from PART X - CEREBROVASCULAR DISORDERS
Published online by Cambridge University Press: 05 August 2016
Intracranial aneurysms and arteriovenous malformations (AVMs) are structural vascular lesions that are life threatening by virtue of their propensity to cause intracranial hemorrhage. The Greek word ‘aneurysma’ is derived from a combination of ‘ana-’ (up, through) and ‘eurynein’ (to widen) (Haubrich, 1984). Peripheral aneurysms were well recognized by Hippocratic times, when physicians were familiar with superficial traumatic vascular lesions (Weir, 1987). The first description of an intracranial aneurysm was probably by Biumi, in 1765 (Biumi, 1778) and the first clinical description differentiating subarachnoid hemorrhage (SAH) from other types of apoplexy was in 1813 (Blackall, 1825). Various surgical attempts were made to treat intracranial aneurysms in the late nineteenth and early twentieth centuries, including proximal ligation by Horsley and others and packing with muscle by Dott (1933), before the first definitive cure by clip application, which was performed by Dandy in 1937 (Dandy, 1938).
Cerebral arteriovenous malformations (AVMs) are some of the more challenging lesions to come under the ambit of neurological surgery. Regarding surgery for AVMs, Cushing considered any attempt at excision ‘foolhardy’ (Cushing & Bailey, 1928) and Northfield stated, ‘The dangers of fatal hemorrhage and the extensive damage to brain forbid any attempt’ (Northfield, 1940). It was not until the mid-twentieth century that these lesions were recognized as malformations rather than neoplasms. With the advent of arteriography and its widespread use by the 1940s and 1950s, an understanding of the configuration of feeding arteries and draining veins of AVMs emerged, along with more favourable surgical results (Bergstrand et al., 1936; Olivecrona & Riives, 1948; Pilcher, 1946).
Clinical presentation
Spontaneous disruption of the abnormal walls of AVMs and aneurysms results in intracranial hemorrhage with obvious catastrophic consequences. Most aneurysms and AVMs are not detected until such a rupture occurs. A minority of lesions will come to clinical attention because they cause mass effect on cranial nerves or the brain, obstruction of cerebrospinal fluid pathways, or epilepsy. Aneurysms occasionally present with ischemic deficits caused by thromboemboli originating from the aneurysm sac. Investigation of neurological symptoms with high resolution CT or MRI is leading to an increase in the incidental detection of vascular abnormalities.
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