Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 4428  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (1,308 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

  In this Article
 »  Abstract
 »  Search Strategy ...
 » Primary Vital Signs
 »  Pulse and Cardia...
 » Blood Pressure
 » Temperature
 » Respiration Rate
 » General Appearance
 » Skin and Hair
 » Auscultation
 » Neck Auscultation
 » Conclusion
 »  References
 »  Article Figures

 Article Access Statistics
    PDF Downloaded107    
    Comments [Add]    
    Cited by others 1    

Recommend this journal


Table of Contents    
Year : 2020  |  Volume : 68  |  Issue : 2  |  Page : 282-287

Role of the Physical Examination in the Determination of Etiology of Ischemic Stroke

1 Hospital Regional de Alta Especialidad del Bajío, Mexico
2 Hospital Nacional “San Juan de Dios”, San Miguel, El Salvador, Mexico
3 Instituto Mexicano del Seguro Social (IMSS) HGZ 2, Aguascalientes, Mexico

Date of Web Publication15-May-2020

Correspondence Address:
Juan M Marquez-Romero
Instituto Mexicano del Seguro Social (IMSS) HGZ 2, Av. de los Conos 102, Fraccionamiento Ojo Caliente, Desarrollo Especial Ojocaliente, Aguascalientes, Mexico - 20190
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.284386

Rights and Permissions

 » Abstract 

The actual investigation of the body of a patient by the clinician in search for the signs of the disease beginning with the primary vital signs and continues with the careful and attentive observation of the patient. This article reviews the key findings in the physical examination of patients with ischemic stroke that have the potential to indicate the etiology of the infarct and to help to choose the use of ancillary tests. Through a systematic search of articles published in English related to the physical examination of patients with stroke, we identified key findings in the vital signs and classic components of the physical exam (appearance of the patient, auscultation, and eye examination) that have shown clinical significance when determining ischemic stroke etiology. We further suggest that the prompt identification of such findings can translate into better use of diagnostic tools and selection of ancillary confirmatory tests, thus, reducing the time to etiology based treatment and secondary prevention of ischemic stroke. in this manuscript, we aim to show that even though nowadays the clinical skills tend to be overlooked due to the overreliance on technology, the physical exam continues to be a valuable tool in the clinician armamentarium when facing the challenge of a patient with ischemic stroke.

Keywords: Clinical exam, ischemic stroke, neurology
Key Message: There are key findings in the physical examination of patients with ischemic stroke that have the potential to indicate the etiology of the infarct and/or to help to choose the use of ancillary tests. Therefore, the physical exam continues to be a valuable tool for the clinician.

How to cite this article:
Garcia-Cazares R, Merlos-Benitez M, Marquez-Romero JM. Role of the Physical Examination in the Determination of Etiology of Ischemic Stroke. Neurol India 2020;68:282-7

How to cite this URL:
Garcia-Cazares R, Merlos-Benitez M, Marquez-Romero JM. Role of the Physical Examination in the Determination of Etiology of Ischemic Stroke. Neurol India [serial online] 2020 [cited 2022 Jul 5];68:282-7. Available from: https://www.neurologyindia.com/text.asp?2020/68/2/282/284386

The determination of the etiology of ischemic stroke (IS) is the initial step in providing specific secondary prevention measures and determining the patient's prognosis. However, it is also a challenge for the physician. A careful medical history and a focused physical examination can be helpful in identifying probable causes of IS and guiding subsequent confirmatory tests.

In this review, we summarize the current literature regarding the physical exam in patients with suspected IS. We describe potential findings in the physical examination of the patient with IS and the implications of these findings for the determination of etiology.

 » Search Strategy and Selection Criteria Top

References for this review were identified by electronic searches of Medline, Lilacs, Scielo, and searches of references from pertinent papers. No date limit was set, and we included papers published up to January 2019. Publication types were reviews, cohort studies, clinical trials, and case series. We systematically searched and reviewed papers published in English and used the following search terms. First term: “stroke,” “cerebrovascular accident,” “cerebrovascular disease,” “ischemic stroke,” “transient ischemic attack,” “cerebral infarction,” “cerebral thrombosis.” Second term: “clinical exam,” “clinical examination,” “physical exam,” “etiology,” “risk factors,” “infarction subtypes,” “vital signs,” “ophthalmology,” “auscultation,” “palpation,” “percussion.” On the basis of abstracts, one or more authors selected the papers for the review.

We did not perform any kind of statistical analysis.

 » Primary Vital Signs Top

The primary vital signs are the simplest and most important part of the physical examination in any patient, including patients with stroke. The clinician should always take into account the bidirectional relationship between brain injury and vital signs. On one hand, certain alterations in vital signs can indicate specific stroke etiologies. On the other hand, these altered vital signs can be the product of the brain injury regardless of the etiology. Brain lesions affecting the insula are known to produce dysautonomic disorders such as hypertension bursts and arrhythmias.[1] Additionally, the predictable pattern of decline in the neurological status known as rostrocaudal deterioration manifests with alterations in respiratory pattern and frequency along with the changes in blood pressure associated with the Cushing response.[2]

 » Pulse and Cardiac Frequency Top

When evaluating the cardiac frequency, one should take into account its regularity and synchrony with the peripheral arterial pulse, since any discrepancy indicates the presence of an arrhythmia. Among stroke patients, the occurrence of any kind of arrhythmia is a probable cause of the initial stroke; it is estimated that up to 35% of the population of >65 years of age have subclinical tachyarrhythmias which increase their stroke risk 2.5 times.[3] By far, the most common arrhythmia associated with IS is nonvalvular atrial fibrillation (AF), although valvular AF in association with rheumatic heart disease continues to be an important cause of stroke in low- and middle-income countries.[4] AF is the cause of IS in approximately 20% of all patients, although some authors believe that this is an underestimation.[5] Due to its intermittent nature, AF can be difficult to detect based solely on clinical grounds, but the assessment of AF during the primary vital signs evaluation is mandatory.

Tachycardia and bradycardia at rest are abnormal findings associated with thyroid disease, which in turn can increase the risk of stroke. The presence of hyperthyroidism is associated with the development of AF, and the metabolic alterations secondary to hypothyroidism have been related to atherosclerotic progression and atherothrombotic stroke.[6]

The pulse wave product of the ventricular systole propagates at an estimated velocity of 8–10 m/s; as mentioned earlier, this pulse wave should be synchronous and regular regardless of the place where it is measured. To correctly assess the pulse, the clinician's fingertips are positioned in places where a horizontal segment of an artery can be pressed over a bone. The finding of a decreased brachial artery pulse and decreased pulsation of one or both brachial arteries is one of the American College of Rheumatology (ACR) criteria for the classification of Takayasu arteritis, also known as the pulseless disease.[7] Such a decrease in pulse intensity correlates with the slowly progressive occlusive disease affecting the aorta, and its major branches are usually found in the angiogram [Figure 1] and with the severity and location of the resulting ischemia.
Figure 1: On the left, magnetic resonance angiography of a patient with Takayasu arteritis showing steno-occlusive disease involving the brachiocephalic trunk, the left common carotid artery, and both subclavian arteries. On the right, Angiogram of the left subclavian artery in a patient with Takayasu arteritis and a difference between arms in systolic pressure of over 20 mmHg

Click here to view

Giant cell arteritis (GCA) is another potential cause of stroke that can be detected through pulse abnormalities. GCA is most commonly associated with retinal ischemia and amaurosis but can also increase the risk of stroke.[8] Pulse abnormalities at the level of the temporal arteries are a part of the ACR criteria for GCA.[9] The temporal arteries can be palpated in front of the tragus and along the mid-portion of the temporal bone.[10] Both sides are usually palpated simultaneously. The absence of a pulse on one side or the presence of pain over the artery suggests temporal arteritis; advanced cases can show thickening or a “string-of-beads appearance” but these are difficult to palpate.

 » Blood Pressure Top

Hypertension (blood pressure values ≥140/90 mmHg) is one of the most important modifiable risk factors for stroke[11] and is present in up to 70% of all stroke patients on arrival.[12] However, these increases in BP are usually transient and resolve spontaneously. Current treatment guidelines[13] recommend the use of antihypertensive medication during the initial 24 h of acute IS only if BP is >220/120 mmHg.

Regarding stroke etiology, for certain patients, it is advisable to register BP values in both arms. Differences in the BP values of >20 mmHg between sides are suggestive of subclavian artery stenosis, which can manifest as syncope and vertebral basilar IS [Figure 1]. A difference of ≥10 mmHg in BP values between arms is also a part of the ACR criteria for Takayasu arteritis.[14] Takayasu arteritis, also known as occlusive thromboaortopathy or Martorell syndrome, is a non-atherosclerotic vasculopathy capable of leading to the brain or retinal ischemic injury.[14]

In addition to accounting for interbrachial differences, it is also important to assess the effect of different body positions on BP. Orthostatic hypotension, defined as a drop of >20 mmHg systolic, 10 mmHg diastolic, or both when an upright position is assumed,[15] has been linked to the presence of watershed infarction,[16] especially in patients with impaired autoregulation of cerebral blood flow.[17]

 » Temperature Top

Approximately one-third of patients with IS have hyperthermia (body temperature >37.3°C) 4–6 h after the stroke onset. However, when hyperthermia appears after 10–12 h, it is related to a poor outcome.[18] In this regard, most elevations in body temperature are related to concomitant infection but in special populations (known valvular heart disease (VHD), the history of intravenous illegal drug use), fever can indicate the presence of infective endocarditis as the source of emboli.[19] Additional factors supporting this diagnosis are subtle vascular phenomena such as conjunctival hemorrhages, Janeway lesions, and splinter hemorrhages.[20] Fever is also a common symptom accompanying GCA.[21]

Spontaneous hypothermia (body temperature <35.0°C) is an ominous sign that confers a higher risk of in-hospital death in patients with stroke; it is more common among patients with hemorrhagic stroke.[22]

 » Respiration Rate Top

Respiration rate and pattern abnormalities are common in rostrocaudal deterioration associated with malignant brain edema in middle cerebral artery infarction.[23] However, these findings are common to all causes of deterioration, and there is not a specific etiology of stroke associated with respiration rate irregularities. Chronic obstructive pulmonary disease (COPD) has been associated with an increased risk of stroke through various mechanisms.[24] Clinical findings of COPD such as diminished breath sounds,[25] increased anterior-posterior chest diameter, and the Hoover sign[26] can be obtained through physical examination alone but the significance of these findings is unclear.

 » General Appearance Top

The general appearance of a patient may provide diagnostic clues to the etiology of stroke. For example, tall and long-limbed individuals may have Marfan's syndrome, while Ehlers-Danlos syndrome features fragile skin and laxity of the joints. Both conditions predispose individuals to cervical artery dissections (CAD) and subsequent IS.[27],[28]

An endomorph somatotype with central obesity and a body mass index >30 kg/m2 has also been related to a higher risk of vascular morbidity, metabolic syndrome, atherosclerosis, and stroke.[29],[30]

 » Skin and Hair Top

The finding of skin and hair abnormalities in patients with IS can indicate the presence of a variety of causes of stroke, either through direct mechanisms (an autoimmune disease) or through indirect mechanisms such as increased prevalence of traditional vascular risk factors. Among young patients with stroke (<45 years of age), autoimmune disorders (AD) constitute up to 35% of all stroke causes.[31] AD usually present with multiple cutaneous manifestations.[32]

For example, systemic lupus erythematosus (SLE) can produce stroke through multiple mechanisms including vasculitis, hypercoagulable states, and cardioembolism due to Libman–Sacks (LS) endocarditis. SLE hair changes include the presence of alopecia areata[33] and subtle changes in hair diameter in the frontal and temporal areas known as “lupic hair.”[34] Another cutaneous manifestation of SLE is livedo (a persistent violaceous, red or blue pattern on the skin of the trunk, arms, or legs that does not disappear on warming). Livedo may consist of a regular pattern of broken circles (livedo racemosa) or a pattern of unbroken circles (livedo reticularis) [Figure 2] and is usually found in conjunction with antiphospholipid antibody syndrome (AAS).[35]Livedo racemosa is also found in patients with a rare noninflammatory thrombotic vasculopathy called Sneddon syndrome that can cause transient ischemic attacks and infarction.[36]
Figure 2: Livedo reticularis (left) and livedo racemosa (right)

Click here to view

SLE patients can also exhibit oral or nasopharyngeal ulcers and the classic malar erythema; both cutaneous findings are part of the clinical criteria for the diagnosis of the disease.[37] Red coloration of the skin can also be found in patients with increases in the hematocrit that result in increased blood viscosity that in turn promotes ischemic heart disease and stroke.[38] Such increases in the hematocrit are observed in patients with polycythemia vera or polycythemia secondary to COPD; in these cases, it is also common to find marked conjunctival erythema and injection. Severe injection and subconjunctival hemorrhage (hyposphagma) can indicate the presence of carotid occlusive disease due to the augmentation of the flow rate through the anastomotic pathway between the internal and external carotid arteries.[39] Hyposphagma can also be a sign of an advanced case of carotid-cavernous sinus fistula and is usually accompanied by chemosis, ophthalmoplegia, and retro-orbital pain.[40]

While examining the eyes, one may observe xanthelasma palpebrarum, the most common form of cutaneous xanthoma frequently associated with primary or secondary hyperlipidemias and known to increase the risk of stroke [Figure 3].[41] Psoriasis, commonly manifested as psoriatic plaques found on the scalp, elbows, and/or knees, is another inflammatory disease that can cause accelerated atherosclerosis and is associated with a higher risk of AF.[42]
Figure 3: An example of xanthelasma palpebrarum in a patient with hypercholesterolemia

Click here to view

 » Auscultation Top

Heart sounds

Cardiac auscultation should be performed in all patients with stroke since cardiac emboli are the cause of approximately 20% of strokes. The likelihood of a cardiac source of stroke is increased when cortical or cerebellar infarcts are present, when patients do not have traditional risk factors for atheroma or lacunar infarct and when patients are young. The occurrence of a stroke during a spontaneous Valsalva maneuver suggests the presence of a paradoxical embolism and should prompt the investigation of a thrombotic source in the lower extremities.[43]

As mentioned earlier, the most common cardiac abnormalities are AF and VHD. These abnormalities, in conjunction with infectious endocarditis, recent acute myocardial infarction, sick sinus syndrome, dilated cardiomyopathy, and cardiac myxoma, constitute the major cardioembolic sources of stroke.[44]

Cardiac auscultation findings associated with AF include variation in the intensity of the first heart sound and absence of a fourth sound that was previously present (while the patient was in sinus rhythm). Atrial flutter may also produce similar findings, except that the rhythm may be regular and rapid venous oscillations may occasionally be visible in the jugular pulse. Since the most common cause of chronic AF is mitral valve disease (MVD),[45] it is always mandatory to auscultate for a systolic murmur over the mitral valve auscultation area of the chest and left axilla.

Cranial and orbital auscultation

Cranial and orbital bruits result from turbulence in the intracranial or extracranial vessels; they are usually systolic and may originate within the cranium or be transmitted from arteries in the neck. The presence of these bruits frequently indicates atherosclerotic stenosis, but the existence of a carotid-cavernous sinus fistula should always be investigated as well.[40]

 » Neck Auscultation Top

Cervical bruits arise from neck arteries, and it is possible to auscultate not only the carotid circulation but also the vertebral and subclavian arteries.

Carotid bruits are the result of turbulent flow across the vessel; thus, intrinsic stenosis or, occasionally, arterial tortuosity and kinking can produce them. They are present during systole and are short and high-pitched.[46] The examiner should always ask the patient to hold his or her breath in order to eliminate breathing sounds and place the diaphragm of the stethoscope under the angle of the mandible, being careful not to apply excessive compression that could lead to rupture or dislodgement of the subjacent atherosclerotic plaque.[47]

Approximately, 75% of patients with carotid bruit have at least 50% stenosis. However, the ability to detect a bruit decreases in high-grade (90–90%) stenosis, resulting in low overall sensitivity.[48]

Supraclavicular bruits during systole are a frequent finding in normal children and in adults with subclavian or vertebral artery stenosis.

Supraclavicular auscultation can be used to evaluate vertebral artery occlusive symptoms, arm claudication, or “subclavian steal” in adults with atherosclerosis or compression of the subclavian artery. Both atherosclerosis and compression of the subclavian artery can lead to brachial ischemia and, in rare cases, retrograde embolism toward the vertebral artery. Frequent additional findings are unilateral Raynaud's phenomenon,[49] brittle nails, and digital ulcers. In addition to supraclavicular auscultation, Adson's test (checking for the loss of the radial pulse in the arm by rotating the head to the ipsilateral side with extended neck following deep inspiration) and Wright's test (looking for weakening or disappearance of the radial pulse when the arm is abducted and externally rotated) can be helpful in determining the presence of subclavian artery compression.

Eye examination

Monocular amaurosis is a well-known symptom of acute retinal ischemia frequently caused by thromboembolic and carotid artery diseases. However, eye symptoms related to carotid artery disease can sometimes have a chronic or subacute course. The resulting syndrome, known as ocular ischemic syndrome (OIS), hypoperfusion/hypotensive retinopathy, or ischemic oculopathy,[50] can be identified by the progressive and painless loss of visual acuity, as well as one or more of the following symptoms: Iris atrophy and neovascularization, secondary glaucoma, peripheral retinal microaneurysms, punctiform retinal hemorrhages, retinal veins dilatation and tortuosity, and papilledema [Figure 4]. These manifestations of OIS are present in 4–18% of patients with severe carotid stenosis or carotid occlusion.[51]
Figure 4: Two cases of complicated hypertensive retinopathy, on the left with ischemic optic neuropathy and on the right with retinal vein thrombosis

Click here to view


Ophthalmoscopic observation of cholesterol embolus (Hollenhorst plaque) in a blood vessel of the retina is a sign that indicates an increased risk of subsequent ipsilateral transient ischemic attack or IS.[52] Interestingly, such plaques infrequently correspond to locations of visual field defects in retinal ischemia.[52]

Hypertensive retinopathy is a much more common finding in patients with IS that can help distinguish between the reactive rise in BP seen during the first hours after IS and chronic undiagnosed hypertension. The presence of hypertensive retinopathy (which includes microaneurysms, soft exudates, hard exudates, macular edema, intraretinal microvascular abnormalities, venous beading, new vessel formation and, generalized arteriolar narrowing) also predicts the long-term risk of stroke, independent of blood pressure in patients without acute stroke.[53]

 » Conclusion Top

Current trends in medical practice tend to place the physical examination in a secondary role when evaluating a patient.[54] Nevertheless, the physical examination of patients continues to provide valuable information, and patients with IS are no exception. Even though the diagnosis of IS cannot be made without the aid of neuroimaging, it is clear that the physical examination can provide helpful indicators regarding the etiology of IS. Information from the physical examination can, thus, lead to better use of diagnostic tools and confirmatory tests, which in turn can reduce the time to etiology-based treatment and/or secondary prevention of IS. We hope that the present review serves as a reminder to all clinicians to not overlook this fundamental tool of the medical profession.


Dr. Thammar Gómez from the Instituto Nacional de Neurologia y Neurocirugia and Dr. Gabriela Calvo Leroux from the Instituto Nacional de Cardiologia in Mexico City provided photographs showed in [Figure 4] from her personal archive to illustrate the present article.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

 » References Top

Christensen H, Boysen G, Christensen AF, Johannesen HH. Insular lesions, ECG abnormalities, and outcome in acute stroke. J Neurol Neurosurg Psychiatry 2005;76:269-71.  Back to cited text no. 1
Marshman LA. Cushing's 'variant' response (acute hypotension) after subarachnoid hemorrhage. Association with moderate intracranial tensions and subacute cardiovascular collapse. Stroke 1997;28:1445-50.  Back to cited text no. 2
Healey JS, Connolly SJ, Gold MR, Israel CW, Van Gelder IC, Capucci A, et al. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med 2012;366:120-9.  Back to cited text no. 3
Seckeler MD, Hoke TR. The worldwide epidemiology of acute rheumatic fever and rheumatic heart disease. Clin Epidemiol 2011;3:67-84.  Back to cited text no. 4
Elijovich L, Josephson SA, Fung GL, Smith WS. Intermittent atrial fibrillation may account for a large proportion of otherwise cryptogenic stroke: A study of 30-day cardiac event monitors. J Stroke Cerebrovasc Dis 2009;18:185-9.  Back to cited text no. 5
Squizzato A, Gerdes VE, Brandjes DP, Buller HR, Stam J. Thyroid diseases and cerebrovascular disease. Stroke 2005;36:2302-10.  Back to cited text no. 6
Chatterjee S, Flamm SD, Tan CD, Rodriguez ER. Clinical diagnosis and management of large vessel vasculitis: Takayasu arteritis. Curr Cardiol Rep 2014;16:499.  Back to cited text no. 7
Unizony S, Menendez ME, Rastalsky N, Stone JH. Inpatient complications in patients with giant cell arteritis: Decreased mortality and increased risk of thromboembolism, delirium and adrenal insufficiency. Rheumatology (Oxford) 2015;54:1360-8.  Back to cited text no. 8
Hunder GG, Bloch DA, Michel BA, Stevens MB, Arend WP, Calabrese LH, et al. The American college of rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum 1990;33:1122-8.  Back to cited text no. 9
Curran RE. Palpation of the superficial temporal artery in normal persons. Arch Ophthalmol 1986;104:1756.  Back to cited text no. 10
Kernan WN, Ovbiagele B, Black HR, Bravata DM, Chimowitz MI, Ezekowitz MD, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: A guideline for healthcare professionals from the American heart association/American stroke association. Stroke 2014;45:2160-2236.  Back to cited text no. 11
Qureshi AI, Ezzeddine MA, Nasar A, Suri MF, Kirmani JF, Hussein HM, et al. Prevalence of elevated blood pressure in 563,704 adult patients with stroke presenting to the ED in the United States. Am J Emerg Med 2007;25:32-8.  Back to cited text no. 12
Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk BM, et al. Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals from the American heart association/American stroke association. Stroke 2013;44:870-947.  Back to cited text no. 13
Johnston SL, Lock RJ, Gompels MM. Takayasu arteritis: A review. J Clin Pathol 2002;55:481-6.  Back to cited text no. 14
Arnold AC, Shibao C. Current concepts in orthostatic hypotension management. Curr Hypertens Rep 2013;15:304-12.  Back to cited text no. 15
Momjian-Mayor I, Baron JC. The pathophysiology of watershed infarction in internal carotid artery disease: Review of cerebral perfusion studies. Stroke 2005;36:567-77.  Back to cited text no. 16
Eigenbrodt ML, Rose KM, Couper DJ, Arnett DK, Smith R, Jones D. Orthostatic hypotension as a risk factor for stroke: The Atherosclerosis risk in communities (ARIC) study, 1987-1996. Stroke 2000;31:2307-13.  Back to cited text no. 17
Boysen G, Christensen H. Stroke severity determines body temperature in acute stroke. Stroke 2001;32:413-7.  Back to cited text no. 18
Ruttmann E, Willeit J, Ulmer H, Chevtchik O, Hofer D, Poewe W, et al. Neurological outcome of septic cardioembolic stroke after infective endocarditis. Stroke 2006;37:2094-9.  Back to cited text no. 19
Li JS, Sexton DJ, Mick N, Nettles R, Fowler VG Jr, Ryan T, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis 2000;30:633-8.  Back to cited text no. 20
Hu Z, Yang Q, Zheng S, Tang J, Lu W, Xu N, et al. Temporal arteritis and fever: Report of a case and a clinical reanalysis of 360 cases. Angiology 2000;51:953-8.  Back to cited text no. 21
Rincon F, Hunter K, Schorr C, Dellinger RP, Zanotti-Cavazzoni S. The epidemiology of spontaneous fever and hypothermia on admission of brain injury patients to intensive care units: A multicenter cohort study. J Neurosurg 2014;121:950-60.  Back to cited text no. 22
Dohmen C, Galldiks N, Bosche B, Kracht L, Graf R. The severity of ischemia determines and predicts malignant brain edema in patients with large middle cerebral artery infarction. Cerebrovasc Dis 2012;33:1-7.  Back to cited text no. 23
Mills NL, Miller JJ, Anand A, Robinson SD, Frazer GA, Anderson D, et al. Increased arterial stiffness in patients with chronic obstructive pulmonary disease: A mechanism for increased cardiovascular risk. Thorax 2008;63:306-11.  Back to cited text no. 24
Badgett RG, Tanaka DJ, Hunt DK, Jelley MJ, Feinberg LE, Steiner JF, et al. Can moderate chronic obstructive pulmonary disease be diagnosed by historical and physical findings alone? Am J Med 1993;94:188-96.  Back to cited text no. 25
Lemyze M, Bart F. Hoover sign. CMAJ 2011;183:E133.  Back to cited text no. 26
Vanakker OM, Hemelsoet D, De Paepe A. Hereditary connective tissue diseases in young adult stroke: A comprehensive synthesis. Stroke Res Treat 2011;2011:712903.  Back to cited text no. 27
Lummus S, Breeze R, Lucia MS, Kleinschmidt-DeMasters BK. Histopathologic features of intracranial vascular involvement in fibromuscular dysplasia, Ehlers-Danlos type IV, and neurofibromatosis I. J Neuropathol Exp Neurol 2014;73:916-32.  Back to cited text no. 28
Kurl S, Laukkanen JA, Niskanen L, Laaksonen D, Sivenius J, Nyyssonen K, et al. Metabolic syndrome and the risk of stroke in middle-aged men. Stroke 2006;37:806-11.  Back to cited text no. 29
Lear SA, Humphries KH, Kohli S, Frohlich JJ, Birmingham CL, Mancini GB. Visceral adipose tissue, a potential risk factor for carotid atherosclerosis: Results of the Multicultural community health assessment trial (M-CHAT). Stroke 2007;38:2422-9.  Back to cited text no. 30
Griffiths D, Sturm J. Epidemiology and etiology of young stroke. Stroke Res Treat 2011;2011:209370.  Back to cited text no. 31
Rashtak S, Pittelkow MR. Skin involvement in systemic autoimmune diseases. Curr Dir Autoimmun 2008;10:344-58.  Back to cited text no. 32
Werth VP, White WL, Sanchez MR, Franks AG. Incidence of alopecia areata in lupus erythematosus. Arch Dermatol 1992;128:368-71.  Back to cited text no. 33
Sánchez-Schmidt JM, Pujol-Vallverdú RM. Diagnóstico diferencial de las lesiones cutáneas en el lupus. Semin Fund Esp Reumatol 2006;07:12-26.  Back to cited text no. 34
Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, Cervera R, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost 2006;4:295-306.  Back to cited text no. 35
Wu S, Xu Z, Liang H. Sneddon inverted question marks syndrome: A comprehensive review of the literature. Orphanet J Rare Dis 2014;9:768.  Back to cited text no. 36
Petri M, Orbai AM, Alarcon GS, Gordon C, Merrill JT, Fortin PR, et al. Derivation and validation of the systemic lupus international collaborating clinics classification criteria for systemic lupus erythematosus. Arthritis Rheum 2012;64:2677-86.  Back to cited text no. 37
Lowe GD, Lee AJ, Rumley A, Price JF, Fowkes FG. Blood viscosity and risk of cardiovascular events: The Edinburgh artery study. Br J Haematol 1997;96:168-73.  Back to cited text no. 38
Schaser KD, Settmacher U, Puhl G, Zhang L, Mittlmeier T, Stover JF, et al. Noninvasive analysis of conjunctival microcirculation during carotid artery surgery reveals microvascular evidence of collateral compensation and stenosis-dependent adaptation. J Vasc Surg 2003;37:789-97.  Back to cited text no. 39
Choi JY, Baek SH, Jung JM, Kwon DY, Park MH. Teaching neuroimages: Ocular bruit in carotid-cavernous sinus fistula. Neurology 2014;83:e87-8.  Back to cited text no. 40
Christoffersen M, Frikke-Schmidt R, Schnohr P, Jensen GB, Nordestgaard BG, Tybjaerg-Hansen A. Xanthelasmata, arcus corneae, and ischaemic vascular disease and death in general population: Prospective cohort study. BMJ 2011;343:d5497.  Back to cited text no. 41
Ahlehoff O, Gislason GH, Jorgensen CH, Lindhardsen J, Charlot M, Olesen JB, et al. Psoriasis and risk of atrial fibrillation and ischaemic stroke: A Danish nationwide cohort study. Eur Heart J 2012;33:2054-64.  Back to cited text no. 42
Weir NU. An update on cardioembolic stroke. Postgrad Med J 2008;84:133-42; quiz 139-140.  Back to cited text no. 43
Arboix A, Alio J. Acute cardioembolic stroke: An update. Expert Rev Cardiovasc Ther 2011;9:367-79.  Back to cited text no. 44
Hinton RC, Kistler JP, Fallon JT, Friedlich AL, Fisher CM. Influence of etiology of atrial fibrillation on incidence of systemic embolism. Am J Cardiol 1977;40:509-13.  Back to cited text no. 45
Sandercock PAG, Kavvadia E. The carotid bruit. Pract Neurol 2002;2:221-4.  Back to cited text no. 46
Stern B, Wityk R. Extracranial and intracranial large artery atherosclerosis. Continuum (Minneap Minn) 2003;9:97-110.  Back to cited text no. 47
McColgan P, Bentley P, McCarron M, Sharma P. Evaluation of the clinical utility of a carotid bruit. QJM 2012;105:1171-7.  Back to cited text no. 48
Yamaguchi R, Kohga H, Kurosaki M, Tamura M, Tanaka S, Tosaka M, et al. Acute basilar artery occlusion in a patient with left subclavian artery occlusion due to first rib anomaly: Case report. Neurol Med Chir (Tokyo) 2008;48:355-8.  Back to cited text no. 49
Kearns TP, Hollenhorst RW. Venous-stasis retinopathy of occlusive disease of the carotid artery. Proc Staff Meet Mayo Clin 1963;38:304-12.  Back to cited text no. 50
Miller NR, Newman NJ. The eye in neurological disease. Lancet 2004;364:2045-54.  Back to cited text no. 51
Schwarcz TH, Eton D, Ellenby MI, Stelmack T, McMahon TT, Mulder S, et al. Hollenhorst plaques: Retinal manifestations and the role of carotid endarterectomy. J Vasc Surg 1990;11:635-41.  Back to cited text no. 52
Ong YT, Wong TY, Klein R, Klein BE, Mitchell P, Sharrett AR, et al. Hypertensive retinopathy and risk of stroke. Hypertension 2013;62:706-11.  Back to cited text no. 53
Ambinder EP. A history of the shift toward full computerization of medicine. J Oncol Pract 2005;1:54-6.  Back to cited text no. 54


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

This article has been cited by
1 Causative Classification of Ischemic Stroke by the Machine Learning Algorithm Random Forests
Jianan Wang, Xiaoxian Gong, Hongfang Chen, Wansi Zhong, Yi Chen, Ying Zhou, Wenhua Zhang, Yaode He, Min Lou
Frontiers in Aging Neuroscience. 2022; 14
[Pubmed] | [DOI]


Print this article  Email this article
Online since 20th March '04
Published by Wolters Kluwer - Medknow