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Ischemic stroke physical examination

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

Overview

Overview

A complete physical examination may be suggestive of initial diagnostic clue about an ischemic stroke presenting as decreased motor strength, sensory loss or cranial nerve involvement. It may also help assess the degree of neurological deficit, identification of cause, localization of site of infarction, selection of patient for appropriate intervention, determination of prognosis and complications, and ruling out differential diagnosis.

Physical Examination

Physical Examination

A complete physical examination in the patient of ischemic stroke is essential for the following reasons:[1]

  • Assess the degree of neurological deficit
  • Identify the cause
  • Locate the site of infarction
  • Selection of patient for appropriate intervention
  • Determine the prognosis and complications
  • Rule out differential diagnosis

Physical assessment may be divided into 1) GPA 2) Systemic examination 3) Neurological examination:

General physical assessment and Systemic Review

Organ System Findings Suggestive of
General Appearance Cachexia[2] Underlying carcinoma
Confused or disoriented Extensive neurological deficit
Vital Signs Fever May suggest concomittant infectious process
Tachycardia (irregularly irregular) Underlying atrial fibrillation[3]
Absent pulse (radial or carotid artery) Atherosclerosis
Tachypnea Congestive heart failure[4], concomittant lung disease
Skin Pallor Anemia of chronic disease from any inflammatory condition
Abnormal bruising Underlying coagulation disorder
Cyanosis Embolism
Wound infection
 Diabetes mellitus
Migratory thrombophlebitis Underlying visceral carcinoma
Eyes Visual field defect Infarct involving posterior cerebral circulation
Absent light reflex Cranial nerve involvement
Speckled appearance of iris with ipsilateral pupil dilatation Carotid artery occlusion
Arteriolar constriction, arteriovenous nicking, yellow hard exudates, Hypertensive changes on fundoscopy [5]
Macular edema, microhemorrhages Diabetic eye disease[6]
Ears Deafness Brain stem infarction
Neck Carotid bruit Presence of occlusive extracranial disease[7][5]
Lungs Cough Congestive heart failure, underlying infection
Heart Arrhythmia Atrial fibrillation[7]
Displaced apical impulse Cardiac enlargement
Murmur Underlying valvular disease[8]
Abdomen Abdominal Tenderness Underlying visceral carcinoma
Palpable abdominal mass Underlying visceral carcinoma
Genitourinary Urinary incontinence Anterior circulation stroke
Erectile dysfunction [9] Anterior, middle or posterior cerebral infarction
Extremities Cyanosis Embolism
Neurological Dysarthria Suggestive of stroke
Muscle weakness Suggestive of stroke
Vertigo, deafness, nystagmus and hemiparesis Posterior circulation stroke
Gait abnormalities/Ataxia Cerebellar stroke
Cranial nerve abnormalities Brain stem infarct

Neurological examination

The physical examination findings in ischemic stroke may vary according to the blood vessel involved and site of infarction:

Vessel involved Physical examination
Anterior cerebral artery [10][11]
Middle cerebral artery[15]
  • Most common site of infarction
Posterior cerebral artery[22][23][24][25][24][26]
Vertebrobasilar artery[30] Midbrain
  • Contralateral decreased motor strength
  • Deviation of eye downwards and outwards-ipsilateral 3rd nerve palsy
Medulla
  • Impaired gag reflex
  • Uvula deviated to the opposite side of lesion
  • Ptosis
  • Miosis
  • Enophthalmos
  • Ipsilateral impaired pain, touch and temperature sensation on the upper half of the face
  • Contralateral decreased motor strength and sensory loss
  • Romberg’s sign
  • Deviation of tongue to the side of lesion-hypoglossal nerve
  • Contralateral decreased motor strength
  • Contralateral loss of position sense, vibration and two point discrimination
Pons
  • Inability to close eyes
  • Deviation of angle of mouth
  • Facial muscle weakness-Facial ner ve
  • Loss of taste sensation on the anterior two thirds of tongue
  • Affected eye deviation inwardsand down-Abducent nerve
  • Locked-in syndrome[36][37]
Cerebellum

Neurological assessment with standardized scales

The neurological assessment of the patient with ischemic stroke may be done using standardized scoring system to assess patient prognosis and treatment strategy. Two types of scoring systems widely used are:


For more information about Glasgow coma scoring system, click here.
For information about NIHSS scoring system, click here

Glasgow coma score

Glasgow coma score helps determine the severity of infarction, extent of damage and prognosis in unconscious or semi conscious patients. The score is determined by adding score in each category with the maximum score of 15 and minimum score of 3.[38][39][40][41][42]

Parameter Patient response Glassgow coma score
Eye opening
  • Spontaneous
  • To speech
  • To pain
  • No response
  • 4
  • 3
  • 2
  • 1
Verbal response
  • Oriented to time, place and person
  • Confused
  • Inappropriate words
  • Incomprehensible words
  • No response
  • 5
  • 4
  • 3
  • 2
  • 1
Motor response
  • Obeys commands
  • Moves to localized pain
  • Flexion withdrawl from pain
  • Abnormal flexion to pain (decorticate posture)
  • Abnormal extension to pain (decerebrate posture)
  • No response
  • 6
  • 5
  • 4
  • 3
  • 2
  • 1

Interpretation of Glasgow coma scale:

The following interpretation of glasgow coma scale may help determine the prognostic outcome in patients with brain injury:

Mild brain injury

Glasgow coma scale of 13-15

Moderate brain injury

Glasgow coma scale of 9-12

Severe brain injury

Glasgow coma scale of 3-8

References

References

  1. ↑ Goldstein L, Simel D (2005). “Is this patient having a stroke?”. JAMA. 293 (19): 2391–402. doi:10.1001/jama.296.16.2012 url=http://jama.ama-assn.org/cgi/content/full/296/16/2012 Check |doi= value (help). PMID 15900010.
  2. ↑ Dearborn JL, Urrutia VC, Zeiler SR (2014). “Stroke and Cancer- A Complicated Relationship”. J Neurol Transl Neurosci. 2 (1): 1039. PMC 4550304. PMID 26322334.
  3. ↑ Dewar RI, Lip GY, Guidelines Development Group for the NICE clinical guideline for the management of atrial fibrillation (2007). “Identification, diagnosis and assessment of atrial fibrillation”. Heart. 93 (1): 25–8. doi:10.1136/hrt.2006.099861. PMC 1861326. PMID 16952973.
  4. ↑ Cuadrado-Godia E, Ois A, Roquer J (2010). “Heart failure in acute ischemic stroke”. Curr Cardiol Rev. 6 (3): 202–13. doi:10.2174/157340310791658776. PMC 2994112. PMID 21804779.
  5. ↑ 5.0 5.1 Thanvi B, Robinson T (2007). “Complete occlusion of extracranial internal carotid artery: clinical features, pathophysiology, diagnosis and management”. Postgrad Med J. 83 (976): 95–9. doi:10.1136/pgmj.2006.048041. PMC 2805948. PMID 17308211.
  6. ↑ Negi A, Vernon SA (2003). “An overview of the eye in diabetes”. J R Soc Med. 96 (6): 266–72. PMC 539505. PMID 12782689.
  7. ↑ 7.0 7.1 Ustrell X, Pellisé A (2010). “Cardiac workup of ischemic stroke”. Curr Cardiol Rev. 6 (3): 175–83. doi:10.2174/157340310791658721. PMC 2994109. PMID 21804776.
  8. ↑ Maganti K, Rigolin VH, Sarano ME, Bonow RO (2010). “Valvular heart disease: diagnosis and management”. Mayo Clin Proc. 85 (5): 483–500. doi:10.4065/mcp.2009.0706. PMC 2861980. PMID 20435842.
  9. ↑ Koehn J, Crodel C, Deutsch M, Kolominsky-Rabas PL, Hösl KM, Köhrmann M; et al. (2015). “Erectile dysfunction (ED) after ischemic stroke: association between prevalence and site of lesion”. Clin Auton Res. 25 (6): 357–65. doi:10.1007/s10286-015-0313-y. PMID 26374302.
  10. ↑ 10.0 10.1 10.2 10.3 Nagaratnam N, Davies D, Chen E (1998). “Clinical effects of anterior cerebral artery infarction”. J Stroke Cerebrovasc Dis. 7 (6): 391–7. PMID 17895117.
  11. ↑ 11.0 11.1 11.2 Kumral E, Bayulkem G, Evyapan D, Yunten N (2002). “Spectrum of anterior cerebral artery territory infarction: clinical and MRI findings”. Eur J Neurol. 9 (6): 615–24. PMID 12453077.
  12. ↑ 12.0 12.1 Alexander MP, Schmitt MA (1980). “The aphasia syndrome of stroke in the left anterior cerebral artery territory”. Arch Neurol. 37 (2): 97–100. PMID 7356415.
  13. ↑ Mizuta H, Motomura N (2006). “Memory dysfunction in caudate infarction caused by Heubner’s recurring artery occlusion”. Brain Cogn. 61 (2): 133–8. doi:10.1016/j.bandc.2005.11.002. PMID 16510225.
  14. ↑ den Heijer T, Ruitenberg A, Bakker J, Hertzberger L, Kerkhoff H (2007). “Neurological picture. Bilateral caudate nucleus infarction associated with variant in circle of Willis”. J Neurol Neurosurg Psychiatry. 78 (11): 1175. doi:10.1136/jnnp.2006.112656. PMC 2117617. PMID 17940169.
  15. ↑ Lemieux F, Lanthier S, Chevrier MC, Gioia L, Rouleau I, Cereda C; et al. (2012). “Insular ischemic stroke: clinical presentation and outcome”. Cerebrovasc Dis Extra. 2 (1): 80–7. doi:10.1159/000343177. PMC 3492997. PMID 23139684.
  16. ↑ Arboix A, Martí-Vilalta JL (2009). “Lacunar stroke”. Expert Rev Neurother. 9 (2): 179–96. doi:10.1586/14737175.9.2.179. PMID 19210194.
  17. ↑ Melo TP, Bogousslavsky J, van Melle G, Regli F (1992). “Pure motor stroke: a reappraisal”. Neurology. 42 (4): 789–95. PMID 1565233.
  18. ↑ Tei H, Uchiyama S, Maruyama S (1993). “Capsular infarcts: location, size and etiology of pure motor hemiparesis, sensorimotor stroke and ataxic hemiparesis”. Acta Neurol Scand. 88 (4): 264–8. PMID 8256570.
  19. ↑ Fridriksson J, Fillmore P, Guo D, Rorden C (2015). “Chronic Broca’s Aphasia Is Caused by Damage to Broca’s and Wernicke’s Areas”. Cereb Cortex. 25 (12): 4689–96. doi:10.1093/cercor/bhu152. PMC 4669036. PMID 25016386.
  20. ↑ Henderson VW (1985). “Lesion localization in Broca’s aphasia. Implications from Broca’s aphasia without hemiparesis”. Arch Neurol. 42 (12): 1210–2. PMID 4062622.
  21. ↑ 21.0 21.1 Soma Y (1997). “[Cerebrovascular disorder and the language areas]”. Rinsho Shinkeigaku. 37 (12): 1117–9. PMID 9577663.
  22. ↑ 22.0 22.1 Brandt T, Steinke W, Thie A, Pessin MS, Caplan LR (2000). “Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature”. Cerebrovasc Dis. 10 (3): 170–82. doi:16053 Check |doi= value (help). PMID 10773642.
  23. ↑ 23.0 23.1 Cereda C, Carrera E (2012). “Posterior cerebral artery territory infarctions”. Front Neurol Neurosci. 30: 128–31. doi:10.1159/000333610. PMID 22377879.
  24. ↑ 24.0 24.1 Yamamoto Y, Georgiadis AL, Chang HM, Caplan LR (1999). “Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry”. Arch Neurol. 56 (7): 824–32. PMID 10404984.
  25. ↑ 25.0 25.1 Fisher CM (1986). “The posterior cerebral artery syndrome”. Can J Neurol Sci. 13 (3): 232–9. PMID 3742339.
  26. ↑ 26.0 26.1 Caplan LR, Hedley-Whyte T (1974). “Cuing and memory dysfunction in alexia without agraphia. A case report”. Brain. 97 (2): 251–62. PMID 4434176.
  27. ↑ Pessin MS, Lathi ES, Cohen MB, Kwan ES, Hedges TR, Caplan LR (1987). “Clinical features and mechanism of occipital infarction”. Ann Neurol. 21 (3): 290–9. doi:10.1002/ana.410210311. PMID 3606035.
  28. ↑ Damasio AR, Damasio H, Van Hoesen GW (1982). “Prosopagnosia: anatomic basis and behavioral mechanisms”. Neurology. 32 (4): 331–41. PMID 7199655.
  29. ↑ 29.0 29.1 Melo TP, Bogousslavsky J (1992). “Hemiataxia-hypesthesia: a thalamic stroke syndrome”. J Neurol Neurosurg Psychiatry. 55 (7): 581–4. PMC 489170. PMID 1640235.
  30. ↑ 30.0 30.1 30.2 Caplan L (2000). “Posterior circulation ischemia: then, now, and tomorrow. The Thomas Willis Lecture-2000”. Stroke. 31 (8): 2011–23. PMID 10926972.
  31. ↑ Nouh A, Remke J, Ruland S (2014). “Ischemic posterior circulation stroke: a review of anatomy, clinical presentations, diagnosis, and current management”. Front Neurol. 5: 30. doi:10.3389/fneur.2014.00030. PMC 3985033. PMID 24778625.
  32. ↑ Sacco RL, Freddo L, Bello JA, Odel JG, Onesti ST, Mohr JP (1993). “Wallenberg’s lateral medullary syndrome. Clinical-magnetic resonance imaging correlations”. Arch Neurol. 50 (6): 609–14. PMID 8503798.
  33. ↑ Shetty SR, Anusha R, Thomas PS, Babu SG (2012). “Wallenberg’s syndrome”. J Neurosci Rural Pract. 3 (1): 100–2. doi:10.4103/0976-3147.91980. PMC 3271596. PMID 22346215.
  34. ↑ Kim JS, Kim HG, Chung CS (1995). “Medial medullary syndrome. Report of 18 new patients and a review of the literature”. Stroke. 26 (9): 1548–52. PMID 7660396.
  35. ↑ Kim K, Lee HS, Jung YH, Kim YD, Nam HS, Nam CM; et al. (2012). “Mechanism of medullary infarction based on arterial territory involvement”. J Clin Neurol. 8 (2): 116–22. doi:10.3988/jcn.2012.8.2.116. PMC 3391616. PMID 22787495.
  36. ↑ Patterson JR, Grabois M (1986). “Locked-in syndrome: a review of 139 cases”. Stroke. 17 (4): 758–64. PMID 3738962.
  37. ↑ Karp JS, Hurtig HI (1974). ““Locked-in” state with bilateral midbrain infarcts”. Arch Neurol. 30 (2): 176–8. PMID 4810896.
  38. ↑ Sternbach GL (2000). “The Glasgow coma scale”. J Emerg Med. 19 (1): 67–71. PMID 10863122.
  39. ↑ Reith FC, Van den Brande R, Synnot A, Gruen R, Maas AI (2016). “The reliability of the Glasgow Coma Scale: a systematic review”. Intensive Care Med. 42 (1): 3–15. doi:10.1007/s00134-015-4124-3. PMID 26564211 : 26564211 Check |pmid= value (help).
  40. ↑ Gabbe BJ, Cameron PA, Finch CF (2003). “The status of the Glasgow Coma Scale”. Emerg Med (Fremantle). 15 (4): 353–60. PMID 14631703.
  41. ↑ Tsao JW, Hemphill JC, Johnston SC, Smith WS, Bonovich DC (2005). “Initial Glasgow Coma Scale score predicts outcome following thrombolysis for posterior circulation stroke”. Arch Neurol. 62 (7): 1126–9. doi:10.1001/archneur.62.7.1126. PMID 16009770.
  42. ↑ Bastos PG, Sun X, Wagner DP, Wu AW, Knaus WA (1993). “Glasgow Coma Scale score in the evaluation of outcome in the intensive care unit: findings from the Acute Physiology and Chronic Health Evaluation III study”. Crit Care Med. 21 (10): 1459–65. PMID 8403953.

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