Stroke (main)
(Redirected from Cerebrovascular event)
Background
- Vascular injury that reduces cerebral blood flow to specific region of brain causing neuro impairment
- Accurate determination of last known time when patient was at baseline is essential
- In-hospital mortality of 5-10% for ischemic stroke and 40-60% for hemorrhagic stroke
- Only 10% of stroke survivors will recover completely
Ischemic stroke causes (87%)
- Thrombotic (80% of ischemic CVA)
- Atherosclerosis
- Vasculitis
- Vertebral and carotid artery dissection
- Often preceded by yoga, spinal manipulation, coughing, vomiting
- Polycythemia
- Hypercoagulable state (oral contraceptives, antiphospholipid antibodies, protein S and C deficiencies, sickle cell anemia)
- Infection
- Toxicologic exposure (cocaine, amphetamines, etc.)
- Embolic (20% of ischemic CVA)
- Valvular vegetations
- Mural thrombi
- Arterial-arterial emboli from proximal source (ex. amaurosis fugax -> emboli from a proximal carotid artery plaque embolizes to the ophthalmic artery, causing transient monocular blindness)
- Fat emboli
- Septic emboli
- Hypoperfusion
- Cardiac failure resulting in systemic hypotension
- Cryptogenic
- Cryptogenic Stroke (CS) is defined as an Ischemic stroke of obscure or unknown origin. Its causes are unknown. It is transitory or reversible.[1]
Hemorrhagic stroke causes (13%)
- Intracerebral
- Hypertension
- Cerebral amyloid angiopathy (usually found in elderly, tends to be lobar in nature)[2]
- Anticoagulation
- Vascular malformations (e.g. AVM, moyamoya
- Cocaine use
- Subarachnoid hemorrhage
- Berry aneurysm rupture
- Arteriovenous malformation
Stroke Types
Clinical Features
Anterior Circulation
Internal Carotid Artery
- Tonic gaze deviation towards lesion
- Global aphasia, dysgraphia, dyslexia, dyscalculia, disorientation (dominant lesion)
- Spatial or visual neglect (non-dominant lesion)
Anterior Cerebral Artery (ACA)
Signs and Symptoms:
- Contralateral sensory and motor symptoms in the lower extremity (sparing hands/face)
- Urinary and bowel incontinence
- Left sided lesion: akinetic mutism, transcortical motor aphasia
- Right sided lesion: Confusion, motor hemineglect
- Presence of primitive grasp and suck reflexes
- May manifest gait apraxia
Middle Cerebral Artery (MCA)
Signs and Symptoms:
- Hemiparesis, facial plegia, sensory loss contralateral to affected cortex
- Motor deficits found more commonly in face and upper extremity than lower extremity
- Dominant hemisphere involved: aphasia
- Wernicke's aphasia (receptive aphasia) -> patient unable to process sensory input and does not understand verbal communication
- Broca's aphasia (expressive aphasia) -> patient unable to communicate verbally, even though understanding may be intact
- Nondominant hemisphere involved: dysarthria (motor deficit of the mouth and speech muscles; understanding intact) w/o aphasia, inattention and neglect side opposite to infarct
- Contralateral homonymous hemianopsia
- Gaze preference toward side of infarct
- Agnosia (inability to recognize previously known subjects)
Posterior circulation
- Blood supply via the vertebral artery
- Branches include, AICA, Basilar artery, PCA and PICA
Signs and Symptoms:
- Crossed neuro deficits (i.e., ipsilateral CN deficits w/ contralateral motor weakness)
- Multiple, simultaneous complaints are the rule (including loss of consciousness, nausea/vomiting, alexia, visual agnosia)
- 5 Ds: Dizziness (Vertigo), Dysarthria, Dystaxia, Diplopia, Dysphagia
- Isolated events are not attributable to vertebral occlusive disease (e.g. isolated lightheadedness, vertigo, transient ALOC, drop attacks)
- Approximately 25% associated with aortic dissection
Basilar artery
Signs and Symptoms:
- Quadriplegia, coma, locked-in syndrome
- "Crossed signs" in which a patient has unilateral cranial nerve deficits but contralateral hemiparesis and hemisensory loss suggest brainstem infarction
- Sparing of vertical eye movements (CN III exits brainstem just above lesion)
- Thus, may also have miosis b/l
- One and a half syndrome (seen in a variety of brainstem infarctions)
- "Half" - INO (internuclear ophthalmoplegia) in one direction
- "One" - inability for conjugate gaze in other direction
- Convergence and vertical EOM intact
- Medial inferior pontine syndrome (paramedian basilar artery branch)
- Medial midpontine syndrome (paramedian midbasilar artery branch)
- Medial superior pontine syndrome (paramedian upper basilar artery branches)
Superior Cerebellar Artery (SCA)
- ~2% of all cerebral infarctions[3]
- May present with nonspecific symptoms - nausea/vomiting, dizziness, ataxia, nystagmus (more commonly horizontal)[4]
- Lateral superior pontine syndrome
- Ipsilateral ataxia, nausea/vomiting, nystagmus, Horner syndrome, conjugate gaze paresis
- Contralateral loss of pain/temperature in face/extremities/trunk, and loss of proprioception/vibration in LE > UE
Posterior Cerebral Artery (PCA)
Signs and Symptoms:
- Common after CPR, as occipital cortex is a watershed area
- Unilateral headache (most common presenting complaint)
- Visual field defects (contralateral homonymous hemianopsia, unilateral blindness)
- Visual agnosia - can't recognize objects
- Possible macular sparing if MCA unaffected
- Motor function is typically minimally affected
- Lateral midbrain syndrome (penetrating arteries from PCA)
- Medial midbrain syndrome (upper basilar and proximal PCA)
Anterior Inferior Cerebellar Artery (AICA)
- Lateral inferior pontine syndrome
- Ipsilateral facial paralysis, loss of corneal reflex (CN VII)
- Ipsilateral loss of pain/temperature (CN V)
- Nystagmus, nausea/vomiting, vertigo, ipsilateral hearing loss (CN VIII)
- Ipsilateral limb and gait ataxia
- Ipsilateral Horner syndrome
- Contralateral loss of pain/temperature in trunk and extremities (lateral spinothalamic)
Posterior Inferior Cerebellar Artery (PICA)
Signs and Symptoms:
- Lateral medullary/Wallenberg syndrome
- Ipsilateral cerebellar signs, ipsilateral loss of pain/temperature of face, ipsilateral Horner syndrome, ipsilateral dysphagia and hoarseness, dysarthria, vertigo/nystagmus
- Contralateral loss of pain/temp over body
- Also caused by vertebral artery occlusion (most cases)
Internal Capsule and Lacunar Infarcts
- May present with either lacunar c/l pure motor or c/l pure sensory (of face and body)[5]
- Pure c/l motor - posterior limb of internal capsule infarct
- Pure c/l sensory - thalamic infarct (Dejerine and Roussy syndrome)
- C/l motor plus sensory if large enough
- Clinically to cortical large ACA + MCA stroke - the following signs suggest cortical rather than internal capsule[6]:
- Gaze preference
- Visual field defects
- Aphasia (dominant lesion, MCA)
- Spatial neglect (non-dominant lesion)
- Others
- Ipsilateral ataxic hemiparesis, with legs worse than arms - posterior limb of internal capsule infarct
- Dysarthria/Clumsy Hand Syndrome - basilar pons or anterior limb of internal capsule infarct
Anterior Spinal Artery (ASA)
Superior ASA
- Medial medullary syndrome - displays alternating pattern of sidedness of symptoms below
- Contralateral arm/leg weakness and proprioception/vibration
- Tongue deviation towards lesion
Inferior ASA
- ASA syndrome
- Watershed area of hypoperfusion in T4-T8
- Bilateral pain/temp loss in trunk and extremities (spinothalamic)
- Bilateral weakness in trunk and extremities (corticospinal)
- Preservation of dorsal columns
Differential Diagnosis
Stroke-like Symptoms
- Stroke
- Seizures/postictal paralysis (Todd paralysis)
- Syncope
- Subdural hemorrhage
- Epidural hemorrhage
- Hypoglycemia
- Hyponatremia
- Meningitis/encephalitis
- Hyperosmotic Coma
- Labyrinthitis
- Drug toxicity
- Bell's Palsy
- Complicated migraine
- Meniere Disease
- Demyelinating disease (MS)
- Conversion disorder
- Transient global amnesia
- Giant cell arteritis
- Cerebral sinus thrombosis
Weakness
- Neuromuscular weakness
- Upper motor neuron:
- CVA
- Hemorrhagic stroke
- Multiple sclerosis
- Amyotrophic Lateral Sclerosis (ALS) (upper and lower motor neuron)
- Lower motor neuron:
- Spinal and bulbar muscular atrophy (Kennedy's syndrome)
- Spinal cord disease:
- Infection (Epidural abscess)
- Infarction/ischemia
- Trauma (Spinal Cord Syndromes)
- Inflammation (Transverse Myelitis)
- Degenerative (Spinal muscular atrophy)
- Tumor
- Peripheral nerve disease:
- Neuromuscular junction disease:
- Muscle disease:
- Rhabdomyolysis
- Dermatomyositis
- Polymyositis
- Alcoholic myopathy
- Upper motor neuron:
- Non-neuromuscular weakness
- Can't miss diagnoses:
- ACS
- Arrhythmia/Syncope
- Severe infection/Sepsis
- Hypoglycemia
- Periodic paralysis (electrolyte disturbance, K, Mg, Ca)
- Respiratory failure
- Emergent Diagnoses:
- Symptomatic Anemia
- Severe dehydration
- Hypothyroidism
- Polypharmacy
- Malignancy
- Aortic disease - occlusion, stenosis, dissection
- Other causes of weakness and paralysis
- Acute intermittent porphyria (ascending weakness)
- Can't miss diagnoses:
Evaluation
Always obtain blood glucose, which is commonly overlooked (more embarrassing if you give tPA) Find out last known normal of affected deficit and write it down in chart
Stroke Work-Up
- Labs
- POC glucose
- CBC
- Chemistry
- Coags
- Troponin
- T&S
- ECG
- In large ICH or stroke, may see deep TWI and prolong QT, occ ST changes
- Head CT (non-contrast)
- Also consider:
MR Imaging (for Rule-Out CVA or TIA)
- MRI Brain with DWI, ADC (without contrast) AND
- Cervical vascular imaging (ACEP Level B in patients with high short-term risk for stroke):[10]
- MRA brain (without contrast) AND
- MRA neck (without contrast)
- May instead use Carotid CTA or US (Carotid US slightly less sensitive than MRA)[11] (ACEP Level C)
Large Vessel Occlusion - Thrombectomy
- "Cortical strokes" of ICA, MCA, and some ACA occlusions are most likely to benefit from thrombectomy
- CT perfusion study is the key factor in determining brain tissue salvageability from symptom onset to thrombectomy of 6-24 hours[12]
- If CT perfusion unavailable, use ASPECT score[13]
VAN Score
- NIHSS score ≥ 6 is nearly 100% sensitive for emergent large vessel occlusion, which may be amenable to thrombectomy[14]
- VAN score is just as sensitive, but also may be more specific (~90%)
- Weakness must be present, plus one or all of the VAN to be VAN positive
- Weakness qualifying findings -- if no weakness, the pt is VAN negative
- Mild (minor drift)
- Moderate (severe drift—touches or nearly touches ground)
- Severe (flaccid or no antigravity)
- Visual disturbance qualifying findings
- Field cut (which side) (4 quadrants)
- Double vision (ask patient to look to right then left; evaluate for uneven eyes)
- Blind new onset
- Aphasia qualifying findings
- Expressive (inability to speak or paraphasic errors); do not count slurring of words (repeat and name 2 objects)
- Receptive (not understanding or following commands) (close eyes, make fist)
- Mixed
- Neglect qualifying findings
- Forced gaze or inability to track to one side
- Unable to feel both sides at the same time, or unable to identify own arm
- Ignoring one side
- Weakness qualifying findings -- if no weakness, the pt is VAN negative
- If VAN positive, CT and CTA of the head should be ordered for consideration of thrombectomy plus/minus tPA
- Weakness must be present, plus one or all of the VAN to be VAN positive
Management
- Depends on type
- Ischemic vs Hemorrhagic
- Acute vs subacute vs old
- Due to risk for hemorrhagic transformation, there is no role in acute completed stroke for:
- Dual antiplatelet therapy (as opposed in select cases of TIA)
- Anticoagulation, with or without atrial fibrillation
BP Goals in Acute Stroke[15]
Stoke Type | Target BP (mm Hg) |
Notes |
Acute ischemic stroke | ||
IV tPA eligble | <185/110 | |
During/after tPA | <180/105 | Monitor BP every 15 min for 2 hr, then every 30 minfor 6 hr, then hourly until 24 hr. |
No tPA | <220/120 | |
Mechanical thrombectomy | ≤180/105 | Maintain during and for 24 h after procedure |
Aneurysmal subarachnoid hemorrhage | ||
Unsecured | SBP <140-160 | Controversy regarding exact number; others recommend <100 MAP |
Secured | Unclear | May depend on ppremorbid BP and presence of vasospasm |
Intraparenchymal hemorrhage | ||
Initial SPB 150-220 | SBP <140 | |
Initial SPB >220 | SBP 140-160 |
Common Medications for BP Control in Acute Stroke
Agent | Typica Dose/Range | Onset of Action | Cautions/Contraindications |
Labetalol | 10-20 mg IV push; may repeat x 1 | 5 min | Avoid in COPD, asthma, heart failure, bradycardia, heart block |
Nicardipine | IV infusion at 5 mg/h; titrate up by 2.5 mh/h q5-15 min; max 15 mg/h | 1-5 min | Avoid in severe aortic stenosis |
Clevidipine | 1-2 mg/h IV; titrate by doubling dose q2-5 min; max 21 mg/h | 2-4 min; short half-life | Avoid in egg/soy allergy |
Hydralazine | 10-20 mg IV; repeat q4-6 h | 10-20 min |
Disposition
- Admit for acute or subacute stroke
See Also
- Transient Ischemic Attack (TIA)
- Thrombolysis in Acute Ischemic Stroke (tPA)
- CVA (Post-tPA Hemorrhage)
- Intracerebral Hemorrhage
- Subarachnoid Hemorrhage (SAH)
- Cervical Artery Dissection
- NIH Stroke Scale
- Cerebellar Stroke
- Focal neurologic signs
External Links
- MDCalc - NIH Stroke Scale/Score
- Emergency medicine cases - ED stroke management in the age of endovascular therapy
References
- ↑ [Finsterer J. Management of cryptogenic stroke. Acta Neurol Belg. 2010 Jun;110(2):135-47. PMID: 20873443].
- ↑ Itoh Y, Yamada M, Hayakawa M, Otomo E, Miyatake T. Cerebral amyloid angiopathy: a significant cause of cerebellar as well as lobar cerebral hemorrhage in the elderly. J Neurol Sci. 1993 Jun;116(2):135-41.
- ↑ Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 18 (5): 849-55.
- ↑ Lee H, Kim HA. Nystagmus in SCA territory cerebellar infarction: pattern and a possible mechanism. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):446-51.
- ↑ Rezaee A and Jones J et al. Lacunar stroke syndrome. Radiopaedia. http://radiopaedia.org/articles/lacunar-stroke-syndrome.
- ↑ Internal Capsule Stroke. Stanford Medicine Guide. http://stanfordmedicine25.stanford.edu/the25/ics.html
- ↑ Mullins ME, Schaefer PW, Sorensen AG, Halpern EF, Ay H, He J, Koroshetz WJ, Gonzalez RG. CT and conventional and diffusion-weighted MR imaging in acute stroke: study in 691 patients at presentation to the emergency department. Radiology. 2002 Aug;224(2):353-60.
- ↑ Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006; 354(4):387–396.
- ↑ Douglas VC, Johnston CM, Elkins J, et al. Head computed tomography findings predict short-term stroke risk after transient ischemic attack. Stroke. 2003;34:2894-2899.
- ↑ ACEP Clinical Policy: Suspected Transient Ischemic Attack full text
- ↑ Nederkoorn PJ, Mali WP, Eikelboom BC, et al. Preoperative diagnosis of carotid artery stenosis. Accuracy of noninvasive testing. Stroke. 2002;33:2003-2008.
- ↑ Albers GW, Marks MP, Kemp S, et al. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging. N Engl J Med. 2018;378(8):708-718.
- ↑ Barber PA, Demchuk AM, Zhang J, Buchan AM. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy. ASPECTS Study Group. Alberta Stroke Programme Early CT Score. Lancet. 2000;355(9216):1670-4.
- ↑ Teleb MS, Ver Hage A, Carter J, et al Stroke vision, aphasia, neglect (VAN) assessment—a novel emergent large vessel occlusion screening tool: pilot study and comparison with current clinical severity indices Journal of NeuroInterventional Surgery 2017;9:122-126.
- ↑ Cocchi MN, Edlow JA. Managing Hypertention in Patients with Acute Stroke. 2020. Annals of EM 75(6):767771