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Cryptogenic stroke is defined as brain infarction that is not attributable to a source of definite cardioembolism, large artery atherosclerosis, or small artery disease despite a thorough vascular, cardiac, and serologic evaluation. Embolic stroke of undetermined source (ESUS) is defined as a nonlacunar brain infarct without proximal arterial stenosis or cardioembolic sources. ESUS represents a subset of cryptogenic stroke.
The pathophysiology of cryptogenic stroke is likely heterogeneous. Proposed mechanisms include cardiac embolism secondary to occult paroxysmal atrial fibrillation, aortic atheromatous disease or other cardiac sources, paradoxical embolism from atrial septal abnormalities such as patent foramen ovale, hypercoagulable states, and preclinical or subclinical cerebrovascular disease.
In our study, 55 CS patients,out of 482 patients, were included representing 11.4% of total ischemic stroke patients included during the study time and Laboratory investigations were done including routine lab (complete blood picture, liver functions, kidney functions, electrolytes), ESR, CRP, ANA, Anti DNA, anticardiolipin antibody, lupus anticoagulant, ANCA P and ANCA C, Protein C, protein S, antithrombin ш.
A panel of investigations were done including 48 hours Holter ECG, TEE and TCD for detection of RLS.
A venous sample was obtained from each patient for detection of homocysteine levels and Alpha Galactosidase A enzyme level as screening tool for Fabry Disease.
Our results showed that considerable percentage of the patients had PFO together with active RLS and ASA while 48 Hours Holter ECG only detected pAF in small proportion of the patients, yet the potential cardiac causes were detected in almost half of the patients.
Our results also showed that TCD is considered a sensitive tool for RLS detection in CS patients.
Our results also showed that thrombophilias, whether inherited or acquired, might play an important role in the etiology of CS.
Homocysteine levels showed statistical significance between cases and controls which shows that hyperhomocysteinemia may play a role in the etiology of CS.
On the other hand, there was statistical significance regarding GLA levels between cases and controls yet none of the patients had levels lower than 0.1 µg/L which is the known cut off of GLA enzyme.
There was no statistical significance regarding MRI parameters between Cardiac and non-cardiac causes.
CS patients constitute a heterogeneous group of patients leading to therapeutic implications based on the potential mechanism. This approach, in addition to risk factor management and lifestyle modifications, will lead to improved stroke prevention strategies in patients with CS. This will allow for targeted clinical trials to improve stroke prevention strategies in this patient population.