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Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
Published on: March 15, 2022
Stopping "transient ischemic attacks" by antiplatelet withdrawal
Lina Palaiodimou1, Aikaterini Theodorou1, Stefanos Lachanis2
1Second Department of Neurology, National and Kapodistrian University of Athens, School of Medicine, "Attikon" University Hospital, Rimini 1, Chaidari, 12462, Athens, Greece.
Insights
Transient focal neurological episodes (TFNE) were misdiagnosed as TIAs in a patient with cerebral amyloid angiopathy. Stopping antiplatelet therapy resolved symptoms, highlighting the importance of recognizing cortical superficial siderosis.
Area of Science:
- Neurology
- Neuroradiology
- Vascular Neurology
Background:
- Transient ischemic attack (TIA) is a significant risk factor for ischemic stroke, necessitating thorough evaluation and secondary prevention.
- Accurate differential diagnosis is crucial to distinguish TIA from mimicking conditions.
Introduction:
Transient ischemic attack (TIA) is considered to be an important risk factor for the development of ischemic stroke and requires complete etiopathogenic evaluation and prompt initiation of secondary prevention treatment. In addition, an accurate differential diagnosis should be performed in order to exclude other disorders mimicking TIA.
Methods:
In this case report, we describe the clinical and neuroimaging evaluation and the differential diagnosis of a patient with suspected crescendo TIAs.
Results:
A 79-year-old man presented with recurrent episodes of right-sided numbness over the past 7 months, despite different single and dual antiplatelet therapies that were sequentially prescribed for suspected TIAs. Brain MRI revealed cortical superficial siderosis, symmetrical periventricular leukoencephalopathy and enlarged perivascular spaces. Cerebral amyloid angiopathy was considered in the differential diagnosis of the patient. Antiplatelet withdrawal was recommended and led to complete remission of the patient's transient focal neurological episodes (TFNE) that were initially misdiagnosed as TIAs.
Discussion:
Cortical superficial siderosis has been implicated as a key neuroimaging feature of cerebral amyloid angiopathy, a diagnosis which can be supported by the additional radiological findings of symmetrical white matter hyperintensities and enlarged perivascular spaces. Antiplatelet treatment in patients with cortical superficial siderosis may increase the frequency and severity of TFNE, while it increases exponentially the risk of intracerebral hemorrhage. The present case highlights that recognition of cortical superficial siderosis is crucial in the management of patients presenting with transient focal neurological symptoms that can be misdiagnosed as recurrent TIAs.
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