(cpni bulletin) - neurointerventional services edition - california

CALIFORNIA PACIFIC Neuroscience Institute BUllETIN

SUMMER 2013

IN THIS ISSUE

Endovascular Treatment of Acute Ischemic Stroke

Hemorrhagic Stroke

California Pacific Neuroscience Institute BULLETIN

SUMMER 2013

CONteNts

2 Endovascular Treatment of Acute Ischemic Stroke

8 Hemorrhagic Stroke

14 Active Neuroscience Research Trials Through California Pacific Medical Center Research Institute

15 Neuroscience Institute Quick-Reference Guide

PROJECT DIRECTOR Brian T. Andrews, M.D., FACS, FAANS

PROJECT COORDINATOR lauren Fleming

CEREBROVASCUlAR SERVICES MANAGER Nila Camino

PHOTOGRAPHER Bill Posner

GRAPHIC DESIGNER Beverly Snydercpmc.org/neuroscience

cpmc.org/neuroscience

In this issue of the CPNI Bulletin, the focus is on our

robust neurointerventional service. since the 1980s

endovascular techniques have continually advanced

in the treatment of cerebrovascular disorders such as

acute stroke, aneurysmal subarachnoid hemorrhage,

arteriovenous malformations and fistulas, and in such

areas as tumor embolization for head, neck and brain

tumors. since the publication of the seminal IsAt

trial, the standard of care for treatment of intracranial

aneurysms has become that of endovascular coil

placement rather than surgical clipping when technically

feasible. the CPNI now offers the highest level of

expertise and technology, with experts from the fields

of neurology, neuroradiology and neurosurgery working

together in our dedicated neurointerventional suite,

located in the operating rooms of the Davies Campus.

this suite, designed for both endovascular and open

microsurgery, provides state-of-the-art diagnostic

imaging, real-time 3-D processing and intraoperative

neurophysiologic monitoring to enhance patient

safety. each patient is offered individualized care

coordinated by our team, and every patient is managed

in the neurointensive care unit by our stroke service

in concert with the neurointerventional experts and

neurosurgeons. I applaud their efforts.

sincerely,

Brian T. Andrews, M.D., FACS, FAANS Chairman, Department of Neurosciences

1

by Joey D. English M.D., Ph.D. Neurointerventional Radiology

ENDOVASCULAR TREATMENT OF Acute Ischemic Stroke

Overview of Acute Ischemic stroke (AIs)

The abrupt occlusion of an intracranial

artery typically results in acute

cerebral ischemia and immediate focal

neurological symptoms. The specific

neurological deficits experienced by the patient

are related to the functional anatomy of the

brain tissue experiencing compromised blood

supply, with common symptoms being unilateral

weakness of the face, arm and/or leg, difficulty

with language production or comprehension,

visual field disturbances, slurred speech,

unilateral incoordination and/or unilateral sensory

loss. Without prompt restoration of blood flow

through the occluded vessel, cerebral infarction

(permanent neuronal cell death) and persistent

neurological deficits can occur.

C A L I F O R N I A P A C I F I C N e u R O s C I e N C e I N s t I t u t e B u L L e t I N 2

ENDOVASCULAR TREATMENT OF

Acute Ischemic Stroke

these acute ischemic strokes account for approximately 85% of all strokes (with the remaining ~15% being related to rupture of a cerebral blood vessel giving a hemorrhagic stroke), and their individual and societal burden is hard to overstate: Approximately 750,000 AIss occur annually in the united states alone, and AIs remains the third leading cause of death and the leading cause of adult disability.

C A L I F O R N I A P A C I F I C M e D I C A L C e N t e R 33


Acute Ischemic Stroke Caused by Large Vessel Occlusions

Acute ischemic stroke pathology can be divided

into small vessel occlusions versus large vessel

occlusions. “small vessel” occlusion refers to an

acute blockage of one of many 200-400 micron

diameter perforating arteries that arise off of

the proximal aspects of the great vessels of the

intracranial circulation (e.g., lenticulostriates of

the proximal middle or anterior cerebral artery,

brainstem perforators of the basilar artery). these

“lacunar” stroke syndromes are likely caused by

in situ thrombotic occlusion of an individual

perforator. Large vessel occlusion (LVO), by

comparison, describes the acute blockage of a

proximal great vessel (e.g., M1 segment of a middle

cerebral artery) or one or more of its distal cortical

branches. LVOs are typically embolic in nature, with

thrombus originating from a proximal source such as

atrial fibrillation or cervical carotid atherosclerosis.

LVOs now account for 40-50% of all acute ischemic

strokes, and this percentage is likely to only increase

as the population ages and the prevalence of atrial

fibrillation rises. Not surprisingly, given the large area

of cortical tissue usually supplied by large intracranial

vessels, LVO-related AIs is clinically more severe

than small vessel lacunar stroke syndromes, leading

to a 4.5-fold increase in mortality and a 3-fold

reduction in the likelihood of a good long-term

functional outcome1. And while both large

vessel and small vessel occlusion AIs patients

benefit from treatment with intravenous tPA,

LVOs respond only very modestly to this

therapy. A patient with an acute occlusion of a

proximal middle cerebral artery will experience

spontaneous recanalization in a clinically

meaningful time window approximately

15-20% of the time; this recanalization rate

increases to 30-35% with intravenous tPA

administration. these data demonstrate that

65-70% of patients with a middle cerebral

artery occlusion will not recanalize with

intravenous tPA therapy. three quarters

of these patients will suffer significant long-

term disability.

While the observations that LVO ischemic

strokes are common, clinically severe and

poor responders to intravenous tPA therapy

are sobering, the encouraging news is that a

significant amount of data demonstrate that

successful recanalization of the occluded

vessel correlates with a markedly improved

chance of a favorable long-term functional

outcome. One meta-analysis of 33 studies of

988 LVO patients found a 58.1% rate of good

functional outcome and 14.4% mortality in

patients that had successful revascularization

of their LVO, compared to a 24.1% rate

of good functional outcome and a 41.6%

mortality in patients without successful

LVO revascularization2. these data suggest

that any treatment that can improve timely

revascularization of an LVO can dramatically

improve a patient’s chance for a good

neurological outcome.the development and

advancements of endovascular therapies for

LVO acute stroke patients has been driven by

this idea.


Endovascular Therapy for Acute Large Vessel Occlusions: Treatment Options and Device Evolution

Direct intra-arterial delivery of a thrombolytic agent

into an intracranial LVO using trans-femoral artery

micro-catheterization has been investigated since

the 1980s. the best data supporting this approach

come from the PROACt-II trial3, a randomized

double-blinded study in which patients with middle

cerebral artery occlusions who were ineligible for

treatment with intravenous tPA were randomized to

intra-arterial infusion of a thombolytic (pro-urokinase)

or intra-arterial sham infusion of saline. successful

recanalization was achieved in 66% of patients

A B

C

treated with intra-arterial thrombolytic but

in only 18% of patients treated with intra

arterial saline. this significant increase in

recanalization correlated with a significant

improvement in neurological outcome (40%

versus 25%). Despite these data, originally

published in 1999, intra-arterial thrombolysis

has never achieved FDA approval, and

pro-urokinase is no longer commercially

available. Many stroke centers, including our

institution, continue to utilize this approach in

specific situations using off-label use of intra

arterial tPA.

the major advances over the past five to

10 years in endovascular acute ischemic

stroke treatment, however, have been in the

development of mechanical thrombectomy

devices. such devices are designed to

engage and physically remove occlusive

thrombus from the target intracranial artery.

the Merci Retriever, a wire-based corkscrew

shaped device, was first approved in 2004.

the Penumbra reperfusion system, a

microcatheter device designed to macerate

and aspirate thrombus, was subsequently

FDA approved in 2008. While both devices

were important mechanical thrombectomy

pioneers, neither proved to have the impact

desired, namely the ability to achieve a high

rate of successful revascularization in a safe

and timely fashion. From this experience,

however, newer and more efficient devices

have emerged.

stent retriever devices are novel self-

expanding non-detachable stents that are

deployed across the thrombus burden of

an LVO. After allowing the stent retriever to

expand and engage the occlusive thrombus,

A. Right internal carotid

angiogram demonstrating

occlusion of the proximal right

middle cerebral artery.

B. Angiogram following removal

of occlusive thrombus using

an endovascular stent retriever

device, showing complete

recanalization.

C. Stent retriever device and

thrombus removed from patient’s

right middle cerebral artery. continued



the device is then retrieved from the intracranial

circulation, thereby physically removing the clot.

two stent retrievers, the solitaire and trevo

devices, were approved by the FDA in 2012 after

clinical trials demonstrated that each was clearly

superior to the Merci Retriever device in both

recanalization rates and safety profiles (e.g., 86%

successful recanalization with trevo compared

to 60% with Merci), with improved clinical

outcomes4,5. Overall, these stent retriever devices

represent a dramatic advancement in the ability

to quickly, safely and successfully treat acute

ischmic stroke patients presenting with large

vessel occlusions.

Endovascular Therapy for Acute Large Vessel Occlusions: Image-Based Patient Selection

the duration of time since symptom onset

has classically been the primary criteria for

identifying which AIs patients might benefit

from either intravenous or endovascular

therapies. Intravenous tPA is typically offered

within 3 to 4.5 hours of symptom onset, while

endovascular therapies were initially studied

within the first 6 to 8 hours of symptoms.

symptom duration, however, is likely a poor

surrogate for predicting an individual patient’s

tissue viability, as this is largely determined by

the nature of the individual’s unique intracranial

collateral circulation and ischemic tolerance.

these observations have driven intense

interest in the use of Ct or MR perfusion

imaging of tissue viability as a better means of

identifying patients most likely to benefit from

endovascular therapy6.

CT perfusion scan of a patient with an occlusion of

the right middle cerebral artery. The mean transit

time data (upper three panels) demonstrates the

volume of tissue at risk for infarction (dark blue

area), while the cerebral blood volume data (lower

three panels) suggests that this territory remains

salvageable if blood flow can be restored.


Endovascular Therapy for Acute Large Vessel Occlusions: Current State of the Art

the development of stent retriever devices has

dramatically improved our ability to quickly and

safely achieve successful recanalization of AIs

patients presenting with a LVO. Advancements

in image-based patient selection, specifically

dynamic perfusion imaging, has allowed us to offer

endovascular therapy beyond the typical 6- to

8-hour time window. the combination of the two

has markedly altered our approach to endovascular

treatment of AIs, and much preliminary data

from our institution and others suggest significant

improvements in the long-term clinical outcomes

in these patients. the use of stent-retrievers and

image-based patient selection is currently being

studied in multiple rigorous clinical trials.

At CPMC, the neurointerventional

service and the stroke neurology service

have worked jointly to advance this

approach to the endovascular treatment

of AIs, and we currently have one of

the most active acute stroke programs

along the West Coast. Our goal is to

be leaders in advancing all aspects of

the endovascular treatment of AIs, with

the ultimate motivation of improving the

long-term neurological outcome of the

patients we are privileged to treat.

References

1. significance of large vessel intracranial occlusion causing acute ischemic stroke and,tIA. smith Ws, Lev MH, english JD, Camargo eC, Chou M, Johnston sC, Gonzalez G, schaefer PW, Dillon WP, Koroshetz WJ, Furie KL. Stroke. 2009 40(12):3834-40.

2. the impact of recanalization on ischemic stroke outcome: a meta-analysis. Rha JH, saver JL. Stroke. 2007 38(3):967-73.

3. Intra-arterial prourokinase for acute ischemic stroke. the PROACt II study: a randomized controlled trial. Prolyse in Acute Cerebral thromboembolism. Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, Kase C, Pessin M, Ahuja A, Callahan F, Clark WM, silver F, Rivera F. JAMA. 1999 282(21): 2003-11.

4. trevo versus Merci retrievers for thrombectomy revascularisation of large vessel occlusions in acute ischaemic stroke (tReVO 2): a randomised trial. Nogueira RG, Lutsep HL, Gupta R, Jovin tG, Albers GW, Walker GA, Liebeskind Ds, smith Ws; tReVO 2 trialists. Lancet. 2012 380(9849):1231-40.

5. solitaire flow restoration device versus the Merci Retriever in patients with acute ischaemic stroke (sWIFt): a randomised, parallel-group, non-inferiority trial. saver JL, Jahan R, Levy eI, Jovin tG, Baxter B, Nogueira RG, Clark W, Budzik R, Zaidat OO; sWIFt trialists. Lancet. 2012 380(9849):1241-9.

6. Advanced imaging to extend the therapeutic time window of acute ischemic stroke. Fisher M, Albers GW. Ann Neurol. 2013 73(1):4-9.


by Warren T. Kim, M.D., Ph.D. Neurointerventional Radiology

HemorrhagicStroke

8 C A L I F O R N I A P A C I F I C N e u R O s C I e N C e I N s t I t u t e B u L L e t I N

Hemorrhagic

Hemorrhagic stroke from acute rupture of a cerebral blood vessel is

a devastating disease, and more common than generally appreciated.

In the united states, the annual incidence of hemorrhagic stroke is

approximately 30 per 100,000 people1 .

While representing only a small (15%) subset of all

strokes, hemorrhagic stroke is particularly

deadly and destructive: thirty-day mortality is

approximately 50%, and 50% of the survivors

suffer significant permanent disability.

Although frequently related to hypertensive small

vessel disease, many hemorrhagic strokes are due to

rupture of a discrete cerebrovascular lesion.

In the case of spontaneous subarachnoid

hemorrhage, about 85% are from a ruptured

intracranial aneurysm. Other vascular causes include

arteriovenous malformation, arteriovenous fistula,

dissection, and vasculopathy/vasculitis.


Emergency Diagnosis and Management: The Crucial Early Steps

emergency medical technicians and emergency

department physicians are often the first responders

in treating hemorrhagic stroke. Patients typically

present with severe “thunderclap” headache,

nausea and vomiting, confusion or altered level

of consciousness, seizure, aphasia, and/or focal

weakness or numbness. Risk factors include

advanced age, hypertension, smoking, alcohol

abuse, amphetamine or cocaine abuse, and

coagulopathy/anticoagulant therapy.

essential initial treatment involves basic life support,

control of blood pressure, treatment of seizures,

management of bleeding/coagulopathy, control

of intracranial pressure, and sometimes emergent

ventriculostomy. Initial diagnostic work-up involves

a detailed neurologic exam and non-invasive

imaging, typically a head Ct scan, which might show

subarachnoid, intracerebral, and/or intraventricular

hemorrhage that implicates an underlying

cerebrovascular lesion such as an aneurysm or

arteriovenous malformation. If the patient has a

compelling story for intracranial hemorrhage, but

presents in a delayed fashion (when Ct may not

detect subacute blood), lumbar puncture and CsF

analysis may be indicated.

High Level Multidisciplinary Care for High-Risk Cerebebrovascular Lesions

When the clinical and radiologic findings confirm

intracranial hemorrhage and suggest an underlying

cerebrovascular lesion, the patient’s survival and

prognosis depend on receiving immediate high

level care at a tertiary center with the facilities and

expertise to manage these complex problems2.

California Pacific Medical Center is a Joint

Commission Certified stroke Center committed to

providing the most advanced and comprehensive

care for patients with stroke. Our stroke

Neurologists employ a telemedicine network to

provide around-the-clock service to many

sutter-affiliated and other hospitals throughout

Northern California.


Biplane high resolution digital subtraction

angiography and 3-D rotational angiography

for the definitive diagnosis and endovascular

treatment of a large bilobed supraclinoid

internal carotid artery aneurysm.

Our neurointerventionalists have unsurpassed training and expertise in the diagnosis and treatment of cerebrovascular diseases, one with additional subspecialty training in stroke Neurology and Neurocritical Care Medicine, the other in Diagnostic Neuroradiology.

In our neurological intensive care unit, close

monitoring, blood pressure control, and

cardiopulmonary support are provided for altered

level of consciousness, neurocardiogenic injury and

respiratory failure. seizures, intracranial pressure,

hydrocephalus, cerebral edema and mass effect

are carefully managed, with ventriculostomy,

craniectomy and open surgery provided by the

Neurosurgery service. using advanced non

invasive imaging technology, including a 64-slice

Ct scanner with Ct angiography and perfusion

mapping capability, as well as a 3-tesla MRI with

MR angiography and venography, we can often

diagnose even small 2-3 mm aneurysms and

other hemorrhagic lesions. If not, our dedicated

neurointerventional suite is a state-of-the-art facility,

with a biplane high-resolution digital angiography

system with rotational capability for real-time 3-D

processing and analysis, optimized to detect

even the subtlest cerebrovascular pathology,

and to provide the most detailed views for

treatment planning.

Cerebral Aneurysms

An intracranial aneurysm is a focal out-pouching

or ballooning of an arterial wall that develops

due to chronic hemodynamic stress at a point

of weakness, typically at a branch point (e.g.,

anterior communicating artery, middle cerebral

artery bifurcation, carotid terminus, posterior

communicating artery and basilar terminus).

Aneurysms are actually quite prevalent, with a

conservative estimate of 5 million people in the

united states thought to have an aneurysm.

However, most are asymptomatic and may never

cause a problem3. Nonetheless, in at least 0.5%

of cases, an aneurysm can slowly grow and

weaken, much like a balloon as it stretches, and

ultimately rupture.

When an acutely ruptured aneurysm is discovered,

the next step is to clearly define its anatomy with

a catheter angiogram, determining its size, shape,

location, and the precise relationship of the parent

vessel, aneurysm neck, and nearby branches. Given

that a recently ruptured aneurysm has a high risk for

catastrophic re-bleed, a decision can immediately be

made about how best to treat the aneurysm, either

endovascularly or by open surgery4,5.

Minimally invasive endovascular treatment involves

navigating a microcatheter through the blood vessels

and into the aneurysm itself, then packing small,

soft, thread-like platinum coils within the aneurysm

sac until it clots and is secured. Where the anatomy

is less favorable, a small balloon can be transiently

inflated in the parent vessel to help position the coils

in the aneurysm. Alternatively, a stent can be placed

in the parent vessel, serving as a retaining lattice to

pack coils in the aneurysm while leaving the parent

vessel patent.

When an aneurysm is not readily amenable to

endovascular treatment (e.g., very small, wide-

based, branch originating off the sac), open

microvascular neurosurgery is the definitive

alternative treatment, where a craniotomy is

performed and a surgical clip closed around the

neck of the aneurysm, occluding its connection with

the parent vessel. When an unruptured aneurysm

is discovered incidentally, it can be thoroughly

evaluated and observed over time, and electively

treated if there are high-risk features, e.g., larger

size (greater than 7 mm), posterior circulation or

posterior communicating artery, daughter lobule,

symptomatic, enlarging, or history of prior

ruptured aneurysm.

continued


At CPMC, our neurology, radiation oncology, neurosurgery, and neurointerventional teams work together to offer coordinated multidisciplinary treatment to maximize the chance of cure and minimize the overall risk.

Arteriovenous Malformations

A cerebral arteriovenous malformation (AVM) is a

cluster or nidus of abnormally formed blood vessels,

with arteriovenous shunting of high-pressure

arterial flow directly into veins,

generally considered congenital/

development in etiology. there

are sometimes aneurysms in the

nidus itself or in a feeding artery,

which are related to the chronic

high flow. Hemorrhage from an

AVM can result from rupture of

a recipient vein under the stress

of high-pressure flow, or of a

nidal or feeding artery aneurysm.

unruptured AVMs often present

with seizures, but also sometimes

headache, progressive neurological

deficit or incidentally.

Diagnosis and characterization of

an AVM involves an MRI and MR

angiography as well as catheter

angiography to determine the size, margins, and

location of the nidus, feeding arteries, draining veins,

and presence of nidal or feeding artery aneurysms.

Ruptured AVMs have a high risk for catastrophic

re-bleed, particularly during the first year after

hemorrhage, while untreated unruptured AVMs

have an annual risk of hemorrhage of approximately

2%. therefore, management of cerebral AVMs

involves considering the patient’s age, co-morbidities,

and life expectancy, and weighing the prospective

lifetime risk of hemorrhage versus the up-front risk

of treatment6.

Options include medical management (e.g. control

of blood pressure and seizures), stereotactic

radiosurgery to precisely target the nidus and slowly

obliterate the AVM (best for small and unruptured

AVMs, given the risk of radiation injury and 3-year

latency to effect), open microsurgical resection

(best for small, superficial AVMs), and endovascular

embolization with n-BCA glue, Onyx, coils, or

PVA particles to occlude the feeding arteries and

penetrate the nidus (usually to decrease the AVM

size or risk of hemorrhage prior to radiosurgery or

open surgery, but occasionally curative alone).

Vasospasm in the Aftermath of Subarachnoid Hemorrhage: “Adding Insult to Injury”

subarachnoid hemorrhage-related vasospasm is

narrowing of the intracranial arteries due to irritation

from surrounding blood breakdown products,

typically occurring during the first 14 days after

hemorrhage, peaking between 7 to 10 days. If

sufficiently severe, this narrowing can become flow-

limiting and cause ischemia and infarcts, resulting in

severe disability and death in up to 10% of patients.



References

1. Roger VL, Go As, Lloyd-Jones DM, Benjamin eJ, Berry JD, Borden WB, et al. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. Jan 3 2012;125(1):e2-e220.

2. Morgenstern LB, Hemphill JC 3rd, Anderson C, Becker K, Broderick JP, Connolly es Jr, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American stroke Association. Stroke. sep 2010;41(9):2108-29.

3. Wiebers DO, Whisnant JP, Huston J 3rd, et al.: unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 362:103–110, 2003.

4. Molyneux AJ, Kerr Rs, Yu LM, Clarke M, sneade M, Yarnold JA, et al. International subarachnoid aneurysm trial (IsAt) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. sep 3-9 2005;366(9488):809-17.

5. McDougall CG, spetzler RF, Zabramski JM, Partovi s, Hills NK, Nakaji P, et al. the Barrow Ruptured Aneurysm trial. J Neurosurgery. Jan 2012;116(1):135-44.

6. Ogilvy Cs, stieg Pe, Awad I, Brown RD Jr, Kondziolka D, Rosenwasser R. AHA scientific statement: Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the stroke Council, American stroke Association. Stroke. Jun 2001;32(6):1458-71.

7. Abruzzo t, Moran C, Blackham KA, eskey CJ, Lev R, Meyers P, et al. Invasive Interventional Management of Post- hemorrhagic Cerebral Vasospasm in Patients With Aneurysmal subarachnoid Hemorrhage. J NeuroIntervent Surg. 2012;4(3):169-177.

Optimal management in the ICu involves vasodilator

therapy, close neurological monitoring and

surveillance transcranial Doppler ultrasounds, Ct

angiography and perfusion

analysis, and so-called “triple

H” therapy (hypertension,

hypervolemia, and

hemodilution). When neurologic

changes or non-invasive

imaging suggests symptomatic

or ominous worsening

vasospasm despite best

medical management, catheter

angiography is performed to

accurately assess the degree

of narrowing and flow limitation.

If significant, selective intra

arterial infusion of vasodilator

or balloon angioplasty can

be performed to treat the

vasospasm aggressively7.

Leaders in Hemorrhagic stroke treatment

We at the California Pacific Medical Center

and Neuroscience Institute have an abiding

commitment to offer the highest quality of

care to patients suffering from cerebrovascular

diseases such as hemorrhagic stroke.

Working as an integral component of a

strong multidisciplinary team that includes

Stroke Neurology, Critical Care Medicine,

Neuroradiology and Neurosurgery, our

Neurointerventional service provides leading

edge technology and unsurpassed expertise

to diagnose and treat the most challenging

cerebrovascular problems with the safest and

most effective techniques.

NEUROINTERVENTIONAL SURGEONS

Joey D. English M.D., Ph.D.

Warren T. Kim, M.D., Ph.D.

Active Neuroscience Research Trials through California Pacific Medical Center Research Institute

It has been a nearly a year since the SUTTER NEUROSCIENCE CLINICAL TRIALS web page was launched.

this system-wide effort was led by edie Zusman, MD. Listed trials cover a wide range of neurological and neurosurgical conditions such as brain tumors, stroke, autism, Alzheimer’s disease, ALs and multiple sclerosis. Information on open and continuing clinical trials can be accessed by physicians and the community. the site is updated monthly and activity to the web page is tracked. to date, there have been 3,725 visits to the site. Responses from physicians on the ease of use of this tool have been positive, and we can see that the community is accessing the information also. the site

can be accessed through the following uRL.


http://www.sutterhealth.org/clinicaltrials/neurology-clinical-trials.html

Active Neuroscience Research Trials through California Pacific Medical Center Research Institute

Neuroscience Institute

Quick Reference Guide For patient referrals or transfers, call 888-637-2762

The California Pacific Neuroscience Institute combines the expertise of physicians, surgeons, and researchers from different neuroscience disciplines with modern diagnostic equipment and surgical technology to understand and care for the most complicated and difficult-to-treat neurological disorders. Our experts are at the forefront of treating patients with complicated neurological conditions.

Acute Rehabilitation

Moshe Lewis, M.D. 415-642-0707

Masato Nagao, M.D. 415-206-7846

Steven Ng, M.D. 415-600-7710

Lisa Pascual, M.D. 415-206-7846

Diokson Rena, M.D. 415-409-7364

Scott Rome, M.D. 415-600-7710

Jules Steimnitz, M.D. 415-641-8631

AlS/Neuromuscular

Jonathan Katz, M.D. 415-600-3604

Robert Miller, M.D. 415-600-3604

Susan Woolly, Ph.D. 415-600-1261

Alzheimer’s and Dementia

Catherine Madison, M.D. 415-600-3604

Louisa Parks, Ph.D. 415-600-5555

Susan Woolley, Ph.D. 415-600-3604

Cerebrovascular Disorders

Nobl Barazangi, M.D., Ph.D. 415-600-5760

Charlene Chen, M.D. 415-600-4610

Jack Rose, M.D. 415-600-5760

David Tong, M.D., FAHA 415-600-5760

Christine Wong, M.D. 415-600-4610

Alan Yee, D.O. 415-600-4610

Brian Andrews, M.D., FACS 415-600-7760 (neurosurgery)

Lewis Leng, M.D. 415-600-7760 (neurosurgery)

Peter B. Weber, M.D. 415-885-8628 (neurosurgery)

Joey English, M.D., Ph.D. 415-600-7760 (neurointerventionalist)

Warren Kim, M.D., Ph.D. 415-600-7760 (neurointerventionalist)

Mark Saleh, M.D. 415-600-3604 (neurology in-house consult)

Epilepsy and Seizure Disorders

Kenneth Laxer, M.D. 415-600-7880

David King-Stephens, M.D. 415-600-7880

William McMullen, Jr., Ph.D., ABCN, ABPP 415-600-7880


cpmc.org/neuroscience 15

Neuroscience Institute Quick Reference Guide continued

General Adult Neurology

Amy Akers, M.D. 415-600-7886

Gary Belaga, M.D. 415-641-6223

Chau-Chun Chien, M.D., Ph.D. 415-981-6013

Max Duncan, D.O. 707-521-7788

William Estrin, M.D. 415-268-0054

Arnold Greenberg, M.D. 415-346-7505

Marina Kasavin, M.D. 415-561-0575

Jonathan Katz, M.D. 415-600-3604

Donald Kitt, M.D. 415-751-7753

Richard Mendius, M.D. 707-521-7788

Robert Miller, M.D. 415-600-3604

Gregory Pauxtis, M.D. 415-864-4482

Carlos Quintana, M.D. 415-751-7753

Marilyn Robertson, M.D. 415-268-3208

Charles Skomer, M.D. 415-923-3164

Mark Strassberg, M.D. 415-749-6820

Smirit Wagie, D.O. 415-464-0411

General Adult Neurosurgery

Brian Andrews, M.D., FACS, FAANS 415-600-7760

Leo W.K. Cheng, M.D. 415-673-3888

Edward F. Eysner, M.D. 415-923-9222

Lewis Leng, M.D. 415-600-7760

Bruce McCormack, M.D. 415-923-9222

Peter B. Weber, M.D. 415-885-8628

Movement Disorders


Marilyn Robertson, M.D. 415-561-1714

Peter Weber, M.D. 415-885-8628

Neurology In-house Consult

Mark Saleh, M.D. 415-600-3604

Neurointerventional Treatments

Brian Andrews, M.D., FACS, FAANS 415-600-7760 (neurosurgery)

Lewis Leng, M.D. 415-600-7760 (neurosurgery)


Joey English, M.D., Ph.D. 415-600-7760 (neurointerventional)

Warren Kim, M.D., Ph.D. 415-600-7760 ((neurointerventional)

Neurodevelopmental Disabilities Lalaine Dimagiba-Sebastian, M.D. 415-600-6200


For patient referrals or transfers, call 888-637-2762

Neurophysiology

Amy Akers, M.D. 415-600-7886

Jon Katz, M.D. 415-600-3604

Gregory Pauxtis, M.D. 415-864-4482

Neuro-Oncology

Brian Andrews, M.D., FACS, FAANS 415-600-7760

Lewis Leng, M.D. 415-600-7760

Peter B. Weber, M.D. 415-885-8628

Neuropsychology


Louisa Parks, Ph.D. 415-600-5555

Susan Woolley, Ph.D. 415-600-1261

Neuroradiology Jerome Barakos, M.D. 415-600-3232

Amy Huang, M.D. 415-884-3418

Kirk Moon, M.D. 415-600-3232

Derk Purcell, M.D. 415-600-6000

Pediatric Neurology

Paul Fisher, M.D. 650-736-0885

Christopher W. Lee-Messer, M.D. 650-736-0885

Farhad Sahebkar, M.D. 415-600-0770

Pediatric Neurosurgery

Kevin Chao, M.D. 650- 497-8775

Samuel H. Cheshier, M.D. 650- 497-8775

Michael S. Edwards, M.D. 650- 497-8775

Pain Medicine/Headache Disorders

Wayne Anderson, D.O. 415-558-8584

Michael Rowbotham, M.D. 415-600-1750

Peripheral Nerve Conditions

Jon Katz, M.D. 415-600-3604

Spinal Surgery

Brian Andrews, M.D., FACS, FAANE 415-600-7760 Lewis Leng, M.D. 415-600-7760

Bruce McCormack, M.D. 415-923-9222

Peter B. Weber, M.D. 415-885-8628

cpmc.org/neuroscience 17

CALIFORNIA PACIFIC Neuroscience Institute

California Pacific Medical Center P.O. Box 7999 san Francisco, CA 94120-7999

415-600-7760 cpmc.org/neuroscience

Printed on 100% recycled paper. Copyright © 2013 California Pacific Medical Center. All rights reserved.

(cpni bulletin) - neurointerventional services edition - california

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