Clinical-Anatomical Syndromes of Ischemic Infarction

Published on 12/04/2015 by admin

Filed under Neurology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 3 (2 votes)

This article have been viewed 5622 times

Chapter 2 Clinical-Anatomical Syndromes of Ischemic Infarction

Ischemic stroke can be defined as a sudden focal neurological deficit corresponding to a vascular distribution. Brain imaging techniques allow us to visualize lesions with great anatomical precision. However, optimal interpretation of the information provided by neuroimaging requires having detailed knowledge of the arterial anatomy (Figures 2-1 through 2-4) and the vascular territories of the brain (Figure 2-5).

Brain imaging has also enhanced our understanding of clinical-anatomical correlations in patients with ischemic infarctions. Before the development of modern neuroimaging modalities, these correlations could only be established by necropsy studies. In fact, clinical research using radiological data has shown that localization based on classical semiological syndromes may often be incorrect. Similar clinical presentations may occur in patients with strokes in different territories and, conversely, infarctions in the same territory may produce dissimilar manifestations in different patients. Nonetheless, accurate diagnosis relies on the recognition of the brain lesion in a defined vascular territory.

This chapter provides illustrations of ischemic infarctions in all major vascular territories and presents the most common clinical correlations. It is conceived as a practical and concise guide to the correct interpretation of brain imaging and not as a comprehensive anatomical or semiological monograph on this important topic. The reader should keep in mind that the variety of distribution of infarctions encountered in practice is enormous. The boundaries of arterial territories are far from invariable across patients, and anatomical variations in the constitution of the cerebral circulation and its interconnections are relatively common.

CAROTID BIFURCATION OCCLUSION

Case Vignette

A 61-year-old man with history of coronary artery disease, previous myocardial infarction, and multiple vascular risk factors presented to the emergency department with global aphasia and right hemiplegia for more than 6 hours. On examination, he was drowsy and exhibited forced left gaze deviation, right hemianopia, right flaccid hemiplegia involving the arm and the leg to similar degree, and absent response to pain on the right side. Diffusion-weighted imagery (DWI) of the brain revealed a large area of ischemia in the left hemisphere, including the territories of the anterior and middle cerebral arteries (Figure 2-6). Fluid-attenuated inversion recovery (FLAIR) sequence showed no parenchymal hyperintensity but disclosed extensive hyperintense signal in the left middle cerebral artery consistent with fresh thrombus (Figure 2-7). Magnetic resonance angiography (MRA) of the intracranial circulation confirmed the presence of a left carotid terminus occlusion (Figure 2-7). The patient was subsequently diagnosed with acute myocardial infarction and a left ventricular mural thrombus. His neurological condition deteriorated over the following 48 hours, and he expired after care was restricted to palliative measures.

An intravascular hyperdensity at the level of the carotid bifurcation may often be seen on CT scan. Thin-section computed tomography (CT) scans1 and T2* gradient echo magnetic resonance (MR) sequence2 may reveal intra-arterial thrombus with greater sensitivity.

MIDDLE CEREBRAL ARTERY OCCLUSION

The MCA is divided in four segments (see Figures 2-1 and 2-2). The M1 or horizontal segment is a single stem that give rise to the penetrating lenticulostriate branches. It branches into two (or occasionally three) M2 or insular segments as it enters the Sylvian fissure. The M3 or opercular segments ascend following the curvature of the operculum. The M4 or cortical segments travel along the sulci and gyri of the cerebral convexity.

Territorial MCA Infarction

Hyperdense MCA sign may be seen on the initial CT scan. Its presence is associated with less chances of recanalization after thrombolysis5,6 and worse likelihood of favorable recovery.57 Still, intravenous thrombolysis remains the standard of care for patients with MCA stroke presenting within 3 hours of symptom onset regardless of the presence of this radiological sign.6 Although preferential use of intra-arterial interventions has been advocated by some groups, the benefits of this approach are thus far unproved.8

Deep Middle Cerebral Artery Infarction

Superficial Divisional Middle Cerebral Artery Infarction

Acute confusional state, often associated with agitated delirium, may predominate in right-sided infarctions of the inferior M2 division.16 It is important to keep this diagnosis in mind when evaluating any patient presenting with acute confusion and agitation, because detailed neurological examination may be difficult in these cases, and sensory, visual, and perceptual deficits may be easily missed.
Infarctions of the inferior division of the MCA are predominantly caused by cardiac embolism.15,16 Carotid artery disease is rarely a cause of infarctions in this vascular distribution.

Superficial Cortical Infarctions

Left20 and right-sided18,19 infarctions have been associated with worse cardiac outcomes in different studies. Hence, the degree of lateralization in the control of autonomic cardiac function in humans remains to be fully elucidated.
Other cortical branch infarctions may be caused by occlusion of M3 branches (Figure 2-12) and may present with distinctive clinical syndromes. Some common examples of localizing clinical features encountered in practice are shown in Table 2-1.

Hemispheric Border-Zone Infarctions

ANTERIOR CEREBRAL ARTERY OCCLUSION

Anatomical variations are often present, including unilateral A1 segment hypoplasia (“threadlike” in 6%-8%, absent in 0.2%-2%, and hypoplastic in 6%-10%), multiple anterior communicating arteries (up to 40% in necropsies); unpaired or azygous ACA (1%-5%); and various anomalies in distal branching.2628 These variations affect the ability of collateral circulation to compensate for ischemia in the event of a stroke (e.g., patients with poor cross-flow through the anterior communicating artery will suffer greater ischemic damage to the frontal lobe ipsilateral to a carotid occlusion). Additionally, anomalies in the anterior communicating artery region are associated with increased frequency of saccular aneurysm.29

ANTERIOR CHOROIDAL ARTERY OCCLUSION

Most AChA infarctions are small (<20 mm) and often manifest clinically as lacunar syndromes.33 Pure motor and ataxia-hemiparesis syndromes predominate. Sometimes the latter is associated with hypesthesia.

POSTERIOR CEREBRAL ARTERY OCCLUSION

The PCAs constitute the terminal branches of the basilar artery. However, persistence of the fetal origin of the PCA from the internal carotid artery is seen in approximately 10% to 30% of individuals.37,38 In these patients, the PCA continues a large posterior communicating artery and does not join the basilar artery. Rarely, this variation is present bilaterally.
The PCAs are also conventionally divided in segments: the P1 segment (mesencephalic or precommunicating) extends from the PCA origin on the top of the basilar to the union with the posterior communicating artery, the P2 segment (ambient or postcommunicating) spans from the posterior communicating artery junction until the posterior midbrain. The main branches of these two proximal PCA segments are the central perforating branches (thalamoperforating, thalamogeniculate, and peduncular arteries), posterior choroidal vessels (medial posterior and lateral posterior choroidal arteries), anterior and posterior temporal arteries, and splenial branches to the posterior aspect of the corpus callosum. The distal PCA segments are the short P3 segment (quadrigeminal), extending within the perimesencephalic cistern from the posterior midbrain to the calcarine fissure, and the terminal P4 segment (calcarine or cortical). The latter gives origin to several cortical branches, including the inferior temporal arteries (anterior, middle, and posterior), the parietooccipital artery, and the calcarine artery itself. The PCA trajectory and branches are shown in Figures 2-3 and 2-4.

In the acute setting, large PCA infarctions may be clinically indistinguishable from MCA strokes.15 Thus brain imaging is essential to make the correct diagnosis and direct further evaluations.

TABLE 2-2 Visual field disturbance caused by PCA infarction.

Bilateral PCA infarction
Cortical blindness
Bilateral altitudinal hemianopia
Unilateral PCA infarction
Macular sparing hemianopia
Temporal crescent paring hemianopia
Quadrantanopia
Isolated macular hemianopia (rare)

VERTEBROBASILAR DISEASE

Case Vignette

A 64-year-old woman was found unresponsive in her bathroom by her husband. She was intubated by the paramedics and transported to our emergency department. On arrival, she was comatose and breathing at a rate of 40 to 45 per minute. She was tachycardic and hypertensive. Her pupils were slightly anisocoric (3.5 mm on the left and 3 mm on the right), and responses to light were minimal on the left and absent on the right. Corneal and oculocephalic reflexes were preserved. Best motor responses to pain were in the form of withdrawal. DWI showed restricted diffusion in the midcerebellum and mesencephalon (Figure 2-34). A hyperintense signal in the basilar artery indicative of acute thrombosis was visualized on FLAIR. Conventional angiography confirmed occlusion of the basilar trunk. She underwent successful basilar recanalization by intra-arterial thrombolysis combined with mechanical disruption of the clot. Despite reperfusion, the patient failed to improve neurologically. Repeat MRI showed established infarction throughout the midbrain. Patient expired shortly after her family requested withdrawal of artificial life support.

The top of the basilar syndrome (or rostral basilar artery syndrome) is characterized by sudden loss of consciousness, sometimes preceded by acute vertigo, ataxia, and diplopia. It is the manifestation of rostral brainstem, occipitotemporal, and thalamic ischemia (Figure 2-37). The area of infarction may also involve the superior cerebellum. Upon awakening, patients may exhibit drowsiness, agitation, disordered visual perception, and oculomotor dysfunction. Motor deficits are typically absent. The mechanism of the stroke is almost invariably embolic (from a cardiac or proximal arterial source).44

TABLE 2-3 Signs suspicious for basilar artery occlusion.

Combination of ophthalmoplegia with motor, sensory, or coordination deficits
Crossed motor or sensory findings
Acute ataxia with inability to walk
Sequential appearance of bilateral Babinski signs*
Sequential appearance of bilateral weakness
Acute reduction in the level of consciousness

* It can also be seen in patients with incipient craniocaudal herniation from massive supratentorial infarctions.

CEREBELLAR INFARCTIONS

MRI, especially DWI, often discloses multiple areas of cerebellar ischemia.4549 Multiple small cerebellar infarctions are frequently associated with atherosclerotic vertebrobasilar disease.48,49

Posterior Inferior Cerebellar Artery Infarction

Case Vignette

A 38-year-old woman presented with severe neck and posterior head pain, dizziness, gait imbalance, and right-hand clumsiness. Her examination predominantly demonstrated right appendicular ataxia. Brain imaging disclosed a large right PICA stroke with incipient mass effect (Figure 2-38). Vascular imaging revealed a right vertebral artery occlusion, most likely due to dissection. The patient was carefully monitored in the stroke unit, and as she developed mild confusion and restlessness, repeat imaging was performed showing worsening swelling with displacement of the fourth ventricle, effacement of the subarachnoid cisterns, distortion of the brainstem, and dilatation of the temporal horn of the right lateral ventricle. The patient immediately underwent suboccipital craniectomy. She improved substantially after surgery and achieved good functional recovery over the ensuing 6 months.

Decompressive suboccipital craniectomy is indicated in patients with a declining level of consciousness.52 However, because clinical decline occurs quickly in these patients, it is reasonable to consider preemptive surgery in patients with incipient clinical signs of swelling or radiological features predictive of deterioration.

Anterior Inferior Cerebellar Artery Infarction

Superior Cerebellar Artery Infarction

Pure SCA strokes manifest with dysarthria, nystagmus, and axial and ipsilateral appendicular ataxia.55 SCA-territory ischemia may be part of the rostral basilar artery syndrome (discussed earlier).56
MRI scans have shown that SCA infarctions are often multiple, with several lesions in the SCA territory (one or both sides) or other cerebellar territories.46,47 They may remain clinically unnoticed, particularly when they occur in the context of other embolic infarctions in more eloquent areas.

BRAINSTEM INFARCTIONS

Medullary Infarctions

The main ischemic medullary syndromes are illustrated in Figure 2-42.

Pontine Infarctions

The main ischemic pontine syndromes are illistrated in Figure 2-44.

Case Vignette

A 63-year-old man developed acute onset of slurred speech, gait imbalance, left-sided weakness, and horizontal diplopia. Initially he did not seek medical attention because “he did not like doctors who always found something wrong with him,” but after more than 12 hours of persistent deficits, his family convinced him to go to the hospital. On examination, he had mild dysarthria, right abducens palsy, right facial weakness, left arm and leg weakness, and mild axial and right appendicular ataxia. CT scan showed an area of possible hypoattenuation of the right pons, which was subsequently confirmed by MRI with DWI (Figure 2-45). MRA of the intracranial vessels disclosed atherosclerotic midbasilar stenosis (see Figure 2-45), which was likely the culprit for the pontine stroke by occluding a paramedian penetrating branch. During the hospitalization the patient was diagnosed with hypertension, diabetes mellitus, and hyperlipidemia. He was discharged on antiplatelet therapy, a statin, an angiotensin-converting enzyme (ACE) inhibitor, and an oral hypoglycemic agent. He achieved fair functional recovery with the help of intensive physical and occupational therapy. He remained compliant with the medications and has not had recurrent symptoms of posterior circulation ischemia.

Midbrain Infarctions

The main ischemic midbrain syndromes are illustrated in Figure 2-46.

References

1 Kim EY, Lee SK, Kim DJ, Suh SH, Kim J, Heo JH, et al. Detection of thrombus in acute ischemic stroke: value of thin-section noncontrast-computed tomography. Stroke. 2005;36:2745-2747.

2 Assouline E, Benziane K, Reizine D, Guichard JP, Pico F, Merland JJ, et al. Intra-arterial thrombus visualized on T2* gradient echo imaging in acute ischemic stroke. Cerebrovasc Dis. 2005;20:6-11.

3 Sugg RM, Malkoff MD, Noser EA, Shaltoni HM, Weir R, Cacayorin ED, et al. Endovascular recanalization of internal carotid artery occlusion in acute ischemic stroke. AJNR Am J Neuroradiol. 2005;26:2591-2594.

4 Rabinstein AA, Wijdicks EF, Nichols DA. Complete recovery after early intraarterial recombinant tissue plasminogen activator thrombolysis of carotid T occlusion. AJNR Am J Neuroradiol. 2002;23:1596-1599.

5 Tomsick T, Brott T, Barsan W, Broderick J, Haley EC, Spilker J, et al. Prognostic value of the hyperdense middle cerebral artery sign and stroke scale score before ultraearly thrombolytic therapy. AJNR Am J Neuroradiol. 1996;17:79-85.

6 Qureshi AI, Ezzeddine MA, Nasar A, Suri MF, Kirmani JF, Janjua N, et al. Is IV tissue plasminogen activator beneficial in patients with hyperdense artery sign? Neurology. 2006;66:1171-1174.

7 Manno EM, Nichols DA, Fulgham JR, Wijdicks EF. Computed tomographic determinants of neurologic deterioration in patients with large middle cerebral artery infarctions. Mayo Clin Proc. 2003;78:156-160.

8 Agarwal P, Kumar S, Hariharan S, Eshkar N, Verro P, Cohen B, et al. Hyperdense middle cerebral artery sign: can it be used to select intra-arterial versus intravenous thrombolysis in acute ischemic stroke? Cerebrovasc Dis. 2004;17:182-190.

9 Marinkovic SV, Kovacevic MS, Marinkovic JM. Perforating branches of the middle cerebral artery. Microsurgical anatomy of their extracerebral segments. J Neurosurg. 1985;63:266-271.

10 Fisher CM. Capsular infarcts: the underlying vascular lesions. Arch Neurol. 1979;36:65-73.

11 Nicolai A, Lazzarino LG, Biasutti E. Large striatocapsular infarcts: clinical features and risk factors. J Neurol. 1996;243:44-50.

12 Marinkovic SV, Milisavljevic MM, Kovacevic MS, Stevic ZD. Perforating branches of the middle cerebral artery. Microanatomy and clinical significance of their intracerebral segments. Stroke. 1985;16:1022-1029.

13 Fenelon G, Houeto JL. Unilateral parkinsonism following a large infarct in the territory of the lenticulostriate arteries. Mov Disord. 1997;12:1086-1090.

14 Caplan LR, Schmahmann JD, Kase CS, Feldmann E, Baquis G, Greenberg JP, et al. Caudate infarcts. Arch Neurol. 1990;47:133-143.

15 Bogousslavsky J, Van Melle G, Regli F. Middle cerebral artery pial territory infarcts: a study of the Lausanne Stroke Registry. Ann Neurol. 1989;25:555-560.

16 Caplan LR, Kelly M, Kase CS, Hier DB, White JL, Tatemichi T, et al. Infarcts of the inferior division of the right middle cerebral artery: mirror image of Wernicke’s aphasia. Neurology. 1986;36:1015-1020.

17 Fink JN, Selim MH, Kumar S, Voetsch B, Fong WC, Caplan LR. Insular cortex infarction in acute middle cerebral artery territory stroke: predictor of stroke severity and vascular lesion. Arch Neurol. 2005;62:1081-1085.

18 Abboud H, Berroir S, Labreuche J, Orjuela K, Amarenco P. Insular involvement in brain infarction increases risk for cardiac arrhythmia and death. Ann Neurol. 2006;59:691-699.

19 Ay H, Koroshetz WJ, Benner T, Vangel MG, Melinosky C, Arsava EM, et al. Neuroanatomic correlates of stroke-related myocardial injury. Neurology. 2006;66:1325-1329.

20 Laowattana S, Zeger SL, Lima JA, Goodman SN, Wittstein IS, Oppenheimer SM. Left insular stroke is associated with adverse cardiac outcome. Neurology. 2006;66:477-483.

21 Ay H, Arsava EM, Koroshetz WJ, Sorensen AG. Middle cerebral artery infarcts encompassing the insula are more prone to growth. Stroke. 2008;39:373-378.

22 Minematsu K, Yamaguchi T, Omae T. “Spectacular shrinking deficit”: rapid recovery from a major hemispheric syndrome by migration of an embolus. Neurology. 1992;42:157-162.

23 Baird AE, Donnan GA, Austin MC, McKay WJ. Early reperfusion in the “spectacular shrinking deficit” demonstrated by single-photon emission computed tomography. Neurology. 1995;45:1335-1339.

24 Sage JI, Van Uitert RL. Man-in-the-barrel syndrome. Neurology. 1986;36:1102-1103.

25 Hurley JP, Wood AE. Isolated man-in-the-barrel syndrome following cardiac surgery. Thorac Cardiovasc Surg. 1993;41:252-254.

26 Riggs HE, Rupp C. Variation in form of circle of Willis. The relation of the variations to collateral circulation: anatomic analysis. Arch Neurol. 1963;8:8-14.

27 Marinkovic S, Kovacevic M, Milisavljevic M. Hypoplasia of the proximal segment of the anterior cerebral artery. Anat Anz. 1989;168:145-154.

28 Dunker RO, Harris AB. Surgical anatomy of the proximal anterior cerebral artery. J Neurosurg. 1976;44:359-367.

29 Ogawa A, Suzuki M, Sakurai Y, Yoshimoto T. Vascular anomalies associated with aneurysms of the anterior communicating artery: microsurgical observations. J Neurosurg. 1990;72:706-709.

30 Caplan LR, Schmahmann JD, Kase CS, Feldmann E, Baquis G, Greenberg JP, et al. Caudate infarcts. Arch Neurol. 1990;47:133-143.

31 Nagaratnam N, Nagaratnam K, Ng K, Diu P. Akinetic mutism following stroke. J Clin Neurosci. 2004;11:25-30.

32 Gelmers HJ. Non-paralytic motor disturbances and speech disorders: the role of the supplementary motor area. J Neurol Neurosurg Psychiatry. 1983;46:1052-1054.

33 Hupperts RM, Lodder J, Heuts-van Raak EP, Kessels F. Infarcts in the anterior choroidal artery territory. Anatomical distribution, clinical syndromes, presumed pathogenesis and early outcome. Brain. 1994;117(Pt 4):825-834.

34 Takahashi S, Ishii K, Matsumoto K, Higano S, Ishibashi T, Suzuki M, et al. The anterior choroidal artery syndrome. II. CT and/or MR in angiographically verified cases. Neuroradiology. 1994;36:340-345.

35 Levy R, Duyckaerts C, Hauw JJ. Massive infarcts involving the territory of the anterior choroidal artery and cardioembolism. Stroke. 1995;26:609-613.

36 Friedman JA, Pichelmann MA, Piepgras DG, Atkinson JL, Maher CO, Meyer FB, et al. Ischemic complications of surgery for anterior choroidal artery aneurysms. J Neurosurg. 2001;94:565-572.

37 Bisaria KK. Anomalies of the posterior communicating artery and their potential clinical significance. J Neurosurg. 1984;60:572-576.

38 Pedroza A, Dujovny M, Artero JC, Umansky F, Berman SK, Diaz FG, et al. Microanatomy of the posterior communicating artery. Neurosurgery. 1987;20:228-235.

39 Waterston JA, Stark RJ, Gilligan BS. Paramedian thalamic and midbrain infarction: the “mesencephalothalamic syndrome.”. Clin Exp Neurol. 1987;24:45-53.

40 Auchus AP, Chen CP, Sodagar SN, Thong M, Sng EC. Single stroke dementia: insights from 12 cases in Singapore. J Neurol Sci. 2002;203–204:85-89.

41 Tay KY, King-Im JM, Trivedi RA, Higgins NJ, Cross JJ, Davies JR, et al. Imaging the vertebral artery. Eur Radiol. 2005;15:1329-1343.

42 Caplan LR, Wityk RJ, Glass TA, Tapia J, Pazdera L, Chang HM, et al. New England Medical Center Posterior Circulation registry. Ann Neurol. 2004;56:389-398.

43 Koch S, Amir M, Rabinstein AA, Reyes-Iglesias Y, Romano JG, Forteza A. Diffusion-weighted magnetic resonance imaging in symptomatic vertebrobasilar atherosclerosis and dissection. Arch Neurol. 2005;62:1228-1231.

44 Caplan LR. “Top of the basilar” syndrome. Neurology. 1980;30:72-79.

45 Kumral E, Kisabay A, Atac C. Lesion patterns and etiology of ischemia in the anterior inferior cerebellar artery territory involvement: a clinical–diffusion weighted–MRI study. Eur J Neurol. 2006;13:395-401.

46 Kumral E, Kisabay A, Atac C. Lesion patterns and etiology of ischemia in superior cerebellar artery territory infarcts. Cerebrovasc Dis. 2005;19:283-290.

47 Barth A, Bogousslavsky J, Regli F. The clinical and topographic spectrum of cerebellar infarcts: a clinical-magnetic resonance imaging correlation study. Ann Neurol. 1993;33:451-456.

48 Canaple S, Bogousslavsky J. Multiple large and small cerebellar infarcts. J Neurol Neurosurg Psychiatry. 1999;66:739-745.

49 Min WK, Kim YS, Kim JY, Park SP, Suh CK. Atherothrombotic cerebellar infarction: vascular lesion-MRI correlation of 31 cases. Stroke. 1999;30:2376-2381.

50 Koh MG, Phan TG, Atkinson JL, Wijdicks EF. Neuroimaging in deteriorating patients with cerebellar infarcts and mass effect. Stroke. 2000;31:2062-2067.

51 Jauss M, Muffelmann B, Krieger D, Zeumer H, Busse O. A computed tomography score for assessment of mass effect in space-occupying cerebellar infarction. J Neuroimaging. 2001;11:268-271.

52 Jauss M, Krieger D, Hornig C, Schramm J, Busse O. Surgical and medical management of patients with massive cerebellar infarctions: results of the German-Austrian Cerebellar Infarction Study. J Neurol. 1999;246:257-264.

53 Chaves CJ, Caplan LR, Chung CS, Tapia J, Amarenco P, Teal P, et al. Cerebellar infarcts in the New England Medical Center Posterior Circulation Stroke Registry. Neurology. 1994;44:1385-1390.

54 Amarenco P, Hauw JJ. Cerebellar infarction in the territory of the anterior and inferior cerebellar artery. A clinicopathological study of 20 cases. Brain. 1990;113:139-155.

55 Sohn SI, Lee H, Lee SR, Baloh RW. Cerebellar infarction in the territory of the medial branch of the superior cerebellar artery. Neurology. 2006;66:115-117.

56 Amarenco P, Hauw JJ. Cerebellar infarction in the territory of the superior cerebellar artery: a clinicopathologic study of 33 cases. Neurology. 1990;40:1383-1390.

57 Kim HA, Lee H, Sohn SI, Yi HA, Cho YW, Lee SR, et al. Bilateral infarcts in the territory of the superior cerebellar artery: clinical presentation, presumed cause, and outcome. J Neurol Sci. 2006;246:103-109.

58 Amarenco P, Kase CS, Rosengart A, Pessin MS, Bousser MG, Caplan LR. Very small (border zone) cerebellar infarcts. Distribution, causes, mechanisms and clinical features. Brain. 1993;116:161-186.

59 Sacco RL, Freddo L, Bello JA, Odel JG, Onesti ST, Mohr JP. Wallenberg’s lateral medullary syndrome. Clinical-magnetic resonance imaging correlations. Arch Neurol. 1993;50:609-614.

60 Sacco RL, Freddo L, Bello JA, Odel JG, Onesti ST, Mohr JP. Wallenberg’s lateral medullary syndrome. Clinical-magnetic resonance imaging correlations. Arch Neurol. 1993;50:609-614.

61 Milandre L, Lucchini P, Khalil R. [Lateral bulbar infarctions. Distribution, etiology and prognosis in 40 cases diagnosed by MRI]. Rev Neurol (Paris). 1995;151:714-721.

62 Frumkin LR, Baloh RW. Wallenberg’s syndrome following neck manipulation. Neurology. 1990;40:611-615.

63 Kitis O, Calli C, Yunten N, Kocaman A, Sirin H. Wallenberg’s lateral medullary syndrome: diffusion-weighted imaging findings. Acta Radiol. 2004;45:78-84.

64 Ross MA, Biller J, Adams HPJr, Dunn V. Magnetic resonance imaging in Wallenberg’s lateral medullary syndrome. Stroke. 1986;17:542-545.

65 Erro ME, Gallego J, Herrera M, Bermejo B. Isolated pontine infarcts: etiopathogenic mechanisms. Eur J Neurol. 2005;12:984-988.

66 Klein IF, Lavallee PC, Schouman-Claeys E, Amarenco P. High-resolution MRI identifies basilar artery plaques in paramedian pontine infarct. Neurology. 2005;64:551-552.

67 Kim JS, Kim J. Pure midbrain infarction: clinical, radiologic, and pathophysiologic findings. Neurology. 2005;64:1227-1232.

68 Kumral E, Bayulkem G, Akyol A, Yunten N, Sirin H, Sagduyu A. Mesencephalic and associated posterior circulation infarcts. Stroke. 2002;33:2224-2231.