Topographic Syndromes
Paciaroni M, Agnelli G, Caso V, Bogousslavsky J (eds): Manifestations of Stroke.
Front Neurol Neurosci. Basel, Karger, 2012, vol 30, pp 162–165
Pontine Infarcts and Hemorrhages
Jorge Moncayo
Neurovascular Unit, Department of Neurology, Eugenio Espejo Hospital, International University of Ecuador, Quito, Ecuador
Abstract
Pontine infarcts are often part of a large ischemia involv-
ing the brainstem, although infarcts may be restricted to
the pons. In both cases, infarcts in the pons are charac-
terized by interesting clinical patterns resulting from a
variety of cranial nerve dysfunctions, eye movement dis-
orders and motor, sensory and cerebellar manifestations,
either isolated or in combination. The anteromedial and
anterolateral territories are the most commonly involved.
Penetrating branch artery disease is the most common
etiology. Ten percent of all intracerebral hemorrhages
are located in the pons, and small hemorrhages in this
brainstem structure may, in some instances, give rise to
unusual clinical manifestations.
Copyright © 2012 S. Karger AG, Basel
Pontine Infarcts
The pons, either in isolation or as part of multi-
level ischemia, is affected by stroke much more
often than other brainstem structures. Infarcts
restricted exclusively to the pons account for
12–27% of posterior circulation ischemia [1, 2].
Transient ischemic attacks preceding pontine in-
farcts may occur in up to one-third of patients
and may include unusual manifestations such as
pontine warning syndrome, pathological laugh-
ter (‘fou rire prodromique’), transient excessive
yawning, several patterns of transient facial pain
(e.g., ‘salt and pepper on the face’ pain) and clon-
ic arm movements. Based on clinical, anatomical
and radiological correlations, the following con-
stant vascular territories have been defined in
pontine ischemia: ventromedial (anteromedial),
anterolateral, lateral (tegmental), dorsal and bi-
lateral infarcts.
Anteromedial Infarcts
Two out of three isolated pontine infarcts may in-
volve the paramedian territory [1, 2]. The medi-
al basis pontis (corticospinal tract) is supplied by
the short midline perforators branching directly
off the basilar artery, from which the long midline
perforators supply the medial tegmentum (includ-
ing the medial part of the medial lemniscus, the
abducens nucleus, medial longitudinal fascicu-
lus and paramedian pontine reticular formation).
Paramedian infarcts often extend to the ventral
surface, whereas ischemia restricted to parame-
dian tegmentum is less common [2, 3]. Moderate
to severe pure motor hemiparesis (PMH), more
marked in the upper extremity and in the distal
part of the limbs, is the main clinical manifestation
in approximately one-half of infarcts due to lesions
of the ventral surface of the paramedian caudal or
middle pons [2]. Distinct lingual, contralateral
palatal-lingual or palatal-lingual-laryngeal hemi-
paresis are uncommon patterns of motor deficit
and resemble those observed in capsular genu syn-
drome. Moderate or marked dysarthria is almost a
constant finding in large paramedian infarcts, par-
ticularly of the upper pons, and is often accompa-
nied by hemiparesis, brachial monoparesis, supra-
nuclear facial palsy and hemiataxia, while isolated
dysarthria is a rare occurrence [3].
Mild and transitory tegmental dysfunction
characterizes most paramedian infarcts and is
noticeable by pure lemniscal sensory loss (in-
cluding cheiro-oral, crural or facial hypesthe-
sia) or associated with motor deficit as well as a
broad spectrum of neuro-ophthalmologic signs.
The main neuro-ophthalmologic manifestations
found in paramedian ischemia, and which almost
never occur in isolation, are one-and-a-half syn-
drome (ipsilateral horizontal gaze palsy to one
side and a restriction for adduction to the other),
internuclear ophthalmoplegia (INO), ipsilateral
horizontal gaze palsy, ocular bobbing, primary-
position downbeating nystagmus, skew deviation,
Horner’s syndrome and abducens nerve palsy
[2, 3]. Smaller infarctions in the ventrotegmen-
tal junction at the middle upper pons may be as-
sociated with dysarthria-clumsy hand syndrome
(DCHS) and its variants, and ataxic hemiparesis
(AH) and its variants [1, 3]. The most common
etiology of anteromedial infarcts is basilar branch
disease (occlusion of a penetrating branch from
the BA). Functional outcome is favorable; most
patients have a mild disability and are indepen-
dent 9 months after pontine infarct [2, 3].
Anterolateral Territory
This is the second most frequent territory in-
volved in pontine infarcts. It is served by antero-
lateral pontine arteries supplying the lateral por-
tion of the corticospinal tract and parts of the
medial lemniscus. Clinical manifestations of small
infarcts include PMH (mild facio-brachio-crural
or, less often, brachio-crural hemiparesis) and,
less commonly, DCHS and AH and its variants.
Tegmental dysfunction is found in nearly 60%
of infarcts. The main manifestations are lemnis-
cal sensory loss (brachial or facio-brachio-crural
Pontine Infarcts and Hemorrhages
hypesthesia), homolateral conjugate gaze palsy,
isolated abducens palsy, one-and-a half syndrome,
nystagmus, skew deviation, Horner’s syndrome
and pursuit movements superimposed with sac-
cades. The causes are basilar artery branch disease
and small artery disease in one-half and one-fifth
of infarcts, respectively. Functional outcome is fa-
vorable in most patients [1, 2].
Lateral Territory
Lateral pontine arteries stemming from the anteri-
or inferior cerebellar artery feed the caudal lateral
pons. These arteries, at the upper level, arise from
the superior cerebellar artery and supply the pon-
tine nuclei, dorsolateral corticospinal tract, medi-
al lemniscus, ventral trigeminothalamic tract and,
more externally, the middle cerebellar peduncle.
Frequency of lateral ischemia ranges from 12 to
30% of all pontine infarcts [1, 2].
Motor deficit is not a constant finding in lateral
infarcts; when present, a mild facio-brachio-crural
hemiparesis, brachio-crural hemiparesis and cru-
ral monoparesis (particularly at the upper level)
are the main clinical patterns [4]. Contralateral
lemniscal or spinothalamic sensory deficits are
not always present. Brachio-crural, facio-brachio-
crural, arm, trunk and leg or crural hypesthesias
have been described; isolated trigeminal weakness
with hypesthesia is very uncommon [1, 2]. Neuro-
ophthalmologic signs are common and quite sim-
ilar to those described in other pontine territori-
al infarcts. These signs are often accompanied by
contralateral motor and sensory deficits or ataxia.
Tiny laterodorsal infarcts, nevertheless, may mani-
fest as isolated single nerve palsies – VI fascicular or
nuclear facial palsy – or painful ipsilateral trigemi-
nal neuropathy. Ischemia at the caudolateral pons
is characterized by absence of oculomotor signs;
isolated vertigo may be a predominating manifes-
tation suggesting acute peripheral vestibulopathy.
Small artery disease is the leading etiology of later-
al pontine infarcts. Prognosis is usually favorable:
over 80% of patients are independent [1, 2].
163
Table 1. Uncommon manifestations of pontine infarcts

Paramedian territorial infarcts

Contralateral pure supranuclear facial palsy
Unilateral hyperhidrosis, pure or associated with hemiparesis
Variants of one-and-a-half syndrome (eight-and-a-half syndrome; sixteen-and-a-half syndrome associated with
ipsilateral supranuclear facial palsy)
Body lateropulsion, pure or associated with INO
Transient bilateral upbeat nystagmus associated with ataxia, INO and hemiparesis
REM sleep behavior disorder; periodic limb movements during sleep
Millard-Gubler syndrome: ipsilateral facial palsy and contralateral hemiplegia
Foville’s syndrome: ipsilateral facial paralysis, conjugate gaze paralysis and contralateral hemiparesis

Lateral territory
Gasperini syndrome: ipsilateral abducens palsy plus complete anterior inferior cerebellar artery syndrome

Posterior territory
Marie-Foix syndrome: homolateral cranial nerve palsies, Horner’s syndrome, hemiataxia, uvulo-palato-pharyngeal
myoclonus, and contralateral spinothalamic sensory loss

Combined anteromedial and anterolateral territories

Raymond-Cestan syndrome (ipsilateral INO, contralateral hemiparesis and hemihypesthesia)

Bilateral infarcts
Peduncular hallucinosis: paramedian rostral pontine infarcts [8]
Freezing of gait: bilateral pedunculopontine nuclei infarcts
Fifteen-and-a-half syndrome (one-and-a-half syndrome with facial diplegia)
Bilateral horizontal gaze palsy and peripheral facial palsy
Hypesthesia in perioral area, hands and distal arms: bilateral tegmental infarcts at the caudal pons

Posterior Infarcts (Dorsomedial) (neuro-ophthalmologic, sensory deficits and cra-

This territory is supplied by long circumferential
branches of the superior cerebellar artery or ante-
rior inferior cerebellar artery. Isolated infarcts of
the extreme lateral pons are extremely rare, often
occurring with concomitant cerebellar infarcts or
more widespread brainstem infarctions due to BA
occlusion [1, 2].
nial nerve palsies) are usual findings. Bilaterally
restricted ventral infarcts at the middle and cau-
dal level can produce disturbed consciousness,
locked-in syndrome, and diverse patterns of mo-
tor deficit (tetraplegia, triparesis, paraplegia and
ataxic tetraparesis), sometimes as isolated features
[1, 2].

Bilateral Infarcts Combined Infarcts

These are most often part of extensive brainstem Large ventromedial infarcts (anteromedial and
ischemia and account for up to 10% of all isolated anterolateral territories) produce severe hemipa-
pontine infarcts. Acute pseudobulbar palsy, bi- resis and dysarthria, whereas small infarcts mani-
lateral motor deficits and tegmental dysfunction fest as DCHS, AH and PMH. Crural monoparesis

164 Moncayo
predominates in combined anterolateral and dor-
solateral infarcts at the rostral level.
Pontine Hemorrhages
One in ten non-traumatic intracerebral hem-
orrhages is located in the pons. Chronic arte-
rial hypertension is the leading etiology; less
common causes are all types of vascular mal-
formations, hematologic disorders, tumors and
drugs [5]. Sudden onset, headache, vomiting
and loss of consciousness occur particularly in
large hemorrhages [6]. Large central hemato-
mas usually extend to the rostral midbrain and
the fourth ventricle, often beginning at the junc-
tion between the basis pontis and tegmentum
and leading to loss of consciousness, quadriple-
gia, cranial nerve dysfunction, small and reac-
tive pinpoint pupils, skew deviation, absence of
horizontal gaze movements and ocular bobbing.
Apneustic respiration or Cheyne-Stokes pattern,
hyperthermia (comatose patients) and contral-
ateral hyperhidrosis in the subacute phase may
be seen. Unilateral basal or tegmentobasal para-
median hemorrhages may present with PMH or
AH with dysarthria. Sensory deficits, ataxia and
oculomotor abnormalities (INO, one-and-a half
syndrome, horizontal gaze palsies and ocular
bobbing) are common findings with hemorrhag-
es restricted to the lateral tegmentum. Reports of
sensory alien hand phenomenon are uncommon
[7] (table 1). Isolated symptoms such as PMH,
pure sensory stroke, oculomotor disorders (lat-
eral gaze palsy of the supranuclear type, INO and
one-and-a half syndrome), isolated abducens and
facial palsies, and pure trigeminal sensory neu-
ropathy have been reported with minute hemor-
rhages. Massive pontine hemorrhages have the
worst prognosis, with death usually occurring in
the first 48 h. Small tegmental hematomas have
the best prognosis.

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Jorge Moncayo, MD
Neurovascular Unit, Department of Neurology
Eugenio Espejo Hospital
PO Box 17-11-6631, Quito (Ecuador)
Tel. +593 2 290 6958, E-Mail jmgaete@panchonet.net

Pontine Infarcts and Hemorrhages 165