{'fraction_non_alphanumeric': 0.02585034013605442, 'fraction_numerical': 0.0, 'mean_word_length': 5.4801762114537445, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
TIAs and the pathology of cerebral ischemia

The term “transient ischemic attack,” or TIA, refers to a clinically detectable event that is neurologically transient. Implicit in the definition is the assumption that the underlying cerebrovascular occlusion is also transient, i.e., that there is an arterial occlusion responsible for the symptoms, the obstruction is relieved and, through the restitution of flow, there is no residual injury but rather a complete recovery from neurologic symptoms. This sequence presumes that any neuron injury is short-lived and that there is no detectable evidence of sustained injury. An alternative to this accepted view of TIA is the hypothesis that, in the setting of transient ischemia, there is residual and permanent injury to neurons and their supporting cells (e.g., glia, astrocytes, microvessels) that remains clinically silent. This section of the supplement examines the evidence supporting the view that the pathologic accompaniment of TIA is a permanent type of neuron injury. I focus on two questions drawn from experimental data: (a) whether a vascular lesion, in this particular case, a carotid artery lesion, can continuously produce local arterial occlusion with downstream embolization into the cerebral microvasculature, and (b) whether experimental transient occlusions of the microvasculature affect neuron integrity of the ischemic territory and whether that impact of emboli produces permanent injury (table).