Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_5776_Библиотеки_им_академика_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

30.08.2026

Размер:

53 Мб

Скачать

☆

<<< < Предыдущая 23 24 25 26 27 28 29 30 31 32 33 3435 / 5035 36 37 38 39 40 41 42 43 44 45 46 47 > Следующая >>>

319Discussion

Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers All rights reserved. Usage subject to terms and conditions of license.

40/17 cm/s to 45/23 cm/s seemed insuﬃ cient to prove a ﬂ ow rise, as small variations can also be caused by a slightly diﬀ erent insonation angle. However, as CTA in our patient demonstrated an unchanged left VA stenosis the ﬂ ow velocity increase was ﬁ nally attributed to a raised collateral ﬂ ow.

Another issue of interest is the exact allocation of VA

segments and the transitions from one segment to another. The V0–V1 transition is usually not further diﬀ er- entiated at the vessel origin. The V1–V2 transition is well deﬁ ned at the place where the VA begins its intraforam- inal course, usually at the level of the sixth transverse process. The V2–V3 transition is only rarely of clinical interest. In contrast, determination of the V3–V4 boundary is important as it permits diﬀ erentiation between the extradural and intradural VA especially in vessel aneurysm. For example, an intracranial location of a VA aneurysm or dissecting aneurysm carries the potential risk of subarachnoid hemorrhage and anticoagulation

treatment should then be avoided. As in our case, an exact anatomic localization of VA pathology might also help to clarify the etiology, as an intracranial localization of vascular pathology is more indicative of atherosclerosis. Transcranial color-coded duplex sonography (TCCS) is usually not able to answer this question. Both distal V3- and proximal V4-VA segments can usually be visualized but ﬁ nding the exact site of the penetration of the dura mater which deﬁ nes the beginning of the intradural course is usually not possible. Sometimes a mild notch is seen in the color-mode image, which may correspond to the VA penetration of the dura mater (for further reading, see also Chapter 2, “V4 and Distal V3 Segment” under “Special Arterial Anatomy and Ultrasound Anatomy”). In our patient, the stenoses seemed to be located intracranially in the most proximal V4-VA segment, but CTA suggested that their location was extracranial, at the border between the extracranial and intracranial parts.

320

Case 17

Ascending Left Middle Cerebral Artery Occlusion in an HIV-positive Patient

Clinical Presentation

A 39-year-old HIV-positive man was admitted to the infectious diseases unit after developing mild speech disturbance and hypesthesia of his right face. An opportunistic infection or lymphoma was suspected, but MRI revealed an ischemic cortical stroke in the left middle cerebral artery (MCA) territory. An intracranial MR angiogram (MRA) demonstrated a proximal M2 branch occlusion of the left MCA (Fig. B17.1 and Fig. B17.2). There were no known vascular risk factors. His symptoms improved spontaneously and a diagnostic workup was initiated. No heparin or antiplatelet therapy was given. Five days later his condition acutely worsened, with severe right-sided hemiparesis and marked aphasia. He was then transferred to the stroke unit for further evaluation and treatment (National Institute of Health Stroke Scale [NIHSS] score: 10).

Initial Neuroradiologic Findings

Following transfer to the stroke unit, a cerebral MRI revealed a large left-sided infarct in the striatum extending into the parietal lobe. The intracranial MRA now demonstrated a left proximal M1-MCA occlusion (Fig. B17.3 and Fig. B17.4).

Suspected Diagnosis

Ischemic reinfarction in the left MCA territory caused by M1-MCA occlusion.

Initial Neurosonologic Findings (Day 1)

Extracranial Sonography

B-mode sonography revealed a single echogenic atherosclerotic plaque in the left carotid bifurcation at the origin of the internal carotid artery (ICA). Doppler spectrum analysis showed a ﬂ ow signal with marked reduced ﬂ ow velocity in the left ICA (ﬂ ow velocity 24/8 cm/s). Flow signals in the right ICA (ﬂ ow velocity 58/23 cm/s) as well as in both external carotid arteries (ECAs) and the vertebral arteries (VAs) were normal (Fig. B17.5, Fig. B17.6, Fig.B17.7).

Transcranial Duplex Sonography

In projection of the left M1-MCA segment within the sylvian ﬁ ssure no ﬂ ow signal was detectable. The termi- nal left C1-ICA segment showed a ﬂ ow pattern similar to the extracranial ICA (31/16 cm/s). In the left A1-ACA (ﬂ ow velocity 147/70 cm/s) and proximal P2-PCA (ﬂ ow velocity 94/47 cm/s) segments there was increased nonturbulent ﬂ ow indicating leptomeningeal collateraliza- tion. Normal ﬂ ow velocities were seen in all the right cerebral arteries and in both ophthalmic arteries (OAs) (Fig. B17.8–Fig. B17.13; see also Video

B17.1).

Conclusion

Left proximal M1-MCA occlusion of unknown origin. Leptomeningeal collateral blood ﬂ ow via the left ACA and PCA.

Conventional Angiography (Day 3)

Questions to Answer by Ultrasound Techniques

• Was there evidence of atherosclerotic change or vasculitis in the extracranial brain-supplying arteries?

• Was there a sustained left M1-MCA occlusion?

• If so, was there evidence of collateral leptomeningeal blood ﬂ ow via the anterior (ACA) and/or posterior (PCA) cerebral arteries?

Digital subtraction angiography (DSA) was performed to exclude or conﬁ rm cerebral vasculitis. Proximal occlusion of the left M1-MCA segment was seen. Smooth borders at the contrast block were suggestive of thrombotic o c c l u s i o n . T h e r e w a s d i s t i n c t l e p t o m e n i n g e a l c o l l a t e r a l i zation via the left anterior and posterior cerebral arteries (Fig. B17.14, Fig. B17.15, Fig. B17.16).

Fig. B17.17 shows a schematic of the patient’s extra-

and intracranial brain-supplying arteries.

321Clinical Course

Fig. B17.1 Cerebral MRI, apparent diﬀ usion coeﬃ cient (ADC) map, axial plane. Territorial MCA infarct in the left-sided temporal lobe and anterior insula 2 days after the initial event (arrowheads).

Fig. B17.3 Cerebral MRI, ADC map, axial plane. Acute infarction predominantly in the left striatum 7 days after the initial event. Note the isointense residual temporal infarct (arrowhead).

Fig. B17.2 Intracranial contrast-enhanced MRA, axial maximal intensity projection (MIP). Absent signal in a prominent M2-MCA branch suggestive of left proximal MCA branch occlusion (arrowhead).

Fig. B17.4 Intracranial 3D TOF-MRA, axial MIP. In contrast with the ﬁ rst MRA, there was a proximal left M1-MCA occlusion (arrowhead). Note the fetal-type PCA in the contralateral side and the increased vessel signal of the left PCA main stem indicating collateral ﬂ ow.

Clinical Course

In view of the recent cerebral infarction, no systemic thrombolysis was performed. Considering the underlying immunosuppressive disease, absence of vascular risk factors (no thrombophilia, no ﬁ ndings predisposing for

cardiac embolism), infective cerebral vasculitis was suspected. However, cerebrospinal ﬂ uid (CSF) analysis did not support this hypothesis, revealing only an intrathecal IgG synthesis, consistent with the known HIV infection. A mild hyperlipidemia was thought to be due to the antiretroviral therapy, but this was not suﬃ cient to be

322 Case 17 Ascending Left Middle Cerebral Artery Occlusion in an HIV-positive Patient

BIF-L

Fig. B17.5 Extracranial duplex, longitudinal plane. B-mode i m a g i n g r e v e a l s a m i l d l y h y p e r e c h o i c a t h e r o s c l e r o t i c p l a q u e i n t h e left carotid bifurcation with extension to the proximal ICA (arrows).

ICA-R

ICA-L

Fig. B17.6 Extracranial duplex, longitudinal plane. Markedly reduced ﬂ ow in the left ICA (ﬂ ow velocity 24/8 cm/s).

C1-ICA-L

Fig. B17.7 Extracranial duplex, longitudinal plane. Normal ﬂ ow sig- nal in the right ICA (ﬂ ow velocity 58/23 cm/s).

the only causal factor. Cardiac embolism was ruled out as far as possible. An artery-to-artery embolism from the extracranial left ICA plaque was considered to be a potential trigger of the initial vessel occlusion that then led to progressive in-situ thrombosis with an adjacent extension of the clot. Besides the two-step embolism from the ICA plaque, primary HIV-related in-situ thrombosis with secondary extension also seemed possible. Secondary stroke prevention was started with aspirin. The patient was transferred to another hospital for rehabilitation. Over the next few weeks his neurologic deﬁ - cits improved only marginally. The patient was then lost to follow-up.

Final Diagnosis

Two-step MCA infarction caused by a progressive left MCA occlusion, presumably due to a growing in-situ thrombosis.

Fig. B17.8 TCCS ( tran stempor al app roach), lef t-si ded in sonation, upper pontine plane. Left terminal C1-ICA with ﬂ ow signal, similar to the extracranial ICA (ﬂ ow velocity 31/16 cm/s). Absent signal within the unusual bright sheath of the left M1-MCA (arrowheads).

Discussion

Clinical Aspects

Here we report on a relatively young HIV-positive patient with a two-step left MCA infarction caused by stepwise left MCA occlusion of unknown etiology. We suspect that an artery-to-artery embolic event, originating from extracranial ICA atherosclerosis, may have triggered the ﬁ rst ischemic event and the proximal M2-MCA occlusion. The secondary clinical worsening and the subsequent ﬁ nding of a proximal M1-MCA occlusion were thought to be caused by a progressing in-situ thrombosis.

In the past, stroke in HIV patients was frequently associated with opportunistic infections, tumors, or an advanced stage of immunosuppression (Pinto 1996). The introduction of combination antiretroviral therapy (cART) has changed the clinical picture of the disease. Patients live longer, and speciﬁ c symptoms as well as concomitant infections can be better controlled. Knowledge of the

323Discussion

M1-MCA-R

Fig. B17.9 TCCS (t ranstem pora l app roac h), r ight -side d in sonat ion, midbrain plane. Normal ﬂ ow in the right M1-MCA (ﬂ ow velocity 116/47 cm/s).

A1-ACA-R

A1-ACA-L

Fig. B17.10 TCCS (t rans tempora l ap proa ch), left -sid ed in sona tion, midbrain plane. Increased nonturbulent ﬂ ow in the left A1-ACA (ﬂ ow velocity 147/70 cm/s).

P2-PCA-L

Fig. B17.11 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normal ﬂ ow in the right A1-ACA (ﬂ ow velocity 102/46 cm/s).

d i s e a s e i s a l w a y s c h a n g i n g a n d n e w h y p o t h e s e s a r e c o n tinually being generated.

Currently it is diﬃ cult to ﬁ nd precise epidemiolog-

ic data on the combination of HIV and stroke. Based on very little data, some authors postulate an increased risk of stroke in HIV infection (Qureshi et al 1997, Cole et al 2004) while others did not conﬁ rm these results (M. Hoﬀ mann et al 2000, Patel et al 2005). Autopsy studies have reported the occurrence of ischemic as well as hemorrhagic stroke in HIV-infected patients. The reported stroke prevalence ranges from 6% to 34% (Berger et al 1990, Connor et al 2000, Kieburtz et al 1993, Pinto 1996, Rabinstein 2003). Most of these were clinically silent and only detected at postmortem examination. The prevalence of clinically diagnosed strokes ranges from 0.5% to 5% (Rabinstein 2003). Population-based studies before the era of cART reported an annual incidence of ischemic stroke and of intracerebral hemorrhage among AIDS patients of 0.14% and 0.11%, respectively (Cole et al 2004). No studies have prospectively assessed the risk of stroke in HIV-infected patients since the introduction of cART

Fig. B17.12 TCCS (t rans tempora l ap proa ch), left -sid ed in sona tion, midbrain plane. Increased nonturbulent ﬂ ow in the left proximal P2-PCA (ﬂ ow velocity 94/47 cm/s).

(Sen et al 2012). In the United States, analysis of discharge data from the U.S. Nationwide Inpatient Sample found that the number of patients with HIV admitted for stroke rose by 43% between 1997 and 2006, adjusting for population size (Ovbiagele and Nath 2011). However, how much of the rise was due to the eﬀ ect of cART on stroke risk in the HIV-positive patients is not clear.

Diﬀ erent mechanisms seem to contribute to the

o b s e r v e d i n c r e a s e d s t r o k e r i s k i n H I V . B e s i d e s t h e l o n g term side eﬀ ects of the cART therapy, HIV-associated inﬂ ammation and immune activation are being discussed. Stroke patients with HIV infection are usually younger than those without HIV infection. One explanation for this ﬁ nding might be the age of the risk group; another is that the pathomechanism of ischemic stroke in HIV might be diﬀ erent and less associated with the classical vascular risk factors. The average age of HIV-positive patients with ischemic stroke ranges from 33 to 49 years, but HIVpositive patients with stroke in lower income-countries are younger (Heikinheimo et al 2012, Ovbiagele and Nath 2011, Tipping et al 2007). Interestingly, although stroke

324 Case 17 Ascending Left Middle Cerebral Artery Occlusion in an HIV-positive Patient

P2-PCA-R

Fig. B17.13 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normal ﬂ ow in the right distal P2-PCA (ﬂ ow velocity 55/27 cm/s).

Fig. B17.14 DSA, left ICA injection (early arterial phase), p o s t e r o - a n t e r i o r v i e w . P r o x i m a l o c c l u s i o n o f t h e l e f t M 1 - M C A w i t h a smooth margin, suggestive of thrombotic occlusion (large arrowhead). Note the distinct leptomeningeal collateralization via the ACA (small arrowheads).

Fig. B17.15 DSA, left ICA injection (late arterial phase), posteroanterior view. Note the leptomeningeal collateralization via the ACA ﬁ lling the insular branches of the MCA indicating excellent collateralization (arrowheads).

patients with HIV are markedly younger, vascular risk factors like hypertension, hyperlipidemia, diabetes, and smoking are more frequently observed.

Ischemic stroke is the predominant pathologic stroke type among patients with HIV (Ovbiagele and Nath 2011). Although data from the pre-cART era in the United States showed nearly equal proportions of cerebral hemorrhage

Fig. B17.16 DSA, left VA injection, posteroanterior view. Note the prominent leptomeningeal collateralization from the PCA via the occipitotemporal artery (single arrowhead) and the parietooccipital artery (arrowheads) toward the MCA territory.

and ischemic stroke, these results were probably in part due to illicit drug use or hospital admission bias (Cole et al 2004). A recent or intercurrent infection seemed to play an important trigger role because it was present in 37% of 64 HIV-positive patients (aged <46 years) 3 months before i s c h e m i c s t r o k e . T h e s e w e r e m o s t l y o p p o r t u n i s t i c i n f e c tions such as tuberculosis, varicella zoster, pneumocystis

Fig. B17.17 Schematic of the patient’s extra- and intracranial brain-supplying arteries. There is proximal M1-MCA occlusion on the left side (circle), and collateral blood ﬂ ow toward the left MCA territory via leptomeningeal collaterals from the left ACA (blue arrow) and the left PCA (green arrow).

pneumonia, and cryptococcal meningitis. In the same study, 28% had a direct opportunistic infection-related stroke (infectious meningitis/vasculitis) and 19% had a coagulopathy, of which 40% were due to raised anticardiolipin antibodies. Cardiac embolism, mainly caused by HIV-related cardiomyopathy, was found in 14%, and HIV-associated vasculopathy in 20%. Multiple etiologies were present in 11% (Tipping et al 2007). In a comparable study including 77 patients with ischemic stroke and a mean age of 42 years the mechanism of stroke was large artery atherosclerosis in 12%, cardiac embolism in 18%, small-vessel occlusion in 18%, other determined etiology in 23%, and undetermined or incomplete evaluation in 29%. Vasculitis was considered to lead to stroke in 10 patients (13%) and hypercoagulability in 7 patients (9%). Protein S deﬁ ciency was detected in 10/22 (45%) and anticardiolip- in antibodies in 9/31 (29%) examined patients (Ortiz et al

2007). Protein S deﬁ ciency and cardiolipin antibodies may, however, be an epiphenomenon associated with the HIV infection itself (Mochan et al 2005).

HIV-associated vasculopathy may aﬀ ect all vessel sizes.

Small-vessel vasculopathy is characterized by hyaline small-vessel thickening, perivascular space dilatation, rarefaction, and pigment deposition with vessel wall mineralization, and occasional perivascular inﬂ amma- tory cell inﬁ ltrates. This type of vasculopathy is often clinically asymptomatic and leads to microinfarctions (Connor et al 2000). Multilocular degenerative ectasia involving the cerebral arterial circle (circle of Willis) and its proximal branches may also occur. All aﬀ ected ves- sels can display aneurysmal and nonaneurysmal lesions with stenoses and occlusions or local thrombi within the intracranial but also extracranial arteries (Gutierrez et al 2012, Nogueras et al 2002, Tipping et al 2007). The pathogenesis of HIV-related vasculopathies remains complex and not well understood. Although HIV antigen and particles were identiﬁ ed in perivascular cells, a direct role of HIV in the development of vasculitis is not conﬁ rmed

325Discussion

(Chetty 2001). Improvement of vessel involvement after initiation of cART is reported (Bhagavati and Choi 2008).

Atherogenesis in HIV-infected patients is a complex

and controversial topic. Independent of cART, an increased carotid IMT and increased “arterial wall stiﬀ ness” have been described as a manifestation of atherosclerosis (Lorenz et al 2008, Oliviero et al 2009, Seaberg et al 2010). A possible explanation for this might be the HIV-induced activation of endothelial and immune cells, the rise in circulating immune cells, and changes in lipid metabolism which subsequently lead to increased atherogenesis (Zanni and Grinspoon 2012).

However, the occurrence of atherosclerosis in HIV patients was rare before the introduction of protease inhibitors, which was explained by the young age of the patients and their reduced life expectancy. As the highly eﬀ ective cART has transformed HIV infection into a chronic disease and dramatically reduced the early mortality, atherosclerosis became more relevant. There is growing evidence that cART increases the risk of stroke and heart disease (d’Arminio et al 2004, Rasmussen et al 2011, Worm et al

2010). Its use may lead to hypertriglyceridemia and hypercholesterolemia, increased serum insulin and peptide C levels with proven insulin resistance, and peripheral lipodystrophy. An ultrasound study of patients treated with cART for at least 1 year demonstrated an increased prevalence of atherosclerosis in the carotid arteries. Atherosclerotic vessel wall changes (plaque or IMT >1 mm) were shown in 51% of HIV patients on cART and 15% of HIV patients not on cART; in the control group of matched healthy volunteers only 7% were aﬀ ected (Maggi et al 2000). One study showed that cART is a predictor of subclinical atherosclerosis (Jericó et al 2006). Menge and coworkers reported a patient on cART who, like our patient, had stepwise symptoms of ischemic stroke over a few weeks. This was, however, caused by rapid development of severe atherosclerotic changes within the MCA and distal ICA (Menge et al 2000). In our patient, the cART might have promoted the development of extracranial atherosclerotic vessel wall changes, as other vascular risk factors were not present. The uncommon accession of the intraluminal thrombus with subsequent M1-MCA occlusion is probably a result of a combination of the above trigger factors.

Angiologic and Anatomic Aspects

In our case, the proximal M1-MCA occlusion at the origin of the artery from the ICA was visualized with all the imaging techniques used, i.e., MRA, DSA, and transcranial color-coded duplex sonography (TCCS); for further discussion on intracranial occlusion, see Case 10. An exact determination of the level of occlusion is important for the evaluation of infarct volume and subsequent clinical outcome. Of particular interest is whether the origins of the lenticulostriate arteries (LSAs) are also aﬀ ected. MCA occlusions can be divided into four types (Saito et al 1987):

• Type 1: proximal M1-MCA occlusion with or without

the involvement of the LSA.

• Type 2: distal M1 occlusion beyond the origin of

the LSA.

• Types 3 and 4: occlusion of one or more M2-MCA

branches.

326 Case 17 Ascending Left Middle Cerebral Artery Occlusion in an HIV-positive Patient

Our patient initially presented with a type 4 MCA occlusion which later progressed to a type 1 occlusion (see also Chapter 5, “MCA Occlusion” under “Intracranial Pathology”).

Another factor inﬂ uencing the extent of infarction and clinical outcome is the quality of the collaterals. For instance, a proximal M1-MCA occlusion might result in complete MCA territory or LSA infarction only, depending on the available collaterals. Even during thrombolysis, the eﬃ cacy of the leptomeningeal collaterals inﬂ uences the ﬁ nal infarct volume, as they provide the blood supply to the border zone of the infarct, i.e., the penumbra. This function seems to be related to the perfusion pressure, which is why a stable perfusion pressure, even if above normal values, is desirable. This hypothesis is supported by isolated case reports of patients in whom perfusion MRI demonstrated that a controlled increase in blood pressure reduces the size of the oligemia area (Hillis et al

2003) and by a small ultrasound case series, in which induced hypertension was found to increase blood ﬂ ow ve- locities in distal MCA and activated collateral vessels (List et al 2013) (see also Chapter 5, “Collateral Pathways”). DSA is the only valid method for direct visualization of the peripheral and leptomeningeal collaterals, e.g., retrograde ﬁ lling of cortical arteries or distal M2-MCA branch- es, as was shown in our case via the hyperperfused ACA. Also, important PCA branches, e.g., the occipitotemporal and the parietooccipital arteries, feeding the leptomeningeal collateral vessels, were identiﬁ ed.

In our patient TCCS also showed clear signs of leptomeningeal collateralization in the form of raised ﬂ ow

velocities in the ACA and PCA. More detailed ultrasound analysis also permits the identiﬁ cation of PCA branches, but this was not done in our patient (see also Chapter 2, “Posterior Cerebral Artery” under “General Arterial Anatomy,” and Case 15). Over all, leptomeningeal collateralization in our patient was rather good, as the secondary proximal MCA occlusion only led to a large striatal infarction with little cortical involvement. Another indirect extracranial ultrasound sign of relevant proximal MCA ﬂ ow obstruction was the reduced ﬂ ow velocity in the nor- mal-sized extracranial ICA, a common ﬁ nding in proximal MCA occlusion. However, a reduced extracranial ICA ﬂ ow signal is not a reliable indicator of proximal MCA occlusion, and normal or nearly normal extracranial ICA ﬂ ow proﬁ les may be found despite the presence of MCA occlu- sion in cases with good leptomeningeal collateralization via the ACA in combination with an ipsilateral fetal-type PCA (see also Fig. A5.98).

The TOF-MRA technique in our patient was able to

demonstrate the M1-MCA occlusion later conﬁ rmed by DSA, but was unable to evaluate the eﬃ ciency of collat- eral function. With respect to the intracranial collaterals from the anterior communicating and posterior communicating arteries, TOF-MRA has a negative predictive value of 53% compared to functional TCCS, and is therefore only of limited value (Hoksbergen et al 2003b). It may, however, reveal a prominent PCA main stem and even peripheral segments as an indirect sign of leptomeningeal collateralization on comparison of the aﬀ ected and unaf- fected sides (Ichijo et al 2013, Uemura et al 2004) which was in part also seen in our patient.

Case 18

Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle Cerebral Artery Occlusion

327

Clinical Presentation

A 27-year-old left-handed woman without relevant medical history or known vascular risk factors was admitted after a severe motor vehicle accident in which her car turned over several times. The initial neurologic examination was normal. A CT of the head showed a left subgaleal hematoma as the only ﬁ nding (not shown). A body CT showed a pelvis fracture and foreign particles in the legs, for which the patient was surgically treated. On the following morning a left-sided hemiparesis with gaze palsy, aphasia, and a decreased level of consciousness were noted. The exact onset of symptoms was not clear (National Institute of Health Stroke Scale [NIHSS] score: 9).

Neuroradiologic Findings (Day 2)

A second cranial CT yielded a dense media sign on the right side and a new hypodense area in the right frontal middle cerebral artery (MCA) territory (Fig. B18.1) conﬁ rmed by CT perfusion. CT angiography showed right-sided extracranial internal carotid artery (ICA) occlusion starting 2 cm distal of the bifurcation together with an ipsilateral proximal MCA occlusion (Fig. B18.2). Furthermore, irregular vessel lumina were seen extracranially in the left ICA and in both V2 segments of the vertebral arteries (VA) (not shown).

ular near-occlusion of the right ICA, multisegmental lumen reduction of the left ICA starting 2 cm distal of the bifurcation with a small submandibular dissecting aneurysm without a stenosis, and left-pronounced mild to moderate dissecting stenosis at the entrance of both V2-VA segments. The right proximal M1-MCA remained occluded. There was no opacity of the right A1 anterior cerebral artery (ACA) which was related to the poststenotic low ﬂ ow state. Leptomeningeal collateralization was assured by the posterior circulation via the right posterior cerebral artery (PCA) (Fig. B18.3, Fig. B18.4, Fig. B.18.5). Using a stent retriever and aspiration device the right MCA was reopened via the occluded ICA under generalized anesthesia (Fig. B18.6). Secondary prevention was started with intravenous partial thromboplastin time (PTT)-guided heparin.

Fig. B18.7 and Fig. B18.8 show sche matics o f the ext ra- and intracranial brain-supplying arteries before and after mechanical thrombectomy of right M1-MCA.

Clinical Course (1)

The patient was transferred to the intensive care unit (ICU). Her neurologic status improved slightly during the next day with partial regression of the aphasic syndrome and hemiparesis. Extracranial and intracranial ultrasound was ﬁ rst requested for vessel status analysis. CT on

no intracranial bleeding.

Suspected Diagnosis

Questions to Answer by Ultrasound

Partial territorial right MCA infarction in proximal MCA occlusion caused by extradural traumatic cervical arterial dissection (CAD) of all four brain-supplying arteries with occlusive dissection of the right ICA and artery-to artery embolic occlusion of the right MCA.

Conventional Angiography with Endovascular Thrombectomy (Day 2)

Urgent mechanical thrombectomy was performed within 1 hour after CT. Digital subtraction angiography (DSA) conﬁ rmed CAD of both ICA and VA with a submandib-

Techniques

• Does ultrasound aﬃ rm dissection in all brain-

supplying arteries?

• Did the right M1-MCA remain open after intervention?

• Did the right extracranial ICA remain occluded?

• If yes, what were the intracranial collaterals to protect

the brain from large hemodynamic ischemic events?

• Could the small dissecting aneurysm be detected by

duplex sonography?

• Was there progress stenosis in the nonoccluded

brain-supplying arteries during anticoagulation with heparin?

328 Case 18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle

Cerebral Artery Occlusion

Fig. B18.1 Unenhanced cranial CT, axial plane. (A) Long-segmented dense media sign on the right side indicating vessel occlusion (arrow). (B) Early parenchymal signs of ischemia can be seen in the right frontal area of the MCA territory (yellow circle).

Fig. B18.2 Intracranial 3D CTA, axial MIP (A) and coronal MIP (B), conﬁ rming M1-MCA occlusion starting at its mid part (arrows).

Fig. B18.3 DSA, superimposed right and left selective ICA injection, posteroanterior view. Right ICA injection, showing dissecting high-grade stenosis submandibular at the entrance to the skull base (large arrowhead) and a distal ICA occlusion (arrow), presumably caused by artery-to artery embolism. Left ICA injection, showing also signs of dissection with a small aneurysm (yellow circle) and a suspicion of mild involvement in the distal part of its vertical petrosal segment (small arrowhead). Ipsilateral ﬂ ow is undisturbed and a collateral ﬂ ow into the right ACA territory via the left A1-ACA is evident (white arrows).

Initial Neurosonologic Findings (Day 3)

Extracranial Duplex Sonography

B-mode imaging revealed no atherosclerotic transformation of carotid vessels. Doppler spectrum analysis in the right common carotid artery (CCA) showed a high resistance ﬂ ow with increased pulsatility suggestive of an ICA occlusion below the origin of the ophthalmic artery (OA). The right proximal ICA itself revealed a tapering of the vessel with a stump signal. No direct signs of a dissecting lesion could be seen. The ipsilateral external carotid artery (ECA) showed an “internalized” ﬂ ow signal (Fig. B18.9, Fig. B18.10, Fig. B18.11). In the left ICA a mas-

Fig. B18.4 DSA, superimposed right and left selective VA injection, posteroanterior view. Long-segmented mild right and a moderate left V2-VA stenoses, starting typically at the entrance to V2-VA ( a r r o w s ) .

sive and lengthy vessel lumen reduction was seen, caused by a hypoechoic lesion indicating a mural hematoma. Doppler spectrum analysis revealed a turbulent ﬂ ow with reduced ﬂ ow velocity (55/9 cm/s) and a markedly increased pulsatility (PI 2.1) indicative of a further distal ﬂ ow obstruction (Fig. B18.12). The left ECA ﬂ ow signal also appeared “internalized.” Despite a submandibular access with adequate inclination of the linear probe the small dissecting aneurysm could not be detected. B-mode imaging of both V2-VAs showed multiple segmental vessel diameter diﬀ erences ranging from 1.5 to 4.2 mm in the left V2-VA and from 1.6 to 3.8 mm in the right V2-VA, also caused by hypoechoic material considered to be mural hematomas. Accordingly, the ﬂ ow velocities varied

<<< < Предыдущая 23 24 25 26 27 28 29 30 31 32 33 3435 / 5035 36 37 38 39 40 41 42 43 44 45 46 47 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
30.08.202663 Мб0Книга_5771_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_5772_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202657 Мб0Книга_5774_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202656 Мб0Книга_5775_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202653 Мб0Книга_5776_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202651 Мб0Книга_5777_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202648 Мб0Книга_5778_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202642 Мб0Книга_5779_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202678 Мб0Книга_578_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202642 Мб0Книга_5780_Библиотеки_им_академика_М_И_Перельмана.pdf