Pearls on Intracranial atherosclerosis

Turan TN, Chimowitz MI.  . 10 questions about intracranial atherosclerosis.The Neurologist. 16:6 400-405 1020.

1.  MRA and TCD have high negative predictive values but low positive predictive values for detecting intracranial stenosis.  (86-91. v. 36-59 % respectively).  They are therefore adequate screening tests but need CTA for diagnosis or catheter angiography.  CTA studies have limited statistical power therefore catheter studies are the "gold standard" to determine the degree of stenosis, but also confer risk.  A single preliminary study showed CTA had a sensitivity and specificity to detect intracranial stenosis greater than 50 % of of 97.1 and 99.5 % respectively.  In ACAS the risk of stroke with catheter angiography was 1.2 %. The SONIA study was the study that helped evaluate the above.

2.  The risk of stroke with intracranial stenosis is the highest of any stroke subtype, with respect to symptomatic stenosis  of greater than 50 %.  The risk of ischemic stroke in any territory within two years was 20 % in aspirin arm and 17 % in the warfarin arm (WASID).  Over 70 % of strokes occurred in the same territory.  Thus the risk in the symptomatic artery was 15/13 % in aspirin and warfarin arms respectively.  This is higher than the risk with atrial fibrillation or cardioembolic stroke.

3.   The risk of stroke was proportional to the severity of stenosis (risk of stroke within the symptomatic artery occurred in 6/18 % of patients, respectively, with < 70 and >70 % stenosis. 

4.  Other risk factors for stroke in the territory included recent symptoms, female gender, and baseline NIHSS >1.  Vertebrobasilar arterial disease was NOT a risk factor. 

5.  Asymptomatic stenosis was very low risk, with a one year risk of stroke of 0 % in one study and 3.5 % in WASID by MRA. 

6.  "Antithrombotic failures" ie patients already on antiplatelet drugs at time of their stroke, were not at higher risk for recurrent stroke than patients who were not on antiplatelet drugs at the time of their qualifying event. 

7.  Most important risk factors for recurrent stroke were dyslipidemia and hypertension  (SBP> 140). 

8.  SSYLVIA (stenting of symptomatic atherosclerotic lesions in the vertebral or intracranial arteries) was a ph I study of a bare metal stent that showed technical success and a 10.9 % stroke rate in one year with all strokes within the same artery. 

9.  SSAMPRIS study is ongoing (Stenting and Aggressive Medical Management of for Prevention of Recurrent Stroke in Intracranial Stenosis) NIH sponsored study.  In 764  patients it compares angioplasty and stenting plus aggressive medical management v. medical management alone in patients with 70-99 % stenosis.  Patients must have a TIA or nondisabling  stroke within 30 days in an appropriate artery to be eligible.  The protocol includes ASPIRIN for duration, plavix for first 90 days, aggressive bp and lipid management.

10.  See http://www.ssampris.org/ or http://www.sammpris.org/.

HINTS to diagnose stroke in acute vestibular syndrome: 3 step oculomotor exam

 

Stroke. 2009 Nov;40(11):3504-10. Epub  2009 Sep 17.
HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging.
Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE.
Department of Neurology, The University of Illinois College of Medicine at Peoria and the Illinois Neurological Institute at OSF Saint Francis Medical Center, Peoria, Ill, USA.

Abstract
BACKGROUND AND PURPOSE: Acute vestibular syndrome (AVS) is often due to vestibular neuritis but can result from vertebrobasilar strokes. Misdiagnosis of posterior fossa infarcts in emergency care settings is frequent. Bedside oculomotor findings may reliably identify stroke in AVS, but prospective studies have been lacking.
METHODS: The authors conducted a prospective, cross-sectional study at an academic hospital. Consecutive patients with AVS (vertigo, nystagmus, nausea/vomiting, head-motion intolerance, unsteady gait) with >or=1 stroke risk factor underwent structured examination, including horizontal head impulse test of vestibulo-ocular reflex function, observation of nystagmus in different gaze positions, and prism cross-cover test of ocular alignment. All underwent neuroimaging and admission (generally <72 hours after symptom onset). Strokes were diagnosed by MRI or CT. Peripheral lesions were diagnosed by normal MRI and clinical follow-up.
RESULTS: One hundred one high-risk patients with AVS included 25 peripheral and 76 central lesions (69 ischemic strokes, 4 hemorrhages, 3 other). The presence of normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation (vertical ocular misalignment) was 100% sensitive and 96% specific for stroke. Skew was present in 17% and associated with brainstem lesions (4% peripheral, 4% pure cerebellar, 30% brainstem involvement; chi(2), P=0.003). Skew correctly predicted lateral pontine stroke in 2 of 3 cases in which an abnormal horizontal head impulse test erroneously suggested peripheral localization. Initial MRI diffusion-weighted imaging was falsely negative in 12% (all <48 hours after symptom onset).
CONCLUSIONS: Skew predicts brainstem involvement in AVS and can identify stroke when an abnormal horizontal head impulse test falsely suggests a peripheral lesion. A 3-step bedside oculomotor examination (HINTS: Head-Impulse-Nystagmus-Test-of-Skew) appears more sensitive for stroke than early MRI in AVS.

neurodoc

Patient foramen ovale

Kent DM, Thaler DE.  Is Patent foramen ovale a modifiable risk factor for stroke recurrence?Stroke 2010: 41 (supplement 1) S 26-S30.

Authors make statistical arguments about PFO management.  Facts that form a basis:

1.  PFO occurs in 25 % of autopsies.
2.  PFO occurs in a higher rate in cryptogenic stroke, but in at least 33 % of strokes with PFO the PFO is incidental.
3.  PFO in Cryptogenic Stroke Study (PICSS) shows near identical stroke recurrence risk in patients with cryptogenic stroke whether or not they have a PFO.  Further, small PFO's had a higher recurrence rate than large ones.  This simply indicates, however, that PICSS included patients who were eventually given a TEE , even if they had a different defined mechanism for their stroke.  Other occult mechanisms such as occult afib or subthreshold aortic atherothrombotic disease may have a higher recurrence rate.
4.  Consistently, studies show that patients with cryptogenic stroke and PFO have less conventional stroke risk factors than patients without PFO.  Since recurrence risk of stroke is about equal in PFO + and - patients, PFO singlehandedly compensates for lack of other risk factors.  Therefore, PFO IS a risk factor for stroke.  Younger patients without DM or HTN are much more likely to have a PFO. 
5.  When a PFO is found in setting with an atrial septal aneurysm, the PFO is rarely incidental to the stroke.
6.  "PFO propensity" is likelihood based on age or other factors that a CS patient has a PFO.  A higher PFO propensity correlates with a lower chance of incidental PFO.  A younger patient without other risk factors may have a very high PFO propensity and therefore probability of nonincidental PFO. 
7.  The margin of benefit in PFO closure is narrow.  Even a low rate of procedure complications could nullify benefit.  "Testing the procedure (closure) in a population in which many incidental PFOs occur may falsely suggest the procedure is of no benefit."

Blackbox contraindication intravenous nimodipine

August 2, 2010 — As if a "black box" warning currently on the label were not enough to get anyone's attention, today the US Food and Drug Administration (FDA) again reminded clinicians that nimodipine (Nimotop; Bayer Pharmaceuticals) should be given only by mouth or through a feeding tube and never by intravenous (IV) administration, a method that could be fatal.

Nimodipine, available only as an oral capsule, is used in critical-care settings to treat neurologic complications from subarachnoid hemorrhage.

The FDA states that it continues to receive reports of IV administration of the drug, which sometimes has resulted in death or near-death events. Intravenous administration of nimodipine can cause cardiac arrest, dramatic drops in blood pressure, and other cardiovascular adverse events, according to the agency.

In 1996, Bayer added a bolded statement to the drug's label to warn against incorrect administration after 1 patient who received nimodipine the wrong way died. In 2006, the company added a boxed warning against giving nimodipine intravenously or by other parenteral routes.

Through its Adverse Event Reporting System (AERS) and other sources, including published literature, the FDA has identified 31 cases of nimodipine errors between 1989 and 2009, with 25 involving the prescription or administration of the drug intravenously. Four patients who received nimodipine intravenously died while another 5 came close. One patient suffered permanent harm, according to the agency.

Errors Sometimes Occur With Patients Who Cannot Swallow Capsule

Sometimes nimodipine is administered intravenously despite repeated warnings to the contrary when a patient is not able to swallow the capsule. Such patients are supposed to receive it through a nasogastric tube. The drug comes with instructions for making a hole in both ends of the capsule with a standard 18 gauge needle, removing the contents with a syringe, and emptying the syringe into the tube.

The agency noted that because a standard needle will not fit on an oral syringe, it must be attached to an intravenous syringe. "The use of intravenous syringes to deliver nimodipine increases the chance that the medication will be given intravenously instead of by mouth or nasogastric tube," the FDA stated.

Clinicians can minimize confusion in these circumstances by labeling the syringe with the words "Not for IV Use" and removing the needle, according to the agency. They then should empty the syringe contents into the nasogastric tube followed by 30 mL of normal saline.

More information about today's announcement is available on the FDA's Web site.

To report adverse events related to nimodipine capsules, contact MedWatch, the FDA's safety information and adverse event reporting program, by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to MedWatch, FDA, 5600 Fishers Lane, Rockville, Maryland 20852-9787.

Mendelsohn maneuver for stroke

The Mendelsohn maneuver is taught by having the patient place


their fingers lightly over the thyroid cartilage and then trying to

swallow. When the thyroid cartilage reaches the top part of its

elevation during the swallow the patient is supposed to try to keep it

in this position for a second or two. The crycopharyngeus upper

esophageal sphincter is stretched by this excursion and is mechanically

opened. There may also be some reflex inhibition of the sphincter, but

the benefit is probably mostly mechanical. Logeman's book on dysphagia

has a much better description.

Homocystinuria and stroke

Testai FD, Gorelick PB.  Hommocystinuria, organic acidurias and urea cycle disorder.  Arch Neurol 2010; 67: 148-153.

Features of homocystinuria
Genetics (classical) Aut rec, chromosome 21, deficient cystathione synthase, 90 + mutations, elevated Homocystine and metabolite, methionine(or elevated homocysteine and normal methionine with MTHFR mutations or errors of B12 metabolism. Levels are over 100
. Stroke is due to atherosclerosis, dissection, or SVD

Clinical  -- myopia, osteoporosis, mental retardation, decreased pigmentation of hair and skin, downwards ectopic lenses, dolichostenomelia, and if untreated, seizures, psychiatric disorders, thromboembolic events (PE, MI, stroke).  Clinically there is an equal distribution of the milder B6 (pyridoxal phosphate) responsive form and more severe unresponsive form. 

Thromboembolic events-- distribution-- 51 % peripheral vein (one fourth PE's), 32 % strokes, 11 % peripheral arterial, 4 % MI, 2 % other. 25 % stroke by age 15, half by age 30.  Treatment of pyrodoxal phosphate responders delays first event.

Mechanism-- of thromboembolism is multi.  Increased homocysteine causes premature atherosclerosis due to endovascular dysfunction due to deficient nitrous oxide and oxidative stress.  Also, hypercoagulability due to increased thrombosis and platelet activation may affect stability of arterial wall and cause dissections, arterial thrombosis, and arteriopathy mimicking FMD.

Diagnosis-- Based on clinical and lab features.  Brand reaction is screening test using urinary cyanide nitroprusside.  Blood usually has elevated homocysteine and methionine and decreased cysteine.  Urine excretion of homocysteine, homocystine (the oxidized form) and methionine occurs.  Cystathionine B synthase cultures in fibroblasts, amniotic fluid and chorionic villi can be assessed.

Treatment-- judicious use of B6 (300-600 mg/day) to prevent PN.  Folate, betaine and B12 cause conversion of homocysteine to methionine.  A methionine free diet with cysteine supplementation is suggested. Vitamin C and antiplatelet agents are commonly used.

Aneurysm presentation-- random clinical pearls

Diagnosis
1.  Of patients with the worst headache of their life, ten percent have aneurysms
2.  Sensitivity of LP to detect aneurysms decreases by seven percent per day
3.  CT-A removes need for catheter angiography in those with more than 5 rbc's
4.  SAH- aneurysmal peaks in April and September and nadirs in June and July
5.  Population prevalence of aneurysm in 2 %
Treatment
6.  **FENESTRATION OF LAMINA TERMINALIS IS EASY, DECREASES HYDROCEPHALUS INCIDENCE FROM 13 TO 2 PERCENT AND ALLOWS LUMBAR DRAINS
7.   EEG is a "pseudoexam " under anesthesia
8.  St Julien NSURG 2008  cardiopulmonary bypass without a chest incision (endovascular)allows fine control of BP and avoids circulatory arrest, hypothermia improves outcomes ( outcome of St Julien)  Grade 0 , 1 (1.5 %), 2 (6.2%), 3 (12.1%), 4 (17.4 %).  CP bypass is good for giant aneurysms
9.  Fisher scale stratifies the risk of vasospasm .  Grade 1: no blood   Grade 2:  vertical layer < 1mm
      Grade 3:    vertical layer > 1 mm, local clot     Grade 4:  ICH/IVH but minimal or no SAH. GRADE  THREE IS MAXIMAL RISK> GRADE FOUR.  Risk of vasospasm is 23 %.   With modified Fisher scale, vasospasm is greatest with grade 4.  About 20-30 % of vasospasms stroke.
10.  Risk of rebleed is 4 % in first 24 hours, then 1-2 % per day for 4 weeks.  Cumulative risk is 20 % at 2 weeks, 30 % at one month, 40 % at 6 months. Ventriculostomy which otherwise can be lifesaving also can precipitate a rebleed.
10.  Risk of rebleed is       

Hemorrhagic shock plus TBI no longer uniformly fatal

Combination is less lethal than formerly provided that CPP is maintained.  Treatment algorithm:  stop bleeding (factor 7), restore volume (whole blood, crystalloid), saline, plasma, platelets, pressors (phenylephrine, vasopressin, norepinephrine, DA), prophylactic phenytoin, for 7 days, treat fevers with tylenol, aggressive nutrition, use hemicraniectomy for impending herniation is efficacious, use GCS to communicate. 

Prehospital care:  avoid hypoxia-- give oxygen, avoid hypotension, hypertonic saline is good; mannitol only if intravascular volume can be maintained, generally avoid hyperventilation unless herniating. 

ICP monitor if GCS < 8 and abnormal CT scan.  Want ICP< 20, intervention threshold around 25.  ICP plateau or A waves are sine qua non of herniation.  These are best seen with changing sweep speed on monitor to minutes.  B waves last from 0.5 to 2 minutes and are associated with changing brain compliance not increased ICP.  C waves are ICP waves associated with respiration. 

Components of a "brain code" are 1) elevated HOB to 45 degrees   2)  HV to pCO2 around 35   3) mannitol .5 grams/kg   4) saline bullet (see    http://neurologyminutiae.blogspot.com/2010/04/saline-bullets-and-hypertonic-saline.html)   5) CSF  drainage

from lecture by Dr Ling

Vasospasm after traumatic brain injury

Unlike its better known couin that occurs after SAH, vasospasm after TBI follows a different time course of 10-21 days is often subclinical and is best treated with nicardipine and endovascular therapy.  It can be monitored with TCD. 

Source-- lecture Col. Geoffrey Ling , MD

Pearls on blood pressure, misc and hemorrhagic stroke care

1.  PET studies do  not support the concept of an ischemic penumbra, hence blood pressure control should be used judiciously (Schellinger et al, Stroke 2003)

2.  The occurrence of ICH is strongly related to prevailing blood pressure, however no definitive evidence exists that recurrent ICH in the acute setting relates to blood pressure or control thereof (Jauch et al. Stroke 2006)

3.  Intracranial hypertension is associated with a worse outcome

4.  Prior statin use is associated with decreased perihemorrhage edema and decreased 30 day mortality ; however this data is retrospective (Naval et al., 2 refs Neurocritical Care 2008)

5. The Stroke Council continues to advocate for 2-4 weeks of prophylactic antiepileptic therapy in patients with SICH and SAH

6.  Hematoma size (Stoke 1997, Brott et al) and growth (Davis et al, Neurology 2006)  are correlated with mortality

7.  The "spot sign" or contrast extravasation in CTA may identify patients at high risk of hematoma expansion

8.  ICH < 30 cc may benefit from intraclot alteplase

9.  MIS minimal invasive surgery is also considered under investigation although certain types of ICH do not benefit

Carotid artery webbing

case report at AAN 2010 also known as "atypical FMD" a 41 year old woman with headache  for months, facial droop and aphasia cutely.  MRI showed an M1 occlusion, and delayed time to peak in entire MCA.  Catheter showed bilateral ICA webbing with stagnant flow.  No standard of care is known.

MCA arrow sign in MCA aneursmal SAH

In a review, arrow sign was present in 4 patients with SAH all Fisher 3.  That is 16 % of total MCA aneurysms and was not seen in any other type of aneurysm.

below is an arrow sign for an MCA trifurcation aneurysm (from neurology.org)

Ptosis and astasia with thalamic infarcts: case report (s)

Jain D. et al.  Cerebral ptosis and astasia  "Lateral pulsion" due to a left anterior thalamic lesion.  Mechanisms are reviewed.AAN 2010:PO2:102

Alderazi Y.  Thalamic infarction causing astasia-abasia, ataxia and asterixis.  clinical and radiological features of two cases.  PO2:108.    Wide based gait past pointing and intention tremor on right, with left posterolateral thalamic infarct.    Second case with left arm drift, left asterixis, inability to stand unassisted with right lateral thalamic acute stroke and old left cerebellar hemorrhage. 

Sneddon's syndrome need for angiography

Faris et al.  Sneddon's syndrome without antiphospholipid antibodies:  a report of 26 cases with cerebral angiography (Rabat).  Neurology 2010 74:9:PO2:099.

Authors emphasize Sneddon's syndrome (stroke  plus livedo racemosa) is NOT identical to APL syndrome.  26 patients were studied retrospectively with a combination of focal motor deficits and dementia.  Imaging always showed infarcts with white matter involvement.  Angio showed a distal arteriopathy in 18 cases with pial networks in  cases.  Two had hematomas.  The authors suggested angiography to prevent the unwarranted and dangerous potential use of anticoagulation.

NSE after cardiac arrest during hypothermia predicts outcome

AN 2010 Po1.048  JEF Fugate, Wijdicks et al.  NSE was measured serially in comatose patients undergoing hypothermia.  A cutoff was used of 33 ug/L.  NSE was measured at day one and day three,  with higher NSE suggesting poor prognosis (defined as one year mortality).  48 patients, 41 had first day NSE, 14 had third day NSE.  For first day NSE, the number with high level is given with number of survivors at one year in parenthesis 19 (3) with a low NSE being 22 (11).  Trend in NSE on day 3 was highly predictive (p<.015).  The sensitivity for first day NSE was 59 % for one year mortality with improvement to 66 % if 3 day NSE is included.

Four score is predictor of outcome in coma after cardiac arrest

Neurology AAN 2010 PO1.045 Wijdicks et al.

The Four Score differs from the GCS because it has 4 components-- eye, motor, brainstem and respiration (latter two are not included in GCS) .  Prospectively looked at patients from 2006-2009 (n=131) and looked at outcome after one year.  91 died.  31 had four score less than 4 at day one and of these, zero survived.  Of patients with GCS of 3, 4 (7 %) survived at one year.  The Four Score had a specificity for absent survival at one year of 100 % versus 90 % for GCS of 3. 

Description of the FOUR Score


The FOUR score has 4 components: eye responses, motor responses, brainstem reflexes, and respiration pattern. Each component has a maximal value of 4 (Figure 1). Assessing all components of this score usually takes only a few minutes.5 The eye response component of the FOUR score allows differentiation between a vegetative state (eyes open but do not track) and a locked-in syndrome (eyes open, blink, and track vertically on command). The motor assessment component of the FOUR score combines the withdrawal reflex and decorticate rigidity responses because these conditions are often difficult to distinguish clinically. The motor component includes a complex command (the patient is asked to produce a thumbs-up hand signal, a fist, and the peace sign) that determines whether patients are alert.7 Similarly, the motor component of the FOUR score can detect signs of severe cerebral dysfunction, such as myoclonic status epilepticus. Such dysfunction is often a poor prognostic sign for patients with suspected anoxic brain injury.8 The brainstem components of the FOUR score assess the pons, the mesencephalon, and the medulla oblongata in various combinations. The FOUR score also includes an assessment of Cheyne-Stokes respiration and irregular breathing; such signs can indicate bihemispheric or lower brainstem dysfunction of respiratory control. For patients who have undergone intubation, the FOUR score records the presence or absence of a respiratory drive.

FIGURE 1.


Description of Full Outline of UnResponsivenes (FOUR) score. Eye response: E4 = eyelids open or opened, tracking, or blinking to command; E3 = eyelids open but not tracking; E2 = eyelids closed but open to loud voice; E1 = eyelids closed but open to pain; E0 = eyelids remain closed with pain. Motor response: M4 = thumbs-up, fist, or peace sign; M3 = localizing to pain; M2 = flexion response to pain; M1 = extension response to pain; M0 = no response to pain or generalized myoclonus status. Brainstem reflexes: B4 = pupil and corneal reflexes present; B3 = one pupil wide and fixed; B2 = pupil or corneal reflexes absent; B1 = pupil and corneal reflexes absent; B0 = absent pupil, corneal, and cough reflex. Respiration pattern: R4 = not intubated, regular breathing pattern; R3 = not intubated, Cheyne-Stokes breathing pattern; R2 = not intubated, irregular breathing; R1 = breathes above ventilatory rate; R0 = breathes at ventilator rate or apnea.

The Broken Heart Syndrome

llan Wittstein has published and given lectures and states there are clinical criteria, diagnostic criteria and treatment and prognosis information that can be readily identified. Synonyms include neurogenic stunned myocardium, acute coronary syndrome, stress myocarditis, and Takotsubo syndrome (named after the japanese pot used to capture octopus).  The syndrome is a REVERSIBLE disorder with very abnormal EKG, U waves, ST elevations, Q waves, elevated troponins, normal coronaries on cath, and return of EF to normal within days to weeks.  The pathology includes contraction band necrosis in myocardium, and is linked to hypersympathetic state.  It is a huge problem involving 2 percent of patients undergoing cath and 5-7 % of women.  Most patients are postmenopausal Caucasian women with risk factors who present with chest pain and shortness of breath.  Many have mood disorders


Diagnostic criteria are divided into "helpful" and "required"
HELPFUL-
1.  Acute trigger-- could be emotional (anxiety, joy, grief, fear, anger) or physical (procedure, respiratory drugs) even surprise party. 
2.  Characteristic EKG-- presenting EKG has steep ST elevation without reciprocal changes, T wave inversions everywhere, QT prolongation,  that becomes milder within 2-4 days
3.  Troponin elevation is mild-- less than 5, never more than 20

REQUIRED
1.  Absent coronary thrombosis
2.  Wall motion abnormalities extend beyond a single coronary artery territory  ( 3 patterns:  apical, basal, and midventricular)
3.  Rapid recovery of systolic function within 2 weeks at most

Diagnostic tests that are helpful (but possibly hard/unlikely to obtain esp. acutely)
1.  MRI heart unlike ECHO differentiates dead and stunned tissue.  Dead cardiac tissue lights up with Gadolinium but stunned heart will not

Therapy:
1.  supportive-- possibly not in ICU- arbs, ACEi's, diuretics.  Anticoag if apex not moving to prevent clot kicking, avoid pressors (catechols are a problem)
2.  Balloon pump better than pressors
3.  HHH  good for brain, bad for heart

Prognosis
1.  recurrence 3-10 percent with 2 % mortality
2.  Death is due to etiology not to cardiac dysfunction per se.

Pathophysiology
contraction band necrosis- direct myocyte injury related to calcium overload.

air embolism and air travel

The Neurologist 2010   A  62 year old woman with cerebral artery air embolism during commercial air travel.  16: 136-137.

 

Notes

usual list of associations with air embolus-- surgery, scuba diving, induced abortion, angiography and pneumothorax, orogenital sex on a woman with cerebral air emboli (see Crit Care Med 1988).

A new one is air travel.  In this case, pulmonary bullae due to emphysema occurred as the bullae expanded as the pressure in the cabin was reduced, leading to rupture of the bullae, pneumothorax and air embolism.  Barotrauma was presumably the proximate cause.

Pearls on pediatric strokes

hat tip to Lori Jordan MD JHU


1.  Strokes in kids are as common as brain tumors, about 2-3/100,000
2.  In children ICH = bland infarcts, different than adults (Fullerton, Neurology, 2003).  ICH is often due to AVM's
3.  Among bland infarcts, 25-35 % are cardioembolic, 25 % are dissections, other unusual causes include moya moya, sickle cell disease, HIV and varicella (not in order).
4.  Subarachnoid hemorrhage in kids is usually aneurysmal
5.  Kids at risk often have an inciting event such as trauma or surgery
6.  Kids have a high risk of delay in diagnosis
7.  Sicklers have 10 % stroke, but 20 % more of silent stroke; with SCA and CVA stat consult Hematology for transfusion
8.  Many barriers to alteplase use exist, including diagnosis, , lack of evidence and mimics, and delays, but document why alteplase is not given
9.  MERCI and multi MERCI are not studied in kids
10.AHA guidelines for pediatric stroke published Stroke 2008
11.  Presentation in children is much more likely to include seizure (25 % v. 5 % in adults)
12 . Suggested eval: MRI, MRA H/N, hypercoagulability workup complete, TTE/bubble, HB electropheresis, HIV,
13 references
Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, et al.
Management of stroke in infants and children: A scientific statement from a
special writing group of the american heart association stroke council and the
council on cardiovascular disease in the young. Stroke 2008;39:2644-91.
• Amlie-Lefond, C. et al. Use of alteplase in childhood arterial ischaemic stroke: a
multicentre, observational, cohort study. 2009: Lancet Neurol. 8, 530-536.
• Jordan LC, Johnston SC, Wu YW, Sidney SS, Fullerton HJ. The importance of
cerebral aneurysms in childhood hemorrhagic stroke: a population-based study.
Stroke 2009;40:400-405.
• Beslow LA, Licht DJ, Smith SE, Storm PB, Heuer GG, Zimmerman RA, Feiler
AM, Kasner SE, Ichord RN, Jordan LC. Predictors of outcome in childhood
intracerebral hemorrhage: a prospective consecutive cohort study. Stroke 2009;

CAA with vasculitis and edema responsive to steroids references

inflammation related CAA as described in : Ann Neurol 2004; 55: 250-256; Brain 2005; 128: 500-515; Neurology 2007; 68 (17); 1411-1416.

ISC Abstract highlights 2010 San Antonio (pruned and edited)

1.  Restrepo et al. (UCLA) Stroke pretreatment screening for fast Mag trial, involved a 90 second screen with a neurologist, focused, 72 % of patients so diagnosed had acute ischemic stroke, 24 % ICH, rest other

2.  Albright et al. (Penn) studied the potential for the use of air ambulances to increase availability of services and found The combination of pre-hospital regionalization & air ambulance transport of acute stroke
patients would reduce the 135.7 million Americans without 60 minute access to a PSC by
half, to 62.9 million.

3.  Kleindorfer et al. (Cincinatti) stratified t-PA eligibility by age and found contrary to hypothesis, the eligibility for rt-PA significantly increased with increasing age.
Age-Based Eligibility for and Treatment with Rt-PA
Age of Pt           #  Patients           % Eligible for rt-PA  % of Eligible Treated
18–44                   97                        4 (4.1%)              2 (50.0%)
45–54                 219                       15 (6.8%)             5 (33.3%)
55–64                 320                       21 (6.6%)            12 (57.1%)
65–74                 392                       32 (8.2%)            20 (62.5%)
75–84                 502                       47 (9.4%)             23 (48.9%)
85                       300                       29 (9.7%)             10 (34.5%)
Total                  1830                     148 (8.1%)             72 (48.6%)

4.  Riccio et al (Buenos Aires) Occult v. non -occult AF compared in TIA and AIS. Age, female gender and left atrial area (LAA) are traditional determinants of AF.  Out of 194 patients, there were 36 with known AF and 24 with occult AF.  Patients with occult AF were younger, showed a higher proportion of males, had
a smaller LAA, and had more severe strokes. Traditional determinants of AF were associated
with known AF.Diabetes was associated with occult AF.

5.   Gupta et al. (multicenter) General anesthesia during stroke resulted in worse outcomes.

Infective endocarditis and stroke: pearls

.  The classic triad of infective endocarditis and stroke of fever, murmur and acute neurologic deficit is uncommon, occurring in less than half of patients, with murmur occurring in less than one third (due to decline of valvular disease as a cause) ; fever, embolism and high sed rate may also be seen in NBTE, arteritis with PAN, other rheumatologic disease, or atrial myxoma. 


2.  Organisms are more diverse than previously with Streptococcus representing only 60 percent, including resistant Group D Strep viridans (enterococcus faecalis) and Strep bovis  (associated with GI neoplasia).  Staph aureus is seen in up to 30 % especially those with i-v drug abuse, recent surgery, and no preexisting valve lesion. Patients with prosthetic valves may get S aureus and S epidermidis.  Others, including immunocompromised may get HACEK bacteria and fungi ( hemophilus, actinobacillus, cardiobacterium, Eikinella, Kinzella).  Among pretreated groups, culture negative disease has increased to 5.5 %.


3. Early onset (at presentation of first 48 hours) of neurologic symptoms is more common with Staph aureus than with streptococcal infections, that can occur late (54 v 19 %).  Late embolism is especially common among patients with prosthetic valves (14/15 late strokes in one series had prosthetic valves).  In native valve endocarditis, anticoagulation is of no benefit , certainly for at least 48 hours or until infection is controlled.


4. Cardiac vegetations initially larger than 10 mm are high risk, and are best seen with TEE rather than TTE.  Embolic rate is much higher in presence of visible lesions, and vice versa, visible lesions are much more common among patients with detectable emboli.  The 10 mm size may "open the debate" about the need for valve replacement.


5.  The discovery of endocarditis without emboli does not dictate the cessation of otherwise needed anticoagulant therapy. 


6.  If cardiac surgery is needed, timing is dictated by common sense.  One such protocol is to wait at least five days (until the edema of the stroke has settled) before considering operation, if possible.


7.  Use heparin fairly early on (certainly within 48 hours) of stroke with prosthetic valves with endocarditis, especially if subclinical INR was found on presentation.  Discontinue anticoagulation if possible in most cases of fungal endocarditis.


8.  Intracranial hemorrhage (3-6 % of patients) occurs with aneurysm rupture, septic arteritis, conversion of a bland infarct, and late effects of immune deposition.  Septic bacterial aneurysms may occur at distal branch points, but mycotic aneurysms, large ones, may occur proximally.  However, one study suggested the vast majority of patients with aneurysms had abnormal CT scan.  Present blood on CT or (if headache is present) pleocytosis on CSF examination weighs towards four vessel angiogram. 


9.  Serial angiography is indicated for mycotic aneurysms which may heal  with antibiotics.


10.  Special concern exists among patients with line induced sepsis and bland infarction that could result in late S Aureus superinfection of an initially bland infarct.  Full infective endocarditis treatment regimen may be warranted in these patients and TEE may alternatively show evidence of vegetations. 


Unknown angles
1.  Role of MRA/ CTA
2.  When surgery is required

Percentage of patients with stroke with prior TIA

Hackam DG, Kapral  MK, Wang JT et al.  Most stroke patients do not get a warning: a population based cohort study.  Neurology 73: 1074-1075, 2008.

cites data suggesting 17 % of CVA patients have prior TIA.  Authors review 16, 409 charts.  Timing of TIA is not addressed. 12.4  % had prior TIA, but 20% of those with large arter TIA's, much lower with hemorrhagic stroke (5%), somewhat higher with ischemic stroke (15 %).  Risk factors to have prior TIA: older, DM, HTN, AF, CHF,angina, PAD. Patients without TIA were more likely to die in  hospital, arrest, or not be discharged to home. 

covered stents for carotids

The use of covered stents for the endovascular treatment of extracranial internal carotid artery stenosis: a prospective study with a 5-year follow-up; Szólics A, Sztriha LK, Szikra P, Szólics M, Palkó A, Vörös E; European Radiology

 

OBJECTIVES: To evaluate the safety and feasibility of the use of covered stents for the treatment of extracranial carotid artery stenosis caused by highly embologenic plaques, and to study the long-term outcome of patients receiving such covered stents. METHODS: Between 2002 and 2007, 46 patients (63% symptomatic, 78.3% male, 67 +/- 8.6 years old) with internal carotid artery stenosis caused by embologenic plaques or restenosis were treated with self-expanding covered stents (Symbiot, Boston Scientific). Pre-dilatation or protecting devices were not used. Post-dilatation was applied in every patient. Each patient was followed long-term. The outcome measures were the occurrence of neurological events, and the development of in-stent restenosis, as detected by clinical examination and duplex ultrasound. RESULTS: The technical success rate of stenting was 100%. There were no neurological complications in the peri-procedural period. The mean follow-up period was 34.3 +/- 27.7 months (the rate of patients lost to follow-up was 15.2%) during which no stroke or stroke-related deaths occurred. Restenosis was detected in 3 patients (6.5%). CONCLUSION: Covered stents provide efficient peri- and post-procedural protection against neurological complications due to embolisation from high-risk plaques during carotid artery stenting. Restenosis of covered stents appears to be infrequent during long-term follow-up.

hemodialysis causes cerebral microbleeds in about one fourth

Cerebral microbleeds in predialysis patients with chronic kidney disease; Shima H, Ishimura E, Naganuma T, Yamazaki T, Kobayashi I, Shidara K, Mori K, Takemoto Y, Shoji T, Inaba M, Okamura M, Nakatani T, Nishizawa Y; Nephrology Dialysis Transplantation (Dec 2009)

BACKGROUND: Gradient-echo T2*-weighted magnetic resonance imaging (T2*-weighted MRI) is highly sensitive for detecting cerebral microbleeds (CMBs). CMBs have been reported to be a risk factor for future cerebrovascular events and a marker of cerebral small vessel disease in the general population. Chronic kidney disease (CKD) is an independent risk factor for cardiovascular disease. The relationship between CKD and CMBs, which has not been clarified to date, is examined. METHODS: In this cross-sectional study, T2*-weighted MRI of brain was performed with a 1.5-T MRI system in 162 CKD patients (CKD stages 1-5, excluding CKD stage 5(D)) and 24 normal subjects. RESULTS: CMBs were found in 35 CKD patients (25.6%), but not in control subjects. CMBs were more prevalent in male patients, in those with higher blood pressure, advanced age and poor kidney function. There was a significant association between the prevalence of CMBs and the CKD stage, with higher prevalence of CMBs as the CKD stages advanced (P<0.01). Estimated glomerular filtration rate was a significant factor associated with the prevalence of CMBs, independent of age, gender and hypertension. There was no significant relationship between CMBs and the presence of diabetes mellitus and dyslipidemia. CONCLUSIONS: Decreased renal function is a significant risk factor for CMBs, independent of the presence of hypertension. Poor kidney function could be associated with future cerebrovascular events.

Viagra and stroke

The effect of sildenafil citrate (Viagra) on cerebral blood flow in patients with cerebrovascular risk factors; Lorberboym M, Mena I, Wainstein J, Boaz M, Lampl Y; Acta Neurologica Scandinavica (Dec 2009)

 

Objectives - Sildenafil citrate is widely used for erectile dysfunction. The present study examined the short-term effects of sildenafil administration in individuals with cerebrovascular risk factors, including patients with a history of stroke. Materials and Methods - Twenty-five consecutive male patients with erectile dysfunction and vascular risk factors were included in the study. A perfusion brain SPECT study was performed at baseline and 1 h after the oral administration of sildenafil. Results - Associations between any of the risk factors and the perfusion scores were not detected, with the exception of stroke. Stroke patients showed significantly more areas with diminished perfusion after sildenafil administration compared to baseline. Conclusions - In patients with diabetes or hypertension, a dose of 50 mg sildenafil does not appear to produce detrimental effects on cerebral blood flow. However, patients with a history of stroke may be at increased risk of hemodynamic impairment after the use of sildenafil.