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Disappearance of a cerebral aneurysm — an unusual angiographic event
Disappearance of a cerebral aneurysm - an unusual angiographic event Sunil Kumar, V.R.K. Rao, K. Ravi Mandalam, and R.V. Phadke
Introduction
Approximately l-2% of ruptured arterial aneurysms may thrombose completely, usually observed at operation or autopsy examination’. Angiographically documented thrombosis in a cerebral aneurysm is even less frequent. Only a few case reports have been published so far2,3. This report describes the observation of angiographically documented spontaneous thrombosis in an aneurysm located at the posterior cerebral-posterior communicating artery junction. The site of the aneurysm is also uncommon. Case report
A 40-year-old housewife developed sudden headache at night, initially in the occipital region but soon becoming diffuse. There was no associated vomiting or loss of consciousness. Lumbar puncture revealed haemorrhagic cerebrospinal fluid. Thirty hours later she became drowsy for 12 hours, but recovered spontaneously. CT scan of the head done on the 10th day revealed a small infarction in the right posterior temporal region. No subarachnoid blood or hydrocephalus was appreciated on the scan. Repeat spinal puncture on 12th day showed xanthochromic fluid. Right carotid angiography done at the referring hospital on the 16th day demonstrated an aneurysm at the right posterior
Summary
Spontaneous thrombosis of cerebral aneurysms demonstrated by angiography is infrequent. This article describes angiographically documented spontaneous thrombosis of an intracranial aneurysm at the posterior cerebralposterior communicating artery junction in a 40-year-old woman. The initial angiogram done on 16th day after an episode of subarachnoid haemorrhage showed a medium sized aneurysm. Subsequent angiograms done on 30th, 40th and 60th day failed to demonstrate the aneurysm. The factors leading to this rare event remain obscure. Key words: Cerebral aneurysm, cerebral angiography, thrombosis, subarachnoid haemorrhage .
cerebral-posterior communicating artery junction (Fig. 1 A & B). The aneurysm measured about 8 mm in diameter with regular margins. Adjacent vessels were normal. On admission to our Institute on the 27th day, she complained of mild headache. There was no neurological deficit. She was normotensive. To evaluate the width of the neck, direction of fundus and relation to the surrounding vessels, angiography was repeated on the 30th day. The aneurysm was not visualised (Fig. 2 A & B). There was no vasospasm either. Conservative management
Department of Radiology, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Address for correspondence and reprint requests: Sunil Kumar, Assistant Professor, Tirunal Institute for Medical Sciences & Technology, Trivandrum -695 011, India.
Trivandrum-695
01 I, India.
Department of Radiology,
Sree Chitra
Accepted 24-4-90 Clin New-01 Neurosurg 1991. Vol. 93-2
151
Fig. 1. [A & B). Right Carotid Angiogram AP (A) and Lateral (B). Aneurysm is shown on 16th day rn Posterior ierebralPosterior communicating Artery junction.
Fig. 2. (A & B). Right Carotid Angiogram (30th day) AP (A) and Lateral (B). No aneurysm is shown.
A Fig. 3. (A & B). Right Carotid Angiogram (40th day) AP (A} and Lateral (B). Still no aneurysm is demonstrated. is evident.
152
No vasospasm
was continued. No antifibrinolytic agents were given. The patient gradually improved during her stay in the hospital and was conscious and well oriented throughout. She was discharged after repeat angiography on 40th day which again did not show the aneurysm (Fig. 3 A & B). Subsequently, a digital subtraction angiogram done 2 months after the ictus also failed to reveal any abnormality. She remained asymptomatic up to the last follow-up 1 year later.
vasospasm, and had disappeared on the subsequent angiographies. Because no antifibrinolytic drugs had been administered, the present case exemplifies that one of the ways of the natural history of cerebral aneurysm is spontaneous and complete thrombosis. In as much as the majority of visualised aneurysms are neurosurgically managed over the past 50 years, no reliable figures are available whether spontaneous thrombosis is much more frequent than one is led to assume.
Discussion Acknowledgements In spite of extensive literature on the natural history of cerebral aneurysms, reports of angiographically documented thrombosis of congenital aneurysms are scant2*3.Thrombosis in giant intracranial aneurysms is more common, about 50% showing partial thrombosis4. Moritake et al were unable to define any single factor responsible for intraaneu~smal thrombosis3. Factors which promote the blood flow stasis or disturb clot lysis, such as vasospasm and a relatively narrow aneurysmal neck, are considered to be mainly responsible3,5. The width of the neck, in the angiogram done at the referring hospital, was not appreciated. To evaluate this, as well as the direction of the fundus, the angiography was repeated at our Institute to aid the neurosurgical approach. Vasospasm has a maximum incidence between 6th and 9th day though it may appear on the 3rd and last up to the 14th day’. The aneurysm in our patient was visualised on the angiogram done on the 16th day and revealed no
We are gratefulto the Director of our Institute for his kind permission to send this for publication. We also wish to thank Mrs. K. Ammukutty for Secretarial assistance and Mr. George for the illustrations.
References EDN~RG,FORSTERDM~,STE~NERL,BERGVALL~. Spontaneous healing of intracranial aneurysms after subarachnoid haemorrhage. Case report. J Neurosurg 1978, 48:450-4. DAVILA
S,OLIVER
B,MOLETJ,BARTUMEUS
F. SpOtltBtle-
thrombosis of an intracranial aneurysm. Surg Neural 1984,22:29-32. MORI'~AKEI<,HANDAH,~~T~URA~,HASW~~~TON. Vanishing Cerebral aneurysm in serial angiography. Surg Neural 1981, l&36-40. WHITT~_EIR,D~RSCHNW,BESSERM. Spontaneousthrombosis in giant intracranial aneurysms. J Neurol Neurosurg Psychiatry 1982; 45:1040-7. SENGUPTA RP, MCALLISTER VL teds). Chapter 12 “Vasospasm” & Chapter 7 - “Cerebral Angiography”. In “Subarachnoid Haemorrhage”. Berlin. Heidelberg: Springer Verlag, 1986, Pages 269-81,117&i. ous
153
Introduction
Approximately l-2% of ruptured arterial aneurysms may thrombose completely, usually observed at operation or autopsy examination’. Angiographically documented thrombosis in a cerebral aneurysm is even less frequent. Only a few case reports have been published so far2,3. This report describes the observation of angiographically documented spontaneous thrombosis in an aneurysm located at the posterior cerebral-posterior communicating artery junction. The site of the aneurysm is also uncommon. Case report
A 40-year-old housewife developed sudden headache at night, initially in the occipital region but soon becoming diffuse. There was no associated vomiting or loss of consciousness. Lumbar puncture revealed haemorrhagic cerebrospinal fluid. Thirty hours later she became drowsy for 12 hours, but recovered spontaneously. CT scan of the head done on the 10th day revealed a small infarction in the right posterior temporal region. No subarachnoid blood or hydrocephalus was appreciated on the scan. Repeat spinal puncture on 12th day showed xanthochromic fluid. Right carotid angiography done at the referring hospital on the 16th day demonstrated an aneurysm at the right posterior
Summary
Spontaneous thrombosis of cerebral aneurysms demonstrated by angiography is infrequent. This article describes angiographically documented spontaneous thrombosis of an intracranial aneurysm at the posterior cerebralposterior communicating artery junction in a 40-year-old woman. The initial angiogram done on 16th day after an episode of subarachnoid haemorrhage showed a medium sized aneurysm. Subsequent angiograms done on 30th, 40th and 60th day failed to demonstrate the aneurysm. The factors leading to this rare event remain obscure. Key words: Cerebral aneurysm, cerebral angiography, thrombosis, subarachnoid haemorrhage .
cerebral-posterior communicating artery junction (Fig. 1 A & B). The aneurysm measured about 8 mm in diameter with regular margins. Adjacent vessels were normal. On admission to our Institute on the 27th day, she complained of mild headache. There was no neurological deficit. She was normotensive. To evaluate the width of the neck, direction of fundus and relation to the surrounding vessels, angiography was repeated on the 30th day. The aneurysm was not visualised (Fig. 2 A & B). There was no vasospasm either. Conservative management
Department of Radiology, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Address for correspondence and reprint requests: Sunil Kumar, Assistant Professor, Tirunal Institute for Medical Sciences & Technology, Trivandrum -695 011, India.
Trivandrum-695
01 I, India.
Department of Radiology,
Sree Chitra
Accepted 24-4-90 Clin New-01 Neurosurg 1991. Vol. 93-2
151
Fig. 1. [A & B). Right Carotid Angiogram AP (A) and Lateral (B). Aneurysm is shown on 16th day rn Posterior ierebralPosterior communicating Artery junction.
Fig. 2. (A & B). Right Carotid Angiogram (30th day) AP (A) and Lateral (B). No aneurysm is shown.
A Fig. 3. (A & B). Right Carotid Angiogram (40th day) AP (A} and Lateral (B). Still no aneurysm is demonstrated. is evident.
152
No vasospasm
was continued. No antifibrinolytic agents were given. The patient gradually improved during her stay in the hospital and was conscious and well oriented throughout. She was discharged after repeat angiography on 40th day which again did not show the aneurysm (Fig. 3 A & B). Subsequently, a digital subtraction angiogram done 2 months after the ictus also failed to reveal any abnormality. She remained asymptomatic up to the last follow-up 1 year later.
vasospasm, and had disappeared on the subsequent angiographies. Because no antifibrinolytic drugs had been administered, the present case exemplifies that one of the ways of the natural history of cerebral aneurysm is spontaneous and complete thrombosis. In as much as the majority of visualised aneurysms are neurosurgically managed over the past 50 years, no reliable figures are available whether spontaneous thrombosis is much more frequent than one is led to assume.
Discussion Acknowledgements In spite of extensive literature on the natural history of cerebral aneurysms, reports of angiographically documented thrombosis of congenital aneurysms are scant2*3.Thrombosis in giant intracranial aneurysms is more common, about 50% showing partial thrombosis4. Moritake et al were unable to define any single factor responsible for intraaneu~smal thrombosis3. Factors which promote the blood flow stasis or disturb clot lysis, such as vasospasm and a relatively narrow aneurysmal neck, are considered to be mainly responsible3,5. The width of the neck, in the angiogram done at the referring hospital, was not appreciated. To evaluate this, as well as the direction of the fundus, the angiography was repeated at our Institute to aid the neurosurgical approach. Vasospasm has a maximum incidence between 6th and 9th day though it may appear on the 3rd and last up to the 14th day’. The aneurysm in our patient was visualised on the angiogram done on the 16th day and revealed no
We are gratefulto the Director of our Institute for his kind permission to send this for publication. We also wish to thank Mrs. K. Ammukutty for Secretarial assistance and Mr. George for the illustrations.
References EDN~RG,FORSTERDM~,STE~NERL,BERGVALL~. Spontaneous healing of intracranial aneurysms after subarachnoid haemorrhage. Case report. J Neurosurg 1978, 48:450-4. DAVILA
S,OLIVER
B,MOLETJ,BARTUMEUS
F. SpOtltBtle-
thrombosis of an intracranial aneurysm. Surg Neural 1984,22:29-32. MORI'~AKEI<,HANDAH,~~T~URA~,HASW~~~TON. Vanishing Cerebral aneurysm in serial angiography. Surg Neural 1981, l&36-40. WHITT~_EIR,D~RSCHNW,BESSERM. Spontaneousthrombosis in giant intracranial aneurysms. J Neurol Neurosurg Psychiatry 1982; 45:1040-7. SENGUPTA RP, MCALLISTER VL teds). Chapter 12 “Vasospasm” & Chapter 7 - “Cerebral Angiography”. In “Subarachnoid Haemorrhage”. Berlin. Heidelberg: Springer Verlag, 1986, Pages 269-81,117&i. ous
153