COVID-19-associated stroke: Difference between revisions

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Revision as of 14:18, 14 July 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Parul Pahal, M.B.B.S [2], Moises Romo M.D.

Synonyms and keywords: COVID-19, SARS-CoV-2, stroke, CT scan, cerebrovascular disease, TPA, alteplase

Overview

Cerebral hemorrhage or cerebral ischemia disrupts cerebral perfusion and can lead to an acute neurologic condition, called stroke. Cerebrovascular complications have been reported in severe Coronavirus Disease 2019 (COVID-19). However, neurological complications are not very common in rapidly spreading COVID-19 which is caused by a novel coronavirus, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The presenting complaints in majority of stroke patients reported in different studies were respiratory complaints (shortness of breath, cough) and non-specific constitutional symptoms such as fever, malaise, etc., and stroke developed later in the course of the disease. This is thought to be due to COVID-19-associated coagulopathy. However, there are few case reports and studies that have mentioned specific neurological presenting complaints such as altered mental status, limb weakness, and aphasia. Various non-pulmonary features are being reported as the COVID-19 understanding is unfolding with the spike of cases and continuously rising number of cases globally.

Historical Perspective

Stroke was first recognized by Hippocrates, in the fourth century BC, almost 2,400 years ago, and it was reffered to as Apoplexy, a Greek medical literature term, which means 'struk down by violence'. Later, renaissance anatomists, in mid-16th century A.D., explained the pathophysiology of stroke, differentiating the causes as bleeding or blockage of A cerebral artery.^[1]

Mao et al., in his study, first reported neurological symptoms in COVID-19 patients hospitalized in Wuhan, China from January 16, 2020, to February 19, 2020. Neurological symptoms were reported in 78 patients out of 214 Covid-19 positive hospitalized patients with COVID-19 in Wuhan, China. The stroke patients reported specifically were 14^[2]. In this study, patients with cardiovascular risk factors who presented with severe systemic symptoms were at higher risk of stroke.

Yaghi et al. retrospectively examined stroke patients admitted across different locations of NYU Langone hospital in New York. In this study, the incidence of 0.9% was observed in laboratory confirmed COVID-19 positive patients included in this study. Stroke diagnosis was proved by imaging, and cryptogenic stroke was seen in most of these patients. The mortality was much higher in stroke patients who were COVID-19 positive.^[3]

The most common type of stroke in patients with COVID-19 is ischemic.^[4]

Stroke should be differentiated from other causes of muscle weakness and paralysis. The differentials include the following:^[5]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]^[16]^[17]^[18]^[19]^[20]

There is no specific classification established for 'Stroke in COVID-19 patients'. It is same as the general classification of stroke.^[1]

The most common type of stroke in patients with COVID-19 is ischemic.^[4]

The exact pathophysiology of 'stroke in COVID-19' is not fully understood. However, it is thought that stroke in COVID-19 could be due to one of the following pathophysiologies-
- Sepsis induced coagulopathy:
  - Sepsis induced coagulopathy in COVID-19 patients is thought to be contributing to microthromobosis. This is supported by elevation of D-dimer and C-reactive protein, which are hypercoagulability and inflammatory markers, in COVID-19 positive patients.
- The angiotensin-converting enzyme II:
  - (ACEII) receptors are also present on the vascular endothelial cells and neural cells in the brain .
  - These receptors expressed in the brain are responsible for sympathoadrenal system regulation, and vascular autoregulation^[21].
  - When the virus binds to these receptors, this vascular autoregulation is hampered and can lead to elevated blood pressure, eventually leading to rupture of the cerebral vessels and intracranial hemorrhage^[22].
  - It does so by altering the balance of renin-angiotensin system which likely triggers endothelium dysfunction, organ damage, which eventually results in stroke^[23].
- Viral Neurotropism and Neuroinvasion:
  - Viral Neurotropism and Neuroinvasion is another possible pathogenic mechanism for cerebrovascular accidents in COVID-19 patients.
  - The coronaviruses usually cause mild respiratory illness, but the beta coronavirues are known to have a role in nervous system involvement^[24].
  - The Novel coronavirus “severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)” is a beta coronavirus, similar to severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV)^[25].
  - It,therefore, has an infection mechanism and potential to invade the nervous system, similar to SARS-Cov and MERS-Cov^[26].
  - The detection of the virus in the cells of the brain on autopsy^[27] (neural and capillary endothelial cells), and viral presence in the cerebrospinal fluid of the encephalitis patient infected with SARS-Cov-2^[28] supports the neuro-invasiveness of the virus. The two possible routes are retrograde axonal transport (via nasal cavity) or hematogenous spread (via blood brain barrier endothelial cells)^[27].
  - Once the virus reaches the brain, it attaches to the ACE II receptors.
- Direct entry into brain tissues:
  - Direct entry into brain tissues from cribriform plate to brain^[29].
  - wwwwThis is one of the proposed mechanism as COVID-19 positive patients also presented with anosmia and hyposmia which possibly occurs due to viral effect on olfactory bulb, which is in close proximity to cribriform plate^[2]

Stroke should be differentiated from other causes of muscle weakness and paralysis. The differentials include the following:^[5]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]^[16]^[17]^[18]^[19]^[20]

Stroke was first recognized by Hippocrates, in the fourth century BC, almost 2,400 years ago, and it was reffered to as Apoplexy, a Greek medical literature term, which means 'struk down by violence'. Later, renaissance anatomists, in mid-16th century A.D., explained the pathophysiology of stroke, differentiating the causes as bleeding or blockage of A cerebral artery.^[1]

Mao et al., in his study, first reported neurological symptoms in COVID-19 patients hospitalized in Wuhan, China from January 16, 2020, to February 19, 2020. Neurological symptoms were reported in 78 patients out of 214 Covid-19 positive hospitalized patients with COVID-19 in Wuhan, China. The stroke patients reported specifically were 14^[2]. In this study, patients with cardiovascular risk factors who presented with severe systemic symptoms were at higher risk of stroke.

Yaghi et al. retrospectively examined stroke patients admitted across different locations of NYU Langone hospital in New York. In this study, the incidence of 0.9% was observed in laboratory confirmed COVID-19 positive patients included in this study. Stroke diagnosis was proved by imaging, and cryptogenic stroke was seen in most of these patients. The mortality was much higher in stroke patients who were COVID-19 positive.^[3]

There is no specific classification established for 'Stroke in COVID-19 patients'. It is same as the general classification of stroke.^[1]

The most common type of stroke in patients with COVID-19 is ischemic.^[4]The exact pathophysiology of 'stroke in COVID-19' is not fully understood.
However, it is thought that stroke in COVID-19 could be due to one of the following pathophysiologies-
- Sepsis induced coagulopathy:
  - in COVID-19 patients is thought to be contributing to microthromobosis. This is supported by elevation of D-dimer and C-reactive protein, which are hypercoagulability and inflammatory markers, in COVID-19 positive patients.
- The angiotensin-converting enzyme II:
  - (ACEII) receptors are also present on the vascular endothelial cells and neural cells in the brain .
  - These receptors expressed in the brain are responsible for sympathoadrenal system regulation, and vascular autoregulation^[21].
  - When the virus binds to these receptors, this vascular autoregulation is hampered and can lead to elevated blood pressure, eventually leading to rupture of the cerebral vessels and intracranial hemorrhage^[22].
  - It does so by altering the balance of renin-angiotensin system which likely triggers endothelium dysfunction, organ damage, which eventually results in stroke^[23].
- Viral Neurotropism and Neuroinvasion:
  - This is another possible pathogenic mechanism for cerebrovascular accidents in COVID-19 patients.
  - The coronaviruses usually cause mild respiratory illness, but the beta coronavirues are known to have a role in nervous system involvement^[24].
  - The Novel coronavirus “severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)” is a beta coronavirus, similar to severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV)^[25].
  - It, therefore, has an infection mechanism and potential to invade the nervous system, similar to SARS-Cov and MERS-Cov^[26].
  - The detection of the virus in the cells of the brain on autopsy^[27] (neural and capillary endothelial cells), and viral presence in the cerebrospinal fluid of the encephalitis patient infected with SARS-Cov-2^[28] supports the neuro-invasiveness of the virus.
  - The two possible routes are retrograde axonal transport (via nasal cavity) or hematogenous spread (via blood brain barrier endothelial cells)^[27].
  - Once the virus reaches the brain, it attaches to the ACE II receptors.
- Direct entry into brain tissues:
  - Direct invasion from cribriform plate to brain^[29]. This is one of the proposed mechanism as COVID-19 positive patients also presented with anosmia and hyposmia which possibly occurs due to viral effect on olfactory bulb, which is in close proximity to cribriform plate^[2]

Stroke should be differentiated from other causes of muscle weakness and paralysis. The differentials include the following:^[5]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]^[16]^[17]^[18]^[19]^[20]

Stroke was first recognized by Hippocrates, in the fourth century BC, almost 2,400 years ago, and it was reffered to as Apoplexy, a Greek medical literature term, which means 'struk down by violence'. Later, renaissance anatomists, in mid-16th century A.D., explained the pathophysiology of stroke, differentiating the causes as bleeding or blockage of A cerebral artery.^[1]

Mao et al., in his study, first reported neurological symptoms in COVID-19 patients hospitalized in Wuhan, China from January 16, 2020, to February 19, 2020. Neurological symptoms were reported in 78 patients out of 214 Covid-19 positive hospitalized patients with COVID-19 in Wuhan, China. The stroke patients reported specifically were 14^[2]. In this study, patients with cardiovascular risk factors who presented with severe systemic symptoms were at higher risk of stroke.

Yaghi et al. retrospectively examined stroke patients admitted across different locations of NYU Langone hospital in New York. In this study, the incidence of 0.9% was observed in laboratory confirmed COVID-19 positive patients included in this study. Stroke diagnosis was proved by imaging, and cryptogenic stroke was seen in most of these patients. The mortality was much higher in stroke patients who were COVID-19 positive.^[3]

Classification

There is no specific classification established for 'Stroke in COVID-19 patients'. It is same as the general classification of stroke.^[1]

Stroke can be classified into
- Ischemic stroke: This can be due to
  - Thrombosis (Large vessel or Small vessel thrombosis)
  - Embolism
  - Systemic hypoperfusion
  - Cryptogenic (unknown origin)
- Hemorrhagic stroke: This can be due to

Pathophysiology

The most common type of stroke in patients with COVID-19 is ischemic.^[4]

The exact pathophysiology of 'stroke in COVID-19' is not fully understood. However, it is thought that stroke in COVID-19 could be due to one of the following pathophysiologies-
- Sepsis induced coagulopathy in COVID-19 patients is thought to be contributing to microthromobosis. This is supported by elevation of D-dimer and C-reactive protein, which are hypercoagulability and inflammatory markers, in COVID-19 positive patients.
- The angiotensin-converting enzyme II (ACEII) receptors are also present on the vascular endothelial cells and neural cells in the brain . These receptors expressed in the brain are responsible for sympathoadrenal system regulation, and vascular autoregulation^[21]. When the virus binds to these receptors, this vascular autoregulation is hampered and can lead to elevated blood pressure, eventually leading to rupture of the cerebral vessels and intracranial hemorrhage^[22]. It does so by altering the balance of renin-angiotensin system which likely triggers endothelium dysfunction, organ damage, which eventually results in stroke^[23].
- Viral Neurotropism and Neuroinvasion is another possible pathogenic mechanism for cerebrovascular accidents in COVID-19 patients. The coronaviruses usually cause mild respiratory illness, but the beta coronavirues are known to have a role in nervous system involvement^[24]. The Novel coronavirus “severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)” is a beta coronavirus, similar to severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV)^[25]. It,therefore, has an infection mechanism and potential to invade the nervous system, similar to SARS-Cov and MERS-Cov^[26]. The detection of the virus in the cells of the brain on autopsy^[27] (neural and capillary endothelial cells), and viral presence in the cerebrospinal fluid of the encephalitis patient infected with SARS-Cov-2^[28] supports the neuro-invasiveness of the virus. The two possible routes are retrograde axonal transport (via nasal cavity) or hematogenous spread (via blood brain barrier endothelial cells)^[27]. Once the virus reaches the brain, it attaches to the ACE II receptors.
- Direct entry into brain tissues from cribriform plate to brain^[29]. This is one of the proposed mechanism as COVID-19 positive patients also presented with anosmia and hyposmia which possibly occurs due to viral effect on olfactory bulb, which is in close proximity to cribriform plate^[2]

Further investigations should be done to better understand the mechanism of Stroke in patients with COVID-19.

Causes

Coronavirus disease 2019 (COVID-19) associated stroke is caused by SARS-CoV-2.

Differentiating COVID-19-associated stroke from other Diseases

Stroke should be differentiated from other causes of muscle weakness and paralysis. The differentials include the following:^[5]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]^[16]^[17]^[18]^[19]^[20]

Diseases	History and Physical								Diagnostic tests		Other Findings
Diseases	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	Other Findings
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.

Stroke associated with COVID-19 should be differentiated from other diseases that can have similar presentation as stroke. These include-^[30]^[31]
- Other COVID-19 associated neurological complications: Encephalitis, Encephalopathy, Meningitis, Seizure, Guillain-Barre syndrome, polyneuritis cranialis
- Neurologic in non-COVID patients: Transient Ischemic Attack, Brain abscess, Hemiplegic Migraine, Seizures^[32], Postictal paralysis, Cerebral venous sinus thrombosis, Cerebral neoplasm^[33]^[34], Cerebral Infections (Meningitis, Encephalitis^[35], Brain Abscess, Progressive multifocal leukoencephalopathy)
- Traumatic: Epidural hematoma, Subdural hematoma, Traumatic brain Injury
- Toxic and/or Metabolic: Hypoglycemia, Hyponatremia, Drug intoxication
- Syncope
- Lyme's disease^[36]
- Ear and Nose diseases^[37]: Benign Paroxysmal Positional Vertigo, Vestibular Neuronitis, Meniere's Disease
- Psychiatric: Malingering, Conversion disorder
- Paraneoplastic syndromes
- Autoimmune disorders: Multiple Sclerosis^[38], Acute inflammatory demyelinating polyradiculoneuropathy(Guillain-Barre syndrome)^[39]

Stroke in COVID-19 positive patients vs. Stroke in non-COVID-19 patients: A retrospective cohort study (15th March,2020 to 19th April,2020) conducted by Yaghi et. al. in hospitalized patients in New York Healthcare systems compared stroke characteristics in patients with and without COVID-19^[3]. This study included 3,556 COVID-19 positive patients, out of which 32 patients were diagnosed with ischemic stroke based on imaging. These COVID-19 positive stroke patients were then compared with 46 hospitalized stroke patients without COVID-19. Based on findings of this study-
- Younger patient population (average age-63 years) as compared to relatively older patient population (average age-70 years) in non-COVID-19 patients.
- Severe stroke (National Institutes of Health Stroke Scale- average score 19) as compared to non-COVID patients with lesser average score (8) seen on National Institutes of Health Stroke Scale
- Higher D-dimer levels which point towards severe blood clotting (10,000 in this study). Relatively lower D-dimer levels (525 in this study) were seen in non-COVID patients.
- Mostly Cryptogenic stroke seen in COVID-19 patients.
- Increased mortality seen in COVID-19 patients.
- Most of COVID-19 patients did not have any history of prior stroke (only 3.1% reported stroke history) as opposed to non-COVID patient group in which prior history of stroke was reported in 13%.
- Non-COVID patients were more likely to have higher blood pressure levels.

Further studies are going on to understand the clinical characteristics specific to stroke in COVID-19 patients. It has been observed that the findings vary in different countries possibly due to racial/ethnicity variations. Since strokes have been reported in critically ill COVID-19 patients, hence, it is difficult to diagnose stroke in intubated and sedated COVID-19 patients.

Stroke in COVID-19 positive patients vs. Stroke in Influenza patients: Out of 1916 COVID-19 patients (Emergency Department visits or were hospitalized with COVID-19) in retrospective cohort study which included patients from two academic hospitals in New York, 31 patients (1.6%) with median age 69 years, experienced acute ischemic stroke. The majority of these patients were men (58%). 8 patients (26%] had initial presentation as stroke while 23 had stroke over the course of the disease after testing positive for COVID-19.

Based on this study, the COVID-19 patients have much higher incidence of stroke when compared to influenza patients.^[40]

Epidemiology and Demographics

The case fatality rate of cerebrovascular accidents is 41.7 deaths per 100, 000 population^[41]. The mortality in patients with COVID-19 associated stroke is higher.^[3]

The incidence of stroke in COVID-19 varies significantly depending on the study population.^[42] The prevalence of COVID-19-associated stroke varies in different studies (Table 1).

Prevalence of stroke in patients with COVID-19
Date of publication	Country	Author	Number of patients	Severe infection	Neurological symptoms	Acute Cerebrovascular disease	Ischemic/Hemorrhagic Stroke
April 10, 2020	Wuhan, China	Mao et al.^[2]	214	88 patients (41.1%), Mean age-58.2 years	78 patients (36.4%)	5 among severe [5.7%] infection group vs 1 [0.8%]) in non-severe group	Ischemic-4, Hemorrhagic-1
May 29, 2020	Wuhan, China	Qin et al.^[43] (Retrospective cohort study)	1875	461 severe on admission		50 patients ie. 15 among severe and 35 among mild on admission (Median age-70 years), 30 males and 20 females	Ischemic-90%, Hemorrhagic-10%
May 20, 2020	New York	Yaghi et al.^[3] (Retrospective cohort study)	3556		Stroke at the time of admission-14/32 (43.8%), eventually developed stroke during hospitalization-18 (56.2%)	32 patients (0.9%)	Ischemic stroke- 32
April 28, 2020	New York city	Oxley et al.^[44]	5				Large vessel stroke-5, Mean age-<50 years
July 12, 2020	New York	Valderrama et al.	1 (52-year old male)				Ischemic stroke
Table 1. Prevalence of COVID-19-associated stroke varies in different studies

The incidence of stroke in hospitalized COVID-19 patients is reported to be 0.9–2%^[45].majority of them being ischemic subtype. The mortality in COVID-19 positive stroke patients is reported to be 39%^[2].

The ischemic stroke prevalence in COVID-19 patients is 1.6%.^[45]

A New York study published in May reported that the proportion of these strokes seem to be higher in younger men.^[3] Most of these strokes are large vessel ischemic strokes and are catastrophic.

In a retrospective observational case series of six stroke patients in a hospital in Italy, with lab confirmed COVID-19, the median age reported was 69 years. Ischemic stroke subtype was seen in 4 patients(67%) as compared to hemorrhagic which was only seen in 2 patients (33%). Vascular risk factors were seen in 5/6 patients, which included diabetes mellitus, arterial hypertension

In a single center retrospective study conducted in Wuhan by Qin C. et al. which included 1875 laboratory-confirmed COVID-19 patients from january 27th, 2020, to March 5th, 2020, 50 patients had history of stroke. The median age of this study group was 63 years, with stroke patients relatively older(70 years) when compared to non-stroke patients (62 years).^[43]

Stroke is one of the neurological manifestations in patients with severe infection. There is limited information on COVID-19 patients with stroke who survived.

Risk Factors

According to one of the study conducted in New York, Stroke in COVID-19 infected patients is seen in relatively young patients as compared to with non COVID-19 patients.^[3]

A study by Mao et. al. reported COVID-19 associated stroke in seen in critically patients. The patients who developed stroke were older population with comorbidities like diabetes, hypertension, etc.

However, due to disparities in the stroke prevalence in different studies, no clear association has been established.

Screening

There is insufficient evidence to recommend routine screening for stroke in COVID-19 patients. However, if the patient presents with stroke, COVID-19 screening should be done.

Natural History, Complications, and Prognosis

Prognosis is generally poor for COVID-19 patients with stroke. A study reported a high proportion of these patients were admitted to the Intensive Care Unit(ICU) and required mechanical ventilation. The mortality of COVID-19 patients with stroke was much higher when compared to COVID-19 patients with no history of stroke^[43].

Diagnosis

Diagnosis of stroke associated to COVID-19 is based on history of symptoms development, physical examination, imaging findings, plus a positive COVID-19 test.
There are no standard criteria for the evaluation of stroke associated to COVID-19.
General management protocols for COVID-19-associated stroke should be established so that brain imaging can be realized as prompt as possible in patients who may be candidates for IV fibrinolysis or mechanical thrombectomy or both.^[46]
The current diagnostic approach for stroke associated to COVID-19 is the same as for people with non-COVID infection.

Diagnostic Study of Choice

Non-contrast CT Scan of the brain within 20 minutes of arrival to the emergency department is the diagnostic test of choice for stroke in patients with COVID-19 infection.^[47]
MRI may detect smaller lesions with certainty if required, once the hemorrhagic stroke is excluded by non-contrast CT Scan.^[48]
In a patient who presents with neurological symptoms, RT-PCR for SARS-CoV-2 should be done as well.

History and Symptoms

The extent of damage and symptoms which may result from stroke associated to COVID-19 highly depends on the site of infarction, the blood vessels involved, and the presence of other risk factors.^[49]^[50]^[51]

The majority of patients with COVID-19-associated stroke initially presented with respiratory symptoms (e.g. cough, shortness of breath etc) and constitutional features. These patients developed cerebrovascular signs and symptoms later in the course of disease.
A few studies reported cases of patients with COVID-19 infection which presented with neurological symptoms suggestive of stroke (Table 2). Most of these patients had underlying history of chronic diseases such as diabetes mellitus, atrial fibrillation, etc.^[52]^[53]

Patient no.	Onset of neurologic symptoms	Age and Gender	Neurologic Signs & Symptoms
1	On Admission	73-year old, Male	Respiratory distress, fever, and altered mental status ^[52]
2	On Admission	83-year old, Female	Fever, slurring of speech, facial droop, and reduced oral intake ^[52]
3	On Admission	80-year old female	Left sided weakness, altered mental status, one week history of frequent falls ^[52]
4	On Admission	88-year old, Female	An 15 minute episode of weakness and numbness of right arm and word finding difficulty ^[52]
5	On Admission	58-year old, Male	Dense Right-sided weakness and acute onset aphasia ^[53]
Table 2. Reported cases of patients with COVID-19 infection and symptoms suggestive of stroke.

Physical Examination

The physical examination findings in stroke associated to COVID-19 will highly depend on the site of infarction, the blood vessels involved, and the presence of other risk factors.^[49]^[50]^[51]
The use of stroke scales helps to measure the degree of neurological impairment, ease communication, may help select patients candidates for fibrinolytic or mechanical therapy, permits the evaluation of changing clinical status, and identifies those patients at higher risk for complications (eg. intracerebral hemorrhage).^[54]
The National Institutes of Health Stroke Scale (NIHSS) (Table 3) is a tool used to measure the neurologic impairment caused by a stroke in a quantitative manner.^[55]^[56] The NIHSS is composed of 11 items, each of which scores a specific ability between a 0 and 4. For each item, a score of 0 typically indicates normal function in that specific ability, while a higher score is indicative of some level of impairment. The individual scores from each item are summed in order to calculate a patient's total NIHSS score. The maximum possible score is 42, with the minimum score being a 0.^[56]

National Institutes of Health Stroke Scale (NIHSS)
Tested item	Title	Response and score
1A	Level of consciousness	0—Alert
		1—Drowsy
		2—Obtunded
		3—Coma/unresponsive
1B	Orientation questions (2)	0—Answers both correctly
		1—Answers 1 correctly
		2—Answers neither correctly
2	Gaze	0—Normal horizontal movements
		1—Partial gaze palsy
		2—Complete gaze palsy
3	Visual fields	0—No visual field defect
		1—Partial hemianopia
		2—Complete hemianopia
		3—Bilateral hemianopia
4	Facial movement	0—Normal
		1—Minor facial weakness
		2—Partial facial weakness
		3—Complete unilateral palsy
5	Motor function (arm) a. Left b. Right	0—No drift
		1—Drift before 10 s
		2—Falls before 10 s
		3—No effort against gravity
		4—No movement
6	Motor function (leg) a. Left b. Right	0—No drift
		1—Drift before 5 s
		2—Falls before 5 s
		3—No effort against gravity
		4—No movement
7	Limb ataxia	0—No ataxia
		1—Ataxia in 1 limb
		2—Ataxia in 2 limbs
8	Sensory	0—No sensory loss
		1—Mild sensory loss
		2—Severe sensory loss
9	Language	0—Norma
		1—Mild aphasia
		2—Severe aphasia
		3—Mute or global aphasia
10	Articulation of words	0—Norma
		1—Mild dysarthria
		2—Severe dysarthria
11	Extinction or inattention	0—Absent
		1—Mild loss (1 sensory modality lost)
		2—Severe loss (2 modalities lost)
Table 3. Adapted from Lyden et al., 1994^[57] American Heart Association, Inc.

The pre-stroke Modified Rankin Score (mRS) (Table 4) is an estimated score used to assess the patient’s pre-stroke level of function. An estimated mRS should be abstracted from current medical record documentation about the patient’s ability to perform activities of daily living prior to the hospitalization for the acute ischemic stroke event.^[58]

Alberta stroke program early CT score (ASPECTS)
Area affected		Score
Subganglionic Nuclei:	M1 - Frontal operculum	1
	M2 - Anterior temporal lobe	1
	M3 - Posterior temporal lobe	1
Supraganglionic Nuclei:	M4 - Anterior MCA	1
	M5 - Lateral MCA	1
	M6 - Posterior MCA	1
Basal Ganglia:	C - Caudate	1
	L - Lentiform Nucleus	1
	I - Insula	1
	IC - Internal Capsule	1
Table 4. Adapted from The University of Calgary ASPECT score in Accute stroke, 2020^[59]

Alberta stroke program early CT score (ASPECTS) (Table 5) is a 10 point quantitative score used to asses early ischemic changes in patients suspected of having acute large vessel anterior circulation occlusion.^[59]

*Pre-Stroke Modified Rankin Score (mRS)*
Score	Item tested
0	The patient had no residual symptoms.
1	The patient had no significant disability; able to carry out all activities.
2	The patient had slight disability; unable to carry out all activities but able to look after self without daily help.
3	The patient had moderate disability; requiring some external help but able to walk without the assistance of another individual.
4	The patient had moderately severe disability; unable to walk or attend to bodily functions without assistance of another individual.
5	The patient had severe disability; bedridden, incontinent, requires continuous care.
6	Unable to determine (UTD) from the medical record documentation.
Table 5. Adapted from Specifications Manual for Joint Commission National Quality Measures, 2018^[58]

Laboratory Findings

Patients with stroke associated to COVID-19 will have a positive test for COVID-19 confirmed either through molecular tests, nucleic acid amplification test, or serological testing.

Serum glucose assessment is the only lab study that should proceed IV alteplase initiation, this should be over 50 mg/dL for its administration.^[46]
Coagulation studies and complete blood count should be delayed until after IV alteplase initiation unless there is suspicion for a coagulopathy disorder.^[46]
Troponin should be assessed in patients presenting with ischemic stroke.^[46]
In adults who are 20 years of age or older and not on lipid-lowering therapy, measurement of either a fasting or a nonfasting plasma lipid profile is effective in estimating atherosclerotic cardiovascular disease (ASCVD) risk and documenting baseline low-density lipoprotein cholesterol (LDL-C). 4 to 12 weeks after statin initiation or dose adjustment and every 3 to 12 months thereafter based on need to assess adherence or safety.^[46]*
In patients older than 75 years of age with clinical ASCVD, it is reasonable to initiate moderate or high-intensity statin therapy after evaluation of the potential for ASCVD risk reduction, adverse effects, and drug interactions.*

Ultrasound

Echocardiography may be necessary in patients with ischemic stroke to identify and prevent secondary causes of stroke.
Carotid ultrasound should be performed in all patients with ischemic stroke to assess for narrowing of carotids and decrease recurrence.

X-ray

There is no evidence of usefulness of chest x-ray in the acute setting of stroke.^[46]

CT scan

Non-contrasted CT scan of the head should should always be performed before initiating IV alteplase.^[46]
Once hemorragic stroke is excluded, CT scan with contrast should be realized in patients with no history of renal disease without measuring creatinine concentration, taking into account that both COVID-19 infection and stroke increase the risk for renal impairment per se.^[4]^[60]
CT angiography of the brain may be needed in patients to make a decision for mechanical thrombectomy.^[4]^[61]^[62]
CT angiography's contrast can increase the risk of acute kidney injury in patients with COVID-19 infection.^[4]
CT perfusion should be done in patients who present within 24 hours of the initiation of symptoms.^[4]
Concurrent CT scan of the head and chest may be ordered at the same time in patients with COVID-19 infection.^[4]^[63]
CT angiography of the extracranial carotid and vertebral arteries, in addition to the intracranial circulation,is recommended in patients who are potential candidates for mechanical thrombectomy.^[46]^[64]

MRI

MRI of the head before IV alteplase administration to exclude microbleeds is not recommended.^[46]
Multimodal MRI of the head should be done in patients who present within 24 hours of the initiation of symptoms.^[4]
In patients who wake up with clinical symptoms of stroke of unknown onset (more than 3 hours?), an MRI with diffusion-positive FLAIR may be useful for selecting those who can benefit from IV alteplase administration.^[46]

Electrocardiogram

Baseline electrocardiographic assessment is recommended in patients presenting with ischemic stroke.^[46]

Treatment

Medical therapy

The reported cases of treatment for COVID-19-associated stroke have followed the same guidelines as patients with no COVID-19 infection. The following recommendations are mainly based on the current guidelines of management for stroke of the AHA 2019.
IV alteplase is always preferred over mechanical thrombectomy when there are no contraindications.^[65]
The usefulness of anticoagulants such as thrombin inhibitors (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) is not well established in the acute setting of stroke.^[66]
The use of thrombolysis via ultrasound waves concomitant to IV fibrinolysis is not recommended.^[67]
In patients who are 75 years of age or younger with clinical ASCVD, high-intensity statin therapy should be initiated or continued with the aim of achieving a 50% or greater reduction in LDL-C levels.*
A clinician-patient risk discussion is recommended before initiation of statin therapy to review net clinical benefit, weighing the potential for ASCVD risk reduction against the potential for statin-associated side effects, statin-drug interactions, and safety, while emphasizing that side effects can be addressed successfully.*
For patients with ischemic stroke who qualify for statin treatment, in-hospital initiation of statin therapy is reasonable.^[68]*
Among patients already taking statins at the time of onset of ischemic stroke, continuation of statin therapy during the acute period is reasonable.*

Alteplase

IV alteplase is recommended for selected patients who can be treated within 3-4.5 hours of ischemic stroke symptom onset or patient last known well or at baseline state.^[69]^[46]^[70]
The dose of IV alteplase is 0.9 mg/kg (maximum dose 90 mg) over 60 min, with 10% of the dose given as a bolus over 1 min.^[46]
IV alteplase should be initiated as soon as possible, having been demonstrated better outcomes the sooner is administered.^[46]
Hyperglycemia should be treated during the first 24 hours after ischemic stroke, to achieve values of 140 to 180 mg/dL.^[46]
IV alteplase may cause bleeding and angioedema.^[46]
Glycoprotein IIb/IIIa inhibitors (tirofiban, apiximab, eptifibatide) should not be coadministered with IV alteplase.^[46]^[71]
IV alteplase may be used in patients under warfarin if the INR is lower than 1.7.^[46]
IV alteplase should not be administered to patients who have received a full dose of low-molecular-weight heparin within the previous 24 hours (including prophylactic doses).^[46]^[72]
Blood pressure should be sustained lower than 180/105 mmHg the first 24 hours after IV alteplase administration. Intensive lowering has been shown to be safe.^[46]^[73]
In case of intracranial bleeding due to alteplase administration, alteplase should be suspended, blood draws should be taken (CBC, coagulation studies), tranexamic acid should be administered (1000 mg IV infused over 10 min), and a subsecuent non-contratested CT scan of the head taken.^[74]
The use of IV alteplase should be used cautiously in patients who undergone a major surgery in the past 2 weeks.^[46]
IV alteplase for ischemic stroke is contraindicated in patients with a severe head trauma or subarachnoid hemorrage in the preceding 3 months.^[46]

Tenecteplase

Tenecteplase may be useful in patients with minor neurological impairment.^[75]
The dose of tenecteplase is a single IV bolus of 0.25-mg/kg (maximum 25 mg).^[76]

Antiplatelet therapy

Administration of aspirin is recommended in patients with AIS within 24 to 48 hours after onset. For those treated with IV alteplase, aspirin administration is generally delayed until 24 hours later.^[77]
The dose of aspirin is usually between 160-300mg daily.^[78]
IV aspirin administration within 90 minutes after the start of IV alteplase is associated with symptomatic intracranial hemorrhage, for which co administration is discouraged but benefits should be assessed in each individual case.^[46]^[79]
Dual antiplatelet therapy with aspirin and clopidogrel (75 mg/d, with a loading dose of 600mg) may be started within 24 hours after symptom onset and continued for 21 days in patients with no cardioembolic ischemic stroke.^[80]
Aspirin should not substitute IV alteplase or mechanical thrombectomy in patients eligible for these therapies.

Surgery

The usefulness of emergency carotid endarterectomy, carotid angioplasty and stenting in the absence of an intracranial clot is not well established.^[46]

Mechanical thrombectomy with a stent retriever

Mechanical thrombectomy with stent retrievers is recommended over intra arterial fibrinolysis as first-line therapy.^[46]
Mechanical thrombectomy may be useful in selected patients with up to 24 hours of initiation of stroke.^[46]^[81]
In patients who undergo mechanical thrombectomy,blood pressure should be maintained below 180/105 mmHg during and for 24 hours after the procedure.^[46]

Patients should receive mechanical thrombectomy with a stent retriever if they meet all the following criteria:^[82]
1. Prestroke mRS score of 0 to 1
2. Causative occlusion of the internal carotid artery or MCA segment 1 (M1)
3. Age ≥18 years
4. NIHSS score of ≥6
5. ASPECTS of ≥6; and
6. Treatment can be initiated within 6 hours of symptom onset

Aspiration thrombectomy

Aspiration thrombectomy has not been shown to be inferior to stent retriever.^[83]

Direct aspiration thrombectomy as first-pass mechanical thrombectomy is recommended as noninferior to stent retriever for patients who meet all the following criteria:^[83]
1. Prestroke mRS score of 0 to 1;
2. Causative occlusion of the internal carotid artery or M1;
3. Age ≥18 years;
4. NIHSS score of ≥6;
5. ASPECTS ≥6; and
6. Treatment initiation within 6 hours of symptom onset.

Intra arterial fibrinolysis

Intra-arterial fibrinolysis may be initiated within 6 hours of stroke onset in selected patients in whom IV alteplase is contraindicated.

Other aspects of management

Volume expansors are not recommended in ischemic stroke.^[46]^[84]
The best head positioning after stroke is not well established.^[46]^[85]

Supplemental oxygen and mechanical ventilation support should be provided when necessary to maintain oxygen saturation higher than 93%.^[46]^[86]

Sources of hyperthermia (>38°C) should be identified and treated with antipyretics in patients with stroke.^[46]^[87]
Hypoglycemia (<60 mg/dL) should be treated in the acute setting in patients with ischemic stroke.^[46]
Blood pressure ≥220/120 in patients who did not receive TPA should be treated within the first 48 to 72 hours after the onset of ischemic stroke.^[88]
Enteral feeding should be started within 7 days of admission after an acute stroke when there is no contraindications.^[89]
Psychological screening is always recommended to exclude poststroke depression.^[90]
Early rehabilitation in patients with stroke is adviced.^[46]

Primary Prevention

There is currently no vaccine to prevent COVID-19. The best way to prevent infection is to avoid being exposed to this virus.
COVID-19 increases the probability of developing ischemic stroke, but there are several measures that can decrease the risk of stroke, among them:
Smoking cessation
Lowering blood pressure
Decreasing alcohol intake
Exercise
Treatment of atrial fibrillation
Weight loss
Procedures such as carotid endarterectomy or carotid angioplasty when necessary

Secondary Prevention

Smoking cessation should be highly encouraged in patients who suffered from stroke, behavioral interventions and nicotine replacement may be necessary.

References

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@@ Line 14: / Line 14: @@
 *Mao et al., in his study, first reported neurological symptoms in [[COVID-19]] patients hospitalized in Wuhan, China from January 16, 2020, to February 19, 2020. Neurological symptoms were reported in 78 patients out of 214 Covid-19 positive hospitalized patients with [[COVID-19]] in Wuhan, China. The stroke patients reported specifically were 14<ref name="MaoJin2020">{{cite journal|last1=Mao|first1=Ling|last2=Jin|first2=Huijuan|last3=Wang|first3=Mengdie|last4=Hu|first4=Yu|last5=Chen|first5=Shengcai|last6=He|first6=Quanwei|last7=Chang|first7=Jiang|last8=Hong|first8=Candong|last9=Zhou|first9=Yifan|last10=Wang|first10=David|last11=Miao|first11=Xiaoping|last12=Li|first12=Yanan|last13=Hu|first13=Bo|title=Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China|journal=JAMA Neurology|volume=77|issue=6|year=2020|pages=683|issn=2168-6149|doi=10.1001/jamaneurol.2020.1127}}</ref>. In this study, patients with cardiovascular risk factors who presented with severe systemic symptoms were at higher risk of stroke.
-*Yaghi et al. retrospectively examined [[stroke]] patients admitted across different locations of NYU Langone hospital in New York. In this study, the incidence of 0.9% was observed in laboratory confirmed COVID-19 positive patients included in this study. [[Stroke]] diagnosis was proved by imaging, and [[cryptogenic]] [[stroke]] was seen in most of these patients. The mortality was much higher in stroke patients who were [[COVID-19]] positive.<ref name="YaghiIshida2020">{{cite journal|last1=Yaghi|first1=Shadi|last2=Ishida|first2=Koto|last3=Torres|first3=Jose|last4=Mac Grory|first4=Brian|last5=Raz|first5=Eytan|last6=Humbert|first6=Kelley|last7=Henninger|first7=Nils|last8=Trivedi|first8=Tushar|last9=Lillemoe|first9=Kaitlyn|last10=Alam|first10=Shazia|last11=Sanger|first11=Matthew|last12=Kim|first12=Sun|last13=Scher|first13=Erica|last14=Dehkharghani|first14=Seena|last15=Wachs|first15=Michael|last16=Tanweer|first16=Omar|last17=Volpicelli|first17=Frank|last18=Bosworth|first18=Brian|last19=Lord|first19=Aaron|last20=Frontera|first20=Jennifer|title=SARS-CoV-2 and Stroke in a New York Healthcare System|journal=Stroke|volume=51|issue=7|year=2020|pages=2002–2011|issn=0039-2499|doi=10.1161/STROKEAHA.120.030335}}</ref>
+*Yaghi et al. retrospectively examined [[stroke]] patients admitted across different locations of NYU Langone hospital in New York. In this study, the incidence of 0.9% was observed in laboratory confirmed COVID-19 positive patients included in this study. [[Stroke]] diagnosis was proved by imaging, and [[cryptogenic]] [[stroke]] was seen in most of these patients. The mortality was much higher in stroke patients who were [[COVID-19]] positive.<ref name="YaghiIshida2020">{{cite journal|last1=Yaghi|first1=Shadi|last2=Ishida|first2=Koto|last3=Torres|first3=Jose|last4=Mac Grory|first4=Brian|last5=Raz|first5=Eytan|last6=Humbert|first6=Kelley|last7=Henninger|first7=Nils|last8=Trivedi|first8=Tushar|last9=Lillemoe|first9=Kaitlyn|last10=Alam|first10=Shazia|last11=Sanger|first11=Matthew|last12=Kim|first12=Sun|last13=Scher|first13=Erica|last14=Dehkharghani|first14=Seena|last15=Wachs|first15=Michael|last16=Tanweer|first16=Omar|last17=Volpicelli|first17=Frank|last18=Bosworth|first18=Brian|last19=Lord|first19=Aaron|last20=Frontera|first20=Jennifer|title=SARS-CoV-2 and Stroke in a New York Healthcare System|journal=Stroke|volume=51|issue=7|year=2020|pages=2002–2011|issn=0039-2499|doi=10.1161/STROKEAHA.120.030335}}</ref><br />
 *The most common type of [[stroke]] in patients with [[COVID-19]] is [[ischemic]].<ref name="QureshiAbd-Allah2020" />
-***
@@ Line 29: / Line 22: @@
 Stroke should be differentiated from other causes of muscle weakness and paralysis. The differentials include the following:<ref name="pmid29433111">{{cite journal |vauthors=Kira R |title=[Acute Flaccid Myelitis] |language=Japanese |journal=Brain Nerve |volume=70 |issue=2 |pages=99–112 |date=February 2018 |pmid=29433111 |doi=10.11477/mf.1416200962 |url=}}</ref><ref name="pmid29433111">{{cite journal |vauthors=Kira R |title=[Acute Flaccid Myelitis] |language=Japanese |journal=Brain Nerve |volume=70 |issue=2 |pages=99–112 |date=February 2018 |pmid=29433111 |doi=10.11477/mf.1416200962 |url=}}</ref><ref name="pmid29181601">{{cite journal |vauthors=Hopkins SE |title=Acute Flaccid Myelitis: Etiologic Challenges, Diagnostic and Management Considerations |journal=Curr Treat Options Neurol |volume=19 |issue=12 |pages=48 |date=November 2017 |pmid=29181601 |doi=10.1007/s11940-017-0480-3 |url=}}</ref><ref name="pmid27422805">{{cite journal |vauthors=Messacar K, Schreiner TL, Van Haren K, Yang M, Glaser CA, Tyler KL, Dominguez SR |title=Acute flaccid myelitis: A clinical review of US cases 2012-2015 |journal=Ann. Neurol. |volume=80 |issue=3 |pages=326–38 |date=September 2016 |pmid=27422805 |pmc=5098271 |doi=10.1002/ana.24730 |url=}}</ref><ref name="pmid29028962">{{cite journal |vauthors=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 |title=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 |journal=Clin. Infect. Dis. |volume=66 |issue=5 |pages=653–664 |date=February 2018 |pmid=29028962 |pmc=5850449 |doi=10.1093/cid/cix860 |url=}}</ref><ref name="pmid29482893">{{cite journal |vauthors=Messacar K, Asturias EJ, Hixon AM, Van Leer-Buter C, Niesters HGM, Tyler KL, Abzug MJ, Dominguez SR |title=Enterovirus D68 and acute flaccid myelitis-evaluating the evidence for causality |journal=Lancet Infect Dis |volume=18 |issue=8 |pages=e239–e247 |date=August 2018 |pmid=29482893 |doi=10.1016/S1473-3099(18)30094-X |url=}}</ref><ref name="pmid30200066">{{cite journal |vauthors=Chen IJ, Hu SC, Hung KL, Lo CW |title=Acute flaccid myelitis associated with enterovirus D68 infection: A case report |journal=Medicine (Baltimore) |volume=97 |issue=36 |pages=e11831 |date=September 2018 |pmid=30200066 |pmc=6133480 |doi=10.1097/MD.0000000000011831 |url=}}</ref><ref name="urlBotulism | Botulism | CDC">{{cite web |url=https://www.cdc.gov/botulism/index.html |title=Botulism &#124; Botulism &#124; CDC |format= |work= |accessdate=}}</ref><ref name="pmid3290234">{{cite journal |vauthors=McCroskey LM, Hatheway CL |title=Laboratory findings in four cases of adult botulism suggest colonization of the intestinal tract |journal=J. Clin. Microbiol. |volume=26 |issue=5 |pages=1052–4 |date=May 1988 |pmid=3290234 |pmc=266519 |doi= |url=}}</ref><ref name="pmid16614251">{{cite journal |vauthors=Lindström M, Korkeala H |title=Laboratory diagnostics of botulism |journal=Clin. Microbiol. Rev. |volume=19 |issue=2 |pages=298–314 |date=April 2006 |pmid=16614251 |pmc=1471988 |doi=10.1128/CMR.19.2.298-314.2006 |url=}}</ref><ref name="pmid17224901">{{cite journal |vauthors=Brook I |title=Botulism: the challenge of diagnosis and treatment |journal=Rev Neurol Dis |volume=3 |issue=4 |pages=182–9 |date=2006 |pmid=17224901 |doi= |url=}}</ref><ref name="pmid23642721">{{cite journal |vauthors=Dimachkie MM, Barohn RJ |title=Guillain-Barré syndrome and variants |journal=Neurol Clin |volume=31 |issue=2 |pages=491–510 |date=May 2013 |pmid=23642721 |pmc=3939842 |doi=10.1016/j.ncl.2013.01.005 |url=}}</ref><ref name="pmid23418763">{{cite journal |vauthors=Walling AD, Dickson G |title=Guillain-Barré syndrome |journal=Am Fam Physician |volume=87 |issue=3 |pages=191–7 |date=February 2013 |pmid=23418763 |doi= |url=}}</ref><ref name="pmid21969911">{{cite journal |vauthors=Gilhus NE |title=Lambert-eaton myasthenic syndrome; pathogenesis, diagnosis, and therapy |journal=Autoimmune Dis |volume=2011 |issue= |pages=973808 |date=2011 |pmid=21969911 |pmc=3182560 |doi=10.4061/2011/973808 |url=}}</ref><ref name="pmid14977560">{{cite journal |vauthors=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA |title=Transverse Myelitis: pathogenesis, diagnosis and treatment |journal=Front. Biosci. |volume=9 |issue= |pages=1483–99 |date=May 2004 |pmid=14977560 |doi= |url=}}</ref><ref name="pmid24305450">{{cite journal |vauthors=Amato AA, Greenberg SA |title=Inflammatory myopathies |journal=Continuum (Minneap Minn) |volume=19 |issue=6 Muscle Disease |pages=1615–33 |date=December 2013 |pmid=24305450 |doi=10.1212/01.CON.0000440662.26427.bd |url=}}</ref><ref name="pmid24365430">{{cite journal |vauthors=Berger JR, Dean D |title=Neurosyphilis |journal=Handb Clin Neurol |volume=121 |issue= |pages=1461–72 |date=2014 |pmid=24365430 |doi=10.1016/B978-0-7020-4088-7.00098-5 |url=}}</ref>
-*Stroke was first recognized by Hippocrates, in the fourth century BC, almost 2,400 years ago, and it was reffered to as [[Apoplexy]], a Greek medical literature term, which means 'struk down by violence'. Later, renaissance anatomists, in mid-16th century A.D., explained the pathophysiology of stroke, differentiating the causes as bleeding or blockage of A cerebral artery.<ref name="Theofanidis2015">{{cite journal|last1=Theofanidis|first1=Dimitrios|title=From Apoplexy to Brain Attack, a Historical Perspective on Stroke to Date|journal=Journal of Nursing & Care|volume=04|issue=01|year=2015|issn=21671168|doi=10.4172/2167-1168.1000e121}}</ref>
-*Mao et al., in his study, first reported neurological symptoms in [[COVID-19]] patients hospitalized in Wuhan, China from January 16, 2020, to February 19, 2020. Neurological symptoms were reported in 78 patients out of 214 Covid-19 positive hospitalized patients with [[COVID-19]] in Wuhan, China. The stroke patients reported specifically were 14<ref name="MaoJin2020">{{cite journal|last1=Mao|first1=Ling|last2=Jin|first2=Huijuan|last3=Wang|first3=Mengdie|last4=Hu|first4=Yu|last5=Chen|first5=Shengcai|last6=He|first6=Quanwei|last7=Chang|first7=Jiang|last8=Hong|first8=Candong|last9=Zhou|first9=Yifan|last10=Wang|first10=David|last11=Miao|first11=Xiaoping|last12=Li|first12=Yanan|last13=Hu|first13=Bo|title=Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China|journal=JAMA Neurology|volume=77|issue=6|year=2020|pages=683|issn=2168-6149|doi=10.1001/jamaneurol.2020.1127}}</ref>. In this study, patients with cardiovascular risk factors who presented with severe systemic symptoms were at higher risk of stroke.
-*Yaghi et al. retrospectively examined [[stroke]] patients admitted across different locations of NYU Langone hospital in New York. In this study, the incidence of 0.9% was observed in laboratory confirmed COVID-19 positive patients included in this study. [[Stroke]] diagnosis was proved by imaging, and [[cryptogenic]] [[stroke]] was seen in most of these patients. The mortality was much higher in stroke patients who were [[COVID-19]] positive.<ref name="YaghiIshida2020">{{cite journal|last1=Yaghi|first1=Shadi|last2=Ishida|first2=Koto|last3=Torres|first3=Jose|last4=Mac Grory|first4=Brian|last5=Raz|first5=Eytan|last6=Humbert|first6=Kelley|last7=Henninger|first7=Nils|last8=Trivedi|first8=Tushar|last9=Lillemoe|first9=Kaitlyn|last10=Alam|first10=Shazia|last11=Sanger|first11=Matthew|last12=Kim|first12=Sun|last13=Scher|first13=Erica|last14=Dehkharghani|first14=Seena|last15=Wachs|first15=Michael|last16=Tanweer|first16=Omar|last17=Volpicelli|first17=Frank|last18=Bosworth|first18=Brian|last19=Lord|first19=Aaron|last20=Frontera|first20=Jennifer|title=SARS-CoV-2 and Stroke in a New York Healthcare System|journal=Stroke|volume=51|issue=7|year=2020|pages=2002–2011|issn=0039-2499|doi=10.1161/STROKEAHA.120.030335}}</ref>

COVID-19-associated stroke: Difference between revisions

Revision as of 14:18, 14 July 2020

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating COVID-19-associated stroke from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Ultrasound

X-ray

CT scan

MRI

Electrocardiogram

Treatment

Medical therapy

Alteplase

Tenecteplase

Antiplatelet therapy

Surgery

Mechanical thrombectomy with a stent retriever

Aspiration thrombectomy

Intra arterial fibrinolysis

Other aspects of management

Primary Prevention

Secondary Prevention

References

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