Cryptic Arteriovenous and Venous Hamartomas of the Brain

Crawford, J. V.; Russell, Dorothy S.

doi:10.1136/jnnp.19.1.1

Cited by 201 publications

(47 citation statements)

References 3 publications

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“…Their reported frequency in series of ICH has varied between 4 and 8% of the cases. 16 ' " The diagnosis is usually established by cerebral angiography or, more commonly, following histologic study of biopsy specimens taken at the time of surgical evacuation of the ICH. With the introduction of CT scanning, an increasing number of these lesions are being diagnosed by the demonstration of calcium deposits in their vicinity or, more commonly, by the post-contrast opacification of abnormal serpiginous vascular channels adjacent to an intracerebral hematoma.…”

Section: Small Vascular Malformationsmentioning

confidence: 99%

Intracerebral hemorrhage: non-hypertensive causes.

Kase¹

1986

Stroke

111

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SPONTANEOUS, non-traumatic intracerebral hemorrhage (ICH) in the adult is most commonly secondary to hypertensive cerebrovascular disease. In 70-90% of cases of spontaneous ICH, arterial hypertension is the presumed cause.1 These hypertensive hemorrhages show a predilection for certain anatomic locations: the basal ganglia (the putamen in particular), the subcortical white matter, and the thalamus account for 35%, 25%, and 20% of ICHs, respectively, whereas the posterior fossa locations, the cerebellum and pons, are responsible for only 10% and 5% of the cases.2 Irrespective of their anatomic locations, the common pathogenesis in these hemorrhages involves the hypertension-induced degeneration of the media of small (50-200 micra) arteries called "lypo-hyalinosis," 3 and/ or the formation of "microaneurysms", both of which occur preferentially in perforating or small sub-cortical arteries, thus resulting in the characteristic anatomic distribution of hypertensive ICH.A significant number of cases of ICH are due to causes other than hypertension. The frequency of such cases varies from 25% to 50% among series, and depends on the anatomic type of ICH being considered: non-hypertensive mechanisms may account for as many as 55% of "lobar" ICH cases, 4 ' 3 while pontine hemorrhage is virtually always (90%) hypertensive, and the deep ganglionic (putaminal, thalamic) and cerebellar varieties occupy an intermediate position (35%, 25%, and 38% being of non-hypertensive mechanism, respectively). Among the many possible mechanisms of ICH not primarily related to hypertension, there are several that occur with high enough frequency to warrant separate discussion. These causes of ICH are related to special types of arterial pathology, to the presence of brain tumors, or to the use of medications, and include: cerebral amyloid angiopathy, small vascular malformations, primary or metastatic brain tumors, oral anticoagulants, and amphetamines and a variety of other sympathomimetic drugs. Cerebral Amyloid AngiopathyThis condition is a unique form of angiopathy due to deposits of amyloid in the media and adventitia of

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Section: Small Vascular Malformationsmentioning

confidence: 99%

Intracerebral hemorrhage: non-hypertensive causes.

Kase¹

1986

Stroke

111

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“…The diagnostic criteria used by Kase et al' to support the diagnosis of lobar haematoma were used. These included: (1) absence of clinically detectable cardiac source of cerebral embolism; (2) CT evidence of a hyperdense lesion located in the subcortical white matter which extended beyond a specific arterial territory; (3) the haematoma was sometimes surrounded by an irregularly marginated hypodense region (representing oedema), but the irregular margination of the hypodense component excluded the diagnosis of infarction; (4) there was sometimes ventricular extension; (5) ring enhancement was sometimes seen if scan was performed 7 to 28 days after the haemorrhage; (6) were 2-2 to 3-3 cm in size. These patients initially had contralateral leg weakness (monoparesis) and this rapidly progressed to hemiparesis.…”

Section: Methods and Patientsmentioning

confidence: 99%

Subcortical lobar intracerebral haemorrhage: clinical-computed tomographic correlations.

Weisberg¹

1985

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY Fifty patients with spontaneous lobar haematomas were reviewed. Thirty-two were normotensive and eighteen were hypertensive. Vomiting, seizures, and altered consciousness were more common in hypertensive than in normotensive patients. Haematoma size (greater than 4-0 cm) and intraventricular extension occurred most commonly in hypertensive and rarely in normotensive patients. Twenty-eight per cent of hypertensive patients died, whereas none of the normotensive patients died.The majority of intracerebral haematomas are hypertensive in aetiology. These are usually located in the thalamic or basal ganglionic region; less commonly, they are in the cerebellum, brain stem, or subcortical white matter of the cerebral hemispheres (lobar haematomas). The finding of a lobar haematoma should initiate a thorough investigation for a specific neuropathological aetiology for the haemorrhage such as angioma, aneurysm, neoplasm, or an underlying medical condition (for example bleeding disorder, collagen vascular disease).The present report is an analysis of the clinicalcomputed tomographic correlations in 50 patients with non-traumatic acute lobar haematoma in whom a thorough clinical and laboratory investigation did not demonstrate a specific aetiology for the intracranial haematoma. Methods and patientsOf 489 consecutive patients who were studied prospectively with CT evidence of intracerebral haematoma, there were 68 patients with lobar haematomas. There were 18 patients in whom neurodiagnostic findings, laboratory studies and/or pathological findings showed a specific aetiology for the lobar haematomas ( There were 50 other patients with CT evidence of lobar haematoma in whom no aetiology was determined by CT findings, angiography, laboratory studies, and in some cases by surgical or necropsy studies. Patients with a history of trauma were excluded from this analysis. In an effort to ensure that patients with traumatic haemorrhagic contusions were not included, patients in whom trauma was even a remote consideration were excluded. The clinical and CT findings were reviewed by the author. The diagnostic criteria used by Kase et al' to support the diagnosis of lobar haematoma were used. These included: (1) absence of clinically detectable cardiac source of cerebral embolism; (2) CT evidence of a hyperdense lesion located in the subcortical white matter which extended beyond a specific arterial territory; (3) the haematoma was sometimes surrounded by an irregularly marginated hypodense region (representing oedema), but the irregular margination of the hypodense component excluded the diagnosis of infarction; (4) there was sometimes ventricular extension; (5) ring enhancement was sometimes seen if scan was performed 7 to 28 days after the haemorrhage; (6) when performed, angiogram showed evidence of an avascular mass and not a cortical branch occlusion (which would be consistent with cerebral embolism). Haematomas which appeared to originate in the ganglionic-thalamic region and then secondarily extended into the white m...

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“…22,23,33) Twenty-six of the 30 reported cases of chiasmal and/or optic nerve apoplexy were angiographically occult. Cryptic vascular malformation, which is not detectable by angiography, was first described in 1956, 5) and is occasionally responsible for spontaneous intracerebral hemorrhage. Such malformations may be angiographically occult for several reasons: very small lesion, hematoma compressing abnormal vessels, rupture of abnormal vessels, spasm of abnormal vessels, thrombus in abnormal vessels, or the technique of angiography used.…”

Section: Discussionmentioning

confidence: 99%

Chiasmal and/or Optic Nerve Apoplexy Due to Rupture of Vascular Malformation -Case Report-

Sasagawa

Akai

Sasaki

et al. 2008

Neurol. Med. Chir.(Tokyo)

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An 8-year-old boy presented with a rare case of optic nerve apoplexy caused by an arteriovenous malformation (AVM) manifesting as severe headache and blurred vision. Computed tomography (CT) showed a hyperdense suprasellar mass. Magnetic resonance (MR) imaging indicated a hematoma in the right optic nerve. MR angiography showed normal vessels. Right fronto-temporal craniotomy identified an aggregate of abnormal, nidus-like vessels adhering to the medial surface of the swollen right optic nerve and a drainer-like ectatic red vein. The diagnosis was probable AVM. To avoid optic nerve damage, the malformation was left intact. Two years later, the boy was readmitted with headache. CT showed bleeding, and angiography revealed feeder arteries and nidus in the suprasellar lesion. The diagnosis was optic nerve apoplexy due to AVM. His symptoms improved without intervention within days. He has not experienced any recurrence of the bleeding for 2 years.

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Cryptic Arteriovenous and Venous Hamartomas of the Brain

Cited by 201 publications

References 3 publications

Intracerebral hemorrhage: non-hypertensive causes.

Intracerebral hemorrhage: non-hypertensive causes.

Subcortical lobar intracerebral haemorrhage: clinical-computed tomographic correlations.

Chiasmal and/or Optic Nerve Apoplexy Due to Rupture of Vascular Malformation -Case Report-

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