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51
Main artery involved Division/branches Clinical features
Middle cerebral artery Cortical branches Paralysis of the contralateral face, arm, and leg (with predominance of arm
and face)
Deep MCA branches Sensory impairment over the contralateral face, arm, and leg (with
disturbance of stereognosis, tactile localization, baragnosis,
cutaneographia)
Total MCA stroke Paralysis of conjugate gaze to the opposite side
Homonymous hemianopia (sometimes superior homonymous
quadrantanopia)
Lesions of the dominant cerebral hemisphere: motor speech disorder
(Broca variants of aphasia), Wernicke’s aphasia, word deafness, anomia,
jargon speech, Gerstmann syndrome (agraphia, acalculia, fi nger agnosia,
right-left confusion)
In nondominant cerebral hemisphere: apractagnosia (amorphosynthesis),
anosognosia, hemiasomatognosia
Unilateral neglect, agnosia for the left half of external space, “dressing
apraxia,” “constructional apraxia”
Inaccurate localization in the half visual fi eld, agitated hyperactive state
Loss or impairment of optokinetic nystagmus
Basal ganglia and internal capsule infarction with more severe motor defi cit of
the opposite limbs (frequent hemiplegia with equal distribution on face-arm-
leg), dysarthria in right hemisphere or in left hemisphere transient mutism or
some features of motor aphasia. Sensory loss is transient and minor
Severe motor defi cit (hemiplegia on opposite side), deviation of gaze toward
lesion, hemianopia on opposite side of lesion, mutism, or severe forms of mixed
aphasia in left hemisphere lesions (Broca and Wernicke’s aphasia); anosognosia,
hemiasomatognosia in right hemisphere lesions, Cheyne-Stokes respiration,
stupor and coma due to edema and brain herniation, often with a fatal outcome
Anterior choroidal artery Hemiparesis of face, arm, leg
Prominent sensory loss, but often temporary
Homonymous hemianopia
Absence of other high cortical function defi cits
Posterior cerebral artery Cortical branches Homonymous hemianopia on opposite side, or quadrant hemianopia
Unformed visual hallucinations, metamorphopsia, teleopsia, illusory visual
spread, palinopsia, distortion of outlines, monocular diplopia
Impairment of movement perception
Transient global amnesia or long-term memory problems
Topographic disorientation
Left-sided lesion : dysmnesia (for verbal material), pure alexia, optic
aphasia (visual anomia), transcortical sensory aphasia
Hemiachromatopsia, color anomia, visual hemineglect, acute confusional
state, acute delirium; dyslexia without agraphia,
Right-sided lesion : dysmnesia (for nonverbal material), visual hemineglect,
palinopsia, impaired mental imagery (Charcot-Wilbrand syndrome)
Bilateral lesions: cortical blindness with visual defi cit agnosia, or tubular
vision in partial bilateral lesions with limited peripheral bilateral fi eld and
preserved central vision; Balint’s syndrome (oculomotor apraxia, optical
ataxia, visual simultanagnosia); altitudinal hemianopia; prosopagnosia;
visual object agnosia; amnesia
Deep PCA branches Thalamic syndrome on the opposite side: sensory loss (all modalities),
spontaneous pain and dysesthesias, choreoathetosis, mild intentional tremor,
pseudo-athetosis posture of hand, cognitive impairment, confusion, agitation
Mild hemiparesis produced by subthalamic or midbrain part of pyramidal tract
Paralysis or paresis of vertical eye movement, skew deviation, possible
third nerve palsy with contralateral ataxia or paresis in midbrain lesions
(continued)
Table 2.1 (continued)
2 Cerebral Vascular Territories and the Major Neurovascular Syndromes
52
Table 2.1 (continued)
Main artery involved Division/branches Clinical features
Vertebral arteries Possible (but rare) cervical spinal cord infarcts
Lesion of medulla and cerebellum but sometimes associated pontine,
midbrain, and PCA artery strokes
Medullar lesion is frequent in the retro-olivar area producing a Wallenberg
syndrome. On the lesion side (Horner syndrome, vestibular signs with
nystagmus, cerebellar signs, ambiguous nucleus palsy with dysarthria,
dysphonia and dysphagia, pain and temperature sensibility trigeminal
hypoesthesia) and on the opposite side of body (complete loss of pain and
temperature sensibility)
Cerebellar infarcts are frequent in postero-inferior cerebellar artery
territory associating vertigo, vomiting, nuchal headache, cerebellar ataxia,
falling, and impossibility of gait; possible evolution toward brainstem
compression and herniation of the cerebellar tonsils with cardiac and
respiratory arrest
Basilar artery Inferior-middle part of basilar
artery
Association of medulla, pons, and cerebellar lesions, frequent on both sides
with miosis (pinpoint pupils), various oculomotor palsy (frequent abducens
palsy, conjugated ocular gaze deviation toward paralyzed members, skew
deviation, one and a half syndrome)
Ocular bobbing, nystagmus, decreased or abolished corneal refl ex, peripheral
facial nerve palsy, dysphonia, dysphagia, various combination of motor limb
defi cits going to tetraplegia, locked-in syndrome, cerebellar ataxia,
decerebration, and respiratory disturbances and fi nally in severe cases coma
and death
Top of basilar Association of lesion in midbrain, superior cerebellar arteries, and posterior
cerebral arteries with bilateral divergent strabismus and mydriasis,
multidirectional nystagmus, ocular infraversion, supranuclear vertical gaze
palsy, tetraparesis, abolished vesibulo-ocular refl exes, various visual fi eld
defects or cortical blindness (detected if patient can cooperate), drowsiness,
decerebrate rigidity, respiratory and circulatory abnormalities, coma, and
death
Small perforating arteries Lacunar strokes Pure motor defi cits
Pure sensitive defi cits
Dysarthria clumsy hand
Ataxic hemiparesis
Combined motor and sensitive defi cits
Pseudobulbar palsy in association of many lacunar strokes
Table 2.2 MEDIAL MEDULLARY SINDROME (DEJERINE)
Clinical manifestation/features Side Structure injured Artery obstructed
Hemilingual paresis ± atrophy I Hypoglossal nerve fi bers (XII) VA
Hemiparesis or hemiplegia/face spared
a
C Corticospinal fi bers Proximal BA
Hemihypoesthesia (or anesthesia) for
discriminative touch, proprioception, and
vibration
b
/face spared c
C Medial lemniscus
I ipsilateral, C contralateral
a
Motor nucleus of the trigeminal nerve located in the pons is spared
b
Pain and temperature sensation preserved: spinothalamic tract not affected
c
Spinal tract of trigeminal nucleus is located more laterally
H. Muresian
53
Table 2.3 LATERAL MEDULLARY SYNDROME (Wallenberg)
Clinical manifestation/features Side Structure injured Artery obstructed
Loss of pain and temperature sensation
from face
I Trigeminal (V) spinal tract and nucleus VA
Loss of pain and temperature sensation
from limbs and body
C Lateral spinothalamic tract PICA
Cerebellar ataxia, dysmetria,
dysdiadokokinesia
I Inferior cerebellar peduncle Superior, lateral, or inferior
medullary arteries
Nausea, vomiting, vertigo, nystagmus,
diplopia
Vestibular nuclei
Palatal myoclonus Central tegmental tract
Dysphagia, hoarseness, paresis of soft
palate and pharynx, diminished gag refl ex
I Nucleus ambiguus: vagal (X, XI cranial)
and glossopharyngeal fi bers
Ageusia I Solitary tract nucleus: glossopharyngeal
(IX) and vagal (X) special visceral
afferent (gustatory) fi bers
Horner syndrome I Descending sympathetic fi bers
I ipsilateral, C contralateral
Table 2.4 MEDIAL PONTINE SYNDROME [MEDIAN INFERIOR PONTINE SYNDROME (FOVILLE)]
Clinical manifestation/features Side Structure injured Artery obstructed
Spastic hemiparesis C Corticospinal tract
Paramedian branches of the BA
Loss of tactile, vibration sensation, and
stereognosis
C Medial lemniscus
Strabismus/diplopia I Lateral rectus muscle paralysis
Facial nerve palsy I Facial (VII) nucleus
I ipsilateral, C contralateral
Table 2.5 LATERAL PONTINE SYNDROME
Clinical manifestation/features Side Structure injured Artery obstructed
Loss of pain and temperature sensation in
trunk and limbs
C Lateral spinothalamic tract
AICA
Loss of pain and temperature sensation from
face (facial hemianesthesia)
I Trigeminal (V) spinal tract and
nucleus
Ataxia (limb ataxia and gait) I Inferior and middle cerebral peduncle
Paralysis of upper and lower face
Loss of lacrimation and salivation
Loss of taste (anterior 2/3 of tongue)
Loss of corneal refl ex
I Facial (VII) nucleus and fi bers
Nystagmus, nausea, vomiting, vertigo I Vestibular nuclei and fi bers
Hearing loss/tinnitus I Cochlear nuclei and fi bers
Horner syndrome I Descending sympathetic fi bers
Table 2.6 SUPERIOR ALTERNATING HEMIPLEGIA (WALLENBERG SYNDROME)
Clinical manifestation/features Side Structure injured Artery obstructed
Parkinsonism C Substantia nigra
Paramedian branches of PICA, of
BA bifurcation
Hemiparesis C Corticospinal fi bers before the
medullary decussation
Paresis of lower hemiface and tongue C Corticobulbar fi bers
Ophthalmoplegia (paralysis of all extrinsic
ocular muscles except inf. Oblique and
lateral rectus; of intrinsic muscles = fi xed
pupil and levator palpebrae
superioris = drooping eyelid)
I Oculomotor (III) nerve fi bers
2 Cerebral Vascular Territories and the Major Neurovascular Syndromes
54
ICA
ACA
MCA
OPHT
Fig. 2.1 General disposition of
the branches of the internal
carotid artery. The internal
carotid artery ( ICA ) divides into
the anterior ( ACA ) and middle
( MCA ) cerebral arteries, after
giving off the ophthalmic branch
( OPHT ). Note the curves of the
ICA and the diverging ACA and
MCA. Frequently, the MCA
appears doubled (see also text for
details)
Image Gallery
H. Muresian
55
ICA
A1
A2
A3
M1 -3
M4
OPHT
a
ICA
A1
A2
A3
M1
M2
M3
M4
OPHT
b
Fig. 2.2 The main branches of the cerebral
arteries. Panel ( a ) lateral view. The course of
the ACA is better visualized in this
projection. A1 extends from origin to the
branching of the anterior communicating
artery; A2 up to the level of the
callosomarginal artery and A3 distal to it.
Panel ( b ) anteroposterior view of the main
cerebral branches. The segments of the
MCA appear clearly: M1 sphenoidal, M2
insular, M3 opercular, and M4 cortical.
From M2 onward, the MCA is frequently
doubled
2 Cerebral Vascular Territories and the Major Neurovascular Syndromes
56
ICA
A1
A2
A3
M1
M2
M3
OPHT
Fig. 2.3 Oblique view of the
terminal part of the ICA. Note
that the MCA continues the main
direction of the ICA and has a
more conspicuous caliber as
compared with the ACA; this
detail explains the more frequent
embolization in the territory of
the MCA
H. Muresian
57
V2
V3
V4
PICA
AICA
SCerA
PCA
BA
VA
PICA
m
m
m
a
c
b
Fig. 2.4 Branches of the vertebral and basilar arteries. Panel ( a ) ante-
rior view of the left vertebral artery ( VA ) continuing with the basilar
artery ( BA ). The latter gives off the anterior inferior cerebellar artery
( AICA ) and the superior cerebellar artery ( SCerA ). The VA gives off the
posterior inferior cerebellar artery ( PICA ). The BA bifurcates into the
two posterior cerebral arteries ( PCA ). The segments of the VA V2
through V4 are also labeled. Panel ( b ) contralateral slender VA termi-
nating with the PICA. Note the small muscular branches ( m ). Panel ( c )
muscular and spinal branches of the VA, appearing more evident in a
case with occlusion of the left VA and vertebral steal syndrome
2 Cerebral Vascular Territories and the Major Neurovascular Syndromes
58
A1
A2
AM
AL
PM
PL
MCA
PCA
VA VA
POST. SP.
ANT. SP.
PICA
LAB
AICA
LAB
Pons
SCerA
MGB
LGB
P1
P2 P3
AP
i
m
pm
VA, MD
MGB
P
Fig. 2.5 The central branches of the arterial circle of Willis. The VA
and the ICA are indicated by red disks. ACA and MCA anterior and
middle cerebral arteries, PCA posterior cerebral arteries, A1 and A2 the
segments of the ACA, P1 – P3 the segments of the PCA. The VAs give
off the anterior and posterior spinal branches ( ANT.SP and POST.SP )
and the posterior inferior cerebellar arteries ( PICA ). The basilar artery
gives off the anterior inferior cerebellar artery ( AICA ), the superior cer-
ebellar artery ( SCerA ) just immediately upon its bifurcation. The pon-
tine branches ( Pons ) may also give off the labyrinthine artery ( LAB )
when this latter one does not have a separate origin from the BA. The
central branches of the CoW are grouped as AM anteromedial, AL
anterolateral, PM posteromedial, and PL posterolateral and are depicted
in pink. The main basal nuclei and thalamic and subthalamic nuclei
vascularized are indicated ( VA , MD , ventral anterior and median dorsal,
P pulvinar, MGB and LGB medial and lateral geniculate body). AP
artery of Percheron (the posterior paramedian thalamo-subthalamic
artery which vascularizes the subthalamus, inferior, and anteromedial
thalamic areas, bilaterally ). See text for more details
H. Muresian
59
SCA
VA
Occ
DeepCer
AscCer
Suprascap
InfThyr
AscCer
InfThyr
Suprascap
ECA
VA
Occ
a
b
c
Fig. 2.6 Cervical anastomoses. These anastomoses are established
between the VA and the carotid and subclavian arterial systems. The
anastomoses become evident and may also facilitate arterial steal, in
cases of obstruction or severe stenosis of one of the major arterial trunks
(carotid, vertebral, subclavian). The direction of fl ow is best appreciated during angiogram. Panel ( a ) the anastomotic channel paralleling
the VA: the deep cervical ( DeepCer ) and ascending cervical ( AscCer )
branches of the subclavian artery, anastomosing with the occipital
artery ( Occ ) from the ECA and the VA. Sometimes, an occluded SCA
may be also fed by means of anastomoses with the suprascapular artery
( Suprascap ). Panel ( b ) conspicuous branches at the base of the neck
and at the root of the superior limb provide important collateral channels as in this case with stenosis of the SCA and of the VA. The same
abbreviations as above. InfThyr inferior thyroid artery (from the thyro-
cervical trunk). Panel ( c ) anastomoses at suboccipital level between the
VA and the ECA. This is the case of an occluded origin of the ECA. The
ECA and its main branches are fi lled through collateral circulation from
the VA, mainly through the occipital artery
2 Cerebral Vascular Territories and the Major Neurovascular Syndromes
60
Fig. 2.7 Extra-intracranial collateral circulation. Panel ( a ) lateral view.
The ICA and its major divisions ( ACA , MCA and the ophthalmic artery)
are feebly fi lled due to a severe stenosis at the origin of the ICA. The
ECA and its branches appear conspicuous. The principal collateral
pathways are offered by the facial artery ( Facial ) and its dorsal nasal
branch, the maxillary artery ( Max ) with the sphenopalatine artery and
the middle meningeal ( MMen ), and the superfi cial temporal artery
( SupTemp ). Note also the well-visible ascending pharyngeal artery
( AscPhar ), paralleling the ICA and offering an additional collateral
pathway. Panel ( b ) anteroposterior view. The same abbreviations as
above. Note the anastomoses at meningeal level ( Mening ). Panel ( c )
lateral view of the carotid bifurcation. Note the severe stenosis at the
origin of the ICA, sparing the bulb. The ascending pharyngeal artery
( AscPhar ) is well visible. The ECA and superior thyroid artery and the
facial, lingual, and superfi cial temporal branches of the ECA are also
well visible. The case is of particular interest, refl ecting the caliber of
the ascending pharyngeal artery in situations with severe stenosis of the
ICA. Note also that the ICA immediately distal to the stenosis appears
somehow dilated, while more distally, it becomes narrower. While measuring the degree of a stenosis, it would be diffi cult to choose which of
the ICA diameters represent the best landmark, as the segment after the
stenosis appears as a poststenotic dilatation. Panel ( d ) leptomeningeal
vessels. A later phase angiogram demonstrates the leptomeningeal
arteries. These vessels become conspicuous and easily recognizable in
cases with severe stenotic lesions of the ICA. Note the normal fi lling of
the ophthalmic artery and anastomoses with the ECA (direction of fl ow
from the ICA to the ECA branches) in an individual with no stenosis of
the ICA ( white arrows )
Facial
OPHT
ICA
ACA
MCA
AscPhar
MMen
Max
SupTemp
a
H. Muresian