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Subarachnoid haemorrhage and cerebrovascular traumatic pathology
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
Daniel du Plessis, Paul Johnson
The degree of trauma is not necessarily severe, but the demonstration of deep paravertebral bruising or a C1 fracture rules out minor trauma. The investigative approach should include assessment of the arterial system for any predisposing anatomical abnormalities and conditions potentially contributing to greater susceptibility for rupture and/or dissection. This includes short upper cervical loop segments (Medcalf 2016) and conditions such as fibromuscular dysplasia, segmental arterial mediolysis (SAM), vascular Ehlers-Danlos disease (type IV EDS) and Marfan's syndrome. In our experience, pre-existing vascular degenerative disease is only identified in a very small minority of cases. Post-mortem genetic testing for vasculopathies can be undertaken and Pickup and Pollanen (2011) demonstrated mutations in the COL3A1 gene associated with vascular Ehlers-Danlos syndrome (type IV EDS) in two cases of traumatic subarachnoid haemorrhage. A common role for this condition as a susceptibility factor though has so far not been confirmed. Whilst exceptionally a tear appears to develop at the edge of an atheromatous plaque, good evidence that atherosclerotic cerebrovascular disease predisposes to traumatic tears and dissections is wanting, but a bias towards younger age group victims may be responsible for this observation. In properly investigated cases, arterial dissections may also be found in the terminal part of the extracranial vertebral artery, usually discontinuous with an intracranial site of rupture. Tears are typically identified on the same side of the causative impact. Rapid hyperextension/flexion of the neck without blunt impact has been reported to lead to tears on occasion (Gee 1982) and the vessels are known to be susceptible to longitudinal extension (Johnson et al. 2000). Elegant flow dynamic studies (Farag et al. 1988) showed that sudden occlusion of the vertebral arteries can induce reverse blood flow and induce tearing in the typical locations found in case work.
Polyarteritis nodosa: an evolving primary systemic vasculitis
Published in Postgraduate Medicine, 2023
Non-vasculitis disorders and vasculopathies can also mimic PAN. Segmental arterial mediolysis (SAM) is a vasculopathy that commonly affects the mesenteric vasculature, with similar radiographic characteristics to PAN. SAM causes vacuolization of the vessel wall, commonly presenting as aneurysms radiographically [27]. Fibromuscular dysplasia (FMD) is an arterial vasculopathy that can lead to stenosis, occlusion, dissection, or aneurysm formation of medium vessels, similar to PAN. Distribution of vessel involvement can be a clue to differentiating PAN from FMD, with PAN more commonly affecting visceral arteries. Involvement of the renal, carotid, and/or vertebral with a ‘bead on a string’ appearance can be important clues in the diagnosis of FMD. Atherosclerosis, thrombotic disorders, embolic disease, ergotism, radiation fibrosis, and malignant atrophic papulosis are other important mimics to consider.
A case of multiple aneurysms with stenosis in the coronary and peripheral arteries of a patient with systemic lupus erythematosus
Published in Modern Rheumatology Case Reports, 2018
Ryosuke Hara, Masahiro Yasumura, Takanori Ichikawa, Tomoki Tanaka, Seiichi Ono, Sadahiro Suzuki, Fusazo Urano
The known causes of CAAs include SLE, congenital disorders (e.g. polycystic kidney disease, Ehlers–Danlos syndrome), Kawasaki disease, syphilis, Takayasu arteritis, polyarteritis nodosa, Behçet’s disease, IgG4-related disease, segmental arterial mediolysis and infectious aneurysm. In this case, the patient had no history of congenital disease or Kawasaki disease, and did not present with infectious disease. Takayasu arteritis often causes lesions in the coronary arteries lesions, as well as vascular obstruction in the extremities; however, no characteristic lesions were detected in the aorta or its branches, and the aneurysms and thrombi occurred in smaller arteries. Although CAA and gangrene of the limbs are rare complications of polyarteritis nodosa, the present case did not satisfy the criteria for this classification. We excluded Behçet’s disease because she lacked oral aphthous ulcers, genital ulcers, abnormal skin lesions and ocular lesions. Her normal level of IgG4 suggests that IgG4-related disease was negative. Segmental arterial mediolysis was also negative because abdominal visceral artery aneurysm was not detected. Therefore, we considered that antiphospholipid antibody syndrome might be responsible for thromboembolism in the peripheral artery. However, this would be a case of chronic inflammation associated with vasculitides, as the onset was not acute and the condition was accompanied by aneurysms.