Stroke or cerebrovascular accident (CVA): Focal (or at times global) neurological impairment of sudden onset, lasting more than 24 hours (or leading to death), and of presumed vascular origin. 80% ischemic and 20% hemorrhagic.
Transient Ischemic Attack: Focal (or at times global) neurological impairment of sudden onset, lasting less than 24 hours, and of presumed vascular origin OR a brief episode of neurological dysfunction caused by a focal disturbance of brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of infarction Most last 20-30 min.
Watershed areas: Areas of brain at periphery of 2 vascular territories (e.g., between ACA and MCA); these areas are the most vulnerable to hypoperfusion esp. during times of ischemia.
DDx: Hemorrhagic stroke, Subdural hematoma, Neoplastic lesions, Focal infxn, Multiple sclerosis
Stroke risk factors: Previous stroke or TIA. 10.5% with TIA will have a stroke in 90 days, 5% w/in 2 days. ABCD2 – Assessing risk of patients with recent TIA (higher points equals greater risk) A – Age (>60 = 1, <60 =0) B – Blood Pressure (>140/90 = 1, lower = 0) C – Clinical signs (unilateral weakness = 2, speech disturbance = 1, anything else = 0) D – Duration (<10 min = 0, 10-59 min = 1, >60 min = 2) D – Diabetes (yes = 1, no = 0) Hypertension Heart disease: Atrial fib, Mitral stenosis, Recent myocardial infarction, Infective endocarditis Diabetes mellitus Smoking Atherosclerosis Hypercholesterolemia Carotid stenosis Older age Male sex Family history of stroke Heavy alcohol use Obesity Cocaine and amphetamine use
Common mechanisms of ischemic stroke: Atherothrombotic, Embolic, Hypoperfusion, Dissection, Hypercoagulability, Vasculitis, Vasospasm, Hemodynamic (watershed infarct)
Localization *** Refer to High-Yield Neuroanatomy for diagrams***
Tips A pure motor stroke involving the face, arm, and leg on one side of the body that is fairly equal in severity in the affected body parts is usually caused by a lesion in the contralateral posterior limb of the internal capsule, corona radiate, or base of pons.
A pure sensory stroke is caused by a lesion in the contralateral thalamus.
The presence of a cranial nerve deficit helps you localize the lesion to the midbrain, pons, or medulla and indicates with side is involved
Vertical gaze problems indicate a lesion in the midbrain (e.g. the medial longitudinal fasciculus) while Horizontal gaze problems indicate a lesion in the pons (such as intranuclear ophthalmoplegia, INO)
Name : CN : Function
Olfactory : I : Smell
Optic:II:Sight (visual afferent)
Oculomotor:III:Eye movement, papillary constriction, lens accommodations, eyelid opening
Trigeminal:V :Chewing, facial sensation, sensation to meninges
Facial:VII:Facial Movement, taste for ant. 2/3 of tongue, eyelid closing
Vestibulocochlear:VIII:Hearing and balance
Glossopharyngeal:IX:Taste for post. 1/3 of tongue, oropharyngeal sensations, swallowing, parotid gland, carotid body and sinus chemo and baroreceptors
Vagus:X:Taste from epiglottic region, swallowing, talking, thoracoabdominal viscera, aortic arch chemo and baroreceptors
Accessory:XI:Head turning and shoulder shrugging
MCA Supplies most of cerebral hemisphere Gives off the lenticulostriate artery branches, which supply blood to the basal ganglia and internal capsule Ischemia causes: Contralateral weakness/hemiplegia and anesthesia, predominantly face and arm Paresis/apraxia of contralateral conjugate gaze (gaze preference toward lesion) Contralateral homonymous hemianopsia Motor apraxia Aphasia (dominant hemisphere) Contralateral hemineglect, impaired prosody (nondominant hemisphere) ACA Supplies the parasagittal cerebral cortex Ischemia causes: Contralateral weakness/hemiplegia and anesthesia, predominantly leg Abulia (impaired ability to perform voluntary actions, show initiative, make decisions) PCA Gives off branches to the midbrain and thalamus before supplying the occipital lobes and inferior portions of the temporal lobes Ischemia causes: Contralateral homonymous hemianopsia w/ macular sparing Visual hallucinations Prosopagnosia (inability to recognize faces) Visual association cortical deficits Visual and color agnosia Alexia w/o agraphia Contralateral sensory loss (if thalamus involved) Anterior Spinal Artery Ischemia causes: Bilateral spastic paresis below lesion (lateral corticospinal tract) Bilateral loss of pain and temperature sensation below lesion (lateral spinothalamic tract) Horner’s syndrome below lesion (hypothalamospinal tract – T2 and above) Bilateral flaccid paralysis at the level of lesion (anterior horns) Bladder/bowel incontinence (corticospinal tracts to S2-S4 parasympathetics)
Brainstem ischemia Paramedian midbrain lesion (Benedikt syndrome) – PCA CN III nerve roots Ipsilateral oculomotor paralysis Ipsilateral eye abduction and depression Ipsilateral internal ophthalmoplegia (pupil fixation and dilation) Ipsilateral ptosis Contralateral cerebellar ataxia with intention tremor (dentatothalamic fibers) Contralateral loss of tactile sensation from trunk and extremities (medial lemniscus) Medial midbrain lesion (Weber syndrome) – paramedian branches of PCA CNIII nerve roots (see above) Contralateral spastic hemiparesis (corticospinal tracts) Contralateral weakness of lower face (CN VII, “central seven” lesion) Contralateral weakness of tongue and palate (CN X and XII) Uvula points away from lesion, tongue protrudes toward lesion Medial inferior pontine syndrome – paramedian branches of basilar artery Contralateral spastic hemiparesis (corticospinal tract) Contralateral loss of tactile sensation from trunk and extremities (medial lemniscus) Ipsilateral lateral rectus paralysis (CN VI) Lateral inferior pontine syndrome – AICA Facial nucleus and CN VII Ipsilateral facial nerve paralysis Ipsilateral loss of taste (ageusia) from anterior 2/3 of tongue Ipsilateral loss of lacrimation and reduced salivation Ipsilateral loss of corneal and stapedial reflexes (efferent limb) Unilateral central deafness (cochlear nucleus and CN VIII) Nystagmus, N/V, and vertigo (vestibular nuclei and CN VIII) Ipsilateral facial hemianesthesia (spinal trigeminal nucleus and tract) Ipsilateral limb and gait ataxia (middle and inferior cerebellar peduncles) Contralat loss of pain and temperature sensation from trunk and extremities (spinothalamic tracts) Ipsilateral Horner’s syndrome (descending sympathetic tract) Left lateral medulla(Wallenberg Syndrome) – PICA Nystagmus, N/V, and vertigo (vestibular nuclei) Ipsilateral dystaxia, dysmetria, dysdiadochokinesia (inferior cerebellar peduncle) Ipsilateral laryngeal, pharyngeal, and palatal hemiparesis (nucleus ambiguous) Contralat loss of pain and temperature sensation from trunk and extremities (spinothalamic tracts) Ipsilateral facial hemianesthesia (spinal trigeminal nucleus and tract) Ipsilateral Horner’s syndrome (descending sympathetic tract)
Locked in syndrome Cranial nerve palsies Apnea “Crossed” weakness and sensory loss affecting the ipsilateral face and contralateral body
Acute management: Diagnosis: H&P (document time of symptom onset) NIH stroke scale – a way of standardizing signs of acute stroke (www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf) Emergent head CT without contrast (to differentiate ischemic from hemorrhagic stroke) CBC, CMP, INR, PTT ECG (always do! – concern about acute coronary syndrome) Echocardiogram (if embolic stroke is suspected) Oximetry MRI/MRA (with diffusion-weighted imaging) ASAP: to identify early ischemic changes (DWI is sensitive for acute stroke) Carotid ultrasound
Therapy: Aspirin 325 mg OR IV tPA, use only if: Less than 3 hrs since symptom onset No hemorrhage on CT No prior stroke or head trauma last 3 months No major surgery in last 14 days No history of intracranial hemorrhage Symptoms not minor or rapidly improving (don’t give in TIA) Symptoms do not suggest SAH No recent GI or GU hemorrhage w/in 21 days No arterial puncture at non-compressible site w/in 14 days No seizure at stroke onset No anticoagulants on board INR/PTT normal, platelets >100,000 Glucose >50 and <400 BP <185 systolic and <110 diastolic Benefit: Use of tPA w/in 3 hrs of stroke onset produces a 30% better chance of minimal or no deficit at 3 months Risk: There is a 6% chance of symptomatic intracerebral hemorrhage with the use of tPA
Heparin/warfarin indicated in ischemic stroke due to carotid/vertebral dissection or A-fib Treat hyperglycemia: initially with insulin Treat BP >220 systolic or >130 MAP for first 4–5 days because autoregulation impairment is likely, you don’t want to tx a lower BP because it may lead to hypoperfusion; thereafter, tx to achieve normal recommended control DVT prophylaxis (have to wait 24 hrs) – can give prophylactic doses of lovenox, can use SCDs Aspiration precautions – need to have formal swallowing evaluation by PT or ST Avoid fluid imbalance
CT vs. MRI in detecting strokes CT Standard MRI Diffusion/Perfusion MRI Ischemic 24–48 hours 12 hours Within 2 hours Hemorrhagic Immediately Immediately Immediately
If patient’s deficits worsen: Consider: Extension of infarction; Increased peri-infarction edema (most likely cause, peaks at 3 days); Hemorrhagic transformation of infarction; Superimposed infection, hypoxemia, or metabolic derangement Need to do repeat CT to r/o possible causes
Secondary prevention Antiplatelet agents Aspirin Anticoagulant effect from inhibition of COX-mediated thromboxane A2 synthesis Side effects: dyspepsia and GI upset, occult GI blood loss, hypersensitivity Clopidogral (Plavix) Inhibits the ADP pathway involved in the binding of platelets to fibrinogen Side effects: bleeding, purpura, GI pain, thrombocytopenia, arthralgia, HA, dizziness Aspirin/dipyridamole (Aggrenox) Best prevention against TIA and stroke, but very expensive Dipyridamole inhibits adenosine deaminase and phosphodiesterase to cause an accumulation of adenine nucleotides. It is also a possible vasodilator Side effects: HA is the most common side effect of dipyridamole; aspirin side effects above
Anticoagulation for: Atrial fibrillation – wait 3–4 days before starting tx Mitral stenosis – wait 3–4 days before starting tx Recent MI/wall motion abnormality, mural thrombus Antibiotics for infective endocarditis BP control for everyone (after 4–5 days - in an ischemic stroke, low BP can be detrimental, thus allow “permissive hypertension” to adequately supply the penumbra. The consensus is blood pressure meds should be withheld unless the systolic blood pressure is greater than 220 mm Hg or the diastolic blood pressure is greater than 120 mm Hg) Normoglycemia for everyone Statins for almost everyone (statins may have anti-inflammatory properties) Smoking cessation Folate for everyone? Carotid endarterectomy Indications: < 50% stenosis – medical management 50-69% stenosis – consider endarterectomy, especially if symptomatic 70-99% stenosis – endarterectomy 100% occlusion of carotid – medical management 3% complication risk Carotid stenting if conventional endarterctomy is too risky
Hemorrhagic stroke Areas of the brain susceptible to hypertensive hemorrhage 35-50% - internal capsule & putamen (especially lateral striate arteries) 30% - subcortical white matter 15% - cerebellum 10% - thalamus 5% - pons
Subarachnoid hemorrhage (SAH) SAH is a neurologic emergency often caused by rupture of an intracranial aneurysm, but can also be caused by trauma, bleeding from AVMs, or drug use. Aneurysms are commonly found at the junction between the ACA and anterior communicating artery, at the bifurcations of the MCA, in the PCA, in the apex of the basilar artery, and at the origin of the PICA Symptoms “Worst HA of my life” – common CC; HA of sudden onset, reaches max intensity in seconds (vs. migraine which reaches peak intensity in >30min.) As ICP increases, pt may have N/V, neck stiffness, loss of consciousness, photophobia, possibly seizures, or focal neurological deficits There may be preceding, short-lived “sentinel” HA Main causes Trauma, especially in patients with dementia or advanced age 80% of spontaneous SAH come from ruptured aneurysm 8% come from ruptured arterio-venous malformation Management if SAH suspected Immediate Head CT w/o contrast: Look for blood in subarachnoid space If CT is negative and suspicion is high: Immediate LP to look for RBCs and xanthochromia (yellowing CSF due to breakdown of RBC’s) Angiography is the “gold standard”
Treatment of SAH Definitive tx is coiling or clipping of the aneurysm
Guidelines for medical and surgical treatment of aneurismal SAH ICU admission Cardiopulmonary monitoring Bed rest Prevent rebleeding by maintain systolic BP <150 until definitive tx IV Calcium channel blockers (e.g. nimodipine to decreases vasospasm) Raising head of bed and hyperventilation may be used to decrease ICP Glucose drip Maintain intravascular volume (give IV fluids) and BP, hemodilution; Anticonvulsants (phenytoin) for symptomatic or prophylactic treatment Antifibrinolytics may be indicated if aneurysm cannot be clipped. This increases the risk of ischemia, but decreases the risk of another bleed Surgical repair within first 3 days after SAH or then wait 2–4 weeks to clip Ventriculostomy or shunt for hydrocephalus Lumbar drain or serial LP’s may also be used to treat hydrochephalus Vasospasm is the leading cause of death in SAH (70%). Signs include new HA, seizures, reduced consciousness, new neurologic findings Monitor with transcranial Doppler (antedates clinical Sx) and treat with nimodipine, hypervolemic hemodilution, and drug-induced HTN Occurs 3–4 days after hemorrhage Nimodipine doesn’t help mortality, but does help long-term recovery (i.e. improved functionality)
Intraparenchymal hemorrhage Causes HTN (most common cause) Hemorrhages caused by HTN are most often found in the basal ganglia, thalamus, pons, and cerebellum Anticoagulants Use of drugs such as cocaine or amphetamines Vascular malformations Diseases affecting the blood vessel walls Amyloid angiopathy is a predisposition to bleeding in the cerebral hemispheres, especially the parietal and occipital lobes Brain tumor Symptoms Focal motor and sensory defects that may progress HA Loss of consciousness (with large hematomas) Seizures (not common, but occur more commonly in intraparenchymal hemorrhages than other causes of stroke) If hemorrhage originates in ventricles, patients may present with HA, vomiting, decreased level of arousal, and neck stiffness Management Immediate non-contrast CT (look for mass effect or edema which increases the risk of herniation) Reversal of anticoagulation d/c anticoagulants Administer vit K Transfuse FFP Cautious control of BP Mechanical ventilation and an osmotic diuretic (e.g., mannitol) may help reduce ICP Surgical drainage or intraventricular drain if expanding and accessible Prevention – control of HTN
Subdural Hematoma: Due to rupture of the bridging veins (usually secondary to head trauma) Common in elderly and alcoholics (due to decreased brain mass) Present w/ headache, contralateral hemiparesis, and mental status abnormalities. May not find signs of trauma on PE. Can be subacute or chronic. May present as pseudodementia in the elderly Dx via head CT: Will see a crescent-shaped, concave, mass that does NOT cross the midline. Mass will be hyperdense if acute, isodense if subacute, and hypodense if chronic) Treatment: Blood may regress spontaneously if chronic. Surgical evacuation is required if pt. is symptomatic.
Epidural Hematoma: Caused by a tear of the middle meningeal artery (usually the result of a lateral skull fracture) History: Blow to head followed by immediate loss of consciousness of followed by a lucid interval (may last minutes to hours) Pt. usually has obvious signs of trauma. Dx: Head CT demonstrates a lens-shaped, convex hyperdensity that does not cross suture lines. Tx: Emergent neurosurgical evacuation. Unlike a subdural hematoma you can’t wait for this to regress on its own because it is an arterial bleed and thus may quickly evolve to brain herniation and subsequent death (a “blown pupil” suggest impending brain stem compression)
Surgery indications (from UpToDate) Surgical removal of hemorrhage with cerebellar decompression should be performed for patients with cerebellar hemorrhages >3 cm in diameter who are deteriorating or who have brainstem compression and/or hydrocephalus due to ventricular obstruction Surgical hematoma evacuation for supratentorial ICH is controversial. Because of the questionable efficacy of surgery, it should only be considered as a life saving procedure to tx refractory increases in ICP; even in these instances, decisions should be addressed on a per patient basis: Surgery should not be considered for patients who are either fully alert/intact or deeply comatose. Patients with intermediate levels of arousal (obtunded-stupor) are more appropriate candidates. Features that support performing surgery include a recent onset of hemorrhage, ongoing clinical deterioration, involvement of the nondominant hemisphere, and location of the hematoma near the cortical surface. For patients with supratentorial ICH, current guidelines suggest consideration of standard craniotomy only for those who have lobar clots within 1 cm of the surface. No other patient group is recommended for surgery.
Vascular abnormalities AVM - Surgical resection indicated Cavernous angiomas - Surgical resection indicated Developmental venous anomalies - Surgical resection is NOT recommended Capillary telangectasias - Surgical resection is NOT recommended