EMCrit.org

Stroke

Ischemic

80-85% of strokes

majority are thrombotic vs. embolic (Mitral Stenosis, MI, A-Fib)

Hallmark of stroke is sudden onset of focal neurological derangement in a vascular area

Differential

Common Major Stroke Syndromes

Anterior Circulation

Frontoparietal Lobes

Anterior Aspect of Temporal Lobes

Optic Nerve and Retina

Deep Gray Matter Structures

Posterior Circulation

Medial Aspect of Temporal Lobes

Visual Occipital Cortex

Thalamus

Brainstem

Upper Spinal Cord

Cerebellum

Auditory and Vestibular Aspects of the Ear

Anterior cerebral artery

Paralysis mainly of opposite leg and mild arm involvement

Sensory deficits paralleling paralysis

Altered mentation, confusion, judgment, and impaired insight

Gait apraxia (clumsiness)

Bowel and bladder incontinence

Middle cerebral artery

Paralysis of opposite side of body; arm and face worse than leg

Sensory deficits paralleling paralysis

Blindness in half of visual field (hemianopsia)

Aphasia (if dominant hemisphere involved, usually left)

Hemineglect (If non-dominant hemisphere, usually right)

Inability to recognize known objects (agnosia)

If Gaze preference, patients look towards the lesion

Posterior cerebral artery

Blindness in one half of visual field (hemianopsia)

Third nerve paralysis

Lack of visual recognition (visual agnosia)

Altered mental status with impaired memory

Cortical blindness

Brainstem/Cerebellum

Crossed Signs-face one side, body the other

Hemiparesis or quadriparesis (or worse yet locked in syndrome)

Sensory loss, hemi or all 4 extremities

Diplopia

Dysconjugate Gaze

Nystagmus

Dysarthria/Dysphagia

Vertigo

Decreased LOC or syncope

Ataxia

Vomitting

Patients presenting with pontine infarction may describe a preceding transient pain radiating from the unilateral eye to the nose, following which they developed numbness or ataxic hemiparesis on the side contralateral to the pain.4 The “beauty parlor syndrome” has been described in elderly patrons receiving shampoo treatments. Mechanical impingement by neck rotation and hyperextension decreases vertebral artery flow and produces hypoperfusion at the atlanto-occipital-distal vertebral artery junction. Patients may present with vertigo and ataxia.5

 

Evaluation

Stroke notification

Check Glucose

Consider Aortic Dissection or if neck pain in the absence of trauma, consider arterial dissection of neck vessels

Obtain a BP in both arms

NIH Stroke Scale (FERNE) , but remember it leaves out some CN, gait, and nystagmus

EKG

Draw Labs-CBC, PT/PTT, Lytes, C-XR, Consider ABG, C-Spine, LFTs

Get a stat CT Minus Head

multimodal MRI including gradient echo is at least as and probably more sensitive for bleeds than CT (J Neuro Neurosurg Psych 2001 Apr;70 suppl 1:I7-11)

Management

BP

SBP>185 or DBP>105, first reconfirm bp in 10 minutes

If SBP>220, DBP 121-140, or MAP >130 give Labetolol 5-10 mg IV over 2 minutes, double and repeat Q10 to max total dose of 300 mg or Nitroprusside .5-1 mcg/kg/min or Enalapril .625-1.25 mg over 5 minutes q6.

If SBP 185-220 or DBP 105-120 and thrombolysis candidate, give labetolol.  If BP less than 185/110 can give lysis

If DBP>140 start nitroprusside, not lysis candidate

Treatment of hypertension if the stroke patient is going to be treated with rt-PA therapy

diastolic blood pressure > 140 mmHg => do not treat with rt-PA => check blood pressure q 5 minutes => nitroprusside infusion if the diastolic blood pressure remains > 140 mmHg to try and decrease the blood pressure by ~ 10% in the first few hours
systolic blood pressure 185 - 220 mmHg or diastolic blood pressure 105 - 140 mmHg => labetalol 5 - 10 mg over 2 minutes IV => double the dose q 10 minutes until the blood pressure < 180 mmHg systolic and < 110 mmHg diastolic (do not decrease the blood pressure by > 10 - 20%) => maintain the blood pressure < 185/110 mmHg with an infusion of labetalol at 1 - 2 mg/min
if > 3 doses of labetalol are required to decrease the blood pressure to < 185/110 mmHg, or if the blood pressure remains > 185/110 mmHg despite optimum labetalol treatment => rt-PA therapy is not recommended
some physicians would recommend nitroprusside therapy if the patient is resistant to labetalol therapy (or if labetalol is contra-indicated)
blood pressure should be checked q 15 minutes for the first 2 hours after starting rt-PA therapy => additional labetalol prn
 

Further Exclusions criteria

elevated PT > 15 seconds or INR > 1.7
platelet count < 100,000/cu.mm
patient has received heparin within 48 hours and the aPTT is abnormally elevated
CT scan shows an ICH, or subarachnoid hemorrhage, or early signs of a cerebral infarct
clinical signs, or radiological chest X-ray signs, suggestive of aortic dissection
inability to adequately control the blood pressure during the initial evaluation period
marked deterioration of the patient's clinical status (suggesting an intracranial bleed) during the initial evaluation period
 

Keep MAP<130

Positioning

Hob flat may increase CPP (Neurology 2005;64:1354)

Cerebral Edema

Elevate head of bed to 30º

Hyperventilation or Mannitol only if acute deterioration

Seizures

Only to prevent recurrent seizures

Anticoagulation

ASA well proven (huge Chinese study)

No harm if you give it in hemorrhagic stroke, but still not advised (Stroke, 2000;31:1240-1249)

No benefit to other anticoagulants unless concerns over pt with current A.Fib (Stroke 33:856, 2002)

TPA

lytics up to 4.5 hours (NEJM 2008;359(13):1317)

Must be read by neuroradiologist (Neurologists, general radiologists, and certainly ER docs are not qualified)

BP must be less than 185/110

If not may administer nitropaste and/or 1-2 doses of Labetolol 10-20 mg IVP 

 The NINDS trial was divided into two parts; in both parts, patients were randomized to receive tPA, 0.9 mg/kg, or placebo within three hours after onset of stroke symptoms. Patients in the treatment arm were given 0.9 mg/kg tPA (maximum dose, 90 mg) in a 10% bolus followed by a constant infusion of the remaining 90% over 60 minutes. The first part enrolled 291 patients and measured whether they had improvement in their NIHSS score of four points or more over baseline or resolution of deficits within 24 hours of onset of stroke. In this portion of the trial, there was no statistical difference between the tPA group and the placebo recipients (P = 0.21). However, in post hoc analysis, the authors point out that the median NIHSS scores were two points lower in the 0- to 90-minute range and four points lower in the 90- to 180-minute range when the tPA group was compared with placebo (P value not provided). The second part enrolled 333 patients and assessed clinical outcomes at three months. Patients who received tPA were at least 30% more likely to have minimal or no disability based on four measures of neurologic disability (NIHSS, modified Rankin, Glasgow outcome scale, and Barthel Index). The primary hypothesis in part two was tested with a global statistic to simultaneously test for effect in all four outcome measures.

Symptomatic intracerebral hemorrhage occurred in 6.4% of tPA recipients but only 0.6% of placebo recipients (P < 0.001). Mortality at three months was 17% in the tPA group and 21% in the placebo group (P = 0.30).

A number-needed-to-treat analysis of the NINDS trial indicates that for every eight acute stroke patients treated, one will benefit. One patient in 17 will suffer an intracranial hemorrhage, and one in 40 will die. These numbers may be helpful in explaining risks and benefits to patients who are eligible for thrombolytic treatment.

Meta-analysis of current thrombolytic for stroke data
Symptomatic ICH 6.2% Absolute Risk Increase
Fatal ICH 2.5% Absolute Risk Increase
(Stroke. 2003 Jun;34(6):1437-42.)

The major risk of t-PA is symptomatic intracerebral hemorrhage, which occurred in 6.4 percent of patients who received t-PA, as compared with 0.6 percent of patients who received placebo.1 These figures represent an absolute difference in the risk of symptomatic intracerebral hemorrhage of 6 percent. Seventy-five percent of the patients with a symptomatic intracerebral hemorrhage were dead at three months. Yet despite the risk of intracerebral hemorrhage, the mortality at three months was insignificantly lower in patients treated with t-PA (17 percent) than in placebo-treated patients (21 percent). Two reasons may underlie the similar mortality of t-PA­treated and placebo-treated patients despite a higher risk of symptomatic intracerebral hemorrhage among patients treated with t-PA. First, most patients who had an intracerebral hemorrhage had large strokes and were likely to do poorly regardless of the presence of intracerebral hemorrhage within the damaged brain. Secondly, t-PA probably makes some "big" strokes much smaller. The patients with small strokes are less likely to die.

Patients treated with t-PA who have very large strokes (very severe neurologic deficits, meaning an NIH stroke scale score greater than 20) and who already have evidence of a large acute ischemic stroke on baseline CT have an increased risk of symptomatic intracerebral hemorrhage. 17 However, patients in these two subgroups who receive t-PA are more likely to return to normal than patients who are treated with placebo. The decision to use t-PA in these patients should be made only after frank discussion of the potential risks and benefits with both the patient and the family.

Figure 1 adapted from Marx J. Classification system for stroke patients. Proceedings of the National Symposium on Rapid Identification and Treatment of Acute Stroke, December 13, 1996. Washington, D.C.: National Institute of Neurological Disorders and Stroke (NINDS), November 1997.



 

Get TEE, eval ekg for A-Fib.  Carotid dopplers.

Only treat HTN if > 220/120, use nitroprusside or labetalol

ASA or plavix

Site for NINDS Group Guidelines for TPA

editorial on why it has not been adopted more widely (Lancet 2006;5:722)

• Infuse 0.9 mg/kg (maximum of 90 mg) over 60 minutes with 10% of the dose given as a bolus dose over 1 minute. • Admit the patient to an intensive care unit or a stroke unit for monitoring. • Perform neurological assessments every 15 minutes during the infusion of rtPA and every 30 minutes for the next 6 hours and then every hour until 24 hours from treatment. • If the patient develops severe headache, acute hypertension, nausea, or vomiting, discontinue the infusion (if agent is still being administered) and obtain a CT scan of brain on an emergent basis. • Measure blood pressure every 15 minutes for the first 2 hours, every 30 minutes for the next 6 hours, and then every hour until 24 hours from treatment. • Increase the frequency of blood pressure measurements if a systolic blood pressure 180 mm Hg or diastolic blood pressure of 105 mm Hg is recorded. Administer antihypertensive medications to maintain blood pressure at or below these levels. • If diastolic blood pressure 105–120 mm Hg or systolic blood pressure 180–230 mm Hg, intravenously administer 10 mg labetalol over 1–2 minutes. May repeat or double the dosage or labetalol every 10 to 20 minutes to a maximum dose of 300 mg. As an alternative, can start with the initial bolus dose of labetalol and then follow with a continuous labetalol infusion given at a rate of 2–8 mg/min. • If diastolic blood pressure 121–140 mm Hg or systolic blood pressure >230 mm Hg, intravenously administer 10 mg labetalol over 1–2 minutes. May repeat or double labetalol every 10 minutes to a maximum dose of 300 mg. As an alternative, can start with the initial bolus dose of labetalol and then follow with a continuous labetalol infusion given at a rate of 2–8 mg/min. If the blood pressure is not controlled, consider starting an infusion of sodium nitroprusside. • If diastolic blood pressure >140 mm Hg, start infusion of sodium nitroprusside at a rate of 0.5 mg/kg/min. • Delay placement of nasogastric tubes, indwelling bladder catheters, or intra-arterial pressure catheters.

AHA Contraindications

Diagnosis of ischemic stroke causing measurable neurological deficit The neurological signs should not be clearing spontaneously The neurological signs should not be minor and isolated Caution should be exercised in treating a patient with major deficits The symptoms of stroke should not be suggestive of subarachnoid hemorrhage Onset of symptoms <3 hours before beginning treatment No head trauma or prior stroke in previous 3 months No myocardial infarction in the previous 3 months No gastrointestinal or urinary tract hemorrhage in previous 21 days No major surgery in the previous 14 days No arterial puncture at a noncompressible site in the previous 7 days No history of previous intracranial hemorrhage Blood pressure not elevated (systolic <185 mm Hg and diastolic <110 mm Hg) No evidence of active bleeding or acute trauma (fracture) on examination Not taking an oral anticoagulant or if anticoagulant being taken, INR 1.7 If receiving heparin in previous 48 hours, aPTT must be in normal range Platelet count 100 000 mm3 Blood glucose concentration 50 mg/dL (2.7 mmol/L) No seizure with postictal residual neurological impairments CT does not show a multilobar infarction (hypodensity >1/3 cerebral hemisphere) The patient or family understand the potential risks and benefits from treatment

Cerebellar Stroke

Neurosurgery consult

Misc.

Elevated CK-MB after stroke are not necessarily indicative of AMI, need elevated Troponin to properly eval. (Stroke 33:286 2002)

Giving ASA even to hemorrhagic stroke did not cause additional mortality or increased bleeds (Stroke 2000; 31:1240-9)

Young Stroke Patients

Strokes in Younger Patients

When evaluating a younger patient in the Emergency Department with a stroke, keep in mind the following:

• Cardiac causes including Right-to-Left shunts from a patent foramen ovale (PFO) or occult atrial septal defect (ASD).
• Cocaine and amphetamine use
• Atrial myxoma
• Cervical artery dissections.   Approximately 20% of strokes in the young are caused by carotid artery and vertebral artery dissections in the neck, compared to 2.5% in older patients.
   

As transesophageal echocardiography (TEE) is considered the most sensitive method to date to detect PFO (1), think to suggest a TEE as part of the evaluation.

"In the absence of other causative conditions, an ASD or PFO may be presumed to be the underlying cause of cerebrovascular thromboembolism. The search for these defects will be more cost-effective in younger stroke patients who, unlike older patients, rarely have the cardiovascular conditions associated with advanced age that commonly cause strokes in the elderly" (2).



References:
(1) Horton SC, Bunch TJ. Patent foramen ovale and stroke  Mayo Clin Proc 2004;79(1): 79-88.
(2)  Jaber WA, et al. Suspect an atrial septal defect if a young patient has a stroke Cleveland Clin J Med  2001; 68: 954-956.
(3) Cabanes L, et al.  Atrial septal aneurysm and patent foramen ovale as risk factors for cryptogenic stroke in patients less than 55 years of age. A study using transesophageal echocardiography. Stroke 1993; 24:1865-1873.
(4)  Jones J, Geninatti M. Cardiology  Emerg Med Clin North Am 1997;15(2):341-63.

Exam

(Jama 2005;293(19):2391)

LR of the absence of facial paresis, arm drift, and abnormal speech is 0.39

TIA

annals review article (Annals of Emergency Medicine  Volume 43, Issue 5 , May 2004, Pages 592-604)

ED protocol for w/u of tia (Ann Emerg Med 2007;50:109)

Old: resolves within 24 hrs, if resolves in > then RIND

New TIA Definition:
TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction (NEJM 2002;347:1713-1716)

We probably should change this definition to one hour (Albers GW,  TIA Working Group.  Transient ischemic attack--proposal for a new definition.  N Engl J Med 2002;347:1713-6).

First, the symptoms are acute in onset; symptoms reach maximum intensity within seconds, and all symptoms begin at the same time. Patients with migraine with aura and partial seizures, on the other hand, often present with symptoms that march from one area to another, over a period of seconds to minutes.

in differential are:

migraines with aura-symptoms typically march over 5 to 30 min

seizures-usually sx precede seizure activity though Todd’s can confuse

In order to be TIA, symptoms must all occur simultaneously within seconds

the reason to get a ct scan is to rule out intracranial lesion, avm, meningioma, or subdural hematoma

Kaiser TIA Study (JAMA 2000; 284:2901-2906)

1700 patients for 90 days after being diagnosed with TIA by the emergency physician.

Neurologist reviewed the ED chart of all patients and felt that TIA was unlikely in only 5.6% of the patients

Stroke occurred in 10.5% of patients at 90 days,

Half of the strokes occurred within the first 48 hours.

Stroke was fatal in 21% and only 7% of patients had non-disabling stroke and were not hospitalized.

5 independent risk-factors for stroke:

1. age greater than 60 years,

2. diabetes mellitus,

3. duration of episode longer than 10 minutes,

4. weakness with the episode,

5. speech impairment with the episode.

Risk of stroke increased with the number of risk factors, from 0% with no risk factors, to 34% with 5 risk factors. Finally, 25% of patients experienced either stroke, cardiovascular hospitalization, death, or recurrent TIA within 90 days after their TIA, and more than half of these events occurred within the first 4 days.

In a prospective cohort study, the risk of recurrent stroke after TIA was 8% at 7 days, 11.5% at one month, and 17.3% at three months.  After mild stroke, the rates were 11.5%, 15%, and 18.5% respectively. (BMJ 26 Jan 2004)

In another with similar numbers (Stroke 34:e138, Aug 2003)

Systematic Review (Ann Emerg Med 2008;51:316)

5% during 1st 48 hours in general risk strat

TIA Scoring

Score to prognosticate TIA patients who require admission (Lancet 2005;366(9479):29)

A score of 4 or greater indicates high risk of stroke within one week; these patients should be admitted

reanalysis of retrospective data dichotomizes risk at greater than 4. Age may be removable. (Emerg Med J 2007;24:92)
 

 added diabetes to make D2. 0-3 Low risk, 4-5 moderate risk, >5 high risk. (Lancet 2007;369:283)

low risk=1% 2 day stroke rate. 1 or less=0% stroke rate. Moderate had a 4.1% two day stroke rate. High risk had an 8% 2 day stroke rate.

Anterior Circulation

Hemiparesis, unilateral sensory loss, visual field defect (monocular), gaze preference, aphasia, left sided neglect

Workup:

carotid dopplers, or possible MRA/CTA

echo

Posterior Circulation

hemiparesis, quadriparesis, hemisensory loss or loss in all 4 extremities, crossed deficits, diplopia, disconjugate gaze, gaze palsy, nystagmus, dysarthria, vertigo, decreased LOC, limb or gait ataxia, intractable vomiting

Workup:

transcranial dopplers or MRA of vertebrobasilar system.

cardiac source (acute or previous MI, AF, valvular disease, new murmur

On the other hand, if the dysphagia was prominent, or especially if the facial weakness was on the right, I'd be concerned about basilar artery ischemia

Diener HC, et al.  Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial.  Lancet 2004;364:331-7

Young TIA Patients

headache and neck pain possible with trauma could be carotid or vertebral artery dissection

Classically in carotid dissection,

head face or neck pain

partial Horner's

amaurosis fugax

will be present

If they are pregnant, consider paradoxical embolism, intracranial hemorrhage from eclampsia, ruptured avm, or venous sinus thrombosis

in Vertebral, occipital headache and brainstem ischemia may be the presentation.

Hypercoagulable states can also cause TIAs and strokes in this age group

Sub-Arachnoid Hemorrhage (SAH)

Radiology 224:353, 2002

METHODS: This retrospective chart review, from Massachusetts General Hospital, compared the accuracy of head CT scanning magnetic resonance imaging (MRI) and diffusion-weighted (DW) MRI in 691 patients presenting to the ED with a diagnosis of acute stroke.

RESULTS: For most patients, the precise interval from symptom onset to presentation or imaging could not be determined The final diagnosis was stroke, intraparenchymal hemorrhage with infarct, and cerebral infarct with transient symptoms in 78% of the patients. The mean time from presentation to a first head CT scan was 2.4 hours, and the sensitivity and specificity of this imaging study were 42% and 91%, respectively. A second CT scan was performed in 173 patients at a mean of 2.9 days after presentation with a sensitivity and specificity of 77% and 79%, respectively MRI was performed in 498 patients at a mean of 1.3 days after presentation, and 411 of these consisted of DW MRI studies. The sensitivity and specificity were 70% and 94%, respectively, for conventional MRI, and 94% and 97%, respectively, for DW MRI. In the subset of studies performed within six hours after presentation, sensitivities and specificities were 40% and 92 respectively, for CT scanning, 58% and 100%, respectively, for conventional MRI, and 97% and 100%, respectively, for DW MRI. The accuracy of DW MRI was superior to that of CT scanning up to twelve hours after presentation, but not thereafter.

CONCLUSIONS Diffusion-weighted MRI was superior to both conventional MRI and head CT scanning for the diagnosis of acute stroke during the initial twelve hours after presentation to the ED.

Fiebach, J.B., et al, Stroke 33:2206, September 2002

METHODS: In this German study, 54 patients presenting within six hours of the onset of symptoms of possible stroke underwent both CT scanning and diffusion-weighted magnetic resonance imaging (DW MRI), in random order. Imaging studies were evaluated by one neurologist, four neuroradiologists (considered "experts") and four second- or third-year neurology or neuroradiology residents (considered "novices"), blinded to specific signs and symptoms The gold standard used for making the final diagnosis is not described.

RESULTS: The ultimate diagnosis was ischemic stroke in 50 patients and transient ischemic attack (TIA) in four. The mean interval from symptom onset to imaging was about three hours and the two studies were typically done within about one-half hour of each other. Interrater agreement was substantially better with DW MRI, both overall and for size of lesion, and both for experts and novices. In addition, DW MRI was more accurate for all observers. When interpreted by the experts, sensitivity specificity and accuracy for the identification of infarcts were 91% and 95% for DW MRI, compared to 61% each for CT scanning Similarly, for novices sensitivity and specificity of DW MRI were 81% and 100%, vs. only 46% and 56% for CT.

CONCLUSIONS: Early DW MRI was more reliable and more accurate than CT scanning for the identification of ischemic stroke within six hours of symptom onset, both among experts and inexperienced readers.

Posterior Circulation Stroke

Neurologists have described acute confusional states and acute agitated delirium with several sites of infarction [4, 5 and 6]. Some have been bilateral, others on the right (non-dominant) or the left (dominant) specifically. Restlessness, agitation and disorientation are common with posterior artery infarctions. Forced crying out, cursing and unintelligible speech often have been reported in these cases, as they were in our patient [2]. Hypertension and generalized slowing on EEG are described in some patients, whereas others have normal CT scans for some time before changes of density can be identified [2]. The course of delirium can last several weeks with varying outcomes. Older age, comorbidity, and extent of the infarction have significant impact. Our patient had a history that included diabetes mellitus, hypertension, adenocarcinoma, and psychiatric disorders, all of which could have produced some of the initial symptoms. It is unlikely that her fever was due to medications, because she had been taking them for weeks, or that it was due to infection, because an organism could not be cultured and the white blood cell count was persistently normal. The maximum outside temperature on that day was 76°C.

The Amitriptyline and Nortriptyline levels were less than 10 ng/ml. It is known that acute strokes can cause elevated temperature, agitation and hypothermia. Although total CK level was not obtained, it is unlikely that agitation caused the fever, as it persisted even after agitation resolved with sedation. The ultimate cause of her fever was puzzling, but the most likely etiology was the stroke. Whether or not the antibiotics prescribed at the onset eradicated an undetected infection was never resolved. The confirmed diagnosis of left posterior cerebral artery infarction certainly could have explained the majority of her signs and symptoms as well as the course.

It is quite important to consider this diagnosis early as it carries a high mortality, particularly in the elderly [2]. Rapid intervention with TPA is increasingly initiated to spare neuronal damage when it can be administered shortly after an event. It would not have been given to this patient 11 h post infarction. Because initial CT scans may not be diagnostic, an MRI or MRA is more definitive. Plan for workup depends on initial clinical evaluation, although in most hospitals the first imaging study would be a CT scan. A CT scan can exclude unexpected large lesions or the presence of bleeding but other investigations are necessary to identify the stenotic or occluded artery. Abnormal diffusion weighted imaging (DWI) is a very sensitive and specific identifier of ischemic stroke in patients presenting within 6 h of stroke. Although DWI can detect areas of ischemia within 15–30 min of onset after only 3 s of imaging, its availability is limited. CT scans are more available, easily obtained and cheaper than MRIs or DWIs, so they are usually ordered first. But when non-diagnostic and at the earliest suspicion of ischemic stroke, the alternatives should be considered. Once the delirium clears, post-stroke depression should be reassessed. Untreated depression has a negative impact on both rehabilitation and long-term prognosis, and a premorbid history for depression significantly increases the risk for recurrence. Post-stroke depression is a well-known phenomenon and consistent with our patient's symptoms [7]. When the anterior limbic system is disconnected from the destroyed posterior, the amygdala and anterior hippocampus can also induce confusion, fever, anger and amnesia. The infarct will also disrupt connections between the temporal neocortex and the limbic system, making it extremely difficult to use language-encoded memories. As time progresses to allow for collateral circulation, the symptoms may resolve if the infarction is not so large that it causes devastating destruction.

In conclusion, infarction of the posterior cerebral artery, whether unilateral or bilateral, may present first as delirium without many focal findings. When suspected, an MRI should be immediately obtained to help clarify a diagnosis. Intervention with TPA in all non-hemorrhagic strokes remains controversial but patients treated within 90 min definitely have improved outcomes. Early identification of the patients who may benefit from this approach is essential [8]. The affected limbic structures can produce early psychiatric symptoms involving delirium and altered affect and the later development of post-stroke depression.

ETIOLOGY, DURATION, AND PROGNOSIS OF TRANSIENT ISCHEMIC ATTACKS AN ANALYSIS FROM THE GERMAN STROKE DATA BANK

Weimar, C., et al Arch Neurol 59:1584, October 2002

METHODS: This German registry prospectively recorded clinical characteristics and outcomes of 6,635 patients admitted to one of 15 hospitals with acute cerebral ischemia, including those with an ultimate diagnosis of ischemic stroke and those with a transient ischemic attack (TIA, defined as a clinical neurologic deficit lasting less than 24 hours).

RESULTS: Of the 1,429 patients (21.5%) in whom the final diagnosis was TIA, the deficit lasted more than one hour in 70%, and more than two hours in over half (precise numbers cannot be calculated from the report). At discharge, platelet inhibitors were prescribed for 82% of the TIA group and oral anticoagulants for 12%. By three months, the mortality rate was 14.0% in the stroke group compared with 1.7% in the TIA group. The authors, in looking after the fact at the data identified a number of differences in the prevalence of various stroke risk factors, as well and as in stroke types among various subgroups of patients. Those with a TIA were less likely to have a history of hypertension, atrial fibrillation, diabetes and smoking, but more likely to have hypercholesterolemia and a prior TIA. The TIA group had a higher rate of small vessel disease, and a lower rate of cardioembolic causes. There also appeared to be some differences according to the TIA duration had a higher rate of large artery atherosclerosis

CONCLUSIONS: This study provides information on the similarities and differences between patients with ischemic stroke, short-duration TIA and longer-duration TIA

ATLANTIS trial:  Mild to moderate strokes 79% completely recover at 90 days vs. 56% for placebo.  In moderate to severe, 33% TPA vs. 5% placebo.  22% change of intracranial hemorrhage.  All symptomatic hemorrhages were fatal. (Stroke 2002, 33:493-496)

Comparison of MRI and CT for Detection of Acute Intracerebral Hemorrhage

JAMA. 2004;292:1823-1830.
Results The study was stopped early, after 200 patients were enrolled, when it became apparent at the time of an unplanned interim analysis that MRI was detecting cases of hemorrhagic transformation not detected by CT. For the diagnosis of any hemorrhage, MRI was positive in 71 patients with CT positive in 29 (P<.001). For the diagnosis of acute hemorrhage, MRI and CT were equivalent (96% concordance). Acute hemorrhage was diagnosed in 25 patients on both MRI and CT. In 4 other patients, acute hemorrhage was present on MRI but not on the corresponding CT—each of these 4 cases was interpreted as hemorrhagic transformation of an ischemic infarct. In 3 patients, regions interpreted as acute hemorrhage on CT were interpreted as chronic hemorrhage on MRI. In 1 patient, subarachnoid hemorrhage was diagnosed on CT but not on MRI. In 49 patients, chronic hemorrhage, most often microbleeds, was visualized on MRI but not on CT.

Prognosis and Decision Making in Severe Stroke

JAMA 2005;294(6):725

Our analysis suggests that EICs are prevalent within 3 hours of stroke onset and correlate with stroke severity. However, EICs are not independently associated with increased risk of adverse outcome after rt-PA treatment. Patients treated with rt-PA did better whether or not they had EICs, suggesting that EICs on CT scan are not critical to the decision to treat otherwise eligible patients with rt-PA within 3 hours of stroke onset. (JAMA. 2001 Dec 12;286(22):2830-8.)
 

Optimal stroke scale to lyse 10-20

Hemorrhagic

Abstract

Early Surgery Versus Initial Conservative Treatment in Patients With Spontaneous Supratentorial Intracerebral Haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): A Randomised Trial

Available online 15 June 2006.




Mendelow AD, for the STICH Investigators (Newcastle Gen Hosp, Newcastle upon Tyne, England; et al) Lancet. 2005;365:387-397

Background: Spontaneous supratentorial intracerebral haemorrhage accounts for 20% of all stroke-related sudden neurological deficits, has the highest morbidity and mortality of all stroke, and the role of surgery remains controversial. We undertook a prospective randomised trial to compare early surgery with initial conservative treatment for patients with intracerebral haemorrhage.

Methods: A parallel-group trial design was used. Early surgery combined haematoma evacuation (within 24 h of randomisation) with medical treatment. Initial conservative treatment used medical treatment, although later evacuation was allowed if necessary. We used the eight-point Glasgow outcome scale obtained by postal questionnaires sent directly to patients at 6 months follow-up as the primary outcome measure. We divided the patients into good and poor prognosis groups on the basis of their clinical status at randomisation. For the good prognosis group, a favourable outcome was defined as good recovery or moderate disability on the Glasgow outcome scale. For the poor prognosis group, a favourable outcome also included the upper level of severe disability. Analysis was by intention to treat.

Findings: 1033 patients from 83 centres in 27 countries were randomised to early surgery (503) or initial conservative treatment (530). At 6 months, 51 patients were lost to follow-up, and 17 were alive with unknown status. Of 468 patients randomised to early surgery, 122 (26%) had a favourable outcome compared with 118 (24%) of 496 randomised to initial conservative treatment (odds ratio 0.89 [95% CI 0.66-n-1.19], p=0.414); absolute benefit 2.3% (−3.2 to 7.7), relative benefit 10% (−13 to 33).

Interpretation: Patients with spontaneous supratentorial intracerebral haemorrhage in neurosurgical units show no overall benefit from early surgery when compared with initial conservative treatment.
 

2007 AHA Guidelines

(Stroke. 2007;38:1655.)

5. Multimodal CT and MRI may provide additional information

that will improve diagnosis of ischemic

stroke (Class I, Level of Evidence A).

This recommendation

has been added since the previous guideline.

Class II Recommendations

1. Nevertheless, data are insufficient to state that, with the

exception of hemorrhage, any specific CT finding (including

evidence of ischemia affecting more than one

third of a cerebral hemisphere) should preclude treatment

with rtPA within 3 hours of onset of stroke (Class

IIb, Level of Evidence A).

This recommendation has not

changed from the previous guideline.

Class I Recommendations
 

1. Airway support and ventilatory assistance are recommended for the treatment of patients with acute stroke who have decreased consciousness or who have bulbar dysfunction causing compromise of the airway (Class I, Level of Evidence C). This recommendation has not changed from previous statements.
    
2. Hypoxic patients with stroke should receive supplemental oxygen (Class I, Level of Evidence C). This recommendation has not changed since the previous guideline.
    
3. It is generally agreed that sources of fever should be treated and antipyretic medications should be administered to lower temperature in febrile patients with stroke (Class I, Level of Evidence C). This recommendation has not changed from previous statements. Medications such as acetaminophen can lower body temperature modestly, but the effectiveness of treating either febrile or nonfebrile patients to improve neurological outcomes is not established. Additional research on utility of emergency administration of antipyretic medications is under way.
    
4. General agreement supports the use of cardiac monitoring to screen for atrial fibrillation and other potentially serious cardiac arrhythmias that would necessitate emergency cardiac interventions. It is generally agreed that cardiac monitoring should be performed during the first 24 hours after onset of ischemic stroke (Class I, Level of Evidence B). This recommendation has not changed from previous statements.
    
5. The management of arterial hypertension remains controversial. Data to guide recommendations for treatment are inconclusive or conflicting. Many patients have spontaneous declines in blood pressure during the first 24 hours after onset of stroke. Until more definitive data are available, it is generally agreed that a cautious approach to the treatment of arterial hypertension should be recommended (Class I, Level of Evidence C). Patients who have other medical indications for aggressive treatment of blood pressure should be treated. This recommendation has not changed from previous statements.
    
6. Patients who have elevated blood pressure and are otherwise eligible for treatment of rtPA may have their blood pressure lowered so that their systolic blood pressure is 185 mm Hg and their diastolic blood pressure is 110 mm Hg (Class I, Level of Evidence B) before lytic therapy is started. This recommendation has not changed from previous statements. If medications are given to lower blood pressure, the clinician should be sure that the blood pressure is stabilized at the lower level before treating with rtPA and maintained below 180/105 mm Hg for at least the first 24 hours after intravenous rtPA treatment. Because the maximum interval from stroke onset until treatment with rtPA is short, many patients with sustained hypertension above recommended levels cannot be treated with intravenous rtPA.
    
7. Until other data become available, consensus exists that the previously described blood pressure recommendations should be followed in patients undergoing other acute interventions to recanalize occluded vessels, including intra-arterial thrombolysis (Class I, Level of Evidence C). This recommendation has been added since the previous guideline.
    
8. It is generally agreed that patients with markedly elevated blood pressure may have their blood pressure lowered. A reasonable goal would be to lower blood pressure by 15% during the first 24 hours after onset of stroke. The level of blood pressure that would mandate such treatment is not known, but consensus exists that medications should be withheld unless the systolic blood pressure is >220 mm Hg or the mean blood pressure is >120 mm Hg (Class I, Level of Evidence C). This recommendation has changed from previous statements in that a potential goal for lowering blood pressure is now included. Research testing the effects of early treatment of arterial hypertension on outcomes after stroke is under way. The panel looks forward to any data that will clarify this management decision.
    
9. It is generally agreed that the cause of arterial hypotension in the setting of acute stroke should be sought. Hypovolemia should be corrected with normal saline, and cardiac arrhythmias that might be reducing cardiac output should be corrected (Class I, Level of Evidence C). This recommendation was not included in previous statements. The utility of volume expansion and the use of medications to increase blood pressure to treat ischemic stroke are discussed elsewhere in the present guideline.
    
10. It is generally agreed that hypoglycemia should be treated in patients with acute ischemic stroke (Class I, Level of Evidence C). The goal is to achieve normoglycemia. Marked elevation of blood glucose levels should be avoided. This recommendation was included in previous statements.
     

Class II Recommendations
 

1. No data are available to guide selection of medications for the lowering of blood pressure in the setting of acute ischemic stroke. The recommended medications and doses included in Table 10 are based on general consensus (Class IIa, Level of Evidence C). The recommendations in Table 10 have changed from the previous statements.
    
2. Evidence from one clinical trial indicates that initiation of antihypertensive therapy within 24 hours of stroke is relatively safe. Thus, it is generally agreed that antihypertensive medications should be restarted at 24 hours for patients who have preexisting hypertension and are neurologically stable unless a specific contraindication to restarting treatment is known (Class IIa, Level of Evidence B). This recommendation was not included in previous statements.
    
3. Evidence indicates that persistent hyperglycemia (>140 mg/dL) during the first 24 hours after stroke is associated with poor outcomes, and thus it is generally agreed that hyperglycemia should be treated in patients with acute ischemic stroke. The minimum threshold described in previous statements likely was too high, and lower serum glucose concentrations (possibly >140 to 185 mg/dL) probably should trigger administration of insulin, similar to the procedure in other acute situations accompanied by hyperglycemia (Class IIa, Level of Evidence C). This is a change from previous statements. Close monitoring of glucose concentrations with adjustment of insulin doses to avoid hypoglycemia is recommended. Simultaneous administration of glucose and potassium also may be appropriate. The results of ongoing research should clarify the management of hyperglycemia after stroke.
    

Class III Recommendations
 

1. Nonhypoxic patients with acute ischemic stroke do not need supplemental oxygen therapy (Class III, Level of Evidence B). This recommendation has not changed from previous statements.
    
2. Data on the utility of hyperbaric oxygen are inconclusive, and some data imply that the intervention may be harmful. Thus, with the exception of stroke secondary to air embolization, this intervention is not recommended for treatment of patients with acute ischemic stroke (Class III, Level of Evidence B). This recommendation has changed from previous statements.
    
3. Although data demonstrate the efficacy of hypothermia for improving neurological outcomes after cardiac arrest, the utility of induced hypothermia for the treatment of patients with ischemic stroke is not established. At the present time, insufficient evidence exists to recommend hypothermia for treatment of patients with acute stroke (Class III, Level of Evidence B). This recommendation has not changed from previous statements. Additional research on the safety and efficacy of induced hypothermia for treatment of patients with stroke is under way.
    

Infuse 0.9 mg/kg (maximum dose 90 mg) over 60 minutes with 10% of the dose given as a bolus over 1 minute. Admit the patient to an intensive care or stroke unit for monitoring. Perform neurological assessments every 15 minutes during the infusion and every 30 minutes thereafter for the next 6 hours, then hourly until 24 hours after treatment. If the patient develops severe headache, acute hypertension, nausea, or vomiting, discontinue the infusion (if rtPA is being administered) and obtain emergency CT scan. Measure blood pressure every 15 minutes for the first 2 hours and subsequently every 30 minutes for the next 6 hours, then hourly until 24 hours after treatment. Increase the frequency of blood pressure measurements if a systolic blood pressure is 180 mm Hg or if a diastolic blood pressure is 105 mm Hg; administer antihypertensive medications to maintain blood pressure at or below these levels (see Table 10). Delay placement of nasogastric tubes, indwelling bladder catheters, or intra-arterial pressure catheters. Obtain a follow-up CT scan at 24 h before starting anticoagulants or antiplatelet agents.

Class I Recommendations
 

1. Intravenous rtPA (0.9 mg/kg, maximum dose 90 mg) is recommended for selected patients who may be treated within 3 hours of onset of ischemic stroke (Class I, Level of Evidence A). Physicians should review the criteria outlined in Table 11 (which are modeled on those used in the NINDS trial) to determine the eligibility of the patient. A recommended regimen for observation and treatment of the patient is described in Table 12. This recommendation has not changed from previous statements.
    
2. Besides bleeding complications, physicians should be aware of the potential side effect of angioedema that may cause partial airway obstruction (Class I, Level of Evidence C). This recommendation has been added since the previous guidelines.
    

Class II Recommendations
 

1. A patient whose blood pressure can be lowered safely with antihypertensive agents may be eligible for treatment, and the physician should assess the stability of the blood pressure before starting rtPA (Class IIa, Level of Evidence B). An elevated blood pressure that requires a continuous infusion of sodium nitroprusside may not be sufficiently stable for the patient to receive rtPA. However, because time is limited, most patients with markedly elevated blood pressure cannot be managed adequately and still meet the 3-hour requirement. This recommendation has not changed from previous guidelines.
    
2. A patient with a seizure at the time of onset of stroke may be eligible for treatment as long as the physician is convinced that residual impairments are secondary to stroke and not a postictal phenomenon (Class IIa, Level of Evidence C). This recommendation differs from the previous statements and represents a broadening of eligibility for treatment with rtPA.
    

Class III Recommendations
 

1. The intravenous administration of streptokinase for treatment of stroke is not recommended (Class III, Level of Evidence A). This recommendation has not changed from previous guidelines.
    
2. The intravenous administration of ancrod, tenecteplase, reteplase, desmoteplase, urokinase, or other thrombolytic agents outside the setting of a clinical trial is not recommended (Class III, Level of Evidence C). This recommendation is new.
    

Dizziness and Stroke

Stroke Among Patients With Dizziness, Vertigo, and Imbalance in the
Emergency Department: A Population-Based Study

Kerber KA, Brown DL, Lisabeth LD, et al. Stroke 2006;37:2484–7

Catherine Ambrose MDa
aDenver Health Medical Center, Denver, Colorado

Available online 30 March 2007.






As part of the Brain Attack Surveillance in Corpus Christi (BASIC)
project, this study sought to determine the percentage of stroke
patients who presented to the Emergency Department (ED) with the
complaints of dizziness, vertigo, or imbalance. This large
population-based study examined all patients over the age of 44 years
who presented to the ED or were directly admitted to the hospital
between January 2000 and June 2003 with the previously mentioned
isolated dizziness symptoms (DS) in Nueces County, Texas. The
association of age, sex, race/ethnicity, and isolated dizziness
symptoms with stroke or transient ischemic attack (TIA) was then
determined using multivariable logistic regression. A total of 1666
patients were included in the study, with 3.2% (53 of 1666) ultimately
diagnosed with stroke/TIA. Of those diagnosed, 23 presented with
dizziness as the chief complaint, 18 with vertigo, 11 with imbalance,
and 1 with more than one of the above symptoms. Isolated DS without
additional neurological findings was a strong negative predictor of
stroke/TIA (odds ratio [OR] 0.05; 95% confidence interval [CI]
0.02–0.11), whereas male sex was associated with an increased
association with stroke/TIA (OR 2.5; 95% CI 1.4–4.4). Patients
diagnosed with stroke/TIA were also found to be significantly older
(69.3 ± 11.7 vs. 65.3 ± 12.9, p = 0.02). No significant difference in
race/ethnicity was found between the stroke and non-stroke groups.
When compared to dizziness, patients with imbalance were found to have
an increased risk of stroke/TIA (OR 3.7; 95% CI 1.3–10.7), whereas no
increased risk was found between those with vertigo versus dizziness
(OR 0.9; 95% CI 0.4–2.0). The authors acknowledge several limitations
to this study, including lack of evaluation of the majority of study
patients in the ED by a neurologist, lack of magnetic resonance
imaging on most study patients leading to possible undiagnosed
strokes, and lack of comparison of symptom onset, duration,
aggravating/alleviating factors, headache, and auditory symptoms
between groups. The authors conclude that dizziness and vertigo are
not associated with stroke/TIA, whereas patients who present with
imbalance, those with additional neurologic findings, male gender, and
older age are at the highest risk for possible stroke/TIA.

Rapid approach to NIHSS

The NIHSS as formulated by the National Institute of Neurological Disorders and Stroke has been applied at our medical center as the SQS and is shown here with maximal deficit scores clustered into 3 groups having a total of 7points each (Fig. 1). The level of consciousness section to the NIHSS is grouped together in the frontal regions with an aggregate deficit score totaling 7 for deficits in alertness, ability to answer questions, and obey commands. A second cluster of 3 consisted of deficits in sensation, extinction, and language being clustered along the motor strip and temporal-parietal regions; the extinction category tests inattention with complete neglect scoring 2. In regards to sensory deficits, this can be tested as withdrawal to noxious stimuli, with a severe loss scoring 2 points. A third cluster was placed in the posterior regions and included the maximal visual deficit score of 3 for bilateral hemianopia, and the near to unintelligible deficit score of 2 for dysarthria was placed alongside the maximal limb ataxia score of 2 in the cerebellar region; although speech dysarthria can be a result of ischemic damage to the motor strip, an alternative possibility would be dysarthria of a cerebellar origin and for convenience is grouped here in the posterior fossa region. The maximal motor deficit score of 4 for each of 4 extremities is grouped together (green circle, Fig. 1). Miscellaneous items that are not part of the 322 groupings are separated by a line parallel to the catho-metal line: best gaze (forced deviation of the eyes scores 2 points) and facial palsy (complete facial palsy scores 3 points).
3. Discussion
Although not yet formally tested under controlled conditions, the SQS diagram may accelerate the time factor in reaching an accurate score, but formal testing of this hypothesis is needed. Although the NIHSS attempts to comprehensively include all regions of the brain that could be affected by stroke, the weighting factors for each functional item might need reassessment. The current equal weighting for arms vs legs remains reasonable for now, because 1 study showed very good reliability for these items with the 15-item NIHSS [6]. However, the same study found the least reliable items to facial palsy and dysarthria with low intraclass correlation coefficients being less than 0.40, and advocated a modified 11-item version of the NIHSS.
In summary, the presented SQS diagram shown in Fig. 1, or similar versions, may facilitate training of examiners to comprehend the overall structure of the NIHSS system. The SQS diagram is intended only to serve as a supplement and not a replacement for current methods of scoring. However, further testing of a single visual composite for the NIHSS as an ancillary tool is needed to determine its actual usefulness. (AJEM 2008;26:189)

From EP Monthly:The year’s top stroke advances by Bobby Desai, MD

Lacunes & Lacunar Infarcts

Less well-established is how many clinically evident lacunar infarcts ever cavitate to become "lacunes". It seems generally assumed that all lacunes start life as an infarct, even if the patient did not notice anything, and therefore share the same risk factors, etiology, prognosis, pathogenesis, etc, as clinically evident lacunar infarcts.^3–5 However, suppose only a proportion of lacunar stroke lesions, perhaps as few as a third, ever cavitate, with the majority that fail to cavitate retaining the appearance of a WML?⁶ Counting lacunes could result in spurious risk factor and etiologic associations for lacunar stroke. We should not assume that the pathogenesis of clinically evident lacunar stroke is the same as for clinically silent lacunes. Equally, similarity in appearance between WMLs and clinically evident acute lacunar infarct could imply similar causation. However, surely the fact that one has caused symptoms (lacunar stroke/infarct) and the other not (WML/lacune) is important in itself and should lead to their careful distinction in any research at least until we know more.