Sandbox Maryam Hadipour

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Stroke Main page

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Overview

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Hemorrhagic stroke
Ischemic stroke

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]Aysha Anwar, M.B.B.S[3],Tarek Nafee, M.D. [4],Sara Mehrsefat, M.D. [5]

Overview

Stroke is the rapidly developing loss of brain functions due to a disturbance in the blood vessels supplying blood to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis or embolism, or due to a hemorrhage.[1]

Stroke is a medical emergency and can cause permanent neurological damage, complications and death if not promptly diagnosed and treated. It is the third leading cause of death and the leading cause of adult disability in the United States and Europe. It is predicted that stroke will soon become the leading cause of death worldwide.[2] WHO defines stroke as, a neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours.

Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischaemic attack (TIA), diabetes mellitus, high cholesterol, cigarette smoking, atrial fibrillation, migraine[3] with aura, and thrombophilia. In clinical practice, blood pressure is the most important modifiable risk factor of stroke; however many other risk factors, such as cigarette smoking cessation and treatment of atrial fibrillation with anticoagulant drugs, are important. Treatment of ischemic stroke is occasionally with thrombolysis, but usually with supportive care (physiotherapy and occupational therapy) and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins and anticoagulation (in selected patients).[4] Hemorrhagic stroke is a medical emergency, rapid diagnosis and management is crucial because early deterioration is common in the first few hours after ICH onset.[5]

Causes

The following table lists causes for stroke.[6][7][8][9][10][11][12][13][14][15]

Causes
Disease Lethal causes Common causes Less common causes
Transient ischemic attack (TIA) Emboli from cardiac source (mostly secondary to AF) Arterial dissection
Ischemic stroke
Intracerebral hemorrhage ---
Subarachnoid hemorrhage

Rupture of an aneurysm

Rupture of an aneurysm

Subdural hemorrhage Rupture of bridging vessels Trauma (motor vehicle accidents, falls, and assaults)
Epidural hemorrhage Rupture of middle meningeal arteries Trauma (motor vehicle accidents, falls, and assaults)
Intraparenchymal hemorrhage --- Trauma (motor vehicle accidents, falls, and assaults) Rupture of an aneurysm

Arteriovenous malformation

Intraventricular hemorrhage (IVH) ---

Classification

Transient ischemic attack

  • A transient ischemic attack is caused by the temporary disturbance of blood supply to a restricted area of the brain, resulting in brief neurologic dysfunction that usually persists for less than 24 hours.

Stroke

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stroke
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ischemic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hemorrhagic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Large vessel thromboembolism
 
Cardioembolic
 
Small vessel or Lacunar infarct
 
Intra-axial
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Extra-axial
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intracerebral (ICH)
 
 
Subarachnoid hemorrhage (SAH)
 
 
 
 
 
 
 
Subdural Hemorrhage
 
 
 
 
 
 
 
 
Epidural Hemorrhage
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intraparenchymal hemorrhage
 
 
 
 
Intraventricular hemorrhage (IVH)
 
 
 
 
Cerebral microbleeds

Differential diagnosis

Stroke, must be differentiated from other diseases that may cause, altered mental status, motor and or somatosensory deficits. The table below, summarizes the differential diagnosis for stroke:

Diseases History Symptoms Physical Examination Diagnostic tests Other Findings
Headache ↓ LOC Motor weakness Abnormal sensory Motor Deficit Sensory deficit Speech difficulty Gait abnormality Cranial nerves CT/MRI CSF Gold standard test
Brain tumor[16][17] + – – – + + + – + + Cancer cells MRI
  • Cachexia
  • Gradual progression of symptoms
Hemorrhagic stroke[18][19] + + + + + + + + – + NA CT scan without contrast
Subdural hemorrhage[18][19][20] + + + + + – – – + + Xanthochromia CT scan without contrast
Neurosyphilis[21][22][23] + – + + + + – + – + ↑ Leukocytes and protein Specific: CSF VDRL

Sensitive: CSF FTA-Ab

Complex or atypical migraine + – + + – – + – – – NA Clinical assesment
Hypertensive encephalopathy + + – – – – + + – + NA Clinical assesment
Wernicke’s encephalopathy
  • History of alcohal abuse
 – + – – – + + + + – NA Clinical assesment and lab findings
CNS abscess + + – – + + + – – + ↑ leukocytes, ↓ glucose and ↑ protien MRI is more sensitive and specific
Drug toxicity Medication history of – + – + + + – + – – NA Drug screen test –
Conversion disorder + + + + + + + + – – NA Diagnosis of exclusion
Metabolic disturbances (electrolyte imbalance, hypoglycemia) – – + + + + + – – + – Hypoglycemia, hyponatremia, hypernatremia, hypokalemia, and hyperkalemia Depends on the cause
Meningitis or encephalitis[24] + – – – – + + – – – ↑ Leukocytes, ↑ protein, ↓ glucose CSF analysis
Multiple sclerosis exacerbation[25]
  • History of relapses and remissions
 – – + + – + + + + + ↑ CSF IgG levels, (monoclonal bands) Clinical assesment and MRI
Seizure[26] + + – – + + – – + – Mass lesion Clinical assesment and EEG

Differential diagnosis

Stroke should be differentiated from other causes of muscle weakness and paralysis. The differentials include the following:[27][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42]

Diseases History and Physical Diagnostic tests Other Findings
Motor Deficit Sensory deficit Cranial nerve Involvement Autonomic dysfunction Proximal/Distal/Generalized Ascending/Descending/Systemic Unilateral (UL)

or Bilateral (BL)

or

No Lateralization (NL)

Onset Lab or Imaging Findings Specific test
Acute Flaccid Myelitis + + + - Proximal > Distal Ascending UL/BL Sudden MRI (Longitudinal hyperintense lesions) MRI and CSF PCR for viral etiology Drooping eyelids

Difficulty swallowing

Respiratory failure

Adult Botulism + - + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Diplopia, Hyporeflexia, Hypotonia, possible respiratory paralysis
Infant Botulism + - + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Flaccid paralysis (Floppy baby syndrome), possible respiratory paralysis
Guillian-Barre syndrome + - - - Generalized Ascending BL Insidious CSF: ↑Protein

↓Cells

Clinical & Lumbar Puncture Progressive ascending paralysis following infection, possible respiratory paralysis
Eaton Lambert syndrome + - + + Generalized Systemic BL Intermittent EMG, repetitive nerve stimulation test (RNS) Voltage gated calcium channel (VGCC) antibody Diplopia, ptosis, improves with movement (as the day progresses)
Myasthenia gravis + - + + Generalized Systemic BL Intermittent EMG, Edrophonium test Ach receptor antibody Diplopia, ptosis, worsening with movement (as the day progresses)
Electrolyte disturbance + + - - Generalized Systemic BL Insidious Electrolyte panel ↓Ca++, ↓Mg++, ↓K+ Possible arrhythmia
Organophosphate toxicity + + - + Generalized Ascending BL Sudden Clinical diagnosis: physical exam & history Clinical suspicion confirmed with RBC AchE activity History of exposure to insecticide or living in farming environment. with : Diarrhea, Urination, Miosis, Bradycardia, Lacrimation, Emesis, Salivation, Sweating
Tick paralysis (Dermacentor tick) + - - - Generalized Ascending BL Insidious Clinical diagnosis: physical exam & history - History of outdoor activity in Northeastern United States. The tick is often still latched to the patient at presentation (often in head and neck area)
Tetrodotoxin poisoning + - + + Generalized Systemic BL Sudden Clinical diagnosis: physical exam & dietary history - History of consumption of puffer fish species.
Stroke +/- +/- +/- +/- Generalized Systemic UL Sudden MRI +ve for ischemia or hemorrhage MRI Sudden unilateral motor and sensory deficit in a patient with a history of atherosclerotic risk factors (diabetes, hypertension, smoking) or atrial fibrillation.
Poliomyelitis + + + +/- Proximal > Distal Systemic BL or UL Sudden PCR of CSF Asymmetric paralysis following a flu-like syndrome.
Transverse myelitis + + + + Proximal > Distal Systemic BL or UL Sudden MRI & Lumbar puncture MRI History of chronic viral or autoimmune disease (e.g. HIV)
Neurosyphilis + + - +/- Generalized Systemic BL Insidious MRI & Lumbar puncture CSF VDRL-specifc

CSF FTA-Ab -sensitive

History of unprotected sex or multiple sexual partners.

History of genital ulcer (chancre), diffuse maculopapular rash.

Muscular dystrophy + - - - Proximal > Distal Systemic BL Insidious Genetic testing Muscle biopsy Progressive proximal lower limb weakness with calf pseudohypertrophy in early childhood. Gower sign positive.
Multiple sclerosis exacerbation + + + + Generalized Systemic NL Sudden ↑CSF IgG levels

(monoclonal)

Clinical assessment and MRI Blurry vision, urinary incontinence, fatigue
Amyotrophic lateral sclerosis + - - - Generalized Systemic BL Insidious Normal LP (to rule out DDx) MRI & LP Patient initially presents with upper motor neuron deficit (spasticity) followed by lower motor neuron deficit (flaccidity).
Inflammatory myopathy + - - - Proximal > Distal Systemic UL or BL Insidious Elevated CK & Aldolase Muscle biopsy Progressive proximal muscle weakness in 3rd to 5th decade of life. With or without skin manifestations.

Epidemiology and Demographics

Stroke in USA

  • Stroke is a leading cause of serious long-term disability
  • In USA, the incidence and mortality rates of stroke has significantly decreased compared to previous years.
  • From year 2003 to 2013, the mortality rates due to stroke declined by 18.5%.[43]
  • In 2013, stroke became the fifth leading cause of death.
  • The case fatality rate of stroke is estimated to be 41.7 deaths per 100, 000 population[43]
  • The incidence of new (610, 000) or recurrent stroke (185, 000) is estimated to be 795000 people annually or 250 cases per 100, 000.[43]
  • It is estimated that one incidence of stroke happens every 4 sec with death occurs every 4 min.[43]
  • About 87% of all strokes are ischemic strokes[44]
  • Stroke costs the United States an estimated $34 billion each year[44]

Worldwide

  • According to WHO, the incidence of stroke is estimated to be 15 million people annually, worldwide.[45].
  • Out of these, 5 million die and 5 million are left permanently disabled.[45].

Age

  • Stroke can occur in all age groups. However, the incidence of stroke is less among individuals age less than 40 years of age and the risk increases with increasing age. [44]
  • According to WHO, stroke also occurs in about 8% of children with sickle cell disease.[45].
  • In 2009, 34% of people hospitalized for stroke were younger than 65 years[44]
  • The incidence of stroke in people aged 18 to 50 years is estimated to be approximately 10%. [43]
  • The rate of decline in mortality rates of stroke in different age groups is as follows:[43]
    • Older then 65 years: from 534.1 to 245.2 per 100,000
    • 45-65 years of age: from 43.5 to 20.2 per 100,000
    • 18 to 44 years of age: from from 3.7 to 2.0 per 100,000

Gender

There is increased incidence of stroke in men as compared to women.

Race

  • The risk of incidence of first stroke is twice in African-American population as compared to Caucasians with increased mortality rates.[44]

Geographical distribution

  • There is increased incidence and mortality rates of stroke in developing countries as compared to developed countries due to low socioeconomic status and heath facilities.
  • In the USA, the highest death rates from stroke are in the southeastern United States.[44]

Diagnosis

Almost 10% of cerebrovascular events that present to the emergency department are not detected during evaluation.[46] This is more common when "presenting neurologic complaints are mild, nonspecific, or transient".[46]

  • Diagnosis is based on history of symptoms development, physical examination and imaging findings.
  • CT scan and magnetic resonance imaging (MRI) are both reasonable for initial evaluation.
  • CT scan without contrast is the initial test performed to diagnose ischemic stroke and rule out hemorrhagic stroke.
  • CT is very sensitive for identifying acute hemorrhage and is considered the gold standard.
  • Gradient echo and T2 susceptibility-weighted MRI are as sensitive as CT for detection of acute hemorrhage and are more sensitive for identification of prior hemorrhage.
  • MR diffusion weighted imaging is the most sensitive and specific test for diagnosing ischemic stroke and may help detect presence of infarction in few minutes of onset of symptoms. It may also help differentiate viable tissue from infarct area if combined with MR perfusion. For diagnosing ischemic stroke in the emergency setting, MRI scan has the sensitivity and specificity of 83% and 98% respectively.[47]
  • MRI scan is superior to CT scan for being more sensitive and specific in detection of lacunar and posterior fossa infarcts, differentiation between acute and chronic stroke and detection of microbleeds. Another additional advantage is absence of ionising radiation compared to CT scan. Some of the disadvantages of MRI scan may include lack of availability in acute setting, higher cost, inability to use it in patients with metallic implants. MRI with contrast cannot be used in patients with renal failure.[48][49]

References

  1. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. ISBN 0-7216-0187-1.
  2. ↑ Feigin VL (2005). "Stroke epidemiology in the developing world". Lancet. 365 (9478): 2160–1. doi:10.1016/S0140-6736(05)66755-4. PMID 15978910.
  3. ↑ headaches.about.com
  4. ↑ Hackam DG, Spence JD (2007). "Combining multiple approaches for the secondary prevention of vascular events after stroke: a quantitative modeling study". Stroke. 38 (6): 1881–5. doi:10.1161/STROKEAHA.106.475525. PMID 17431209.
  5. ↑ Moon JS, Janjua N, Ahmed S, Kirmani JF, Harris-Lane P, Jacob M; et al. (2008). "Prehospital neurologic deterioration in patients with intracerebral hemorrhage". Crit Care Med. 36 (1): 172–5. doi:10.1097/01.CCM.0000297876.62464.6B. PMID 18007267.
  6. ↑ Kishimoto M, Arakawa KC (2003). "A patient with wegener granulomatosis and intraventricular hemorrhage". J Clin Rheumatol. 9 (6): 354–8. doi:10.1097/01.rhu.0000089967.51779.d7. PMID 17043443.
  7. ↑ Challa VR, Richards F, Davis CH (1981). "Intraventricular hemorrhage from pituitary apoplexy". Surg Neurol. 16 (5): 360–1. PMID 7336321.
  8. ↑ Flint AC, Roebken A, Singh V (2008). "Primary intraventricular hemorrhage: yield of diagnostic angiography and clinical outcome". Neurocrit Care. 8 (3): 330–6. doi:10.1007/s12028-008-9070-2. PMID 18320145.
  9. ↑ Fukutake T (2011). "Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL): from discovery to gene identification". J Stroke Cerebrovasc Dis. 20 (2): 85–93. doi:10.1016/j.jstrokecerebrovasdis.2010.11.008. PMID 21215656.
  10. ↑ Meretoja A, Strbian D, Putaala J, Curtze S, Haapaniemi E, Mustanoja S; et al. (2012). "SMASH-U: a proposal for etiologic classification of intracerebral hemorrhage". Stroke. 43 (10): 2592–7. doi:10.1161/STROKEAHA.112.661603. PMID 22858729.
  11. ↑ Hart, Robert G., Bradley S. Boop, and David C. Anderson. "Oral anticoagulants and intracranial hemorrhage facts and hypotheses." Stroke 26.8 (1995): 1471-1477.
  12. ↑ Knudsen, Katherine A., et al. "Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria." Neurology 56.4 (2001): 537-539.
  13. ↑ Lovelock, C. E., A. J. Molyneux, and P. M. Rothwell. "Change in incidence and aetiology of intracerebral haemorrhage in Oxfordshire, UK, between 1981 and 2006: a population-based study." The Lancet Neurology 6.6 (2007): 487-493.
  14. ↑ Rümke CL (1975). "Letter: Implications of the statement: No side effects were observed". N Engl J Med. 292 (7): 372–3. PMID 1117973.
  15. ↑ Hanley DF (2009). "Intraventricular hemorrhage: severity factor and treatment target in spontaneous intracerebral hemorrhage". Stroke. 40 (4): 1533–8. doi:10.1161/STROKEAHA.108.535419. PMC 2744212. PMID 19246695.
  16. ↑ Morgenstern LB, Frankowski RF (1999). "Brain tumor masquerading as stroke". J Neurooncol. 44 (1): 47–52. PMID 10582668.
  17. ↑ Weston CL, Glantz MJ, Connor JR (2011). "Detection of cancer cells in the cerebrospinal fluid: current methods and future directions". Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
  18. ↑ 18.0 18.1 Birenbaum D, Bancroft LW, Felsberg GJ (2011). "Imaging in acute stroke". West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
  19. ↑ 19.0 19.1 DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). "ACR Appropriateness Criteria® on cerebrovascular disease". J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
  20. ↑ Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). "Cerebrospinal fluid in cerebral hemorrhage and infarction". Stroke. 6 (6): 638–41. PMID 1198628.
  21. ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). "Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients". J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
  22. ↑ Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
  23. ↑ Ho EL, Marra CM (2012). "Treponemal tests for neurosyphilis--less accurate than what we thought?". Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
  24. ↑ Carbonnelle E (2009). "[Laboratory diagnosis of bacterial meningitis: usefulness of various tests for the determination of the etiological agent]". Med Mal Infect. 39 (7–8): 581–605. doi:10.1016/j.medmal.2009.02.017. PMID 19398286.
  25. ↑ Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). "Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group". Arch Neurol. 51 (1): 61–6. PMID 8274111.
  26. ↑ Manford M (2001). "Assessment and investigation of possible epileptic seizures". J Neurol Neurosurg Psychiatry. 70 Suppl 2: II3–8. PMC 1765557. PMID 11385043.
  27. ↑ 27.0 27.1 Kira R (February 2018). "[Acute Flaccid Myelitis]". Brain Nerve (in Japanese). 70 (2): 99–112. doi:10.11477/mf.1416200962. PMID 29433111.
  28. ↑ Hopkins SE (November 2017). "Acute Flaccid Myelitis: Etiologic Challenges, Diagnostic and Management Considerations". Curr Treat Options Neurol. 19 (12): 48. doi:10.1007/s11940-017-0480-3. PMID 29181601.
  29. ↑ Messacar K, Schreiner TL, Van Haren K, Yang M, Glaser CA, Tyler KL, Dominguez SR (September 2016). "Acute flaccid myelitis: A clinical review of US cases 2012-2015". Ann. Neurol. 80 (3): 326–38. doi:10.1002/ana.24730. PMC 5098271. PMID 27422805.
  30. ↑ Chong PF, Kira R, Mori H, Okumura A, Torisu H, Yasumoto S, Shimizu H, Fujimoto T, Hanaoka N, Kusunoki S, Takahashi T, Oishi K, Tanaka-Taya K (February 2018). "Clinical Features of Acute Flaccid Myelitis Temporally Associated With an Enterovirus D68 Outbreak: Results of a Nationwide Survey of Acute Flaccid Paralysis in Japan, August-December 2015". Clin. Infect. Dis. 66 (5): 653–664. doi:10.1093/cid/cix860. PMC 5850449. PMID 29028962.
  31. ↑ Messacar K, Asturias EJ, Hixon AM, Van Leer-Buter C, Niesters H, Tyler KL, Abzug MJ, Dominguez SR (August 2018). "Enterovirus D68 and acute flaccid myelitis-evaluating the evidence for causality". Lancet Infect Dis. 18 (8): e239–e247. doi:10.1016/S1473-3099(18)30094-X. PMID 29482893. Vancouver style error: initials (help)
  32. ↑ Chen IJ, Hu SC, Hung KL, Lo CW (September 2018). "Acute flaccid myelitis associated with enterovirus D68 infection: A case report". Medicine (Baltimore). 97 (36): e11831. doi:10.1097/MD.0000000000011831. PMC 6133480. PMID 30200066.
  33. ↑ "Botulism | Botulism | CDC".
  34. ↑ McCroskey LM, Hatheway CL (May 1988). "Laboratory findings in four cases of adult botulism suggest colonization of the intestinal tract". J. Clin. Microbiol. 26 (5): 1052–4. PMC 266519. PMID 3290234.
  35. ↑ Lindström M, Korkeala H (April 2006). "Laboratory diagnostics of botulism". Clin. Microbiol. Rev. 19 (2): 298–314. doi:10.1128/CMR.19.2.298-314.2006. PMC 1471988. PMID 16614251.
  36. ↑ Brook I (2006). "Botulism: the challenge of diagnosis and treatment". Rev Neurol Dis. 3 (4): 182–9. PMID 17224901.
  37. ↑ Dimachkie MM, Barohn RJ (May 2013). "Guillain-Barré syndrome and variants". Neurol Clin. 31 (2): 491–510. doi:10.1016/j.ncl.2013.01.005. PMC 3939842. PMID 23642721.
  38. ↑ Walling AD, Dickson G (February 2013). "Guillain-Barré syndrome". Am Fam Physician. 87 (3): 191–7. PMID 23418763.
  39. ↑ Gilhus NE (2011). "Lambert-eaton myasthenic syndrome; pathogenesis, diagnosis, and therapy". Autoimmune Dis. 2011: 973808. doi:10.4061/2011/973808. PMC 3182560. PMID 21969911.
  40. ↑ Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA (May 2004). "Transverse Myelitis: pathogenesis, diagnosis and treatment". Front. Biosci. 9: 1483–99. PMID 14977560.
  41. ↑ Amato AA, Greenberg SA (December 2013). "Inflammatory myopathies". Continuum (Minneap Minn). 19 (6 Muscle Disease): 1615–33. doi:10.1212/01.CON.0000440662.26427.bd. PMID 24305450.
  42. ↑ Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
  43. ↑ 43.0 43.1 43.2 43.3 43.4 43.5 Writing Group Members. Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ; et al. (2016). "Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart Association". Circulation. 133 (4): e38–360. doi:10.1161/CIR.0000000000000350. PMID 26673558.
  44. ↑ 44.0 44.1 44.2 44.3 44.4 44.5 http://www.cdc.gov/stroke/facts.htm Accessed on November 3, 2016
  45. ↑ 45.0 45.1 45.2 Mackay, Judith, et al. The atlas of heart disease and stroke. World Health Organization, 2004 Accessed on November 3 2016
  46. ↑ 46.0 46.1 Tarnutzer AA, Lee SH, Robinson KA, Wang Z, Edlow JA, Newman-Toker DE (2017). "ED misdiagnosis of cerebrovascular events in the era of modern neuroimaging: A meta-analysis". Neurology. 88 (15): 1468–1477. doi:10.1212/WNL.0000000000003814. PMC 5386439. PMID 28356464.
  47. ↑ Chalela JA, Kidwell CS, Nentwich LM, Luby M, Butman JA, Demchuk AM, Hill MD, Patronas N, Latour L, Warach S (2007). "Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison". Lancet. 369 (9558): 293–8. doi:10.1016/S0140-6736(07)60151-2. PMC 1859855. PMID 17258669.
  48. ↑ Wintermark M, Sanelli PC, Albers GW, Bello J, Derdeyn C, Hetts SW; et al. (2013). "Imaging recommendations for acute stroke and transient ischemic attack patients: A joint statement by the American Society of Neuroradiology, the American College of Radiology, and the Society of NeuroInterventional Surgery". AJNR Am J Neuroradiol. 34 (11): E117–27. doi:10.3174/ajnr.A3690. PMC 4072500. PMID 23907247.
  49. ↑ Leiva-Salinas C, Wintermark M (2010). "Imaging of acute ischemic stroke". Neuroimaging Clin N Am. 20 (4): 455–68. doi:10.1016/j.nic.2010.07.002. PMC 2965616. PMID 20974371.

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