Transient ischemic attack

Neurovascular Syndromes of the Carotid Territory

Involvement of the carotid system arteries produces prominent focal symptoms. The middle cerebral artery is most frequently affected.

With occlusion of the main stem of the middle cerebral artery, a total involvement syndrome develops:

• On the side contralateral to the lesion: hemiplegia, hemianopia, and hemianesthesia.
• Central paresis of the tongue and facial muscles occurs.
• Cortical gaze palsy is characteristic.
• In the case of dominant hemisphere involvement, total aphasia develops, while involvement of the nondominant hemisphere leads to body schema disorders and anosognosia.

With occlusion of the branches of the middle cerebral artery, the contralateral side shows hemiparesis (most pronounced in the arm) or isolated monoparesis of the arm, hemi- or monohypesthesia, superior quadrantanopia, as well as higher cortical function disorders (apraxia, aphasia).

Anterior cerebral artery involvement causes contralateral hemiparesis with predominant weakness in the leg and proximal arm, or isolated leg monoparesis. Urinary incontinence or retention frequently joins, while sensory disorders in the affected limbs are usually mild.

Internal carotid artery occlusion can mimic the clinical picture of anterior and middle cerebral artery involvement, yet its hallmark is considered to be oculopyramidal syndrome. It manifests as unilateral blindness (due to ophthalmic artery ischemia) combined with contralateral hemihypesthesia and hemiparesis.

Vertebrobasilar Territory Infarction

Includes brainstem syndromes and cerebellar structure involvement.

Occlusion of the vertebral or posterior inferior cerebellar artery leads to the formation of Wallenberg–Zakharchenko bulbar syndrome (involvement of the dorsolateral medulla oblongata):

• Vestibular and general cerebral manifestations (vomiting, nausea, dizziness).
• On the side of ischemia: Horner syndrome, cerebellar ataxia, facial hypesthesia (temperature and pain), as well as dysphonia, dysarthria, and dysphagia due to paralysis of the palatal, laryngeal, and pharyngeal muscles.
• On the contralateral side: temperature and pain hypesthesia of the trunk and limbs.

Involvement of pontine structures (occlusion of basilar artery branches) produces alternating syndromes. Millard–Gubler syndrome manifests as peripheral facial nerve palsy on the side of the lesion and contralateral hemiplegia. Foville syndrome is distinguished by the addition of abducens nerve (sixth cranial nerve) palsy on the affected side.

Occlusion of midbrain structures manifests with the following syndromes:

• Weber syndrome (crus cerebri involvement): oculomotor nerve palsy on the ischemic side and contralateral hemiplegia.
• Benedikt syndrome (tegmentum involvement): ipsilateral oculomotor palsy and contralateral hemiataxia.
• Parinaud syndrome (tegmentum involvement): convergence disorder, upward gaze palsy, bilateral partial ptosis.

Basilar artery occlusion proceeds extremely severely, causing tetraplegia, disruption of vital functions (circulation, respiration), loss of consciousness, and pronounced oculomotor disorders. Posterior cerebral artery occlusion leads to visual agnosia, memory impairments, and contralateral homonymous hemianopia.

Lacunar Infarcts

A lacunar infarct occurs due to small vessel pathology, usually develops abruptly (sometimes symptoms progress gradually), and is frequently asymptomatic. Five classic variants are distinguished:

1. Pure motor stroke: unilateral central paresis of the face, tongue, arm, and leg (involvement of the pons, internal capsule, or frontal lobe white matter).
2. Sensomotor stroke: a combination of hemihypesthesia and mild central hemiparesis (internal capsule involvement).
3. Pure sensory stroke: isolated hemihypesthesia (involvement of the thalamus, parietal white matter, or internal capsule).
4. Dysarthria–clumsy hand syndrome: dysarthria combined with mild arm weakness (lesion in the internal capsule or pons).
5. Ataxic hemiparesis: central hemiparesis accompanied by ataxia in the paretic limbs.

Diagnostic methods

The diagnosis is based on the sudden onset of a neurovascular syndrome, the presence of risk factors (advanced age, hypertension, atrial fibrillation), and instrumental examination data.

Neuroimaging:

• Non-contrast CT: serves as the "gold standard," reliably ruling out hemorrhage and tumors, but ischemic signs are visualized only several hours later.
• Perfusion CT: highly informative at the earliest stages (within the first hour).
• Diffusion-weighted MRI: detects lesions at the earliest timeframes, when conventional CT/MRI does not yet visualize them.
• Standard MRI: optimal for searching for small ischemic lesions in the cerebellum and brainstem.

Vascular examination: To assess the state of arteries, ultrasound methods (duplex scanning, transcranial Doppler) and angiography are used. X-ray cerebral angiography is the most informative yet invasive method; it is strictly indicated when planning surgical intervention or in young patients with an unclear cause of stroke. MR and CT angiography are safer, yet cannot visualize small intracranial vessel pathology.

Class and exam questions

What else to study on this topic

• Alternating Brainstem Syndromes (Foville, Millard–Gubler)
• Wallenberg–Zakharchenko Bulbar Syndrome
• Differential Diagnosis of Lacunar Infarct Types
• Indications for Selective X-ray Angiography

Other topics in "Chapter 19. Cerebrovascular Disorders"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.