing vasospasm ; cerebral infarction due to vasospasm also has occurred . Although vasospasm due to ruptured AVM with no influence over outcome has been reported [10}, it &-f fected the outcome in our case . It is important for clinicians to keep in mind the possibility of cerebral vasospasm and infarction in cases of ruptured AVM .

Figure 4. Magnetic resonance imaging repealedleftparieto-occipitalAV, ,M . A hypointensity area on T I-weighted image and a hyperintensity area on T2-weighted image were observed around the AVM . (Right) T2-weighted image (SE 2,500/80) . (Left) TI-weighted image (SE 600/20) .



Surg Neurol 199238 :63-7

Vasospasm After Intraventricular Hemorrhage

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The authors thank Takao Kamezaki, M .D ., and Eiki Kobayashi, M .D ., of the Department of Neurosurgery, Tsukuha Memorial Hospital, for their help in the preparation of this article .

References 1 . Armstrong FS, Hayes GJ . Segmental cerebral arterial constriction associated with pheochromocytoma : report of a case with arteriogram. J Neurosurg 1961 ;18 :843-6 . 2 . Bads HS, Hajjar W, Chua C, Sumner DS . Noninvasive diagnosis of neonatal asphyxia and intraventricular hemorrhage by Doppler ultrasound . J Pediatr 1979J5 :775-9 . 3 . Friedman P, Gass H, Magidson M . Vasospasm with an unruptured and unoperated aneurysm. Surg Neurol 1983 ;19 :21-5 . 4 . Kobayashi H, Hayashi M, Kobayashi S, Kabuto M, Handa Y, Kawano H, Ide H . Cerebral vasospasm and vasoconstriction caused by endothelin . Neurosurgery 1991 ;28 :673-9 . 5 . Matsumori K, Asahi S, Nakayama K, Miyasaka Y, Beppu T . Cerebral vasospasm after subarachnoid hemorrhage from arteriovenous malformation . No Shinkei Geka 1983 ;11 :829-34 .

Figure5 . Left caroeidangiogramafter theappearance ofcembralinfarcticn repeated diffuse varorpurm . The nidus is not illustrated in this figure, but it appeared in the late arterial phase Leith decrease in size .

6 . Nishimura K, Hawkins TD . Cerebral vasospasm with suharachnoid haemorrhage from arteriovenous malformations of the brain . Ncuroradiology 1975 ;8 :201-? . Sasaki T, Mayanagi Y, Y ano H, Kim S . Cerebral vasospasm with subarachnoid hemorrhage from cerebral arteriovenous malformations . Surg Neural 1981 ;16 :183-7 . 8 . Smith RA, Collier HF, Underwood FO . Cerebral vasospasm following myelography . Sung Neurol 1973 :18 7-90 . 9 . Stornelli SA, French ID . Subarachnoid hemorrhage-factors on prognosis and management . J Neurosurg 1961 ;21 :769-80 . 10 . von Hoist H, Ericson K, Haberbeck-Modesro M, Steiner L. Angiographic investigation of cerebral vasospasm in subarachnoid haemorrhage due to arteriovenous malformation . Acts Neurochir (Wien) 1988;94 :129-32 . 11 . Wilkios RH . Rengachai-y SS . Neurosurgery update, 11. New York : McGraw-Hill, 1991 :78-94 .