MATRIZ DE CONSISTENCIA

anterior circulation

Most ischemic strokes and transient ischemic attacks are caused by embolic and acute, in situ (usually thrombotic) occlusion of an artery in the brain. How-ever, in some patients severe stenosis or occlusion of carotid or vertebral arteries may cause a critical reduction of blood flow, particularly when collateral circulation is compromised because the circle of Willis is incomplete or diseased. Mechanisms to com-pensate for the reduction of blood flow are vasodila-tation by autoregulation and an increase of the oxygen extraction fraction. If the vascular bed is maximally dilated the supplied brain is particularly vulnerable to any fall in perfusion pressure. Under these circumstances a small drop in systemic blood

pressure may cause transient or permanent focal ischemia.

Boundary-zone infarcts

The evidence that at least some boundary-zone infarcts are caused by low flow rather than acute arterial occlusion is that a sudden, profound and relatively prolonged hypotension (e.g. as a result of cardiac arrest or cardiac surgery) sometimes causes infarction bilaterally in the posterior boundary zones between the supply territories of the middle cerebral artery (MCA) and the posterior cerebral artery in the parieto-occipital regions. The clinical features include visual disorientation and agnosia, and amnesia.

Hemianopia is the most common symptom in unilateral posterior boundary-zone infarction, usually with macular sparing and predominating in the lower quadrant. Brachiofacial hypoesthesia is frequent, while motor weakness is rare and remains mild. In the dominant hemisphere, lesions manifest as either isolated word-finding difficulty or transcortical sens-ory aphasia (impaired comprehension but preserved word repetition and speech output). In the non-dominant hemisphere contralateral hemispatial neg-lect and anosognosia are usually found.

Anterior boundary-zone infarction is recognized in severe carotid stenosis or occlusion. The boundary zone is located in the frontoparasagittal region, between the supply territories of the MCA and the anterior cerebral artery in the frontoparasagittal region. The clinical features are contralateral weakness of the leg, more than the arm and sparing the face, some impaired sensation of the same distribution and transcortical motor aphasia (intact comprehension and repetition with impaired speech output), which may be preceded by mutism if in the dominant hemisphere.

Textbook of Stroke Medicine, Second Edition, ed. Michael Brainin and Wolf-Dieter Heiss. Published by Cambridge University

Press. © Michael Brainin and Wolf-Dieter Heiss 2014.

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There is an internal or subcortical boundary zone in the corona radiate and centrum semiovale, lateral and/or above the lateral ventricle. This lies between the supply areas of the lenticulostriate perforating branches from the MCA trunk and the medullary perforating arteries which arise from the cortical branches of the MCA and the anterior and, perhaps, posterior cerebral arteries. Infarction can occur within this internal boundary zone, usually causing lacunar or partial anterior circulation syndrome, in association with severe carotid disease and sometimes an obvious hemodynamic precipitating cause.

A sudden and profound hypotension sometimes causes boundary-zone infarction.

A fall in cerebral perfusion pressure as a cause of focal brain ischemia should be suspected if the symptoms start under certain circumstances [1]:

 on standing up very quickly, even if postural hypotension cannot be demonstrated in the clinic

 immediately after a heavy meal

 in very hot weather

 with exercise, coughing, or hyperventilation

 during Valsalva maneuver (but embolism is another possibility)

 during a clinically obvious episode of cardiac dysrhythmia (chest pain, palpitations, etc.) but embolism from heart is also possible

 during operative hypotension

 if the patient has recently been started on or increased the dose of any drug likely to cause hypotension.

Limb-shaking TIA

A transient ischemic attack which is typically associ-ated with severe large artery disease with exhausted hemodynamic reserve is “limb-shaking TIA”. It is characterized by 30–60 sec episodes of repetitive jerking movements of contralateral arm and/or leg and has been described with carotid occlusion but also with stenosis of intracranial vessels, e.g. middle cerebral artery or anterior cerebral artery. “Limb-shaking TIA” is elicited in situations which dispose to low flow, e.g. orthostatic dysregulation, hyper-ventilation in Moyamoya disease, or by carotid com-pression. The symptoms usually point towards a seizure-like activity and are often misdiagnosed as focal seizures. In contrast to seizure activity, limb shaking shows no somatotopic spread of movement

activity (no Jacksonian march) and usually has a low frequency (about 3 Hz). It is reported that limb shaking disappears with revascularization, e.g. carotid endarterectomy or extracranial–intracranial bypass (Figure 10.1).

A transient ischemic attack which is typically associated with severe large artery disease with exhausted

hemodynamic reserve is “limb-shaking TIA”.

Ischemic ophthalmopathy

Another symptom of low flow is monocular transient retinal ischemia occurring when looking into bright light. Objects appear bleached and a brief visual loss may follow. This symptom has been related to retinal claudication: an increase in the metabolic demand during exposure to bright light cannot be met because of an already marginal perfusion. Ischemic ophthal-mopathy is a specific, concomitant disorder of uncompensated, critically reduced perfusion pressure due to internal carotid artery occlusive disease. Quite characteristic is the history of a gradual, progressive loss of visual acuity, occasionally with bouts of obscuration, leading to a slowly progressive, irrevers-ible damage of the retinal neuronal layer. Further typical findings are neovascularization of the retina and iris (rubeosis iris) [2].

Ischemic strokes and transient ischemic attacks caused by low cerebral flow – posterior circulation

Rotational vertebral artery occlusion (RVAO) and stroke Rotational vertebral artery occlusion (RVAO) is caused by mechanical compression of vertebral arter-ies during head rotation. The vertebral artery is usu-ally compressed at the atlantoaxial C1–C2 level.

Tendinous insertions, osteophytes or degenerative changes resulting from cervical spondylosis may be the cause of compression. Most RVAO patients exhibit an ipsilateral stenosis or vessel malformation (e.g. hypoplasia) and a contralateral dominant verte-bral artery. With ispilateral head rotation, the (con-tralateral) dominant vertebral artery is compressed.

The leading symptom is vertigo, followed by tinnitus.

Video-oculography showed that RVAO is associated with a mixed downbeat torsional and horizontal beat-ing nystagmus which may spontaneously reverse dir-ection [3]. The labyrinth is predominantly supplied

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by the internal auditory artery, which is usually a branch of the anterior inferior cerebellar artery (AICA). As AICA usually takes off the basilar artery at its lower portion, reduced blood flow from the vertebral artery would result in ischemia. Approxi-mately 50% of RVAO patients treated conservatively suffered from infarction or residual neurological def-icits [4]. Brief episodes of rotational vertigo can also be caused by compression of the vestibular nerve as caused by close contact with intracranial vessels, par-ticularly the posterior inferior cerebellar artery (PICA).

Rotational vertebral artery occlusion(RVAO) is caused by mechanical compression of vertebral arteries during head rotation. The leading symptom is vertigo, followed by tinnitus.

Drop attack and vertebrobasilar ischemia

“Drop attacks” are episodes of sudden loss of postural tone which cause the subject to fall to the ground without apparent loss of consciousness, vertigo or other sensation. The attack occurs without warning and is not induced by a change of posture or move-ment of the head. The patient may be unable to rise

immediately after the fall despite being uninjured.

Not a single patient in the New England Medical Center Posterior Circulation Registry had a drop attack as the only symptom of posterior circulation ischemia [5]. With vertebrobasilar ischemia, sudden falls are usually preceded by and associated with symptoms such as vertigo, diplopia or blurred vision (Figure 10.2). A “drop attack” has been described in a patient with parasagittal motor cortex/subcortex ischemia in the territory of both anterior cerebral arteries [6].

In “drop attacks” a sudden loss of postural tone causes a fall to the ground without loss of consciousness.

Subclavian steal syndrome and hemodynamic effects of proximal vertebral artery disease

Most patients with subclavian artery stenosis or occlusion are asymptomatic. In a large series, only 15 out of 324 patients (4.6%) had objective signs of brachial ischemia such as aching after exercise or coolness of the arm. Among 116 patients with unilat-eral steal as shown by ultrasonography none had

Figure 10.1.Limb-shaking TIA.

A 55-year-old woman with risk factors (metabolic syndrome, smoking) presented with a limb shaking of the left leg when standing. The right internal carotid artery (ICA) was occluded.

Occlusion was presumably acute.

Territory of the ICA was supplied from the left ICA via the anterior

communicating artery. There was no collateral blood flow from the posterior communicating artery. Initially, the symptom was considered to be focal epileptic. Perfusion MR showed reduction of blood flow in the anterior territory of the right middle cerebral artery and the right anterior cerebral artery.

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symptoms of brain ischemia [7]. Among more than 400 patients with posterior circulation TIAs or ische-mic stroke only two had symptoms (TIAs) attribut-able to significant subclavian or innominate artery disease [8]. Symptoms which have been associated with decreased anterograde flow or retrograde flow in the vertebral artery are episodes with dizziness, diplopia, decreased vision or oszillopsia. The attacks are brief and may be elicited by exercise of the arm.

A difference in the wrist or the antecubital pulses and a difference of blood pressure between the two arms are reliable signs which indicate subclavian steal syn-drome. Causes of stenosis or occlusion of the verte-bral artery are: arteriosclerosis, Takayashu disease and temporal arteritis or mechanical trauma, as have been reported by bowlers or baseball pitchers.

Most patients with subclavian artery stenosis or occlusion are asymptomatic. Associated symptoms may include episodes with dizziness, diplopia, decreased vision or oszillopsia.

Severe stenosis or occlusion of the proximal vertebral artery is more likely to be a cause of embolism than to have hemodynamic effects: among 407 patients in the New England Medical Center Posterior Circulation Registry 80 of 407 patients had severe stenosis or occlusion of the proximal vertebral artery. In 45 of the 80 (56%) embolization was the most likely cause of cerebral ischemia. Only in 13 of 80 were hemody-namic effects considered to be the cause of cerebral

ischemia. Twelve of these 13 patients had severe bilat-eral occlusive disease of the vertebral artery [8].