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- , MD, FAHA, , MEDITERRANEO HOSPITAL

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NON-ATHEROSCLEROTIC VASCULOPATHIESNon-Inflammatory

1. Arterial dissection (traumatic and spontaneous)2. Fibromuscular dysplasia3. Moyamoya disease4. Radiation-induced vasculopathy

ATHENS YOUNG STROKE REGISTRY(Spengos and Vemmos, Eur J Neurol 2010)253 first ever ischemic stroke patients collected over 10 years

Dissection was present in 6,7% of cases

(Saver, Stroke Pathophysiology, Diagnosis and Management 1998) 70 ) - , , ( ) >50 mm/h ( 75% ) : , , , , - ,

33

(Wilkinson and Russell, Arch Neurol 1972; Gonzalez-Gay et al, Medicine 2000) , , ; ( ) (arteritic AION) 1/3

Wallenberg ( ), top of the basilar (. ), ( .) (Caselli et al, Neurology 1988; Gibb et al, J Neurol Neurosurg Psychiatry 1985; Ruegg et al, Medicine 2003) (Caselli et al, Neurology 1990) (De Keyser et al, BMJ 1991; Foroozan et al, Ophthalmology 2002)

, , (Peyo-Reygosa et al, Clin Exp Rheumatol 2004; Ray et al, Heart 2005) (Evans et al, Ann Int Med 1995;Gonzalez-Gay et al, Medicine 2004) (Nesher et al, Arthritis Rheumatol 2004)

, , 0.7 1,8 100000 (Brown and Swash, Handbook of Clinical Neurology 1989) , 40-60 (Guillevin et al, Neurol Clin 1997) , 1970 (Trpo and Thivolet, Vox Sang 1970; Gocke et al, Lancet 1970)

(Colmegna and Maldonado-Cocco, Curr Rheumatol Rep 2005) 36% 1970 7-10% ( ) , , ,

, , . : ,

(Cohen et al, Mayo Clin Proc 1980; Conn, Rheum Dis Clin North Am 1990; Moore, Ann Neurol 1995)

VZV DNA- , VZV 2 :

VZV , , (C) / (ACA) (Doyle et al, Ann Neurol 1983; Gasperetti and Son, J Neurol Neurosurg Psychiatry 1985; Hilt et al, Ann Neurol 1983)

VZV , 60 , 25% 34% (Hilt et al, Ann Neur 1983) AEE , (Reshef et al, J Neurol Neurosurg Psychiatry 1985), / MCA ACA :

VZV 1981 (Horton et al, Ann Neurol 1981) (Amlie-Lefond et al, Ann Neurol 1995; Baudrimont et al,Neuropathol Appl Neurobiol 1994; Kronenberg et al; Clin Infect Dis 2002) , ,

VZV , , , - (Amlie-Lefond et al, Ann Neurol 1995) , :

Sjgren

SLE and StrokeCNS involvement in SLE was first described by Kaposi in 1869The first reference to recurrent focal cerebral ischemia in SLE was made by Osler in 1903 who reported a patient with 5-6 episodes of aphasia and hemiplegiaDue to vasculitic changes observed in the skin of patients with SLE, Osler postulated that similar vascular changes in the brain could be responsible for the focal neurologic symptomsLibman and Sacks described endocarditis in SLE in 1924 (Arch Intern Med 1924); they suggested that the left leg paralysis in one of their patients was caused by a cerebral embolus from the heartBowie et al in 1963 described the association of lupus anticoagulant and thrombosis in pts with SLE (J Lab Clin Med 1963)

SLE and StrokeJohnson and Richardson in 1968 reported the neuropathologic findings in 24 patients with SLE and noted that true cerebral arteritis was rare (Medicine 1968)Devinsky et al in 1988 reported an autopsy study of 50 SLE patients; 10 patients had embolic cerebral infarcts, 5 of them due to Libman-Sacks endocarditis, and no case of active intracranial vasculitis was observed (Ann Neur 1988)SLE is an uncommon cause of stroke even in young persons, being found in 3,5% of patients presenting with stroke before the age of 45 (Adams et al, Arch Neur 1995)

SLE and Stroke 3-20% 5 (Futrell and Millikan, Stroke 1989; Kitagawa et al, Stroke 1990) , ,

SLE and Stroke

Etiology of Stroke in SLECardiogenic emboli

Hypercoagulable states

Atherosclerosis

Thrombogenic cytokines

Vasculitis

Cardioembolic Strokes in SLELibman-Sacks vegetations were found and considered the most frequent probable mechanism of stroke in patients with SLE (Roldan et al NEJM 1996, Roldan et al JACC Cardiovasc Imaging 2013)Libman-Sacks endocarditis is a verrucous endocarditis with deposition of hyalinized blood and platelet thrombus, not covered by endothelium. They involve cardiac valves and endocardium, and can produce emboliThe most frequently diseased valve is the mitral valveZuily et al studied SLE patients with Libman-Sacks endocarditis and found antiphospholipid antibodies in 30% (Curr Rheumatol Rep 2013)The hypercoagulability from APA leads to thrombotic manifestations on the cardiac valves

Atherosclerosis as cause of stroke in SLEAtherosclerosis is more frequent in SLE patients than in the general population, and is present at a younger ageSteroids which are frequently administered are associated with a lipid profile that is atherogenic (MacGregor et al, Ann Rheum Dis 1992)Mikdashi et al followed 238 consecutive patients with SLE and no history of stroke (Stroke 2007); 19% developed a first ischemic stroke, and the baseline predictors were disease activity, hypertension and hyperlipidemia

Hypercoagulable states as cause of stroke in SLEThe most frequent cause is related to the presence of antiphospholipid antibodies (including lupus anticoagulant and anticardiolipin antibodies)The presence of antiphospholipid antibodies in SLE patients increases most of all the incidence of stroke (Sanna et al, J Rheumatol 2003)The thrombogenic tendency of lupus anticoagulant and anticardiolipin antibodies is multifactorial, with contributions from defects in protein C (Amer et al, Thromb Res 1990) and protein S (Amster et al, J Am Acad Dermatol 1993), and low functional levels of antithrombin III (Cosgriff and Martin, Arthritis Rheum 1981)

Vasculitis as a cause of stroke in SLESystemic vasculitis is commonly observed in the kidneys and skinNeuropathological studies do not confirm the presence of vasculitis (Johnson and Richardson 1968, Devinsky et al 1988, Hanly et al 1991)The most common pathology is a vasculopathyIn cases with inflammatory changes within brain tissue and brain blood vessels, infection is an important consideration, as it is commonFutrell and Millikan in a study of 105 patients with SLE found cerebral vasculitis occurring only in association with infection (Stroke 1989)

Protein C deficiencyProtein S deficiencyAntithrombin III deficiencyFactor V Leyden mutationProthrombin G20210A mutationHomocysteine levelsMTHFRAntiphospholipid antibodies (LA and aCL)