REVISIÓN DE TEMA ENFERMEDAD CEREBROVASCULAR

1. STROKE
KAREN ALEJANDRA RIVERA RIVERA MD

2. Stroke
Inicio súbito de déficit neurológico de origen vascular por infarto del tejido cerebral (confirmado por
neuroimagen)
ACCIDENTE ISQUEMICO TRANSITORIO: Episodio temporal, de menos de 60 minutos de duración, con déficit
neurológico causado por isquemia focal cerebral, espinal o retiniana, sin ataque agudo y sin cambios en las
imágenes de resonancia magnética. ( muchos se presentan con amaurosis fugaz)
2 TIPOS PRINCIPALES
ISQUEMICO (~80%)
HEMORRAGICO (~20%)
ES LA SEGUNDA CAUSA DE MUERTE A NIVEL
TERCERA CAUSA MAS COMUN DE DISCAPACIDAD

3. STROKE
SUBTYPE
CLINICAL COURSE RISK FACTORS OTHER CLUES
Intracerebral
hemorrhage
Gradual progression during minutes or
hours
Hypertension, trauma, bleeding
diatheses, illicit drugs (eg,
amphetamines, cocaine), vascular
malformations. More common in blacks
and Asians than in whites.
May be precipitated by sex or
other physical activity. Patient
may have reduced alertness.
Subarachnoid
hemorrhage
Abrupt onset of sudden, severe
headache. Focal brain dysfunction less
common than with other types.
Smoking,hypertension, moderate to
heavy alcohol use, genetic susceptibility
(eg, polycystic kidney disease, family
history of subarachnoid hemorrhage)
and sympathomimetic drugs (eg,
cocaine)
May be precipitated by sex or
other physical activity. Patient
may have reduced alertness.
Ischemic
(thrombotic)
Stuttering progression with periods of
improvement. Lacunes develop over
hours or at most a few days; large
artery ischemia may evolve over longer
periods.
Atherosclerotic risk factors (age,
smoking, diabetes mellitus, etc.). Men
affected more commonly than women.
May have history of TIA.
May have neck bruit.
Ischemic (embolic) Sudden onset with deficit maximal at
onset. Clinical findings may improve
quickly.
Atherosclerotic risk factors as listed
above. Men affected more commonly
than women. History of heart disease
(valvular, atrial fibrillation, endocarditis).
Can be precipitated by getting up
at night to urinate, or sudden
coughing or sneezing.

4. PATHOPHYSIOLOGIC CLASSIFICATION OF ISCHEMIC STROKE
ARTERIAL THROMBOSIS
LARGE VESSEL
SMALL VESSEL -
LACUNAR
CARDIOEMBOLIC
AF MOST COMMON
RHEUMATIC VALVE DISEASE
PROSTHETIC HEART VALVE
RECENT MI
FIBROUS AND INFECTIOUS
ENDOCARDITIS
SYSTEMIC HYPOPERFUSION
INTERNAL CAROTID
VERTEBRAL, OR
INTRACRANIAL
ARTERIES
SMALL PENETRATING
ARTERIES OF ANTERIOR,
MIDDLE, AND
POSTERIOR CEREBRAL
AND BASILAR ARTERIES
INADEQUATE BLOOD FLOW
TO BRAIN SECONDARY TO
HEART PUMP FAILURE
(ARRHYTHMIA AND MI)
KAREN ALEJANDRA RIVERA RIVERA MD

6. FACTOR
POPULATION-
ATTRIBUTABLE RISK
RISK REDUCTION WITH
TREATMENT
LIFESTYLE
Cigarette smoking 12-14%
50% within 1 year of
quitting
Physical inactivity 30% ?
Excess alcohol
consumption
7% ?
MEDICAL
Hypertension >90% 32%
Diabetes 5-27% —
Atrial fibrillation 2-24% 64%
Carotid stenosis 2-7% 50%
Sickle cell disease —
91% with transfusion
therapy in children
Data from Goldstein LB, Bushnell CD, Adams RJ, et al. Guidelines for the primary
prevention of stroke: a guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke. 2011;42:517-584.
FACTORES DE
RIESGO
COMUNES

7. FR MODIFICABLES
Hipertension arterial > 90%
Diabetes 5-27%
Fumar 12-14%
Dislipidemia
Inactividad física 30%
FR NO MODIFICABLES
Edad mayor a 80 años
Los hombres tienen una incidencia mayor en edades mas
jóvenes , la incidencia se aumenta y es mayor en las
mujeres con edad mayor o igual a 75 años
Los hispanos y los negros tienen riesgo aumentado
Historia familiar de gemelos monocigoticos , enfermedad
de células falciformes o arteriopatia cerebral dominante
con infartos subcorticales y leucoencefalopatia

8. SOSPECHAR EN PACIENTES MENORES DE 45 AÑOS
● Sickle cell anemia
● Polycythemia vera
● Essential thrombocytosis
● Heparin induced thrombocytopenia
● Protein C or S deficiency, acquired or congenital
● Prothrombin gene mutation
● Factor V Leiden(resistance to activated proteinC)
● Antithrombin III deficiency
● Antiphospholipid syndrome
● Hyperhomocysteinemia

9. NUCLEO ISQUEMICO FLUJO < 10
CC/100 G DE TEJ /MIN
ZONA PENUMBRA FLUJO 10-20
CC/100 G DE TEJ/MIN ( TIENE
VIABILIDD HASTA DE 18 HORAS EN
ALGUNOS ESTUDIOS)
ZONA DE OLIGOHEMIA 20-50
CC/100 G DE TEJ /MIN

12. HEMORRAGIA INTRACEREBRAL
Hipertensión más común—derivado de arteriolas o arterias
pequeñas, ruptura de pequeños micro aneurismas ( aneurismas
de Charcot Bouchard ) produciendo hemorragia intra
parenquimatosa
La acumulación de sangre ocurre minutos a horas y los síntomas
neurológicos aumentan gradualmente de minutos a horas
Sitios más comunes: putamen ,talamo cerebelo y Puente
Otros: trauma angiopatia amiloide ( asociados con hemorragia
lobar ),malformaciones vasculares, vasculitis, uso de
medicamentos cocaína o metanfetamina

13. HEMORRAGIA SUBARACNOIDEA
Ruptura de un aneurisma liberando sangre directamente
al L cefalorraquídeo
Aumenta la presión intracraneal rápido
Los síntomas iniciales abruptamente
La cefalea es severa y global, rigidez de cuello perdida
conciencia na hostia náusea bonito y fotofobia
Predisposición genética
Enfermedad renal poli quística
Síndrome de Marfan
Síndrome de Ehlers Danlos
.

14. Si es dominante ( usulamente el izquierdo) Afasia
motora y deficit sensitivo ( mayor en rostro y
miembro superior )
Si no es dominante ( usualmente el derecho) –
heminegligencia corporal , anosognosia
Hemiplejia si compromete la cápsula interna

15. Deficit sensitivo /motor mayor en miembro inferior –rostro
Reflejos de succion, agarre
Abulia, rigidez paratonica, apraxia de la marcha , confusion ,
incontinencia urinaria
Cambios comportamentales y alteracion en la memoria
marcados
ARTERIA CEREBRAL ANTERIOR

16. Hemianopsia homonima
Alexia sin agrafia ( hemisferio dominante)
Alucinaciones visuales (corteza calcarina)
Coreoatetosis
Dolor espontánea ( talamo)
Parálisis del tercer par
Paresia de los movimientos verticales del globo ocular
ARTERIA CEREBRAL
POSTERIOR

17. VASOS PENETRANTES
Hemiparesia motora pura
Deficit sensitivo puro
Hemiparesia
Ataxia homolateral
Disartria/síndrome de mano torpe
ARTERIA CEREBELAR POSTERIOR INFERIOR
rostro
Lesión de noveno y 10 pc
Ataxia
Sx HORNER
Síndrome vertiginoso por afección de núcleos vestibular es
Disartria y disfagia por paresia de la cuerda vocal, faringe Y velo del
paladar ipsilateral por lesión del núcleo ambiguo
VERTEBROBASILAR
Deficit sensitivos cruzados –hemiparesia y
hemihipoestesia contralaterales y
afectacion ipsiltareral de pares craneales
Diplopia , mareo, vertigo, disartria ,
disfagia, marcha ataxica
Signos bilaterales sugieren arteria basilar

18. POSTERIOR CIRCULATION SYNDROMES

19. EVALUACION INICIAL
v ABC MONITORIA SIGNOS VITALES
v CODIGO ECV <4.5 h DESDE EL INICIO –TROMBOLISIS
v TAC CEREBRAL NO CONTRASTADO ES EL TEST MAS SENSINLE PARA DETECTAR HEMORRAGIA
v LA RMN POR DIFUSION ES EL METODO MAS PRECISO PARA DETECTAR ISQUEMIA CEREBRAL (< 1 H
EVOLUCION)
v ECG: FA (cardioembolismo)
v National Institutes of Health Stroke Scale (NIHSS)
KAREN ALEJANDRA RIVERA RIVERA MD

20. v Severidad del Evento cerebrovascular
v Seguimiento de respuesta tratamiento
v 11 items :
nivel de conciencia
Sistema visual
sistema motor
sistema sensitivo
lenguaje
v Puntaje (x/42):
v 0=no 1-4= leve 5-15=moderado 15-20=moderado a severo 21-42=severo
v rtPA se consdiera si ≥6
The National Institute of Health Stroke Scale (NIHSS)

21. CASO CLINICO
PACIENTE FEMENINA DE 59 AÑOS DE EDAD HIPERTENSA,
FUMADORA 10 CIGARRILLOS AL DIA
DE FORMA SUBITA PRESENTO PERDIDA DE FUERZA EN
EXTREMIDADES DERECHAS JUNTO A ALTERACION DEL LENGUAJE
DE DOS HORAS DE EVOLUCION
AL EXAMEN FISICO
PARESIA FACIAL COMPLETA
PARESIA BRAQUIAL 2/5
PARESIA CRURAL 1/5
MODERADA DISARTRIA Y PARAFASIAS
NIHSS ???
TAC HIPERATENUACION ACM
ANGIOTAC
ESTENOSIS SUBOCLUSIVA DE ARTERIA
CAROTIDA INTERNA IZQUIERDA QUE SE
EXTIENDE HASTA LA CEREBRAL MEDIA
IZQUIERDA
POSTERIOR A ESTUDIOS DE IMAGEN
EMPEORAMIENTO CLINICO
AFASIA MIXTA DE PREDOMINIO MOTOR
NIHSS ???

22. La sensibilidad del TAC aumenta después de 24 h para isquemia
Dentro de 6 horas del inicio del stroke
Prevalencia de signos tempranos 61%
Early signs of brain infarction at CT: observer reliability and
outcome after thrombolytic treatment--systematic
review.AUWardlaw JM, Mielke O SORadiology. 2005;
SIGNOS TEMPRANOS ISQUEMICOS EN TAC NO C
1. Hipo atenuación de 1/3 o mas del territorio de ACM
2. Oscurecimiento del núcleo lentiforme
3. Borramiento del surco cortical
4. Hipoatenuacion parenquimatosa focal
5. Perdida de cordón insular u obscurecimiento de la fisura silviana
6. Hiperatenuacion de grandes vasos
7. Perdida de la diferenciación de la sustancia blanca a nivel ganglio
basal

23. diffuse hypodensity in the right lentiform
nucleus, with mass effect upon the frontal
horn of the right lateral ventricle.
The patient is a 70-year-old female with
history of left-sided weakness for several
hours duration.
HYPOATTENUATION INVOLVING ONE THIRD OR MORE
OF THE (MCA)TERRITORY

24. CORTICALSULCAL EFFACEMENT
Noncontrast CT in this 52-year-old male with
history of worsening right-sided weakness and
apahasia demonstrates diffuse hypodensity and
sulcal effacement involving the left anterior and
middle cerebral artery territories consistent with
acute infarction.
Scattered curvilinear areas of hyperdensity are
suggestive of developing petechial hemorrhage in
this large area of infarction.

25. LOSS OF THE NORMAL GRAY-
WHITE DIFFERENTIATION
Noncontrast CT was obtained to evaluate this
64-year-old male who awoke with aphasia and
right-sided weakness. Loss of the normal gray-
white differentiation between the normally
denser insular cortex and the less attenuating
subinsular white matter is seen; this is
consistent with loss of the "insular ribbon."

26. Noncontrast CT scanning was performed
to evaluate this 70-year-old female with
a history of acute onset of right-hand
weakness and aphasia.
Loss of gray-white differentiation in the
left insular cortex and in the immediately
adjacent cortical and subcortical portions
of the left temporal operculum is seen;
this is strongly suggestive of an acute
infarction.

27. Noncontrast CT scan in an 80-year-old female
who presented with acute onset of right-sided
weakness.
The left middle cerebral artery (MCA) trunk
appears highly attenuated ,suspicious for acute
thrombosis or embolism. A follow-up
noncontrast CT demonstrated an evolving
infarct of the lentiform nucleus.
HYPERATTENUATION OF LARGE VESSEL
(EG,"HYPERDENSE MCA SIGN")

28. Dense middle cerebral artery (MCA)
sign: noncontrast ct in another patient
with strokelike symptoms
demonstrates a hyperdense
appearance of the right MCA with
subtle loss of gray-white differentiation
of the anterior right temporal lobe.

29. Axial noncontrast CT scan demonstrates focal low density, loss of gray-white differentiation, and mild sulcal
effacement in the right parietal region (left image, arrow) in a 62-year-old female presenting with acute stroke. A
follow-up noncontrast CT scan obtained 10 days later demonstrates diminished sulcal effacement and isodensity
with a near-normal appearance (middle image), thought to be secondary to the CT "FOGGING EFFECT" that may be
seen during the evolution of an infarct. The axial diffusion-weighted image (right) confirms the right parietal infarct.

30. Noncontrast CT of the brain in a patient
with history of remote CVA demonstrates
low density in the right frontal and
anterior temporal regions in the MCA
distribution. Evidence of parenchymal
volume loss with ex-vacuo dilatation of
the right lateral ventricle is present,
indicating chronicity infarction.

31. Chronic infarction: Noncontrast CT
scan demonstrates a well-defined
area of volume loss in the right
temporal lobe with a low-density
appearance consistent with
encephalomalacia. No mass effect
exists.

32. CUANTIFICACION DE LA ZONA DE ISQUEMIA
ASPECTS ( Alberta Stroke Program Early CT Score) , se
extrae de dos cortes axiales tomograficos, uno a nivel del
talamo y ganglio basal y el otro a nivel rostral al ganglio basal
10 puntos
Normal 10
< 4/10 alto riesfo de sangrado con rtPA
< 7 mas riesgo de mortalidad a los tres meses
El valor de ASPECTS se relaciona inversamente con la
severidad del Stroke
Las estructuras subcorticales representan tres puntos ( uno
por cada estructura caudado, nucelo lentiforme y la capsula
interna )
La corteza de la arteria cebral media ---7 puntos del corte a
nivel de ganglio basal ( 1 p para corrteza insular, un punto
para m1 , m2 y m3 respectivamente)

33. One point is subtracted for each
area demonstrating signs of early
ischemic change, such as focal
parenchymal hypoattenuation or
edema.
A normal scan would be scored a
10, and diffuse edema involving all
points would be scored 0.
Noncontrast CT scan performed in a 60-year-old male who presented with acute stroke
demonstrates the use of the ASPECTS. Diffuse hypodensity is noted throughout the middle
cerebral artery (MCA) distribution involving the M1-M6 regions and insula. Seven points
are then subtracting from the 10-point ASPECTS, yielding a score of 3. C = caudate nucleus,
L = lentiform nucleus, I = insular cortex, and IC = internal capsule.

34. CT scans in a 65-year-old woman with left-sided hemiplegia,
hemianopia, and neglect less than 3 hours after symptom
onset.
A and B, Baseline CT scans show hypoattenuation with
swelling and effacement in regions M1, M2, insula (I), M4,
and M5 (ASPECTS = 5). Intravenous thrombolysis was
administered.
C and D, Follow-up CT scans show a large area of
hypoattenuation involving much of the MCA territory. The
patient was dependent at 3 months.

35. DIFFUSION-WEIGHTED IMAGING DWI
Can detect abnormalities due to ischemia within 3 to 30
minutes of onset
DWI contains an additional component of T2 effect, and
increased T2 signal due to vasogenic edema can "shine
through" on DWI images, making it difficult to distinguish
vasogenic from cytotoxic edema on these images.
This problem can be overcome by use of the apparent
diffusion coefficient (ADC).
The ADC provides a quantitative measure of the water
diffusion. In acute ischemic stroke with cytotoxic edema,
decreased water diffusion in infarcted tissue causes
increased (hyperintense) DWI signal and a decreased ADC,
visualized as hypointense signal on ADC maps of the brain.

37. TIEMPO ES CEREBRO
ü Evaluation by physician – 10 minutes
ü Stroke or neurologic expertise contacted (ie, stroke team) –
15 minutes
ü Head CT or MRI scan – 25 minutes
ü Interpretation of neuroimaging scan – 45 minutes
ü Start of treatment – 60 minutes from arrival

38. Si trombolisis --anti hta ---METAS TAS ≤185 mmHgs y td ≤110 mmHg
No trombolisis—TS >220 MMHG O TD >120 MMHG
Disminucion gradual de la presion 15% durante las primeras 24 h
despues del inicio del Stroke ( grado 2 C)
TERAPIA ANTIHIPERTENSIVA

39. TERAPIA
ANTIHIPERTENSIVA

40. The benefit of intravenous alteplase beyond the initial 3hour time window was established by the ECASS 3 trial, which
randomly assigned 821 patients (18 to 80 years old) with acute ischemic stroke to treatment with intravenous alteplase or
placebo
Significantly more patients had a favorable outcome with alteplase than with placebo (52versus45percent,odds
ratio 1.34, 95% CI 1.021.76).The number needed to treat to achieve a favorable outcome was 14.
There was no difference in mortality between the alteplase and placebo groups (7.7 and8.4percent).
DOSING : 0.9 mg/kg, maximum dose of 90 mg.
10% of the dose is given as an intravenous bolus over 1 minute and the remainder is infused over 1 hour.
ACTIVADOR RECOMBINANTE DEL PLASMINGENO TISULAR
INTRAVENOSO (TPA OR ALTEPLASE)

44. TROMBECTOMIA INTRAARTERIAL MECANICA
Para oclusiones arteriales grandes en la circulación próximal anterior—se recomienda el uso stent
independiente el tratamiento con rtPA si se cumple las siguientes condiciones(Grade 1A)
v Neuroimagen consistente con zonas pequeñas de infarto excluyendo hemorragia ASPECTS >6
v El paciente tiene un deficit neurologico persistente e incapacitante
v Centro de experticia
v Se inicia seis dentro de las seis horas del inicio síntomas
KAREN ALEJANDRA RIVERA RIVERA MD

46. For patients with ischemic stroke or TIA of any type who have an established blood pressure ≥140 mmHg systolic or ≥90
mmHg diastolicà initiation of antihypertensive therapy (Grade 1A)
For patients with ischemic stroke or TIA of atherothrombotic, lacunar (small vessel occlusive), or cryptogenic type, and an
established blood pressure >120 mmHg systolic or >70 mmHg diastolic-àinitiation of antihypertensive therapy (Grade 2C).
High intensity statin therapy, independent of the LDL, to reduce the risk of stroke and cardiovascular events (Grade 2B).
atorvastatin 80 mg/day
Treatment with an antiplatelet agent (Grade 1A). using either clopidogrel (75 mg daily) as monotherapy or the combination
of aspirin extended release dipyridamole (25 mg/200 mg twice a day), rather than aspirin (Grade 2A)
SECONDARY PREVENTION OF STROKE

49. For patients with recently symptomatic carotid stenosis of 70 to 99% who have a life expectancy of at
least five years, we recommend carotid endarterectomy (CEA) rather than medical management
alone (Grade 1A)
Symptomatic carotid disease is defined as focal neurologic symptoms that are sudden in onset and
referable to the carotid artery distribution within the previous four to six months. These symptoms
may be transient ischemic attacks, episodes of transient monocular blindness, or minor (nondisabling)
ischemic strokes.

50. For select patients with recently symptomatic carotid stenosis of 70 to 99 percent, we suggest carotid
artery stenting CAS rather than CEA if any of the following conditions are present (Grade 2C):
•A carotid lesion that is not suitable for surgical access.
•Radiation-induced stenosis.
•Clinically significant cardiac, pulmonary, or other disease that greatly increases the risk of
anesthesia and surgery; however, it is not clear if revascularization with endarterectomy or stenting is
better than medical management for this group.
KAREN ALEJANDRA RIVERA RIVERA MD