Clinical manifestations of carotid transient ischemic attacks include loss of blood flow in the region supplied by the anterior and middle cerebral arteries. In older individuals, only one carotid artery may supply the anterior and posterior cerebral arteries. Ischemia on one side of the cerebral hemisphere usually results in symptoms on the opposite side. Motor dysfunction may include numbness and dullness in one or both limbs on the opposite side of the affected cerebral hemisphere. It is true that this sensation may not manifest objectively when a patient is examined for seizures. 95% of patients have left hemisphere dominance. Both sensory aphasia and motor aphasia are present. When the former is present, patients and their families may dictate comprehension difficulties. Dysphonia may present as a result of a transient ischemic attack in the nondominant hemisphere. However, when dysphonia is present as a single symptom, it is more likely to be an episode of transient ischemia of the vertebrobasilar artery. Other non-dominant-side dysfunctions include the patient’s personal inattention to the environment contralateral to the lesion. Functional deficits in these areas have also been interpreted as comprehension deficits. Transient visual deficits (transient blackouts) or blurred vision are among the most reliable symptoms of transient ischemic attacks in the main carotid artery. This symptom may be described as a shuttering phenomenon (high degree of) or as quadrant visual field loss. Conjugate ocular deviations such as those seen in epilepsy and complete stroke are not seen. The co-occurrence of ipsilateral hemianopia and any of the symptoms described above supports a carotid transient ischemic attack. This is the result of ischemia in the optic radiation area originating from the optic nerve crossings, which explains the visual deficit in the ipsilateral temporal visual field of the lesion versus the contralateral nasal visual field. When transient ischemic episodes are secondary to carotid artery disease, these visual field deficits are usually confined to the quadrant area associated with the optic radiation distribution. When complete hemianopia is present, it cannot be distinguished from vertebrobasilar TIAs. In 10% of cases, optic nerve ischemia is characterized by blindness and associated with giant cell arteritis. In the other 90% of cases it was idiopathic. Berguer found an important association between extracranial occlusive disease and idiopathic optic neuropathy. In fact, significant extracranial occlusive disease was found in 12 out of 20 (60%) symptomatic eye examinations. Embolic mechanisms are thought to be the cause of optic nerve infarction. There is a more severe form in patients with severe extracranial disease, usually with occlusion on one side and high stenosis on the other. These patients develop ischemic eye disease characterized by iris neovascularization. rubeosis (redness of the iris) is used as a term to describe this feature. This suggests that the optic nerve not secondary to giant cell arteritis does not patients should undergo extracranial vascular examination. Twitching may be present but is more suggestive of a complete or hemorrhagic stroke. When secondary or primary symptoms are present, they all occur at once and do not have a clear indication of a partial seizure. Multiple symptoms may be more diagnostically reliable than the presence of a single symptom. In right carotid TIA, the co-presentation of ipsilateral visual loss and any contralateral arm symptoms increases the association between the two. In left-sided carotid TIA, the diagnostic reliability is increased when speech disorders are combined with right-sided facial or hand and foot weakness or sensory loss. Altered consciousness or syncope may be present, but this is rarely the only symptom and is usually associated with other conditions, such as cardiac arrhythmias. Other symptoms that can make the initial evaluation difficult are dizziness, amnesia, impaired comprehension, and visual deficits with altered consciousness. These clinical symptoms cannot be considered as clinical manifestations of TIA when they are not accompanied by other specific symptoms, as they are most often associated with other diseases.