Vascular Distribution Holmstedt

8/11/2019 Vascular Distribution Holmstedt

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VASCULAR DISTRIBUTIONS AND STROKE

SYNDROMES :

APPROACH TO THE PATIENT SUFFERING STROKE

Christine Holmstedt, D.O.

Assistant Professor of Neurology

Medical Director of Clinical Stroke Services

MUSC


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OBJECTIVES

Help develop a systematic approach to

the patient suffering stroke

Recognize specific stroke syndromes

based on clinical presentations and

physical exam findings

Correlate syndrome to vascular

distribution


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Sidenotes

These are the SICKESTpatients in your ED

WE NEED YOUR HELP

Dont leave the bedside

Concurrent medical issues

Get the right story

LAST KNOWN NORMAL

MEDICATIONS


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Question

You are called emergently to see a stroke

patient in the ED, the first thing you assess on

arrival is?


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INITIALPATIENTSURVEY

ABCs, ABC, ABCs,

Vital signsBlood pressure

Pulse rate and rhythmRespiratory rate

Saturations

General survey

Mental Status Level of consciousness

Distress

Trauma


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SECONDARYSURVEY

Quick patient neurologic overview

Forced deviation

Plegia

AphasicDysarthria

Which hemisphere is affected

Anterior verses posterior Cortical verses subcortical

Large vessel verses small vessel


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NIHSS

Standardized exam designed to improvecommunication between health care providers

Measure the level of impairment caused by astroke.

Scores should reflect what the patient does, notwhat the clinician thinks the patient can do

Main use in clinical medicine is during theassessment of whether or not the degree of

disability caused by a given stroke meritstreatment with tPA

Useful for data collection

Not a neurologic exam


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Physical Exam

Complete physical exam

Neurologic exam


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Question?

While doing the NIHSS, do you include a

patients previous neurologic disability?


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Anterior circulation

Internal Carotid arteries

Anterior cerebral arteries

Middle cerebral arteries


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Internal Carotid Artery

Internal carotid artery

Branch of the common carotid

Bifurcates in the neck

Divides into

ACA

MCA Posterior communicating artery

Circle of Willis
http://upload.wikimedia.org/wikipedia/commons/9/9c/Gray513.png


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Internal Carotid Artery

Cervical C1

Petrous C2

Lacerum C3

Cavernous C4

Clinoid C5

Ophthalmic C6

Communicating C7
http://upload.wikimedia.org/wikipedia/commons/3/33/ICAs.jpg


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Clinical Syndromes

Variable depending on territorial strokeMCA

ACA

MCA/ACA

MCA/ACA/Occipital lobe

Depends on hemisphere involved

Depends on dominance of brain

Depends on acuity of occlusionYounger more acute occlusion typically more

devastating

More chronic occlusion may by asymptomatic


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Clinical Syndrome

Dominant hemisphere

Aphasia

Contralateral hemiplegia/paresis face, arm and leg

Visual field cut

Sensory loss

Gaze preference

Dysarthria

Non-Dominant hemisphere

Contralateral hemiplegia/paresis face, arm and leg

Visual field cut

Sensory loss

Gaze preference

Dysarthria

Neglect

Personality changes

Apraxia


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Anterior Cerebral Arteries

Surface branches supply cortex and white matter of : inferior frontal lobe

medial surface of the frontal and parietal lobes

anterior corpus callosum

Penetrating branches supply:deeper cerebrum

diencephalon

limbic structures

head of caudateanterior limb of internal capsule


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http://en.wikipedia.org/wiki/File:Circle_of_Willis_en.svg


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Clinical Syndrome

Left ACA

Right leg weakness

Right leg sensory loss

Grasp reflex

Frontal lobe behavior abnormalities

Motor aphasia

Larger infarcts can cause hemiplegia


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Clinical Syndrome

Right ACA

Left leg weakness

Left leg sensory loss

Grasp reflex

Frontal lobe behavior abnormalities

Left hemi-neglect


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Middle Cerebral Arteries

Surface branches supply

Cortex & white matter of hemispheric

convexity

All four lobes.

Penetrating branches

Deep matter

Some diencephalic structures


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Horizontal segment M1

Lateral lenticulostriate vessels

Sylvian segment M2

Cortical Segment M3


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Left MCA Stem M1

Right hemiplegia/paresis

Right sensory loss

Right VF cut

Global aphasia

Left Gaze preference


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Left anterior (superior) division

Right face, arm>leg weakness

Motor aphasia

Some right face and arm

sensory loss


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Left posterior (inferior) MCA

Fluent sensory aphasia

Right VF cut

Right face, arm and leg sensory loss

May appear confused or crazy


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Right MCA Branch (M1)

Left hemiplegia/paresis

Left sensory loss

Left VF cut

Left hemi-neglect

Right gaze preference
http://www.canadianmedicaljournal.ca/content/vol170/issue7/images/large/28ff1.jpeg


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Right anterior (superior) division

Left face, arm>leg weakness

Left hemi-neglect

Gaze preference


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Right posterior (inferior) division

Left hemi-neglect

Left VF cut

Left sensory loss

Decreased voluntary movements

Left motor neglect (normal strength)


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Lacunar infarcts

Occlusion of one of the penetrating arteries thatprovides blood to the brain's deep structures

Lacunes are caused by occlusion of a single deeppenetrating arteries that arises directly from the

constituents of the Circle of Willis, cerebellararteries, and basilar artery.

37% putamen

14% thalamus

10% caudate

16% pons

10% posterior limb of the internal capsule


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Lacunar infarcts Pure motor stroke/hemiparesis33-50%

Posterior limb of the internal capsule, or the basis pontis Weakness face, arm, or leg

May have dysarthria, dysphagia and transient sensory symptoms

Ataxic hemiparesis

Posterior limb of the internal capsule, basis pontis, and corona radiata Weakness and clumsiness arm, or leg

Dysarthria/clumsy hand Basis pontis

Dysarthria and clumsiness (i.e., weakness) of the hand, which often are most prominentwhen the patient is writing.

Pure sensory stroke

Thalamus Persistent or transient numbness, tingling, pain, burning, or another unpleasant sensation on

one side of the body. Mixed sensorimotor stroke

Thalamus and adjacent posterior internal capsule Hemiparesis or hemiplegia with ipsilateral sensory impairment


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Posterior circulation

Posterior cerebral arteries

Cerebellar arteries

Vertebral arteries

Basilar artery


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Posterior cerebral Artery

Supply midbrain, cerebral peduncles, medial

temporal lobes, medial thalami, splenium of

the corpus callosum,lateral ventriclar

choroid plexus and bilateral occipital lobes. Arises at the intersection of the posterior

communicating artery and the basilar artery

Connects with the ipsilateral MCA andinternal cerebral artery via the posterior

communicating artery PCommA


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Clinical Syndrome

Contralateral weakness

Contralateral VF cut with macular sparing

Contralateral sensory loss

Posterior headache


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Cerebellar arteries

Posterior inferior cerebellar artery

Anterior inferior cerebellar artery

Superior cerebellar artery


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Posterior inferior cerebellar artery

Last branch off the vertebral artery

Supplies lateral medulla

Most of the inferior cerebellum and

inferior vermis


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Clinical syndrome

Dysphagia

Dysarthria

Gait unsteadiness

Ipsilateral limb ataxia

Vertigo

Hoarseness

Ipsilateral Horners syndrome

Ipsilateral hemianesthesia of the face

Contralateral hemianesthesia of the limbs


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Anterior inferior cerebellar artery

First paired branches off the basilar

Supplies the inferior, lateral pons

Middle cerebellar peduncle

Strip of the ventral, anterior

cerebellum(between the PICA and the

SCA)


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Clinical syndrome

Vertigo

Nystagmus

Facial weakness

Gait ataxia

Acute unilateral deafness (internal

auditory artery)


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Superior cerebellar artery

Paired branches off basilar artery

Supplies upper, lateral pons

Superior cerebellar peduncle

Most of the superior cerebellar

hemisphere

Superior vermis
https://rad.usuhs.edu/synapse/include/medpix_image.php3?imageid=51399


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Clinical syndrome

Ipsilateral cerebellar ataxias (middle and/orsuperior cerebellar peduncles)

Nausea and vomiting

Slurred (pseudobulbar) speech

Loss of pain and temperature over theopposite side of the body

Partial deafness

Tremor of the upper extremity

Ipsilateral Horner syndrome

Palatal myoclonus


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Brainstem infarctions

Basilar occlusion

Small vessel lacunar infarctions


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Basilar artery occlusion

Most important artery in the posterior

circulation (the body)

Formed at the pontomedullary junction by the

confluence of both vertebral arteries

Lies on the ventral surface of the pons

Gives off its median, paramedian, short, and

long circumferential branches


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Clinical presentation

Hemiparesis or tetraparesis and facial paresis - 40-67% of cases Dysarthria and speech impairment - 30-63% of cases

Vertigo, nausea, and vomiting - 54-73% of cases

Visual disturbances - 21-33% of cases

Altered consciousness - 17-33% of cases

Convulsive-like movements along with hemiparesis (herald hemiparesis)

Oculomotor signsIpsilateral abducens palsy

Ipsilateral conjugate gaze palsy

Internuclear ophthalmoplegia

One-and-a-half syndromeOcular bobbing

Skew deviation


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Clinical presentation

Locked-in syndrome: Infarction of the basis pontis

Secondary to occlusive disease of the proximal and middle segments of the basilarartery, which leads to quadriplegia. spared level of consciousness, preserved vertical eyemovements, and blinking.

Coma associated with oculomotor abnormalities and quadriplegia also indicatesproximal basilar and midbasilar occlusive disease with pontine ischemia.

Top-of-the-basilar syndrome: Upper brainstem and diencephalic ischemia caused by occlusion of the rostral basilar

artery

Patients present with changes in the level of consciousness

Visual symptoms Hallucinations and/or blindness.

Third nerve palsy and pupillary abnormalities are also frequent.

Motor abnormalities include abnormal movements or posturing. Other reported signs of pontine ischemia include limb shaking, ataxia (usually

associated with mild hemiparesis), facial weakness, dysarthria, dysphagia, andhearing loss.


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Syndrome?


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Vascular Distribution Holmstedt

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