Circulatory disturbances in the ophthalmic artery lead to monocular hemianopia due to retinal infarction that can be directly visualized on ophthalmoscopy. Acute occlusion of the central retinal artery may occur in isolation or as a partial symptom of carotid occlusion (Fig. 1.4-6).
The same applies to infarction of the anterior choroidal artery, which—after the ophthalmic artery and posterior communicating branch—originates as the third branch from the internal carotid artery, before the latter divides into the anterior and middle cerebral arteries. The main symptoms are sensory or, more rarely, motor hemisyndromes and homonymous hemianopia if the optic tract is affected after the optic chiasm.
The severity of stroke in the acute stage is classified using the National Institutes of Health Stroke Scale (NIHSS), in which points are assigned to neurological deficits and added, leading to maximum score of 42. These are summed up briefly in Table 1.4-1.
As a rule of thumb, thrombolysis is indicated starting from NIHSS 4. Up to NIHSS 9, the condition is described as minor stroke. From NIHSS 10, an occluded cerebral vessel is identified angiographically in over 95% of cases. From NIHSS 12, a large cerebral vessel is affected in over 90% of cases—such as the internal carotid artery (diameter 4–6 mm), the M1 segment of the middle cerebral artery (approx. 3 mm), or the basilar artery (3–4 mm). The recanalization rate with intravenous thrombolysis after occlusions of large cerebral vessels is relatively low.
Fig. 1.4–5a, b The CT (a) shows a subacute, already partly demarcated left-sided posterior infarction due to occlusion of the posterior cerebral artery (b), displayed as a secondary 3D reconstruction from the CT angiogram.
Fig. 1.4–6 Occlusion of the central retinal artery by a cholesterol crystal that is clearly visible on ophthalmoscopy, as is the occluded vessel and retinal edema due to an “ocular stroke.” (Image kindly provided by Dr. Wolf, Dept. of Ophthalmology, University of Berne, Switzerland.)
Table 1.4–1 National Institutes of Health Stroke Scale (NIHSS).
1.4.3 Differential diagnosis
Approximately 20% of stroke cases are caused by bleeding, while the remainder (80–85%) are due to an acute onset of circumscribed hypoperfusion or ischemia. Approximately 60% of the cases of bleeding involve spontaneous intracerebral hematoma as a result of arterial or venous hemorrhage into the cerebral tissue. The remainder consist of subarachnoid bleeding, usually resulting from aneurysmal rupture (Figs. 1.4-7 and 1.4-8).
Approximately 3–5% of stroke cases are caused by bland or septic thrombosis of the cerebral veins or dural sinuses (sinus thrombosis). The symptoms have a wide range of severity and acuteness. The symptoms occur acutely in around 30% of cases, not rarely in the form of epileptic seizures—e.g., when the inferior anastomotic vein (Labbé vein) is affected, which opens into the transverse sinus and drains the ipsilateral temporal lobe. Treatment consists of heparin administration, even if signs of typical venous congestion and hemorrhagic infarction are already visible. Extensive sinus thromboses that progress during systemic anticoagulation treatment represent an indication for local endovascular treatment. Large-lumen catheters can be used that allow aspiration (Fig. 1.4-9).
Fig. 1.4–7a-c (a) Intracerebral bleeding with ventricular penetration on CT. Subarachnoid bleeding is seen on CT (b) and MRI (c). In the fluid-attenuated inversion recovery (FLAIR) sequence, the MRI shows subarachnoid bleeding with a high level of sensitivity as a signal enhancement in the subarachnoid space in the right insular cistern.
Fig. 1.4–8a-e Intracerebral bleeding, right basal ganglia with diffusion restriction on the b1000 diffusion-weighted image (a) and apparent diffusion coefficient (ADC) image (b). The bleeding has a hyperintense appearance on T2-weighted imaging (c) and shows a flow void on susceptibility-weighted imaging (SWI) (d). There was no evidence of a bleeding source on intracranial time-of-flight (TOF) magnetic resonance angiography (e).
Fig. 1.4–9a-f Thrombosis in the superior sagittal sinus. (a) The CT shows a “negative triangle sign” (absence of contrast in the lumen, while the sinus wall takes up contrast). (b) The sagittal T1-weighted MRI shows the thrombus in the sinus. (c) The late venous catheter angiogram shows the congested cerebral veins and an absence of contrast in the superior sagittal sinus. (d) A 5F aspiration catheter (VASCO-ASP) in the transverse sinus. (e) Venogram showing the tip of the aspiration catheter in the anterior third of the partly recanalized superior sagittal sinus. (f) Thrombus material aspirated from the sinus.
Dissections of the carotid artery (approximately 75% of all dissections) and vertebral artery (approximately 20%), which may also occur multiply and in intracranial locations (approximately 5%), are rare causes of infarction in children and adolescents. The resulting stenoses can lead to infarction directly by reducing blood flow, or indirectly due to arterioarterial transport of thrombi out the false lumen into the cerebral circulation. If the dissection expands intradurally, it can also lead to severe intracranial bleeding. When there are progressive symptoms in spite of anticoagulation and/or the dissection is expanding intracranially, stenting with several overlapping stents and/or a flow diverter may be able to stabilize the situation (Figs. 1.4-10 and 1.4-11).
Fig. 1.4–10 Follow-up after a bilateral carotid dissection. Starting on day 4, the wall hematoma with the bright signal on the fat-saturated T1-weighted axial MRI can be easily distinguished from the dark residual lumen (flow void).
Fig. 1.4–11a-c Symptomatic dissection in the distal cervical segment of the internal carotid artery. (a) Digital subtraction angiography (DSA), (b) angiography without subtraction, (c) DSA after implantation of two carotid Wallstents.
Extremely rare causes of ischemic infarction include cerebral auto-somal-dominant arteriopathy with subcortical infarcts and leuko-encephalopathy (CADASIL), vasculitides such as temporal arteritis, Takayasu arteritis, and in particular central nervous system angiitis, which is difficult to diagnose.
1.4.4