Case reports / Journal of Clinical Neuroscience 14 (2007) 775–777 18. Veras LM, Pedraza-Gutierrez S, Castellanos J, et al. Vertebral artery occlusion after acute cervical spine trauma. Spine 2000;25: 1171–7.
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19. Lehmer SM, Steffee AD, Gaines Jr RW. Treatment of L5–S1 spondyloptosis by staged L5 resection with reduction and fusion of L4 onto S1 (Gaines procedure). Spine 1994;19:1916–25.
doi:10.1016/j.jocn.2006.03.003
Simultaneous supra and infratentorial hypertensive intracerebral haemorrhage Ozgur Ozdemir a
a,*
, Tarkan Calisaneller a, Erkan Yildirim b, Nur Altinors
a
Neurosurgery Department, Baskent University Faculty of Medicine, Ankara, Turkey Radiology Department, Baskent University Faculty of Medicine, Ankara, Turkey
b
Received 23 November 2005; accepted 18 February 2006
Abstract Spontaneous intracerebral haemorrhage is a devastating illness with highmortality and morbidity. Multiple simultaneous intracerebral haemorrhages (MSIHs) in different arterial territories occur rarely. This multiplicity complicates management and increases the mortality rate. A 67-year-old right-handed man with a long history of hypertension was admitted to our hospital with acute loss of consciousness. After the diagnosis of MSIH he was medically treated in the intensive care unit and died 2 days after initial admission. Diagnosis and management of MSIH are discussed with refence to the current literature. 2006 Elsevier Ltd. All rights reserved. Keywords: Hypertension; Multiple simultaneous intracerebral haemorrhages
1. Introduction Spontaneous intracerebral haemorrhages account for approximately 10–15% of all strokes.1,2 Hypertensive multiple simultaneous intracerebral haemorrhages (MSIHs) are rare, particularly in the supra and infratentorial compartments.3,4 We present a patient with simultaneous supra and infratentorial hypertensive intracerebral haemorrhages.
2. Case report A 67-year-old right-handed man with a long history of hypertension was admitted to our hospital with acute loss of consciousness. His neurological examination revealed decerebrate posture to central painful stimulus. His pupils were dilated with a very weak reaction to light. His Glas-
*
Corresponding author. Address: Baskent Universitesi Hastanesi, Beyin Cerrahisi B-blok zemin kat, Hoca Cihan Mahallesi, Saray caddesi, No: 1 Selcuklu / KONYA, 42080 Turkey. Tel.: +90 0332 257 060; fax: +90 0332 257 0637. E-mail address:
[email protected] (O. Ozdemir).
cow Coma Scale score (GCS) was four. Blood pressure was measured at 220/110 mmHg in the emergency room. A CT scan was performed 1 hour after the insult and showed a left-sided thalamic haematoma extending into the ventricles (Fig. 1) and haemorrhage in the right cerebellar peduncle that opened into the 4th ventricle (Fig. 2). His blood biochemistry was normal except for a blood sugar level of 130 mg/dL. He had no history of tobacco use or alcohol consumption. He was intubated and anti-edema and anti-hypertensive treatments were started immediately. Despite vigorous intravenous anti-hypertensive medication, his blood pressure level persisted over 160/100 mmHg. His neurological condition did not improve and he died 2 days after admission.
3. Discussion Approximately 10–15% of all strokes are intracerebral haemorrhages (ICHs).1,2 Among ICHs, multiple simultaneous intracerebral haemorrhages (MSIHs) in different arterial territories are rare and the incidence is reported between 0.7–2.8% of all ICHs.3–6
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Case reports / Journal of Clinical Neuroscience 14 (2007) 775–777
Fig. 1. Non-contrast axial brain CT scan showing a large left thalamic hematoma extending into the ventricles.
Known etiological factors for MSIHs include haematological disorders, vasculitis, anticoagulant therapy, drug abuse, cerebral amyloid angiopathy in the elderly and the transformation of multiple ischemic infarctions into haemorrhagic infarctions.4,5,7 However, chronic hypertension is the best known cause of ICH.8 The underlying pathophysiology of hypertensive MSIH is still unclear. In the early course of bleeding, most of patients remain hypertensive despite antihypertensive medication and this may cause an increase in the haematoma volume during this period.9 Komiyama et al. reported MSIH in a hypertensive patient and suggested that MSIH can be caused by simultaneous haemorrhages from different arteries or sustained hypertension due to an intracerebral haemorrhage which can trigger another haemorrhage in a different arterial territory.6 Because of the degenerative effects of hypertension on penetrating arteries, both single and multiple hypertensive haemorrhages are mostly located in the basal ganglia, thalamus and posterior fossa.3 Our patient had a history of inadequate blood pressure control that could be the major contributing factor for this ICH. The location of the haemorrhages and the history of uncontrolled hypertension are compatible with the other reports in the literature. Treatment may be either medical or surgical, based on the GCS of the patient, location and size of the haematomas or presence of additional medical problems. Patients with GCS less than five or those with additional medical problems as in our case should be treated medically.10 The majority of patients with MSIHs have poor outcome because of severely impaired consciousness, tetraparesis and pseudobulbar palsy caused by thalamic or putaminal haemorrhages, even when the hematomas are not large at onset.4,6 In conclusion, supra and infratentorial MSIHs are rare. Because of high mortality and morbidity, treatment of this devastating condition is difficult and preventive measures must be taken. References
Fig. 2. Non-contrast axial brain CT scan shows a hematoma in the right cerebellar peduncle and in 4th ventricle.
1. Bogousslavsky J, Van Melle G, Regli F. The Lausanne Stroke Registry: analysis of 1,000 consecutive patients with first stroke. Stroke 1988;19:1083–92. 2. Davis SM, Kaye AH. Therapy for intracerebral haemorrhage. J Clin Neurosci 2005;12:219–20. 3. Maurino J, Saposnik G, Lepera S, et al. Multiple simultaneous intracerebral haemorrhages: clinical features and outcome. Arch Neurol 2001;58:629–32. 4. McCormick WF, Rosenfield DB. Massive brain haemorrhage: a review of 144 cases and an examination of their causes. Stroke 1973;4:946–54. 5. Weisberg L. Multiple spontaneous intracerebral haematomas: clinical and computed tomographic correlations. Neurology 1981;31:897–900. 6. Komiyama M, Yasui T, Tamura K, et al. Simultaneous bleeding from multiple lenticulostriate arteries in hypertensive intracerebral haemorrhage. Neuroradiology 1995;37:129–30.
Case reports / Journal of Clinical Neuroscience 14 (2007) 777–779 7. Gilles C, Brucher JM, Khoubesserian P, et al. Cerebral amyloid angiopathy as a cause of multiple intracerebral haemorrhages. Neurology 1984;34:730–5. 8. Juvela S, Hillbom M, Palomaki H. Risk factors for spontaneous intracerebral haemorrhage. Stroke 1995;26:1558–64.
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9. Broderick JP, Brott TG, Tomsick T, et al. Ultra-early evaluation of intracerebral haemorrhage. J Neurosurg 1990;72:195–9. 10. Butcher K, Laidlaw J. Current intracerebral haemorrhage management. J Clin Neurosci 2003;10:158–67.
doi:10.1016/j.jocn.2006.02.009
Saccular bilobed aneurysm of an azygos anterior cerebral artery Anita Jagetia *, Pratap N. Kumar, Sanjiv Sinha, Ajay Sharma G.B. Pant Hospital and Maulana Azad Medical College, Department of Neurosurgery, 1-JL Nehru Marg, New Delhi 110002, India Received 19 October 2005; accepted 5 February 2006
Abstract An azygos anterior cerebral artery is an anatomical variant in which the anterior communicating artery is absent and both the A1 segments unite to form a single A2 segment of the artery. This anatomical variant may be associated with holoprosencephaly and may predispose to aneurysm formation, however the association of such an anomaly with an aneurysm is rare. When associated with an aneurysm, it poses management difficulties due to the single distal anterior cerebral artery. Most of the reported aneurysms with such an anomaly are saccular and located in the distal part of the artery. We report a patient with a wide neck saccular multilobed aneurysm who presented after a grade 3 subarachnoid haemorrhage. A right pterional craniotomy and clipping of the aneurysm was performed following cerebral angiography. The mechanism of formation and difficulties in management of such an aneurysm is discussed. 2006 Elsevier Ltd. All rights reserved. Keywords: Azygos anterior cerebral artery; Saccular aneurysm; Clipping
1. Introduction Azygos anterior cerebral artery (ACA) is an uncommon developmental anomaly in adults with an incidence of less than 1% in the general population.1 In this anatomical variant, the distal A2 segment of both ACAs is represented by a single common trunk and is the source of arterial supply to both the basifrontal regions. This type of anomaly is associated with neural migration defects and is prone to the formation of aneurysms.2 This anomaly is rarely encountered in neurosurgical practice and to the best of our knowledge only 54 cases of aneurysms associated with this anomaly have been reported in the literature.3 When this anomaly is associated with an aneurysm, it creates technical difficulties in surgical management. The morphology of such an aneurysm reported in the literature is generally saccular and single-lobe. We report a patient with an azygos ACA and subarachnoid hemorrhage. The morphology of the aneurysm was com*
Corresponding author. Tel.: + 91 11 22725525; fax: +91 11 23234242. E-mail address:
[email protected] (A. Jagetia).
plex, that is wide-neck, saccular and multilobed. The mechanism of formation and problems encountered in the management of such an aneurysm are discussed. 2. Case report A 58-year-old woman was referred to us for the management of subarachnoid hemorrhage. CT scan of the head revealed diffuse blood in the basal cisterns, Sylvian fissure and inter-hemispheric fissure and the fourth ventricle (Fig. 1). The patient had acute onset of headache 10 days previously. When admitted to our institute, she was World Federation of Neurosurgeons Grade 3. She had neck rigidity with normal fundus examination. The routine hematological and biochemical examinations were normal. In view of the subarachnoid hemorrhage, digital subtraction cerebral angiography was done which revealed a wide-neck saccular bilobed aneurysm arising from the A2 segment of the ACA just proximal to its bifurcation, filling from the right ACA. The aneurysm appeared to be a few millimeters from the site of the anterior communicating artery. There was focal spasm of the ACA (Figs. 2 and 3) Based on the angiographic